Topic: General Cardiology

Abstract
<div><h4>Long-Term Outcomes of Resynchronization-Defibrillation for Heart Failure.</h4><i>Sapp JL, Sivakumaran S, Redpath CJ, Khan H, ... Tang ASL, RAFT Long-Term Study Team</i><br /><b>Background</b><br />The Resynchronization-Defibrillation for Ambulatory Heart Failure Trial (RAFT) showed a greater benefit with respect to mortality at 5 years among patients who received cardiac-resynchronization therapy (CRT) than among those who received implantable cardioverter-defibrillators (ICDs). However, the effect of CRT on long-term survival is not known.<br /><b>Methods</b><br />We randomly assigned patients with New York Heart Association (NYHA) class II or III heart failure, a left ventricular ejection fraction of 30% or less, and an intrinsic QRS duration of 120 msec or more (or a paced QRS duration of 200 msec or more) to receive either an ICD alone or a CRT defibrillator (CRT-D). We assessed long-term outcomes among patients at the eight highest-enrolling participating sites. The primary outcome was death from any cause; the secondary outcome was a composite of death from any cause, heart transplantation, or implantation of a ventricular assist device.<br /><b>Results</b><br />The trial enrolled 1798 patients, of whom 1050 were included in the long-term survival trial; the median duration of follow-up for the 1050 patients was 7.7 years (interquartile range, 3.9 to 12.8), and the median duration of follow-up for those who survived was 13.9 years (interquartile range, 12.8 to 15.7). Death occurred in 405 of 530 patients (76.4%) assigned to the ICD group and in 370 of 520 patients (71.2%) assigned to the CRT-D group. The time until death appeared to be longer for those assigned to receive a CRT-D than for those assigned to receive an ICD (acceleration factor, 0.80; 95% confidence interval, 0.69 to 0.92; P = 0.002). A secondary-outcome event occurred in 412 patients (77.7%) in the ICD group and in 392 (75.4%) in the CRT-D group.<br /><b>Conclusions</b><br />Among patients with a reduced ejection fraction, a widened QRS complex, and NYHA class II or III heart failure, the survival benefit associated with receipt of a CRT-D as compared with ICD appeared to be sustained during a median of nearly 14 years of follow-up. (RAFT ClinicalTrials.gov number, NCT00251251.).<br /><br />Copyright © 2024 Massachusetts Medical Society.<br /><br /><small>N Engl J Med: 18 Jan 2024; 390:212-220</small></div>
Sapp JL, Sivakumaran S, Redpath CJ, Khan H, ... Tang ASL, RAFT Long-Term Study Team
N Engl J Med: 18 Jan 2024; 390:212-220 | PMID: 38231622
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<div><h4>Aspirin-free antiplatelet strategies after percutaneous coronary interventions.</h4><i>Capranzano P, Moliterno D, Capodanno D</i><br /><AbstractText>Dual antiplatelet therapy (DAPT) with aspirin and a platelet P2Y12 receptor inhibitor is the standard antithrombotic treatment after percutaneous coronary interventions (PCI). Several trials have challenged guideline-recommended DAPT after PCI by testing the relative clinical effect of an aspirin-free antiplatelet approach-consisting of P2Y12 inhibitor monotherapy after a short course (mostly 1-3 months) of DAPT-among patients undergoing PCI without a concomitant indication for oral anticoagulation (OAC). Overall, these studies have shown P2Y12 inhibitor monotherapy after short DAPT to be associated with a significant reduction in the risk of bleeding without an increase in thrombotic or ischaemic events compared with continued DAPT. Moreover, the effects of the P2Y12 inhibitor monotherapy without prior DAPT or following a very short course of DAPT after PCI are being investigated in emerging studies, of which one has recently reported unfavourable efficacy results associated with the aspirin-free approach compared with conventional DAPT. Finally, P2Y12 inhibitor alone has been compared with aspirin alone as chronic therapy after DAPT discontinuation, thus challenging the historical role of aspirin as a standard of care for secondary prevention following PCI. A thorough understanding of study designs, populations, treatments, results, and limitations of trials testing P2Y12 inhibitor monotherapy vs. DAPT or vs. aspirin is required to consider adopting this treatment in clinical practice. This review addresses the use of aspirin-free antiplatelet strategies among patients undergoing PCI without a concomitant indication for OAC, providing an overview of clinical evidence, guideline indications, practical implications, ongoing issues, and future perspectives.</AbstractText><br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Eur Heart J: 18 Jan 2024; epub ahead of print</small></div>
Capranzano P, Moliterno D, Capodanno D
Eur Heart J: 18 Jan 2024; epub ahead of print | PMID: 38240716
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<div><h4>Merging machine learning and patient preference: a novel tool for risk prediction of percutaneous coronary interventions.</h4><i>Hamilton DE, Albright J, Seth M, Painter I, ... Sukul D, Gurm HS</i><br /><b>Background:</b><br/>and aims</b><br />Predicting personalized risk for adverse events following percutaneous coronary intervention (PCI) remains critical in weighing treatment options, employing risk mitigation strategies, and enhancing shared decision-making. This study aimed to employ machine learning models using pre-procedural variables to accurately predict common post-PCI complications.<br /><b>Methods</b><br />A group of 66 adults underwent a semiquantitative survey assessing a preferred list of outcomes and model display. The machine learning cohort included 107 793 patients undergoing PCI procedures performed at 48 hospitals in Michigan between 1 April 2018 and 31 December 2021 in the Blue Cross Blue Shield of Michigan Cardiovascular Consortium (BMC2) registry separated into training and validation cohorts. External validation was conducted in the Cardiac Care Outcomes Assessment Program database of 56 583 procedures in 33 hospitals in Washington.<br /><b>Results</b><br />Overall rate of in-hospital mortality was 1.85% (n = 1999), acute kidney injury 2.51% (n = 2519), new-onset dialysis 0.44% (n = 462), stroke 0.41% (n = 447), major bleeding 0.89% (n = 942), and transfusion 2.41% (n = 2592). The model demonstrated robust discrimination and calibration for mortality {area under the receiver-operating characteristic curve [AUC]: 0.930 [95% confidence interval (CI) 0.920-0.940]}, acute kidney injury [AUC: 0.893 (95% CI 0.883-0.903)], dialysis [AUC: 0.951 (95% CI 0.939-0.964)], stroke [AUC: 0.751 (95%CI 0.714-0.787)], transfusion [AUC: 0.917 (95% CI 0.907-0.925)], and major bleeding [AUC: 0.887 (95% CI 0.870-0.905)]. Similar discrimination was noted in the external validation population. Survey subjects preferred a comprehensive list of individually reported post-procedure outcomes.<br /><b>Conclusions</b><br />Using common pre-procedural risk factors, the BMC2 machine learning models accurately predict post-PCI outcomes. Utilizing patient feedback, the BMC2 models employ a patient-centred tool to clearly display risks to patients and providers (https://shiny.bmc2.org/pci-prediction/). Enhanced risk prediction prior to PCI could help inform treatment selection and shared decision-making discussions.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Eur Heart J: 17 Jan 2024; epub ahead of print</small></div>
Hamilton DE, Albright J, Seth M, Painter I, ... Sukul D, Gurm HS
Eur Heart J: 17 Jan 2024; epub ahead of print | PMID: 38233027
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<div><h4>Risk of Death in Patients With Coronary Artery Disease Taking Nitrates and Phosphodiesterase-5 Inhibitors.</h4><i>Trolle Lagerros Y, Grotta A, Freyland S, Grannas D, Andersson DP</i><br /><b>Background</b><br />Phosphodiesterase-5 inhibitor (PDE5i) treatment for erectile dysfunction is associated with lower mortality compared with no treatment for erectile dysfunction after myocardial infarction (MI). There are conflicting results regarding the impact of PDE5i treatment on mortality in conjunction with nitrate medication.<br /><b>Objectives</b><br />The purpose of this study was to investigate the association between PDE5i treatment and cardiovascular outcomes in men with stable coronary artery disease treated with nitrate medication.<br /><b>Methods</b><br />Using the Swedish Patient Register and the Prescribed Drug Register we included men with previous MI or revascularization in 2006-2013 who had 2 dispensed nitrate prescriptions within 6 months. Exposure was defined as at least 2 filled prescriptions of any PDE5i. We performed multivariable Cox proportional hazard regression to estimate HRs with 95% CIs for all-cause, cardiovascular, and noncardiovascular mortality, MI, heart failure, cardiac revascularization, and major cardiovascular events (MACE).<br /><b>Results</b><br />In total, 55,777 men were treated with nitrates and 5,710 men with nitrates and a PDE5i. The combined use of PDE5i treatment with nitrates was associated with higher mortality (HR: 1.39; 95% CI: 1.28-1.51), cardiovascular mortality (HR: 1.34; 95% CI: 1.11-1.62), noncardiovascular mortality (HR: 1.40; 95% CI: 1.27-1.54), MI (HR: 1.72; 95% CI: 1.55-1.90), heart failure (HR: 1.67; 95% CI: 1.48-1.90), cardiac revascularization (HR: 1.95; 95% CI: 1.78-2.13), and MACE (HR: 1.70; 95% CI: 1.58-1.83).<br /><b>Conclusions</b><br />The use of a PDE5i in combination with nitrate medication in men with stable coronary artery disease may pose an increased hazard for cardiovascular morbidity and mortality. Careful patient-centered consideration before prescribing PDE5is to patients with cardiovascular disease using nitrate medication is warranted.<br /><br />Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.<br /><br /><small>J Am Coll Cardiol: 23 Jan 2024; 83:417-426</small></div>
Trolle Lagerros Y, Grotta A, Freyland S, Grannas D, Andersson DP
J Am Coll Cardiol: 23 Jan 2024; 83:417-426 | PMID: 38233015
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<div><h4>Clonal haematopoiesis of indeterminate potential and atrial fibrillation: an east Asian cohort study.</h4><i>Ahn HJ, An HY, Ryu G, Lim J, ... Koh Y, Choi EK</i><br /><b>Background:</b><br/>and aims</b><br />Both clonal haematopoiesis of indeterminate potential (CHIP) and atrial fibrillation (AF) are age-related conditions. This study investigated the potential role of CHIP in the development and progression of AF.<br /><b>Methods</b><br />Deep-targeted sequencing of 24 CHIP mutations (a mean depth of coverage = 1000×) was performed in 1004 patients with AF and 3341 non-AF healthy subjects. Variant allele fraction ≥ 2.0% indicated the presence of CHIP mutations. The association between CHIP and AF was evaluated by the comparison of (i) the prevalence of CHIP mutations between AF and non-AF subjects and (ii) clinical characteristics discriminated by CHIP mutations within AF patients. Furthermore, the risk of clinical outcomes-the composite of heart failure, ischaemic stroke, or death-according to the presence of CHIP mutations in AF was investigated from the UK Biobank cohort.<br /><b>Results</b><br />The mean age was 67.6 ± 6.9 vs. 58.5 ± 6.5 years in AF (paroxysmal, 39.0%; persistent, 61.0%) and non-AF cohorts, respectively. CHIP mutations with a variant allele fraction of ≥2.0% were found in 237 (23.6%) AF patients (DNMT3A, 13.5%; TET2, 6.6%; and ASXL1, 1.5%) and were more prevalent than non-AF subjects [356 (10.7%); P < .001] across the age. After multivariable adjustment (age, sex, smoking, body mass index, diabetes, and hypertension), CHIP mutations were 1.4-fold higher in AF [adjusted odds ratio (OR) 1.38; 95% confidence interval 1.10-1.74, P < .01]. The ORs of CHIP mutations were the highest in the long-standing persistent AF (adjusted OR 1.50; 95% confidence interval 1.14-1.99, P = .004) followed by persistent (adjusted OR 1.44) and paroxysmal (adjusted OR 1.33) AF. In gene-specific analyses, TET2 somatic mutation presented the highest association with AF (adjusted OR 1.65; 95% confidence interval 1.05-2.60, P = .030). AF patients with CHIP mutations were older and had a higher prevalence of diabetes, a longer AF duration, a higher E/E\', and a more severely enlarged left atrium than those without CHIP mutations (all P < .05). In UK Biobank analysis of 21 286 AF subjects (1297 with CHIP and 19 989 without CHIP), the CHIP mutation in AF is associated with a 1.32-fold higher risk of a composite clinical event (heart failure, ischaemic stroke, or death).<br /><b>Conclusions</b><br />CHIP mutations, primarily DNMT3A or TET2, are more prevalent in patients with AF than non-AF subjects whilst their presence is associated with a more progressive nature of AF and unfavourable clinical outcomes.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Eur Heart J: 17 Jan 2024; epub ahead of print</small></div>
Ahn HJ, An HY, Ryu G, Lim J, ... Koh Y, Choi EK
Eur Heart J: 17 Jan 2024; epub ahead of print | PMID: 38231881
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<div><h4>Changes in frailty and incident cardiovascular disease in three prospective cohorts.</h4><i>He D, Wang Z, Li J, Yu K, ... Zhou D, Zhu Y</i><br /><b>Background:</b><br/>and aims</b><br />Previous studies found that frailty was an important risk factor for cardiovascular disease (CVD). However, previous studies only focused on baseline frailty status, not taking into consideration the changes in frailty status during follow-up. The aim of this study was to investigate the associations of changes in frailty status with incident CVD.<br /><b>Methods</b><br />This study used data of three prospective cohorts: China Health and Retirement Longitudinal Study (CHARLS), English Longitudinal Study of Ageing (ELSA), and Health and Retirement Study (HRS). Frailty status was evaluated by the Rockwood frailty index and classified as robust, pre-frail, or frail. Changes in frailty status were assessed by frailty status at baseline and the second survey which was two years after the baseline. Cardiovascular disease was ascertained by self-reported physician-diagnosed heart disease (including angina, heart attack, congestive heart failure, and other heart problems) or stroke. Cox proportional hazard models were used to calculate the hazard ratio (HR) and 95% confidence interval (95% CI) after adjusting for potential confounders.<br /><b>Results</b><br />A total of 7116 participants from CHARLS (female: 48.6%, mean age: 57.4 years), 5303 from ELSA (female: 57.7%, mean age: 63.7 years), and 7266 from HRS (female: 64.9%, mean age: 65.1 years) were included according to inclusion and exclusion criteria. The median follow-up periods were 5.0 years in the CHARLS, 10.7 years in the ELSA, and 9.5 years in the HRS. Compared with stable robust participants, robust participants who progressed to pre-frail or frail status had increased risks of incident CVD (CHARLS, HR = 1.84, 95% CI: 1.54-2.21; ELSA, HR = 1.53, 95% CI: 1.25-1.86; HRS, HR = 1.59, 95% CI: 1.31-1.92). In contrast, frail participants who recovered to robust or pre-frail status presented decreased risks of incident CVD (CHARLS, HR = 0.62, 95% CI: 0.47-0.81; ELSA, HR = 0.49, 95% CI: 0.34-0.69; HRS, HR = 0.70, 95% CI: 0.55-0.89) when compared with stable frail participants. These decreased risks of incident CVD were also observed in pre-frail participants who recovered to robust status (CHARLS, HR = 0.66, 95% CI: 0.52-0.83; ELSA, HR = 0.65, 95% CI: 0.49-0.85; HRS, HR = 0.71, 95% CI: 0.56-0.91) when compared with stable pre-frail participants.<br /><b>Conclusions</b><br />Different changes in frailty status are associated with different risks of incident CVD. Progression of frailty status increases incident CVD risks, while recovery of frailty status decreases incident CVD risks.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Eur Heart J: 18 Jan 2024; epub ahead of print</small></div>
He D, Wang Z, Li J, Yu K, ... Zhou D, Zhu Y
Eur Heart J: 18 Jan 2024; epub ahead of print | PMID: 38241094
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<div><h4>Artificial intelligence-derived risk score for mortality in secondary mitral regurgitation treated by transcatheter edge-to-edge repair: the EuroSMR risk score.</h4><i>Hausleiter J, Lachmann M, Stolz L, Bedogni F, ... Rudolph V, EuroSMR Investigators </i><br /><b>Background:</b><br/>and aims</b><br />Risk stratification for mitral valve transcatheter edge-to-edge repair (M-TEER) is paramount in the decision-making process to appropriately select patients with severe secondary mitral regurgitation (SMR). This study sought to develop and validate an artificial intelligence-derived risk score (EuroSMR score) to predict 1-year outcomes (survival or survival + clinical improvement) in patients with SMR undergoing M-TEER.<br /><b>Methods</b><br />An artificial intelligence-derived risk score was developed from the EuroSMR cohort (4172 and 428 patients treated with M-TEER in the derivation and validation cohorts, respectively). The EuroSMR score was validated and compared with established risk models.<br /><b>Results</b><br />The EuroSMR risk score, which is based on 18 clinical, echocardiographic, laboratory, and medication parameters, allowed for an improved discrimination of surviving and non-surviving patients (hazard ratio 4.3, 95% confidence interval 3.7-5.0; P < .001), and outperformed established risk scores in the validation cohort. Prediction for 1-year mortality (area under the curve: 0.789, 95% confidence interval 0.737-0.842) ranged from <5% to >70%, including the identification of an extreme-risk population (2.6% of the entire cohort), which had a very high probability for not surviving beyond 1 year (hazard ratio 6.5, 95% confidence interval 3.0-14; P < .001). The top 5% of patients with the highest EuroSMR risk scores showed event rates of 72.7% for mortality and 83.2% for mortality or lack of clinical improvement at 1-year follow-up.<br /><b>Conclusions</b><br />The EuroSMR risk score may allow for improved prognostication in heart failure patients with severe SMR, who are considered for a M-TEER procedure. The score is expected to facilitate the shared decision-making process with heart team members and patients.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Eur Heart J: 19 Jan 2024; epub ahead of print</small></div>
Hausleiter J, Lachmann M, Stolz L, Bedogni F, ... Rudolph V, EuroSMR Investigators
Eur Heart J: 19 Jan 2024; epub ahead of print | PMID: 38243773
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<div><h4>Legacy benefits of blood pressure treatment on cardiovascular events are primarily mediated by improved blood pressure variability: the ASCOT trial.</h4><i>Gupta A, Whiteley WN, Godec T, Rostamian S, ... Sever PS, ASCOT-10 Investigators </i><br /><b>Background:</b><br/>and aims</b><br />Visit-to-visit systolic blood pressure variability (BPV) is an important predictor of cardiovascular (CV) outcomes. The long-term effect of a period of blood pressure (BP) control, but with differential BPV, is uncertain. Morbidity and mortality follow-up of UK participants in the Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure-Lowering Arm has been extended for up to 21 years to determine the CV impact of mean systolic blood pressure (SBP) control and BPV during the trial, and amongst those allocated to amlodipine- and atenolol-based treatment.<br /><b>Methods</b><br />Eight thousand five hundred and eighty hypertensive participants (4305 assigned to amlodipine ± perindopril-based and 4275 to atenolol ± diuretic-based treatment during the in-trial period (median 5.5 years) were followed for up to 21 years (median 17.4 years), using linked hospital and mortality records. A subgroup of participants (n = 2156) was followed up 6 years after the trial closure with a self-administered questionnaire and a clinic visit. In-trial mean SBP and standard deviation of visit-to-visit SBP as a measure of BPV, were measured using >100 000 BP measurements. Cox proportional hazard models were used to estimate the risk [hazard ratios (HRs)], associated with (i) mean with SBP and BPV during the in-trial period, for the CV endpoints occurring after the end of the trial and (ii) randomly assigned treatment to events following randomization, for the first occurrence of pre-specified CV outcomes.<br /><b>Results</b><br />Using BP data from the in-trial period, in the post-trial period, although mean SBP was a predictor of CV outcomes {HR per 10 mmHg, 1.14 [95% confidence interval (CI) 1.10-1.17], P < .001}, systolic BPV independent of mean SBP was a strong predictor of CV events [HR per 5 mmHg 1.22 (95% CI 1.18-1.26), P < .001] and predicted events even in participants with well-controlled BP. During 21-year follow-up, those on amlodipine-based compared with atenolol-based in-trial treatment had significantly reduced risk of stroke [HR 0.82 (95% CI 0.72-0.93), P = .003], total CV events [HR 0.93 (95% CI 0.88-0.98), P = .008], total coronary events [HR 0.92 (95% CI 0.86-0.99), P = .024], and atrial fibrillation [HR 0.91 (95% CI 0.83-0.99), P = .030], with weaker evidence of a difference in CV mortality [HR 0.91 (95% CI 0.82-1.01), P = .073]. There was no significant difference in the incidence of non-fatal myocardial infarction and fatal coronary heart disease, heart failure, and all-cause mortality.<br /><b>Conclusions</b><br />Systolic BPV is a strong predictor of CV outcome, even in those with controlled SBP. The long-term benefits of amlodipine-based treatment compared with atenolol-based treatment in reducing CV events appear to be primarily mediated by an effect on systolic BPV during the trial period.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.<br /><br /><small>Eur Heart J: 31 Jan 2024; epub ahead of print</small></div>
Gupta A, Whiteley WN, Godec T, Rostamian S, ... Sever PS, ASCOT-10 Investigators
Eur Heart J: 31 Jan 2024; epub ahead of print | PMID: 38291599
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<div><h4>C-reactive protein modifies lipoprotein(a)-related risk for coronary heart disease: the BiomarCaRE project.</h4><i>Arnold N, Blaum C, Goßling A, Brunner FJ, ... Koenig W, Waldeyer C</i><br /><b>Background:</b><br/>and aims</b><br />Recent investigations have suggested an interdependence of lipoprotein(a) [Lp(a)]-related risk for cardiovascular disease with background inflammatory burden. The aim the present analysis was to investigate whether high-sensitive C-reactive protein (hsCRP) modulates the association between Lp(a) and coronary heart disease (CHD) in the general population.<br /><b>Methods</b><br />Data from 71 678 participants from 8 European prospective population-based cohort studies were used (65 661 without/6017 with established CHD at baseline; median follow-up 9.8/13.8 years, respectively). Fine and Gray competing risk-adjusted models were calculated according to accompanying hsCRP concentration (<2 and ≥2 mg/L).<br /><b>Results</b><br />Among CHD-free individuals, increased Lp(a) levels were associated with incident CHD irrespective of hsCRP concentration: fully adjusted sub-distribution hazard ratios [sHRs (95% confidence interval)] for the highest vs. lowest fifth of Lp(a) distribution were 1.45 (1.23-1.72) and 1.48 (1.23-1.78) for a hsCRP group of <2 and ≥2 mg/L, respectively, with no interaction found between these two biomarkers on CHD risk (Pinteraction = 0.82). In those with established CHD, similar associations were seen only among individuals with hsCRP ≥ 2 mg/L [1.34 (1.03-1.76)], whereas among participants with a hsCRP concentration <2 mg/L, there was no clear association between Lp(a) and future CHD events [1.29 (0.98-1.71)] (highest vs. lowest fifth, fully adjusted models; Pinteraction = 0.024).<br /><b>Conclusions</b><br />While among CHD-free individuals Lp(a) was significantly associated with incident CHD regardless of hsCRP, in participants with CHD at baseline, Lp(a) was related to recurrent CHD events only in those with residual inflammatory risk. These findings might guide adequate selection of high-risk patients for forthcoming Lp(a)-targeting compounds.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Eur Heart J: 18 Jan 2024; epub ahead of print</small></div>
Arnold N, Blaum C, Goßling A, Brunner FJ, ... Koenig W, Waldeyer C
Eur Heart J: 18 Jan 2024; epub ahead of print | PMID: 38240386
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<div><h4>Air pollutants, genetic susceptibility, and abdominal aortic aneurysm risk: a prospective study.</h4><i>Ma Y, Li D, Cui F, Wang J, ... Liu R, Tian Y</i><br /><b>Background:</b><br/>and aims</b><br />Air pollutants are important contributors to cardiovascular diseases, but associations between long-term exposure to air pollutants and the risk of abdominal aortic aneurysm (AAA) are still unknown.<br /><b>Methods</b><br />This study was conducted using a sample of 449 463 participants from the UK Biobank. Hazard ratios and 95% confidence intervals for the risk of AAA incidence associated with long-term exposure to air pollutants were estimated using the Cox proportional hazards model with time-varying exposure measurements. Additionally, the cumulative incidence of AAA was calculated by using the Fine and Grey sub-distribution hazards regression model. Furthermore, this study investigated the combined effects and interactions between air pollutants exposure and genetic predisposition in relation to the risk of AAA onset.<br /><b>Results</b><br />Long-term exposure to particulate matter with an aerodynamic diameter <2.5 µm [PM2.5, 1.21 (1.16, 1.27)], particulate matter with an aerodynamic diameter <10 µm [PM10, 1.21 (1.16, 1.27)], nitrogen dioxide [NO2, 1.16 (1.11, 1.22)], and nitrogen oxides [NOx, 1.10 (1.05, 1.15)] was found to be associated with an elevated risk of AAA onset. The detrimental effects of air pollutants persisted even in participants with low-level exposure. For the joint associations, participants with both high levels of air pollutants exposure and high genetic risk had a higher risk of developing AAA compared with those with low concentrations of pollutants exposure and low genetic risk. The respective risk estimates for AAA incidence were 3.18 (2.46, 4.12) for PM2.5, 3.09 (2.39, 4.00) for PM10, 2.41 (1.86, 3.13) for NO2, and 2.01 (1.55, 2.61) for NOx.<br /><b>Conclusions</b><br />In this study, long-term air pollutants exposure was associated with an increased risk of AAA incidence.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Eur Heart J: 18 Jan 2024; epub ahead of print</small></div>
Ma Y, Li D, Cui F, Wang J, ... Liu R, Tian Y
Eur Heart J: 18 Jan 2024; epub ahead of print | PMID: 38241289
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<div><h4>Exposome in ischaemic heart disease: beyond traditional risk factors.</h4><i>Montone RA, Camilli M, Calvieri C, Magnani G, ... Crea F, Niccoli G</i><br /><AbstractText>Ischaemic heart disease represents the leading cause of morbidity and mortality, typically induced by the detrimental effects of risk factors on the cardiovascular system. Although preventive interventions tackling conventional risk factors have helped to reduce the incidence of ischaemic heart disease, it remains a major cause of death worldwide. Thus, attention is now shifting to non-traditional risk factors in the built, natural, and social environments that collectively contribute substantially to the disease burden and perpetuate residual risk. Of importance, these complex factors interact non-linearly and in unpredictable ways to often enhance the detrimental effects attributable to a single or collection of these factors. For this reason, a new paradigm called the \'exposome\' has recently been introduced by epidemiologists in order to define the totality of exposure to these new risk factors. The purpose of this review is to outline how these emerging risk factors may interact and contribute to the occurrence of ischaemic heart disease, with a particular attention on the impact of long-term exposure to different environmental pollutants, socioeconomic and psychological factors, along with infectious diseases such as influenza and COVID-19. Moreover, potential mitigation strategies for both individuals and communities will be discussed.</AbstractText><br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.<br /><br /><small>Eur Heart J: 18 Jan 2024; epub ahead of print</small></div>
Montone RA, Camilli M, Calvieri C, Magnani G, ... Crea F, Niccoli G
Eur Heart J: 18 Jan 2024; epub ahead of print | PMID: 38238478
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<div><h4>Aerobic, resistance, or combined exercise training and cardiovascular risk profile in overweight or obese adults: the CardioRACE trial.</h4><i>Lee DC, Brellenthin AG, Lanningham-Foster LM, Kohut ML, Li Y</i><br /><b>Background:</b><br/>and aims</b><br />To determine the comparative efficacy of resistance, aerobic, and combined resistance plus aerobic exercise on cardiovascular disease (CVD) risk profile.<br /><b>Methods</b><br />This randomized controlled trial enrolled 406 adults aged 35-70 years with overweight or obesity and elevated blood pressure. Participants were randomly assigned to resistance (n = 102), aerobic (n = 101), combined resistance plus aerobic exercise (n = 101), or no-exercise control (n = 102). All exercise participants were prescribed 1 h of time-matched supervised exercise (the combination group with 30 min of each resistance and aerobic exercise) three times per week for 1 year. The primary outcome was the change from baseline to 1 year in the standardized composite Z-score of four well-established CVD risk factors: systolic blood pressure, low-density lipoprotein (LDL) cholesterol, fasting glucose, and per cent body fat.<br /><b>Results</b><br />Among 406 participants (53% women), 381 (94%) completed 1-year follow-up. Compared with the control group, the composite Z-score decreased at 1 year, which indicates improved CVD risk profile, in the aerobic {mean difference, -0.15 [95% confidence interval (CI): -0.27 to -0.04]; P = .01} and combination [mean difference, -0.16 (95% CI: -0.27 to -0.04); P = .009] groups, but not in the resistance [mean difference, -0.02 (95% CI: -0.14 to 0.09); P = .69] group. Both aerobic and combination groups had greater reductions in the composite Z-score compared with the resistance group (both P = .03), and there was no difference between the aerobic and combination groups (P = .96). Regarding the four individual CVD risk factors, only per cent body fat decreased in all three exercise groups at 1 year, but systolic blood pressure, LDL cholesterol, and fasting glucose did not decrease in any exercise groups, compared with the control group.<br /><b>Conclusions</b><br />In adults with overweight or obesity, aerobic exercise alone or combined resistance plus aerobic exercise, but not resistance exercise alone, improved composite CVD risk profile compared with the control.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.<br /><br /><small>Eur Heart J: 17 Jan 2024; epub ahead of print</small></div>
Lee DC, Brellenthin AG, Lanningham-Foster LM, Kohut ML, Li Y
Eur Heart J: 17 Jan 2024; epub ahead of print | PMID: 38233024
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<div><h4>Clinical Presentation, Classification, and Outcomes of Cardiogenic Shock in Children.</h4><i>Puri K, Jentzer JC, Spinner JA, Hope KD, ... Cabrera AG, Price JF</i><br /><b>Background</b><br />Despite growing cardiogenic shock (CS) research in adults, the epidemiology, clinical features, and outcomes of children with CS are lacking.<br /><b>Objectives</b><br />This study sought to describe the epidemiology, clinical presentation, hospital course, risk factors, and outcomes of CS among children hospitalized for acute decompensated heart failure (ADHF).<br /><b>Methods</b><br />We examined consecutive ADHF hospitalizations (<21 years of age) from a large single-center retrospective cohort. Patients with CS at presentation were analyzed and risk factors for CS and for the primary outcome of in-hospital mortality were identified. A modified Society for Cardiovascular Angiography and Interventions shock classification was created and patients were staged accordingly.<br /><b>Results</b><br />A total of 803 hospitalizations for ADHF were identified in 591 unique patients (median age 7.6 years). CS occurred in 207 (26%) hospitalizations. ADHF hospitalizations with CS were characterized by worse systolic function (P = 0.040), higher B-type natriuretic peptide concentration (P = 0.032), and more frequent early severe renal (P = 0.023) and liver (P < 0.001) injury than those without CS. Children presenting in CS received mechanical ventilation (87% vs 26%) and mechanical circulatory support (45% vs 16%) more frequently (both P < 0.001). Analyzing only the most recent ADHF hospitalization, children with CS were at increased risk of in-hospital mortality compared with children without CS (28% vs 11%; OR: 1.91; 95% CI: 1.05-3.45; P = 0.033). Each higher CS stage was associated with greater inpatient mortality (OR: 2.40-8.90; all P < 0.001).<br /><b>Conclusions</b><br />CS occurs in 26% of pediatric hospitalizations for ADHF and is independently associated with hospital mortality. A modified Society for Cardiovascular Angiography and Interventions classification for CS severity showed robust association with increasing mortality.<br /><br />Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.<br /><br /><small>J Am Coll Cardiol: 06 Feb 2024; 83:595-608</small></div>
Puri K, Jentzer JC, Spinner JA, Hope KD, ... Cabrera AG, Price JF
J Am Coll Cardiol: 06 Feb 2024; 83:595-608 | PMID: 38296404
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<div><h4>CRISPR Activation Reverses Haploinsufficiency and Functional Deficits Caused by Truncation Variants.</h4><i>Ghahremani S, Kanwal A, Pettinato A, Ladha F, ... Wei CL, Hinson JT</i><br /><b>Background</b><br /><i>TTN</i> truncation variants (TTNtvs) are the most common genetic lesion identified in individuals with dilated cardiomyopathy, a disease with high morbidity and mortality rates. TTNtvs reduce normal TTN (titin) protein levels, produce truncated proteins, and impair sarcomere content and function. Therapeutics targeting TTNtvs have been elusive because of the immense size of TTN, the rarity of specific TTNtvs, and incomplete knowledge of TTNtv pathogenicity.<br /><b>Methods</b><br />We adapted CRISPR activation using dCas9-VPR to functionally interrogate TTNtv pathogenicity and develop a therapeutic in human cardiomyocytes and 3-dimensional cardiac microtissues engineered from induced pluripotent stem cell models harboring a dilated cardiomyopathy-associated TTNtv. We performed guide RNA screening with custom TTN reporter assays, agarose gel electrophoresis to quantify TTN protein levels and isoforms, and RNA sequencing to identify molecular consequences of TTN activation. Cardiomyocyte epigenetic assays were also used to nominate DNA regulatory elements to enable cardiomyocyte-specific TTN activation.<br /><b>Results</b><br />CRISPR activation of TTN using single guide RNAs targeting either the <i>TTN</i> promoter or regulatory elements in spatial proximity to the <i>TTN</i> promoter through 3-dimensional chromatin interactions rescued TTN protein deficits disturbed by TTNtvs. Increasing TTN protein levels normalized sarcomere content and contractile function despite increasing truncated TTN protein. In addition to <i>TTN</i> transcripts, CRISPR activation also increased levels of myofibril assembly-related and sarcomere-related transcripts.<br /><b>Conclusions</b><br />TTN CRISPR activation rescued TTNtv-related functional deficits despite increasing truncated TTN levels, which provides evidence to support haploinsufficiency as a relevant genetic mechanism underlying heterozygous TTNtvs. CRISPR activation could be developed as a therapeutic to treat a large proportion of TTNtvs.<br /><br /><br /><br /><small>Circulation: 18 Jan 2024; epub ahead of print</small></div>
Ghahremani S, Kanwal A, Pettinato A, Ladha F, ... Wei CL, Hinson JT
Circulation: 18 Jan 2024; epub ahead of print | PMID: 38235591
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<div><h4>Novel Role for Cardiolipin as a Target of Therapy to Mitigate Myocardial Injury Caused by Venoarterial Extracorporeal Membrane Oxygenation.</h4><i>Swain L, Bhave S, Qiao X, Reyelt L, ... Chin MT, Kapur NK</i><br /><b>Background</b><br />Cardiolipin is a mitochondrial-specific phospholipid that maintains integrity of the electron transport chain (ETC) and plays a central role in myocardial ischemia/reperfusion injury. Tafazzin is an enzyme that is required for cardiolipin maturation. Venoarterial extracorporeal membrane oxygenation (VA-ECMO) use to provide hemodynamic support for acute myocardial infarction has grown exponentially, is associated with poor outcomes, and is under active clinical investigation, yet the mechanistic effect of VA-ECMO on myocardial damage in acute myocardial infarction remains poorly understood. We hypothesized that VA-ECMO acutely depletes myocardial cardiolipin and exacerbates myocardial injury in acute myocardial infarction.<br /><b>Methods</b><br />We examined cardiolipin and tafazzin levels in human subjects with heart failure and healthy swine exposed to VA-ECMO and used a swine model of closed-chest myocardial ischemia/reperfusion injury to evaluate the effect of VA-ECMO on cardiolipin expression, myocardial injury, and mitochondrial function.<br /><b>Results</b><br />Cardiolipin and tafazzin levels are significantly reduced in the left ventricles of individuals requiring VA-ECMO compared with individuals without VA-ECMO before heart transplantation. Six hours of exposure to VA-ECMO also decreased left ventricular levels of cardiolipin and tafazzin in healthy swine compared with sham controls. To explore whether cardiolipin depletion by VA-ECMO increases infarct size, we performed left anterior descending artery occlusion for a total of 120 minutes followed by 180 minutes of reperfusion in adult swine in the presence and absence of MTP-131, an amphipathic molecule that interacts with cardiolipin to stabilize the inner mitochondrial membrane. Compared with reperfusion alone, VA-ECMO activation beginning after 90 minutes of left anterior descending artery occlusion increased infarct size (36±8% versus 48±7%; <i>P</i><0.001). VA-ECMO also decreased cardiolipin and tafazzin levels, disrupted mitochondrial integrity, reduced electron transport chain function, and promoted oxidative stress. Compared with reperfusion alone or VA-ECMO before reperfusion, delivery of MTP-131 before VA-ECMO activation reduced infarct size (22±8%; <i>P</i>=0.03 versus reperfusion alone and <i>P</i><0.001 versus VA-ECMO alone). MTP-131 restored cardiolipin and tafazzin levels, stabilized mitochondrial function, and reduced oxidative stress in the left ventricle.<br /><b>Conclusions</b><br />We identified a novel mechanism by which VA-ECMO promotes myocardial injury and further identify cardiolipin as an important target of therapy to reduce infarct size and to preserve mitochondrial function in the setting of VA-ECMO for acute myocardial infarction.<br /><br /><br /><br /><small>Circulation: 18 Jan 2024; epub ahead of print</small></div>
Swain L, Bhave S, Qiao X, Reyelt L, ... Chin MT, Kapur NK
Circulation: 18 Jan 2024; epub ahead of print | PMID: 38235580
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<div><h4>2024 Heart Disease and Stroke Statistics: A Report of US and Global Data From the American Heart Association.</h4><i>Martin SS, Aday AW, Almarzooq ZI, Anderson CAM, ... Palaniappan LP, American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee</i><br /><b>Background</b><br />The American Heart Association (AHA), in conjunction with the National Institutes of Health, annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascular risk factors, including core health behaviors (smoking, physical activity, nutrition, sleep, and obesity) and health factors (cholesterol, blood pressure, glucose control, and metabolic syndrome) that contribute to cardiovascular health. The AHA Heart Disease and Stroke Statistical Update presents the latest data on a range of major clinical heart and circulatory disease conditions (including stroke, brain health, complications of pregnancy, kidney disease, congenital heart disease, rhythm disorders, sudden cardiac arrest, subclinical atherosclerosis, coronary heart disease, cardiomyopathy, heart failure, valvular disease, venous thromboembolism, and peripheral artery disease) and the associated outcomes (including quality of care, procedures, and economic costs).<br /><b>Methods</b><br />The AHA, through its Epidemiology and Prevention Statistics Committee, continuously monitors and evaluates sources of data on heart disease and stroke in the United States and globally to provide the most current information available in the annual Statistical Update with review of published literature through the year before writing. The 2024 AHA Statistical Update is the product of a full year\'s worth of effort in 2023 by dedicated volunteer clinicians and scientists, committed government professionals, and AHA staff members. The AHA strives to further understand and help heal health problems inflicted by structural racism, a public health crisis that can significantly damage physical and mental health and perpetuate disparities in access to health care, education, income, housing, and several other factors vital to healthy lives. This year\'s edition includes additional global data, as well as data on the monitoring and benefits of cardiovascular health in the population, with an enhanced focus on health equity across several key domains.<br /><b>Results</b><br />Each of the chapters in the Statistical Update focuses on a different topic related to heart disease and stroke statistics.<br /><b>Conclusions</b><br />The Statistical Update represents a critical resource for the lay public, policymakers, media professionals, clinicians, health care administrators, researchers, health advocates, and others seeking the best available data on these factors and conditions.<br /><br /><br /><br /><small>Circulation: 24 Jan 2024; epub ahead of print</small></div>
Martin SS, Aday AW, Almarzooq ZI, Anderson CAM, ... Palaniappan LP, American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee
Circulation: 24 Jan 2024; epub ahead of print | PMID: 38264914
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<div><h4>The American Heart Association Emergency Cardiovascular Care 2030 Impact Goals and Call to Action to Improve Cardiac Arrest Outcomes: A Scientific Statement From the American Heart Association.</h4><i>Merchant RM, Becker LB, Brooks SC, Chan PS, ... Sasson C, American Heart Association</i><br /><AbstractText>Every 10 years, the American Heart Association (AHA) Emergency Cardiovascular Care Committee establishes goals to improve survival from cardiac arrest. These goals align with broader AHA Impact Goals and support the AHA\'s advocacy efforts and strategic investments in research, education, clinical care, and quality improvement programs. This scientific statement focuses on 2030 AHA emergency cardiovascular care priorities, with a specific focus on bystander cardiopulmonary resuscitation, early defibrillation, and neurologically intact survival. This scientific statement also includes aspirational goals, such as establishing cardiac arrest as a reportable disease and mandating reporting of standardized outcomes from different sources; advancing recognition of and knowledge about cardiac arrest; improving dispatch system response, availability, and access to resuscitation training in multiple settings and at multiple time points; improving availability, access, and affordability of defibrillators; providing a focus on early defibrillation, in-hospital programs, and establishing champions for debriefing and review of cardiac arrest events; and expanding measures to track outcomes beyond survival. The ability to track and report data from these broader aspirational targets will potentially require expansion of existing data sets, development of new data sets, and enhanced integration of technology to collect process and outcome data, as well as partnerships of the AHA with national, state, and local organizations. The COVID-19 (coronavirus disease 2019) pandemic, disparities in COVID-19 outcomes for historically excluded racial and ethnic groups, and the longstanding disparities in cardiac arrest treatment and outcomes for Black and Hispanic or Latino populations also contributed to an explicit focus and target on equity for the AHA Emergency Cardiovascular Care 2030 Impact Goals.</AbstractText><br /><br /><br /><br /><small>Circulation: 22 Jan 2024; epub ahead of print</small></div>
Merchant RM, Becker LB, Brooks SC, Chan PS, ... Sasson C, American Heart Association
Circulation: 22 Jan 2024; epub ahead of print | PMID: 38250800
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<div><h4>Atlas of Cell Repertoire Within Neointimal Lesions Is Metabolically Altered in Hypertensive Rats.</h4><i>Sun X, Wu J, Zhang X, Xie C, ... Cheng J, Xu Q</i><br /><b>Background</b><br />High blood pressure has been suggested to accelerate vascular injury-induced neointimal formation and progression. However, little is known about the intricate relationships between vascular injury and hypertension in the context of arterial remodeling.<br /><b>Methods</b><br />Single-cell RNA-sequencing analysis was used to depict the cell atlas of carotid arteries of Wistar Kyoto rats and spontaneously hypertensive rats with or without balloon injury.<br /><b>Results</b><br />We found that hypertension significantly aggravated balloon injury-induced arterial stenosis. A total of 36 202 cells from carotid arteries with or without balloon injury were included in single-cell RNA-sequencing analysis. Cell composition analysis showed that vascular injury and hypertension independently induced distinct aortic cell phenotypic alterations including immune cells, endothelial cells (ECs), and smooth muscle cells. Specifically, our data showed that injury and hypertension-induced specific EC phenotypic alterations, and revealed a transition from functional ECs to hypermetabolic, and eventually dysfunctional ECs in hypertensive rats upon balloon injury. Importantly, our data also showed that vascular injury and hypertension-induced different smooth muscle cell phenotypic alterations, characterized by deferential expression of synthetic signatures. Interestingly, pathway analysis showed that dysregulated metabolic pathways were a common feature in monocytes/macrophages, ECs, and smooth muscle cells in response to injury and hypertension. Functionally, we demonstrate that inhibition of mitochondrial respiration significantly ameliorated injury-induced neointimal formation in spontaneously hypertensive rats.<br /><b>Conclusions</b><br />This study provides the cell landscape changes of the main aortic cell phenotypic alterations in response to injury and hypertension. Our findings suggest that targeting cellular mitochondrial respiration could be a novel therapeutic for patients with hypertension undergoing vascular angioplasty.<br /><br /><br /><br /><small>Hypertension: 19 Jan 2024; epub ahead of print</small></div>
Sun X, Wu J, Zhang X, Xie C, ... Cheng J, Xu Q
Hypertension: 19 Jan 2024; epub ahead of print | PMID: 38240164
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<div><h4>Role of the CCL5 and Its Receptor, CCR5 in the Genesis of Aldosterone-Induced Hypertension, Vascular Dysfunction, and End-Organ Damage.</h4><i>Costa RM, Cerqueira DM, Bruder-Nascimento A, Alves JV, ... Ho J, Bruder-Nascimento T</i><br /><b>Background</b><br />Aldosterone has been described to initiate cardiovascular diseases by triggering exacerbated sterile vascular inflammation. The functions of CCL5 (C-C motif chemokine ligand 5) and its receptor CCR5 (C-C motif chemokine receptor 5) are well known in infectious diseases, their contributions to aldosterone-induced vascular injury and hypertension remain unknown.<br /><b>Methods</b><br />We analyzed the vascular profile, blood pressure, and renal damage in wild-type (CCR5<sup>+/+</sup>) and CCR5 knockout (CCR5<sup>-/-</sup>) mice treated with aldosterone (600 µg/kg per day for 14 days) while receiving 1% saline to drink. Vascular function was analyzed in aorta and mesenteric arteries, blood pressure was measured by telemetry and renal injury and inflammation were analyzed via histology and flow cytometry. Endothelial cells were used to study the molecular signaling whereby CCL5 induces endothelial dysfunction.<br /><b>Results</b><br />Aldosterone treatment resulted in exaggerated CCL5 circulating levels and vascular CCR5 expression in CCR5<sup>+/+</sup> mice accompanied by endothelial dysfunction, hypertension, and renal inflammation and damage. CCR5<sup>-/-</sup> mice were protected from these aldosterone-induced effects. Mechanistically, we demonstrated that CCL5 increased Nox1 (NADPH oxidase 1) expression, reactive oxygen species formation, NFκB (nuclear factor kappa B) activation, and inflammation and reduced NO production in isolated endothelial cells. These effects were abolished by antagonizing CCR5 with Maraviroc. Finally, aorta incubated with CCL5 displayed severe endothelial dysfunction, which is prevented by blocking Nox1, NFκB, or CCR5.<br /><b>Conclusions</b><br />Our data demonstrate that CCL5/CCR5, through activation of NFkB and Nox1, is critically involved in aldosterone-induced vascular and renal damage and hypertension placing CCL5 and CCR5 as potential therapeutic targets for conditions characterized by aldosterone excess.<br /><br /><br /><br /><small>Hypertension: 19 Jan 2024; epub ahead of print</small></div>
Costa RM, Cerqueira DM, Bruder-Nascimento A, Alves JV, ... Ho J, Bruder-Nascimento T
Hypertension: 19 Jan 2024; epub ahead of print | PMID: 38240165
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<div><h4>Hypertrophic cardiomyopathy dysfunction mimicked in human engineered heart tissue and improved by SGLT2 inhibitors.</h4><i>Wijnker PJM, Dinani R, van der Laan NC, Algül S, ... Kuster DWD, van der Velden J</i><br /><b>Aims</b><br />Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiomyopathy, often caused by pathogenic sarcomere mutations. Early characteristics of HCM are diastolic dysfunction and hypercontractility. Treatment to prevent mutation-induced cardiac dysfunction is lacking. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are a group of antidiabetic drugs that recently showed beneficial cardiovascular outcomes in patients with acquired forms of heart failure. We here studied if SGLT2i represent a potential therapy to correct cardiomyocyte dysfunction induced by a HCM sarcomere mutation.<br /><b>Methods and results</b><br />Contractility was measured of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) harbouring a HCM mutation cultured in 2D and in 3D engineered heart tissue (EHT). Mutations in the gene encoding β-myosin heavy chain (MYH7-R403Q) or cardiac troponin T (TNNT2-R92Q) were investigated. In 2D, intracellular [Ca2+], action potential and ion currents were determined. HCM mutations in hiPSC-CMs impaired relaxation or increased force, mimicking early features observed in human HCM. SGLT2i enhance relaxation of hiPSC-CMs, to a larger extent in HCM compared to control hiPSC-CMs. Moreover, SGLT2i-effects on relaxation in R403Q EHT increased with culture duration, i.e. hiPSC-CMs maturation. Canagliflozin effects on relaxation were more pronounced than empagliflozin and dapagliflozin. SGLT2i acutely altered Ca2+ handling in HCM hiPSC-CMs. Analyses of SGLT2i-mediated mechanisms that may underlie enhanced relaxation in mutant hiPSC-CMs excluded SGLT2, Na+/H+ exchanger, peak and late Nav1.5 currents, and L-type Ca2+ current, but indicate an important role for the Na+/Ca2+ exchanger. Indeed electrophysiological measurements in mutant hiPSC-CM indicate that SGLT2i altered Na+/Ca2+ exchange current.<br /><b>Conclusions</b><br />SGLT2i (canagliflozin>dapagliflozin> empagliflozin) acutely enhance relaxation in human EHT, especially in HCM and upon prolonged culture. SGLT2i may represent a potential therapy to correct early cardiac dysfunction in HCM.<br /><b>Translational perspective</b><br />HCM is the most common inherited cardiomyopathy and treatment to prevent mutation-induced cardiac dysfunction is lacking. Early HCM characteristics are diastolic dysfunction and hypercontractility. We show in hiPSC-CM models that SGLT2i represent a potential therapy to correct cardiomyocyte dysfunction induced by HCM sarcomere mutations. SGLT2i acutely enhanced relaxation and altered Ca2+ handling in HCM hiPSC-CMs, targeting important early HCM disease hallmarks.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.<br /><br /><small>Cardiovasc Res: 18 Jan 2024; epub ahead of print</small></div>
Wijnker PJM, Dinani R, van der Laan NC, Algül S, ... Kuster DWD, van der Velden J
Cardiovasc Res: 18 Jan 2024; epub ahead of print | PMID: 38240646
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<div><h4>Protein Kinase A Is a Master Regulator of Physiological and Pathological Cardiac Hypertrophy.</h4><i>Bai Y, Zhang X, Li Y, Qi F, ... Houser SR, Chen X</i><br /><b>Background</b><br />The sympathoadrenergic system and its major effector PKA (protein kinase A) are activated to maintain cardiac output coping with physiological or pathological stressors. If and how PKA plays a role in physiological cardiac hypertrophy (CH) and pathological CH (PaCH) are not clear.<br /><b>Methods</b><br />Transgenic mouse models expressing a PKA inhibition peptide-GFP fusion protein in a cardiac-specific and inducible manner (cPKAi) were used to determine the roles of PKA in physiological CH during postnatal growth or induced by swimming, and in PaCH induced by transaortic constriction (TAC) or augmented Ca<sup>2+</sup> influx. Kinase profiling was used to determine cPKAi specificity. Echocardiography was used to determine cardiac morphology and function. Western blotting and immunostaining were used to measure protein abundance and phosphorylation. Protein synthesis was assessed by puromycin incorporation and protein degradation by measuring protein ubiquitination and proteasome activity. Neonatal rat cardiomyocytes (NRCMs) infected with AdGFP or AdPKAi-GFP were used to determine the effects and mechanisms of cPKAi on myocyte hypertrophy. rAAV9.PKA inhibition peptide-GFP was used to treat TAC mice.<br /><b>Results</b><br />(1) cPKAi delayed postnatal cardiac growth and blunted exercise-induced physiological CH; (2) PKA was activated in hearts after TAC due to activated sympathoadrenergic system, the loss of endogenous PKIα (PKA inhibitory peptide α), and the stimulation by noncanonical PKA activators; (3) cPKAi ameliorated PaCH induced by TAC and increased Ca<sup>2+</sup> influxes and blunted neonatal rat cardiomyocyte hypertrophy by isoproterenol and phenylephrine; (4) cPKAi prevented TAC-induced protein synthesis by inhibiting mTOR signaling through reducing Akt activity, but enhancing inhibitory GSK-3α and GSK-3β signals; (5) cPKAi reduced protein degradation by the ubiquitin-proteasome system via decreasing RPN6 phosphorylation; (6) cPKAi increased the expression of antihypertrophic ANP; (7) cPKAi ameliorated established PaCH and improved animal survival.<br /><b>Conclusions</b><br />Cardiomyocyte PKA is a master regulator of physiological CH and PaCH through regulating protein synthesis and degradation. cPKAi can be a novel approach to treat PaCH.<br /><br /><br /><br /><small>Circ Res: 26 Jan 2024; epub ahead of print</small></div>
Bai Y, Zhang X, Li Y, Qi F, ... Houser SR, Chen X
Circ Res: 26 Jan 2024; epub ahead of print | PMID: 38275112
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<div><h4>Reducing the risk of atherosclerotic cardiovascular disease in people with haemophilia, the importance of primary prevention.</h4><i>Dix C, Dolan G, Hunt BJ</i><br /><AbstractText>Revolutionary advances in the treatment of haemophilia has led to a significant improvement in life expectancy. Associated with this has been an increase in age-related diseases especially atherosclerotic cardiovascular disease (CVD). While people with haemophilia (PWH) develop atherosclerosis at rates similar to the general population, rates of atherothrombosis and mortality related to CVD have been much lower, due to their hypocoagulable state. Changing treatment paradigms, aimed at reducing the risk of bleeding by improving haemostasis to levels approaching normality, has meant the protection they are thought to have had may be lost. CVD risk factors are just as common in PWH as in the general population but appear to be under-treated. In particular primary prevention of CVD is vital in all individuals, but particularly in PWH as treatment of established CVD can be difficult. Active identification and management of CVD risk factors, such as obesity, physical inactivity, hypertension and hypercholesterolaemia, is required. In particular, statins have been shown to significantly reduce cardiovascular and all-cause mortality with few adverse events and no increased risk of bleeding in the general population, and their use needs urgent assessment in PWH. Further longitudinal research into preventing CVD in PWH, including accurate CVD risk assessment, is required to optimise prevention and management.</AbstractText><br /><br />Copyright © 2024 International Society on Thrombosis and Haemostasis. Published by Elsevier Inc. All rights reserved.<br /><br /><small>J Thromb Haemost: 01 Feb 2024; epub ahead of print</small></div>
Dix C, Dolan G, Hunt BJ
J Thromb Haemost: 01 Feb 2024; epub ahead of print | PMID: 38309435
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<div><h4>C-reactive protein, pharmacological treatments and diet: how to target your inflammatory burden.</h4><i>Bay B, Arnold N, Waldeyer C</i><br /><b>Purpose of review</b><br />This article focuses on pharmacological agents as well as dietary changes aimed at the reduction of the inflammatory burden measured by circulating C-reactive protein concentrations.<br /><b>Recent findings</b><br />Over the last years, repurposed as well as new anti-inflammatory agents have been investigated in outcome trials in the cardiovascular field. Currently, a specific inhibition of the inflammatory cascade via the interleukin-6 ligand antibody ziltivekimab is being explored in large-scale outcome trials, after the efficacy of this agent with regard to the reduction of inflammatory biomarkers was proven recently. Next to the investigated pharmacological agents, specific dietary patterns possess the ability to improve the inflammatory burden. This enables patients themselves to unlock a potential health benefit ahead of the initiation of a specific medication targeting the inflammatory pathway.<br /><b>Summary</b><br />Both pharmacological agents as well as diet provide the opportunity to improve the inflammatory profile and thereby lower C-reactive protein concentrations. Whilst advances in the field of specific anti-inflammatory treatments have been made over the last years, their broad implementation is currently limited. Therefore, optimization of diet (and other lifestyle factors) could provide a cost effective and side-effect free intervention to target low-grade vascular inflammation.<br /><br />Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.<br /><br /><small>Curr Opin Lipidol: 26 Jan 2024; epub ahead of print</small></div>
Bay B, Arnold N, Waldeyer C
Curr Opin Lipidol: 26 Jan 2024; epub ahead of print | PMID: 38277208
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<div><h4>Remnant cholesterol as a new lipid-lowering target to reduce cardiovascular events.</h4><i>Raggi P, Becciu ML, Navarese E</i><br /><b>Purpose of review</b><br />Remnant cholesterol has become increasingly recognized as a direct contributor to the development of atherosclerosis and as an additional marker of cardiovascular risk. This review aims to summarize the pathophysiological mechanisms, and the current evidence base from epidemiological investigations and genetic studies that support a causal link between remnant cholesterol and atherosclerotic cardiovascular disease. Current and novel therapeutic approaches to target remnant cholesterol are discussed.<br /><b>Recent findings</b><br />A recent Mendelian randomization study of over 12 000 000 single-nucleotide polymorphisms associated with high levels of remnant cholesterol, demonstrated a genetic association between remnant cholesterol and adverse cardiovascular events among 958 434 participants.<br /><b>Summary</b><br />In this light, the emerging role of remnant cholesterol as an independent lipid risk marker warrants a reevaluation of lipid management guidelines and underscores the potential for novel therapeutic targets in cardiovascular disease prevention.<br /><br />Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.<br /><br /><small>Curr Opin Lipidol: 24 Jan 2024; epub ahead of print</small></div>
Raggi P, Becciu ML, Navarese E
Curr Opin Lipidol: 24 Jan 2024; epub ahead of print | PMID: 38276967
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<div><h4>PCSK9-directed therapies: an update.</h4><i>Katzmann JL, Laufs U</i><br /><b>Purpose of review</b><br />Two large cardiovascular outcomes trials of monoclonal antibodies against proprotein convertase subtilisin/kexin type 9 (PCSK9) demonstrated that therapeutic inhibition of extracellular PCSK9 markedly reduces LDL cholesterol concentration and cardiovascular risk. Several novel strategies to inhibit PCSK9 function are in development. Different mechanisms of action may determine specific properties with potential relevance for patient care.<br /><b>Recent findings</b><br />For the monoclonal antibodies evolocumab und alirocumab as first-generation PCSK9 inhibitors, follow-up data of up to 8 years of exposure complement the information on efficacy and safety available from outcome trials. For the small-interfering RNA inclisiran as second-generation PCSK9 inhibitor, several phase III trials have been published and a cardiovascular outcome trial has completed recruitment and is ongoing. Third-generation PCSK9 inhibitors encompass, among others, orally available drugs such as MK-0616 and the fusion protein lerodalcibep. Additional strategies to inhibit PCSK9 include vaccination and gene editing.<br /><b>Summary</b><br />Long-term inhibition of PCSK9 with monoclonal antibodies is safe and conveys sustained cardiovascular benefit. Novel strategies to inhibit PCSK9 function such as orally available drugs, RNA targeting, and one-time treatment with gene editing may further enhance the therapeutic armamentarium and enable novel preventive strategies.<br /><br />Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.<br /><br /><small>Curr Opin Lipidol: 22 Jan 2024; epub ahead of print</small></div>
Katzmann JL, Laufs U
Curr Opin Lipidol: 22 Jan 2024; epub ahead of print | PMID: 38277255
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<div><h4>Long-Term Durability of High- and Very High-Power Short-Duration PVI by Invasive Remapping: The HPSD Remap Study.</h4><i>Szegedi N, Salló Z, Nagy VK, Osztheimer I, ... Merkely B, Gellér L</i><br /><b>Background</b><br />High-power short-duration ablation has shown impressive efficacy and safety for pulmonary vein isolation (PVI); however, initial efficacy results with very high power short-duration ablation were discouraging. This study compared the long-term durability of PVI performed with a 90 versus 50 W power setting.<br /><b>Methods</b><br />Patients were randomized 1:1 to undergo PVI with the QDOT catheter using a power setting of 90 or 50 W. Three months after the index procedure, patients underwent a repeat electrophysiology study to identify pulmonary vein reconnections. Patients were followed for 12 months to detect AF recurrences.<br /><b>Results</b><br />We included 46 patients (mean age, 64 years; female, 48%). Procedure (76 versus 84 minutes; <i>P</i>=0.02), left atrial dwell (63 versus 71 minutes; <i>P</i>=0.01), and radiofrequency (303 versus 1040 seconds; <i>P</i><0.0001) times were shorter with 90W versus 50W procedures, while the number of radiofrequency applications was higher with 90W versus 50W (77 versus 67; <i>P</i>=0.01). There was no difference in first-pass isolation (83% versus 82%; <i>P</i>=1.0) or acute reconnection (4% versus 14%; <i>P</i>=0.3) rates between 90W and 50W. Forty patients underwent a repeat electrophysiology study. Durable PVI on a per PV basis was present in 72/78 (92%) versus 68/77 (88%) PVs in the 90W and 50W energy setting groups, respectively; effect size: 72/78-68/77=0.040, lower 95% CI=-0.051 (noninferiority limit=-0.1, ie, noninferiority is met). No complications occurred. There was no difference in 12-month atrial fibrillation-free survival between the 90W and 50W groups (<i>P</i>=0.2).<br /><b>Conclusions</b><br />Similarly high rates of durable PVI and arrhythmia-free survival were achieved with 90W and 50W. Procedure, left atrial dwell, and radiofrequency times were shorter with 90W compared with 50W. The sample size is too small to conclude the safety and long-term efficacy of the high and very high-power short-duration PVI; further studies are needed to address this topic.<br /><b>Registration</b><br />URL: https://www.clinicaltrials.gov; Unique identifier: NCT05459831.<br /><br /><br /><br /><small>Circ Arrhythm Electrophysiol: 29 Jan 2024:e012402; epub ahead of print</small></div>
Szegedi N, Salló Z, Nagy VK, Osztheimer I, ... Merkely B, Gellér L
Circ Arrhythm Electrophysiol: 29 Jan 2024:e012402; epub ahead of print | PMID: 38284286
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<div><h4>Complete Coronary Revascularization and Outcomes in Patients Undergoing CABG: Insights from the REGROUP Trial.</h4><i>Belyayev L, Stock EM, Hattler B, Bakaeen FG, ... Biswas K, Zenati MA</i><br /><AbstractText>There is growing evidence in support of complete coronary revascularization (CR). Nonetheless there is no universally accepted definition of CR in patients undergoing CABG. We sought to investigate the outcomes of CR defined as surgical revascularization of any territory supplied by a suitable coronary artery with at least 50% stenosis. We performed a pre-planned subanalysis of the REGROUP clinical trial cohort. Of 1,147 patients who underwent CABG, 810 (70.6%) received CR. The primary outcome was a composite of major adverse cardiac events (MACE), including death from any cause, nonfatal myocardial infarction (MI), or repeat revascularization over a median 4.7 years of follow-up. MACE occurred in 175 patients (21.6%) in the CR group and 86 patients (25.5%) in the incomplete revascularization (IR) group (hazard ratio (HR) =0.87; 95% confidence interval [CI] 0.67 to 1.13; p=0.29). A total of 97 patients (12.0%) in the CR group and 48 patients (14.2%) in the IR group died (HR=0.93; 95% CI, 0.65 to 1.32; p=0.67); nonfatal MI occurred in 49 patients (6.0%) in the CR group and 30 patients (8.9%) in the IR group (HR=0.76; 95% CI, 0.48 to 1.2; p=0.24), and repeat revascularization occurred in 62 patients (7.7%) in the CR group and 39 patients (11.6%) in the IR group (HR=0.64; 95% CI, 0.42 to 0.95; p=0.027). In conclusion among patients with a high burden of comorbidities undergoing CABG in the REGROUP trial over a median follow-up period of a median 4.7 years, CR was associated with similar MACE rates but a reduced risk of repeat revascularization. Longer-term follow-up is warranted.</AbstractText><br /><br />Copyright © 2024. Published by Elsevier Inc.<br /><br /><small>Am J Cardiol: 22 Jan 2024; epub ahead of print</small></div>
Belyayev L, Stock EM, Hattler B, Bakaeen FG, ... Biswas K, Zenati MA
Am J Cardiol: 22 Jan 2024; epub ahead of print | PMID: 38266796
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<div><h4>Coronary Flow Reserve and Myocardial Resistance Reserve Changes After Transcatheter Aortic Valve Implantation in Aortic Stenosis.</h4><i>Gutiérrez-Barrios A, Cañadas-Pruaño D, Alfaro LM, Gheorghe L, ... Vázquez-García R, Toro-Cebada R</i><br /><AbstractText>Aortic valve stenosis (AS) induces an alteration in haemodynamic conditions that are responsible of coronary microvasculature impairment. Relief of AS by transcatheter aortic valve implantation (TAVI) is expected to improve coronary hemodynamic. We aimed to assess the mid-term effects of TAVI in coronary flow reserve (CFR) and myocardial resistance reserve (MRR) by continuous intracoronary thermodilution technique. Resting and hyperemic coronary flow was measured by continuous thermodilution technique in 23 AS patients and compared to 17 matched controls, and repeated 6±3 months after TAVI in 11 of the AS patients. In AS patients, Resting absolute coronary flow (Q, rest) was significantly higher and absolute resistance at rest (Ru, Rest) were significantly lower compared to controls (p<0.01 for both), resulting, in lower CFR and MRR (1.73±0.4 versus 2.85±1.1; P<0.01 and 1.95±0.4 versus 3.22±1.4; P<0.01 respectively). TAVI implantation yielded a significant 35% increase in CFR (p>0.01) and a 39% increase in MRR (p<0.01) driven by Q, rest reduction (p=0.03). In AS patients CFR and MRR determined by continuous thermodilution are significantly impaired. At 6 months follow-up TAVI improves these indices and partially relieves the pathophysiologic alterations leading to a partial restoration of CFR and MRR.</AbstractText><br /><br />Copyright © 2024. Published by Elsevier Inc.<br /><br /><small>Am J Cardiol: 15 Jan 2024; epub ahead of print</small></div>
Gutiérrez-Barrios A, Cañadas-Pruaño D, Alfaro LM, Gheorghe L, ... Vázquez-García R, Toro-Cebada R
Am J Cardiol: 15 Jan 2024; epub ahead of print | PMID: 38232809
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<div><h4>Minimally Invasive Epicardial Surgical Left Atrial Appendage Exclusion for Atrial Fibrillation Patients at High Risk of Stroke and of Bleeding.</h4><i>Rose DZ, DiGiorgi P, Ramlawi B, Pulungan Z, Teigland C, Calkins H</i><br /><b>Background</b><br />Atrial fibrillation (AF) patients at high risk for stroke and also at high risk for bleeding may be unsuitable for either oral anticoagulation or endocardial left atrial appendage (LAA) occlusion. However, minimally invasive, epicardial LAA exclusion (LAAE) may be an option.<br /><b>Objective</b><br />To evaluate outcomes of LAAE in high-risk AF patients not on oral anticoagulation.<br /><b>Methods</b><br />A retrospective analysis of Medicare claims data was conducted to evaluate thromboembolic events in AF patients who underwent LAAE compared to a 1:4 propensity score-matched group of patients who did not receive LAAE (control). Neither group was on any oral anticoagulation at baseline or follow-up. Fine-Gray models estimated hazard ratios and evaluated between-group differences; bootstrapping was applied to generate 95%-confidence intervals (CIs).<br /><b>Results</b><br />The LAAE group (N=243) was 61% male with a mean age of 75 years; AF was non-paroxysmal in 70% (mean CHA<sub>2</sub>DS<sub>2</sub>-VASc was 5.4 and mean HAS-BLED was 4.2); the matched control group (N=972) had statistically similar characteristics. One-year adjusted estimates of thromboembolic events were 7.3% (95% CI 4.3-11.1%) in LAAE and 12.1% (95% CI 9.5-14.8%) in the control group. Absolute risk reduction was 4.8% (95% CI 0.6-8.9%, P=0.028). The adjusted hazard ratio for thromboembolic events for LAAE versus non-LAAE was 0.672 (95% CI 0.394-1.146).<br /><b>Conclusions</b><br />In AF patients not taking oral anticoagulation, at high risk of stroke and of bleeding, minimally invasive, thoracoscopic, epicardial LAAE was associated with a lower rate of thromboembolic events.<br /><br />Copyright © 2024. Published by Elsevier Inc.<br /><br /><small>Heart Rhythm: 29 Jan 2024; epub ahead of print</small></div>
Rose DZ, DiGiorgi P, Ramlawi B, Pulungan Z, Teigland C, Calkins H
Heart Rhythm: 29 Jan 2024; epub ahead of print | PMID: 38296011
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<div><h4>Comparison of interleukin-6 and high-sensitivity C-reactive protein for cardiovascular risk assessment: Findings from the MESA study.</h4><i>Ferreira JP, Vasques-Nóvoa F, Neves JS, Zannad F, Leite-Moreira A</i><br /><b>Background:</b><br/>and aims</b><br />Inflammation is a risk factor for major adverse cardiovascular events (MACE). Elevated levels of both high-sensitivity C-reactive protein (hsCRP) and interleukin-6 (IL6) have been associated with MACE. However, few studies have compared IL6 to hsCRP for cardiovascular risk assessment. Using the MESA (Multi-Ethnic Study of Atherosclerosis) study cohort, we aim to compare IL6 to hsCRP.<br /><b>Methods</b><br />We divided IL6 and hsCRP by their median values and created 4 groups i.e., low-low, high-low, low-high and high-high. The median follow-up was 14 years.<br /><b>Results</b><br />6614 (97 %) participants had complete baseline IL6 and hsCRP data. The correlation between hsCRP and IL6 was modest (Rho = 0.53). IL6 ≥1.2 pg/mL (median) was present in 3309 participants, and hsCRP ≥1.9 mg/L (median) was present in 3339 participants. Compared to participants with low IL6 and low hsCRP, those with high IL6 and high hsCRP were older (64 vs. 60 years), more frequently women (63 % vs. 45 %), and with more cardiovascular co-morbidities. hsCRP outcome associations lost statistical significance when adjusting for IL6: MACE HR (95 %CI) 1.06 (0.93-1.20), p =0.39, whereas IL6 associations remained significant after adjusting for hsCRP: HR (95 %CI) 1.44 (1.25-1.64), p <0.001. The C-index of Framingham score for did not improve with hsCRP but improved with IL6. Compared to participants with low IL6 and low hsCRP, those with high IL6, regardless of hsCRP, experienced an increased risk of MACE, heart failure and mortality.<br /><b>Conclusions</b><br />In a diverse and asymptomatic population, IL6 showed a stronger association with atherosclerotic, heart failure and fatal outcomes than hsCRP.<br /><br />Copyright © 2024 Elsevier B.V. All rights reserved.<br /><br /><small>Atherosclerosis: 24 Jan 2024; 390:117461</small></div>
Ferreira JP, Vasques-Nóvoa F, Neves JS, Zannad F, Leite-Moreira A
Atherosclerosis: 24 Jan 2024; 390:117461 | PMID: 38306764
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<div><h4>The effect of sodium-glucose cotransporter 2 inhibitors on left cardiac remodelling in heart failure with reduced ejection fraction: Systematic review and meta-analysis.</h4><i>Usman MS, Januzzi JL, Anker SD, Salman A, ... Metra M, Butler J</i><br /><b>Aims</b><br />The therapeutic mechanism of sodium-glucose cotransporter 2 inhibitors (SGLT2i) on left cardiac remodelling in patients with heart failure with reduced ejection fraction (HFrEF) is not well-established. This study meta-analysed the impact of SGLT2i on left cardiac structure and function in patients with HFrEF.<br /><b>Methods and results</b><br />Online databases were queried up to April 2023 for trials reporting indicators of left cardiac structure and function in patients with HFrEF treated with SGLT2i. Data from studies were pooled using a random-effects model to derive weighted mean differences (WMDs) and 95% confidence intervals (CIs). Six trials were included (n = 555). Compared with control, SGLT2i significantly improved left ventricular end-diastolic volume (LVEDV; WMD: -17.07 ml [-23.84, -10.31]; p < 0.001), LVEDV index (WMD: -5.62 ml/m<sup>2</sup> [-10.28, -0.97]; p = 0.02), left ventricular end-systolic volume (LVESV; WMD: -15.63 ml [-26.15, -5.12]; p = 0.004), LVESV index (WMD: -6.90 ml/m<sup>2</sup> [-10.68, -3.11]; p = 0.001), left ventricular ejection fraction (WMD: 2.71% [0.70, 4.72]; p = 0.008), and left atrial volume index (WMD: -2.19 ml/m<sup>2</sup> [-4.26, -0.11]; p = 0.04) in patients with HFrEF. SGLT2i use was associated with a non-significant trend towards a reduction in left ventricular mass index (WMD: -6.25 g/m<sup>2</sup> [-12.79, 0.28]; p = 0.06). No significant impact on left ventricular global longitudinal strain was noted (WMD: 0.21% [-0.25, 0.67]; p = 0.38).<br /><b>Conclusions</b><br />Sodium-glucose cotransporter 2 inhibitors improve cardiac structure and function in patients with HFrEF.<br /><br />© 2024 European Society of Cardiology.<br /><br /><small>Eur J Heart Fail: 18 Jan 2024; epub ahead of print</small></div>
Usman MS, Januzzi JL, Anker SD, Salman A, ... Metra M, Butler J
Eur J Heart Fail: 18 Jan 2024; epub ahead of print | PMID: 38235936
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<div><h4>Practical Guide on Left Atrial Appendage Closure for the Non-implanting Physician. An International Consensus Paper.</h4><i>Potpara T, Grygier M, Haeusler KG, Nielsen-Kudsk JE, ... Kovac J, Camm AJ</i><br /><AbstractText>A significant proportion of patients who suffer from atrial fibrillation and are in need of thromboembolic protection are not treated with oral anticoagulation or discontinue this treatment shortly after its initiation. This undertreatment has not improved sufficiently despite the availability of direct oral anticoagulants which are associated with less major bleeding than vitamin K antagonists. Multiple reasons account for this, including bleeding events or ischaemic strokes whilst on anticoagulation, a serious risk of bleeding events, poor treatment compliance despite best educational attempts or aversion to drug therapy. An alternative interventional therapy, which is not associated with long-term bleeding and is as effective as vitamin K anticoagulation, was introduced over 20 years ago. Because of significant improvements in procedural safety over the years left atrial appendage closure, predominantly achieved using a catheter-based, device implantation approach, is increasingly favoured for the prevention of thromboembolic events in patients who cannot achieve effective anticoagulation. This management strategy is well-known to the interventional cardiologist/electrophysiologist but is not more widely appreciated within cardiology or internal medicine. This article introduces the devices and briefly explains the implantation technique. The indications and device follow-up are more comprehensively described. Almost all physicians who care for adult patients will have many with atrial fibrillation. This practical guide, written within guideline/guidance boundaries, is aimed at those non-implanting physicians who may need to refer patients for consideration of this new therapy, which is becoming increasingly popular.</AbstractText><br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.<br /><br /><small>Europace: 31 Jan 2024; epub ahead of print</small></div>
Potpara T, Grygier M, Haeusler KG, Nielsen-Kudsk JE, ... Kovac J, Camm AJ
Europace: 31 Jan 2024; epub ahead of print | PMID: 38291925
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<div><h4>Comparative efficacy of vericiguat to sacubitril/valsartan for patients with heart failure reduced ejection fraction: Systematic review and network meta-analysis.</h4><i>Kang DW, Kang SH, Lee K, Nam K, ... Yoon JC, Park SK</i><br /><b>Background</b><br />Despite the established efficacy of vericiguat compared to placebo, uncertainties remain regarding its comparative efficacy to sacubitril/valsartan for patients with heart failure reduced ejection fraction (HFrEF). This study aimed to assess the relative efficacy of vericiguat and sacubitril/valsartan through a systematic review, network meta-analysis, and non-inferiority tests.<br /><b>Methods</b><br />A systematic review was conducted to identify the randomized phase 3 clinical trials involving vericiguat and sacubitril/valsartan. The hazard ratios (HRs) with 95% confidence intervals (CI) for cardiovascular death (CVD) and hospitalization due to HF (hHF) were extracted from these trials and synthesized via network meta-analysis. Non-inferiority testing of vericiguat was performed using a fixed-margin method with a predefined non-inferiority margin (1.24). Sensitivity analyses explored the impact of the time from hHF to screening.<br /><b>Results</b><br />Among the 1366 studies, two trials (VICTORIA and PARADIGM-HF) met the inclusion criteria. Network meta-analysis demonstrated that the HR for CVD or hHF with vericiguat did not significantly differ from that for sacubitril/valsartan (HR: 0.88, 95% CI:0.62-1.23). The upper limit of the 95% CI was less than the predefined margin of 1.24, confirming vericiguat\'s non-inferiority to sacubitril/valsartan. Sensitivity analyses affirmed the robustness of the base-case results.<br /><b>Conclusion</b><br />Vericiguat exhibited a comparable risk of CVD or hHF when contrasted with sacubitril/valsartan. Importantly, in patients with HFrEF, vericiguat\'s efficacy was not statistically inferior to that of sacubitril/valsartan. These findings reinforce the potential of vericiguat as a viable treatment option for this patient population.<br /><br />Copyright © 2024. Published by Elsevier B.V.<br /><br /><small>Int J Cardiol: 17 Jan 2024:131786; epub ahead of print</small></div>
Kang DW, Kang SH, Lee K, Nam K, ... Yoon JC, Park SK
Int J Cardiol: 17 Jan 2024:131786; epub ahead of print | PMID: 38242507
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<div><h4>Clinical characteristics and outcome of end stage hypertrophic cardiomyopathy: Role of age and heart failure phenotypes.</h4><i>Musumeci B, Tini G, Biagini E, Merlo M, ... Boni L, Autore C</i><br /><b>Background</b><br />A minority of patients with hypertrophic cardiomyopathy (HCM) presents advanced heart failure (HF) during their clinical course, in the context of left ventricular (LV) remodeling with reduced LV ejection fraction (LVEF), or of severe diastolic dysfunction without impaired LVEF. Aim of this study was to describe a multicentric end stage (ES) HCM population and analyze clinical course and outcome among its different phenotypes.<br /><b>Methods</b><br />Data of all HCM patients from 7 Italian referral centres were retrospectively evaluated. ES was diagnosed in presence of: LVEF <50% (ES-rEF) or NYHA functional class ≥II with severe diastolic dysfunction (ES-pEF). Outcomes were: HCM-related and all-cause mortality; combined arrhythmic events; advanced HF treatments.<br /><b>Results</b><br />Study population included 331 ES patients; 87% presented ES-rEF and 13% ES-pEF. At ES recognition, patients with ES-pEF were more commonly females, had more frequently NYHA III/IV, atrial fibrillation and greater maximal LV wall thickness. Over a median follow-up of 5.6 years, 83 (25%) patients died, 46 (15%) experienced arrhythmic events and (26%) 85 received advanced HF treatments. Incidence of HCM-related and all-cause mortality, and of combined arrhythmic events did not differ in ES-pEF and ES-rEF patients, but ES-pEF patients were less likely to receive advanced HF treatments. Older age at ES recognition was an independent predictor of increased HCM-related mortality (p = 0.01) and reduced access to advanced HF treatments (p < 0.0001).<br /><b>Conclusions</b><br />Two different HCM-ES phenotypes can be recognized, with ES-pEF showing distinctive features at ES recognition and receiving less frequently advanced HF treatments. Older age at ES recognition has a major impact on outcomes.<br /><br />Copyright © 2024. Published by Elsevier B.V.<br /><br /><small>Int J Cardiol: 17 Jan 2024:131784; epub ahead of print</small></div>
Musumeci B, Tini G, Biagini E, Merlo M, ... Boni L, Autore C
Int J Cardiol: 17 Jan 2024:131784; epub ahead of print | PMID: 38242504
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<div><h4>Geographic disparity of pathophysiological coronary artery disease characteristics: Insights from ASET trials.</h4><i>Kotoku N, Ninomiya K, Masuda S, Tsai TY, ... Serruys PW, ASET Japan and ASET Brazil Investigators</i><br /><b>Background</b><br />The geographical disparity in the pathophysiological pattern of coronary artery disease (CAD) among patients undergoing percutaneous coronary intervention (PCI) is unknown.<br /><b>Objectives</b><br />To elucidate the geographical variance in the pathophysiological characteristics of CAD.<br /><b>Methods</b><br />Physiological indices derived from angiography-based fractional flow reserve pullbacks from patients with chronic coronary syndrome enrolled in the ASET Japan (n = 206) and ASET Brazil (n = 201) studies, which shared the same eligibility criteria, were analysed. The pathophysiological patterns of CAD were characterised using Murray law-based quantitative flow ratio (μQFR)-derived indices acquired from pre-PCI angiograms. The diffuseness of CAD was defined by the μQFR pullback pressure gradient index.<br /><b>Results</b><br />Significant functional stenoses pre-PCI (μQFR≤0.80) were more frequent in ASET Japan compared to ASET Brazil (89.9% vs. 67.5%,p < 0.001), as were rates of a post-PCI μQFR<0.91(22.1% vs. 12.9%,p = 0.013). In the multivariable analysis, pre-procedural μQFR and diffuse disease were independent factors for predicting a post-PCI μQFR<0.91, which contributed to the different rates of post-PCI μQFR≥0.91 between the studies. Among vessels with a post-PCI μQFR<0.91, a consistent diffuse pattern of CAD pre- and post-PCI occurred in 78.3% and 76.7% of patients in ASET Japan and Brazil, respectively; only 6.3% (Japan) and 10.0% (Brazil) of vessels had a major residual gradient. Independent risk factors for diffuse disease were diabetes mellitus in ASET Japan, and age and male gender in Brazil.<br /><b>Conclusions</b><br />There was geographic disparity in pre-procedural angiography-based pathophysiological characteristics. The combined pre-procedural physiological assessment of vessel μQFR and diffuseness of CAD may potentially identify patients who will benefit most from PCI.<br /><br />Copyright © 2024. Published by Elsevier B.V.<br /><br /><small>Int J Cardiol: 23 Jan 2024:131805; epub ahead of print</small></div>
Kotoku N, Ninomiya K, Masuda S, Tsai TY, ... Serruys PW, ASET Japan and ASET Brazil Investigators
Int J Cardiol: 23 Jan 2024:131805; epub ahead of print | PMID: 38272132
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<div><h4>High-risk Brugada Syndrome: Factors Associated with Arrhythmia Recurrence and Benefits of Epicardial Ablation in Addition to ICD implantation.</h4><i>Santinelli V, Ciconte G, Manguso F, Anastasia L, ... Giannelli L, Pappone C</i><br /><b>Aims</b><br />This study aims to evaluate the prognostic impact of the arrhythmogenic substrate size in symptomatic Brugada Syndrome (BrS) as well as to validate the long-term safety and effectiveness of epicardial radiofrequency ablation (RFA) compared to No-RFA group.<br /><b>Methods and results</b><br />In this prospective investigational long-term registry study, 257 selected symptomatic BrS patients with ICD implantation were included. Among them, 206 patients underwent radiofrequency epicardial ablation (RFA) and were monitored for over 5 years post-ablation (RFA group) while 51 patients received only ICD implantation declining RFA. Primary endpoints included risk factors for ventricular fibrillation (VF) events pre-ablation and freedom from VF events post-ablation. In the RFA group, BrS substrates were identified in the epicardial surface of the right ventricle. During the pre-RFA follow-up period (median 27 months), VF episodes and VF storms were experienced by 53 patients. Independent risk factors included substrate size (HR, 1.13; 95% CI, 1.08-1.18; P < 0.001), aborted cardiac arrest (HR, 2.98; 95% CI, 1.68-5.28; P < 0.001), and SCN5A variants (HR, 2.22; 95% CI, 1.15-4.27; P = 0.017). In the post-RFA follow-up (median 40 months), the RFA group demonstrated superior outcomes compared to No-RFA (P < 0.001) without major procedure-related complications.<br /><b>Conclusion</b><br />Our study underscores the role of BrS substrate extent as a crucial prognostic factor for recurrent VF and validates the safety and efficacy of RFA when compared to a No-RFA group. Our findings highlight the importance of ajmaline in guiding epicardial mapping/ablation in symptomatic BrS patients, laying the groundwork for further exploration of non-invasive methods to guide informed clinical decision-making.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.<br /><br /><small>Europace: 22 Jan 2024; epub ahead of print</small></div>
Santinelli V, Ciconte G, Manguso F, Anastasia L, ... Giannelli L, Pappone C
Europace: 22 Jan 2024; epub ahead of print | PMID: 38252933
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<div><h4>Association of GAL-8 promoter methylation levels with coronary plaque inflammation.</h4><i>Xia B, Lu Y, Liang J, Li F, ... Shen Z, Huang J</i><br /><b>Background:</b><br/>and aims</b><br />Coronary heart disease (CHD) is a condition that carries a high risk of mortality and is associated with aging. CHD is characterized by the chronic inflammatory response of the coronary intima. Recent studies have shown that the methylation level of blood mononuclear cell DNA is closely associated with adverse events in CHD, but the roles and mechanisms of DNA methylation in CHD remain elusive.<br /><b>Methods and results</b><br />In this study, the DNA methylation status within the epigenome of human coronary tissue in the sudden coronary death (SCD) group and control (CON) group of coronary heart disease was analyzed using the Illumina® Infinium Methylation EPIC BeadChip (850 K chip), resulting in the identification of a total of 2553 differentially methylated genes (DMGs). The differentially methylated genes were then subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and significant differential DNA methylation was found. Among the differentially hypomethylated genes were GAL-8, LTF, and RFPL3, while the highly methylated genes were TMEM9B, ANK3, and C6orF48. These genes were mainly enriched in 10 significantly enriched pathways, such as cell adhesion junctions, among which the differentially methylated gene GAL-8 was involved in inflammatory pathway signaling. For functional analysis of GAL-8, we first examined the differences in GAL-8 promoter methylation levels among different subgroups of human coronary tissue in the CON, CHD, and SCD groups using pyrophosphate sequencing. The results revealed reduced GAL-8 promoter methylation levels in the SCD group, while the difference between the CHD and CON groups was not statistically significant (P > 0.05). The reduced GAL-8 promoter methylation level was associated with upregulated GAL-8 expression, which led to increased expression of the inflammatory markers TNF-α, IL-1β, MCP-1, MIP-2, MMP-2, and MMP-9. This enhanced inflammatory response contributed to the accumulation of foam cells, thickening of the intima of human coronary arteries, and increased luminal stenosis, which promoted the occurrence of sudden coronary death. Next, we found that GAL-8 promoter methylation levels in PBMC were consistent with human coronary tissue. The unstable angina group (UAP) had significantly lower GAL-8 promoter methylation levels than stable angina (SAP) and healthy controls (CON) (P < 0.05), and there was a significant correlation between reduced GAL-8 promoter methylation levels and risk factors for coronary heart disease. These findings highlight the association between decreased GAL-8 promoter methylation and the presence of coronary heart disease risk factors. ROC curve analysis suggests that methylation of the GAL 8 promoter region is an independent risk factor for CHD. In conclusion, our study confirmed differential expression of GAL-8, LTF, MUC4D, TMEM9B, MYOM2, and ANK3 genes due to DNA methylation in the SCD group. We also established the consistency of GAL-8 promoter methylation alterations between human coronary tissue and patient peripheral blood monocytes. The decreased methylation level of the GAL-8 promoter may be related to the increased expression of GAL-8 and the coronary risk factors.<br /><b>Conclusions</b><br />Accordingly, we hypothesized that reduced levels of GAL-8 promoter methylation may be an independent risk factor for adverse events in coronary heart disease.<br /><br />Copyright © 2024 Elsevier Ireland Ltd. All rights reserved.<br /><br /><small>Int J Cardiol: 19 Jan 2024:131782; epub ahead of print</small></div>
Xia B, Lu Y, Liang J, Li F, ... Shen Z, Huang J
Int J Cardiol: 19 Jan 2024:131782; epub ahead of print | PMID: 38246423
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<div><h4>Waitlist Outcomes in Candidates With Rare Causes of Heart Failure After Implementation of the 2018 French Heart Allocation Scheme.</h4><i>Legeai C, Coutance G, Cantrelle C, Jasseron C, ... Kerbaul F, Dorent R</i><br /><b>Background</b><br />In 2018, an algorithm-based allocation system for heart transplantation (HT) was implemented in France. Its effect on access to HT of patients with rare causes of heart failure (HF) has not been assessed.<br /><b>Methods</b><br />In this national study, including adults listed for HT between 2018 and 2020, we analyzed waitlist and posttransplant outcomes of candidates with rare causes of HF (restrictive cardiomyopathy [RCM], hypertrophic cardiomyopathy, and congenital heart disease). The primary end point was death on the waitlist or delisting for clinical deterioration. Secondary end points included access to HT and posttransplant mortality. The cumulative incidence of waitlist mortality estimated with competing risk analysis and incidence of transplantation were compared between diagnosis groups. The association of HF cause with outcomes was determined by Fine-Gray or Cox models.<br /><b>Results</b><br />Overall, 1604 candidates were listed for HT. At 1 year postlisting, 175 patients met the primary end point and 1040 underwent HT. Candidates listed for rare causes of HF significantly differed in baseline characteristics and had more frequent score exceptions compared with other cardiomyopathies (31.3%, 32.0%, 36.4%, and 16.7% for patients with hypertrophic cardiomyopathy, RCM, congenital heart disease, and other cardiomyopathies). The cumulative incidence of death on the waitlist and probability of HT were similar between diagnosis groups (<i>P</i>=0.17 and 0.40, respectively). The adjusted risk of death or delisting for clinical deterioration did not significantly differ between candidates with rare and common causes of HF (subdistribution hazard ratio (HR): hypertrophic cardiomyopathy, 0.51 [95% CI, 0.19-1.38]; <i>P</i>=0.18; RCM, 1.04 [95% CI, 0.42-2.58]; <i>P</i>=0.94; congenital heart disease, 1.82 [95% CI, 0.78-4.26]; <i>P</i>=0.17). Similarly, the access to HT did not significantly differ between causes of HF (hypertrophic cardiomyopathy: HR, 1.18 [95% CI, 0.92-1.51]; <i>P</i>=0.19; RCM: HR, 1.19 [95% CI, 0.90-1.58]; <i>P</i>=0.23; congenital heart disease: HR, 0.76 [95% CI, 0.53-1.09]; <i>P</i>=0.14). RCM was an independent risk factor for 1-year posttransplant mortality (HR, 2.12 [95% CI, 1.06-4.24]; <i>P</i>=0.03).<br /><b>Conclusions</b><br />Our study shows equitable waitlist outcomes among HT candidates whatever the indication for transplantation with the new French allocation scheme.<br /><br /><br /><br /><small>Circ Heart Fail: 01 Feb 2024:e010837; epub ahead of print</small></div>
Legeai C, Coutance G, Cantrelle C, Jasseron C, ... Kerbaul F, Dorent R
Circ Heart Fail: 01 Feb 2024:e010837; epub ahead of print | PMID: 38299331
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<div><h4>Three-Year Cardiovascular Outcomes of Telmisartan in Patients with Hypertension: An Electronic Health Record-Based Cohort Study.</h4><i>Yum Y, Kim JH, Joo HJ, Kim YH, Kim EJ</i><br /><b>Background</b><br />Telmisartan exhibits superior efficacy in controlling 24-hour blood pressure (BP) compared with other angiotensin receptor blockers (ARBs). However, data on its cardiovascular effects in patients with hypertension are limited. This study aimed to evaluate the cardiovascular outcomes in patients taking telmisartan compared to those taking other ARBs.<br /><b>Methods</b><br />This multicenter retrospective study used data from the Korea University Medical Center database, built from electronic health records. A total of 19,247 patients taking two or more antihypertensive medications were identified. Patients prescribed telmisartan (telmisartan users) were compared with those prescribed an ARB other than telmisartan (other ARB users). The primary outcome was major adverse cardiac events (MACE), a composite of cardiovascular death, myocardial infarction, stroke, and hospitalizations due to heart failure. The adjusted outcomes were compared using 1:1 propensity score (PS) matching.<br /><b>Results</b><br />Overall, 3,437 (17.9%) patients were telmisartan users. These patients were more likely to be younger and male and less likely to have a history of chronic kidney disease, dialysis, or heart failure. In the PS-matched cohort, BP control was similar in both groups; however, telmisartan users exhibited significantly lower visit-to-visit BP variability. The adjusted 3-year MACE rate was similar between telmisartan users (4.6%) and other ARB users (4.7%, log-rank p = 0.75), with comparable safety profiles.<br /><b>Conclusions</b><br />In real-world practice, telmisartan showed cardiovascular outcomes similar to those of other ARBs in patients with hypertension taking two or more antihypertensive drugs.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of American Journal of Hypertension, Ltd. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Am J Hypertens: 29 Jan 2024; epub ahead of print</small></div>
Yum Y, Kim JH, Joo HJ, Kim YH, Kim EJ
Am J Hypertens: 29 Jan 2024; epub ahead of print | PMID: 38285627
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<div><h4>Tolerability and effectiveness of beta-blockers in patients with cardiac amyloidosis: A systematic review and meta-analysis.</h4><i>Kang Y, Qu N, Zhang Z, Zhang Q, Chen X, Michael Fu MD</i><br /><b>Objective</b><br />This systematic review aimed to assess the tolerability of patients with cardiac amyloidosis (CA) to beta-blockers (BBs) and evaluate its association with adverse outcomes.<br /><b>Methods</b><br />We performed a comprehensive search from January 1, 2000 to October 20, 2023. Studies examining BB use and tolerance or the relationship between BB use and outcomes in patients with CA were included. Pooled adjusted hazard ratios (aHRs) for all-cause mortality were calculated using random- and fixed-effects models.<br /><b>Results</b><br />Eight observational studies involving 4002 patients with CA (87.5% with transthyretin CA [ATTR-CA] and 12.5% with immunoglobulin light chain CA [AL-CA]) were assessed. BBs were used by 52.5% of the patients. However, 26.3% of the patients discontinued BBs because of hypotension, bradycardia, or fatigue. Regarding the association between BB use and all-cause death, four studies were identified that included 2874 patients with ATTR-CA and 16 patients with AL-CA. The meta-analysis revealed no apparent relationship between BB use and all-cause mortality (pooled aHR = 0.78, 95% confidence interval (CI) = 0.40-1.51). Two studies on patients with ATTR-CA found no impact of BB use on all-cause mortality in the subgroup with left ventricular ejection fraction (LVEF) > 40%, but conflicting results exist for those with LVEF ≤40% (pooled aHR = 0.78, 95% CI = 0.40-1.54).<br /><b>Conclusion</b><br />The limited number of observational studies that predominantly enrolled patients with ATTR-CA showed that BBs were used in almost half of the patients with CA, with varying tolerability. However, no significant association was observed between BB use and all-cause mortality.<br /><br />Copyright © 2024. Published by Elsevier B.V.<br /><br /><small>Int J Cardiol: 24 Jan 2024:131813; epub ahead of print</small></div>
Kang Y, Qu N, Zhang Z, Zhang Q, Chen X, Michael Fu MD
Int J Cardiol: 24 Jan 2024:131813; epub ahead of print | PMID: 38278490
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<div><h4>Trends and Outcomes Associated With Bariatric Surgery and Pharmacotherapies With Weight Loss Effects Among Patients With Heart Failure and Obesity.</h4><i>Mentias A, Desai MY, Aminian A, Patel KV, ... Nissen SE, Pandey A</i><br /><b>Background</b><br />Utilization patterns of bariatric surgery among older patients with heart failure (HF), and the associations with cardiovascular outcomes, are not well known.<br /><b>Methods</b><br />Medicare beneficiaries with HF and at least class II obesity from 2013 to 2020 were identified with Medicare Provider Analysis and Review 100% inpatient files and Medicare 5% outpatient files. Patients who underwent bariatric surgery were matched to controls in a 1:2 ratio (matched on exact age, sex, race, body mass index, HF encounter year, and HF hospitalization rate pre-surgery/matched period). In an exploratory analysis, patients prescribed pharmacotherapies with weight loss effects (semaglutide, liraglutide, naltrexone-bupropion, or orlistat) were identified and matched to controls with a similar strategy in addition to HF medical therapy data. Cox models evaluated associations between weight loss therapies (as a time-varying covariate) and mortality risk and HF hospitalization rate (calculated as the rate of HF hospitalizations following index HF encounter per 100 person-months) during follow-up.<br /><b>Results</b><br />Of 298 101 patients with HF and body mass index ≥35 kg/m<sup>2</sup>, 2594 (0.9%) underwent bariatric surgery (45% men; mean age, 56.2 years; mean body mass index, 51.5 kg/m<sup>2</sup>). In propensity-matched analyses over a median follow-up of 4.7 years, bariatric surgery was associated with lower risk of all-cause mortality (HR, 0.55 [95% CI, 0.49-0.63]; <i>P</i><0.001), greater reduction in HF hospitalization rate (rate ratio, 0.72 [95% CI, 0.67-0.77]; <i>P</i><0.001), and lower atrial fibrillation risk (HR, 0.78 [95% CI, 0.65-0.93]; <i>P</i>=0.006). Use of pharmacotherapies with weight loss effects was low (4.8%), with 96.3% prescribed GLP-1 (glucagon-like peptide-1) agonists (semaglutide, 23.6%; liraglutide, 72.7%). In propensity-matched analysis over a median follow-up of 2.8 years, patients receiving pharmacotherapies with weight loss effects (versus matched controls) had a lower risk of all-cause mortality (HR, 0.82 [95% CI, 0.71-0.95]; <i>P</i>=0.007) and HF hospitalization rate (rate ratio, 0.87 [95% CI, 0.77-0.99]; <i>P</i>=0.04).<br /><b>Conclusions</b><br />Bariatric surgery and pharmacotherapies with weight loss effects are associated with a lower risk of adverse outcomes among older patients with HF and obesity; however, overall utilization remains low.<br /><br /><br /><br /><small>Circ Heart Fail: 26 Jan 2024:e010453; epub ahead of print</small></div>
Mentias A, Desai MY, Aminian A, Patel KV, ... Nissen SE, Pandey A
Circ Heart Fail: 26 Jan 2024:e010453; epub ahead of print | PMID: 38275114
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<div><h4>Efficacy and safety of CDR132L in patients with reduced left ventricular ejection fraction after myocardial infarction: Rationale and design of the HF-REVERT trial.</h4><i>Bauersachs J, Solomon SD, Anker SD, Antorrena-Miranda I, ... Hauke W, Thum T</i><br /><b>Aim</b><br />Inhibition of microRNA (miR)-132 effectively prevents and reverses adverse cardiac remodelling, making it an attractive heart failure (HF) target. CDR132L, a synthetic antisense oligonucleotide selectively blocking pathologically elevated miR-132, demonstrated beneficial effects on left ventricular (LV) structure and function in relevant preclinical models, and was safe and well tolerated in a Phase 1b study in stable chronic HF patients. Patients with acute myocardial infarction (MI) and subsequent LV dysfunction and remodelling have limited therapeutic options, and may profit from early CDR132L treatment.<br /><b>Methods</b><br />The HF-REVERT (Phase 2, multicenter, randomized, parallel, 3-arm, placebo-controlled Study to Assess Efficacy and Safety of CDR132L in Patients with Reduced Left Ventricular Ejection Fraction after Myocardial Infarction) evaluates the efficacy and safety of CDR132L in HF patients post-acute MI (n = 280), comparing the effect of 5 and 10 mg/kg CDR132L, administered as three single intravenous doses 28 days apart, in addition to standard of care. Key inclusion criteria are the diagnosis of acute MI, the development of systolic dysfunction (LV ejection fraction ≤45%) and elevated N-terminal pro-B-type natriuretic peptide. The study consists of a 6-month double-blinded treatment period with the primary endpoint LV end-systolic volume index and relevant secondary endpoints, followed by a 6-month open-label observation period.<br /><b>Conclusion</b><br />The HF-REVERT trial may underpin the concept of miR-132 inhibition to prevent or reverse cardiac remodelling in post-MI HF. The results will inform the design of subsequent outcome trials to test CDR132L in HF.<br /><br />© 2024 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.<br /><br /><small>Eur J Heart Fail: 25 Jan 2024; epub ahead of print</small></div>
Bauersachs J, Solomon SD, Anker SD, Antorrena-Miranda I, ... Hauke W, Thum T
Eur J Heart Fail: 25 Jan 2024; epub ahead of print | PMID: 38269451
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<div><h4>Effect of a transitional care model following hospitalization for heart failure: 3-year outcomes of the Patient-Centered Care Transitions in Heart Failure (PACT-HF) randomized controlled trial.</h4><i>Averbuch T, Lee SF, Zagorski B, Mebazaa A, ... Thabane L, Van Spall HGC</i><br /><b>Aims</b><br />Patients are at high risk of death or readmission following hospitalization for heart failure (HF). We tested the effect of a transitional care model that included month-long nurse-led home visits and long-term heart function clinic visits - with services titrated to estimated risk of clinical events - on 3-year outcomes following hospitalization.<br /><b>Methods and results</b><br />In a pragmatic, stepped-wedge cluster randomized trial, 10 hospitals were randomized to the intervention versus usual care. The primary outcome was a composite of all-cause death, readmission, or emergency department (ED) visit. Secondary outcomes included components of the primary composite outcomes, HF readmissions and healthcare resource utilization. There were 2494 patients (50.4% female) with mean age of 77.7 years. The primary outcome was reached in 1040 (94.2%) patients in the intervention and 1314 (94.5%) in the usual care group at 3 years. The intervention did not reduce the risk of the primary composite outcome (hazard ratio [HR] 0.92, 95% confidence interval [CI] 0.81-1.05) nor the component outcomes overall, although numerically reduced the risk of ED visits in women but not men (HR 0.79, 95% CI 0.63-1.00 vs. HR 0.98, 95% CI 0.80-1.19; sex-treatment interaction p = 0.23). The uptake of guideline-directed medical therapy was no different with the intervention than with usual care, with the exception of sacubitril/valsartan, which increased with the intervention (3.3% vs 1.5%; relative risk 6.2, 95% CI 1.92-20.06).<br /><b>Conclusions</b><br />More than 9 of 10 patients hospitalized for HF experienced all-cause death, readmission, or ED visit at 3 years. A transitional care model with services titrated to risk did not improve the composite of these endpoints, likely because there were no major differences in uptake of medical therapies between the groups.<br /><b>Clinical trial registration</b><br />ClinicalTrials.gov Identifier NCT02112227.<br /><br />© 2024 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.<br /><br /><small>Eur J Heart Fail: 01 Feb 2024; epub ahead of print</small></div>
Averbuch T, Lee SF, Zagorski B, Mebazaa A, ... Thabane L, Van Spall HGC
Eur J Heart Fail: 01 Feb 2024; epub ahead of print | PMID: 38303550
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<div><h4>Proteomic Associations of NT-proBNP (N-Terminal Pro-B-Type Natriuretic Peptide) in Heart Failure With Preserved Ejection Fraction.</h4><i>Azzo JD, Dib MJ, Zagkos L, Zhao L, ... Cappola TP, Chirinos JA</i><br /><b>Background</b><br />NT-proBNP (N-terminal pro-B-type natriuretic peptide) levels are variably elevated in heart failure with preserved ejection fraction (HFpEF), even in the presence of increased left ventricular filling pressures. NT-proBNP levels are prognostic in HFpEF and have been used as an inclusion criterion for several recent randomized clinical trials. However, the underlying biologic differences between HFpEF participants with high and low NT-proBNP levels remain to be fully understood.<br /><b>Methods</b><br />We measured 4928 proteins using an aptamer-based proteomic assay (SOMAScan) in available plasma samples from 2 cohorts: (1) Participants with HFpEF enrolled in the PHFS (Penn Heart Failure Study; n=253); (2) TOPCAT (Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist Trial) participants in the Americas (n=218). We assessed the relationship between SOMAScan-derived plasma NT-proBNP and levels of other proteins available in the SOMAScan assay version 4 using robust linear regression, with correction for multiple comparisons, followed by pathway analysis.<br /><b>Results</b><br />NT-proBNP levels exhibited prominent proteome-wide associations in PHFS and TOPCAT cohorts. Proteins most strongly associated with NT-proBNP in both cohorts included SVEP1 (sushi, von Willebrand factor type-A, epidermal growth factor, and pentraxin domain containing 1; β<sub>TOPCAT</sub>=0.539; <i>P</i><0.0001; β<sub>PHFS</sub>=0.516; <i>P</i><0.0001) and ANGPT2 (angiopoietin 2; β<sub>TOPCAT</sub>=0.571; <i>P</i><0.0001; β<sub>PHFS</sub>=0.459; <i>P</i><0.0001). Canonical pathway analysis demonstrated consistent associations with multiple pathways related to fibrosis and inflammation. These included hepatic fibrosis and inhibition of matrix metalloproteases. Analyses using cut points corresponding to estimated quantitative concentrations of 360 pg/mL (and 480 pg/mL in atrial fibrillation) revealed similar proteomic associations.<br /><b>Conclusions</b><br />Circulating NT-proBNP levels exhibit prominent proteomic associations in HFpEF. Our findings suggest that higher NT-proBNP levels in HFpEF are a marker of fibrosis and inflammation. These findings will aid the interpretation of NT-proBNP levels in HFpEF and may guide the selection of participants in future HFpEF clinical trials.<br /><br /><br /><br /><small>Circ Heart Fail: 01 Feb 2024:e011146; epub ahead of print</small></div>
Azzo JD, Dib MJ, Zagkos L, Zhao L, ... Cappola TP, Chirinos JA
Circ Heart Fail: 01 Feb 2024:e011146; epub ahead of print | PMID: 38299345
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<div><h4>Proximal optimization technique and percutaneous coronary intervention for left main disease: POTENTIAL-LM.</h4><i>Volet C, Puricel S, Cook ST, di Cicco P, ... Togni M, Cook S</i><br /><b>Background</b><br />Optimal stent deployment in left main (LM) bifurcation is paramount, and incomplete stent apposition may cause major adverse cardiac events (MACE). Bench studies show that the proximal optimization technique (POT) provides the best stent apposition.<br /><b>Aims</b><br />We aimed to investigate the impact of POT on clinical outcomes in patients treated for unprotected LM (ULM) disease at our institution.<br /><b>Methods</b><br />We identified 162 patients who underwent percutaneous coronary intervention (PCI) for ULM coronary disease in the Cardio-FR database. Out of these, 99 (61%) had undergone POT, while 63 patients were treated without POT. The primary outcome was the bifurcation-oriented composite endpoint (BOCE) of cardiac death, target-bifurcation myocardial infarction and target-bifurcation revascularization at maximal follow-up.<br /><b>Results</b><br />Mean age was 76 years, and 69% presented with acute coronary syndrome. Mean follow-up was 2.25 years (822 days). The BOCE occurred in 43 (27%) of which 20 (20%) in the POT group and 23 (37%) in the no-POT group (p = 0.009). Cardiac death occurred in 15 (15%) patients in the POT- and 17 (27%) in no-POT group (p = 0.26). Target bifurcation revascularization occurred in 4 (4%) patients in the POT- and 6 (10%) patients in the no-POT group (p = 0.19). POT In the multivariate analysis, POT was the strongest parameter and was associated with BOCE, cardiac death, occurrence of any revascularization and all-cause mortality.<br /><b>Conclusion</b><br />The POT improves clinical outcomes. These findings strongly support the systematic use of POT in patients undergoing ULM-PCI.<br /><br />© 2024 The Authors. Catheterization and Cardiovascular Interventions published by Wiley Periodicals LLC.<br /><br /><small>Catheter Cardiovasc Interv: 31 Jan 2024; epub ahead of print</small></div>
Volet C, Puricel S, Cook ST, di Cicco P, ... Togni M, Cook S
Catheter Cardiovasc Interv: 31 Jan 2024; epub ahead of print | PMID: 38297989
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<div><h4>Transcatheter aortic valve replacement in heart failure.</h4><i>Parikh PB, Mack M, Stone GW, Anker SD, ... Skopicki HA, Butler J</i><br /><AbstractText>Patients with severe aortic stenosis (AS) may develop heart failure (HF), the presence of which has traditionally been deemed as a final stage in AS progression with poor outcomes. The use of transcatheter aortic valve replacement (TAVR) has become the preferred therapy for most patients with AS and concomitant HF. With its instant afterload reduction, TAVR offers patients with HF significant haemodynamic benefits, with corresponding changes in left ventricular structure and improved mortality and quality of life. The prognostic covariates and optimal timing of TAVR in patients with less than severe AS remain unclear. The purpose of this review is to describe the association between TAVR and outcomes in patients with HF, particularly in the setting of left ventricular systolic dysfunction, acute HF, and right ventricular systolic dysfunction, and to highlight areas for future research.</AbstractText><br /><br />© 2024 European Society of Cardiology.<br /><br /><small>Eur J Heart Fail: 31 Jan 2024; epub ahead of print</small></div>
Parikh PB, Mack M, Stone GW, Anker SD, ... Skopicki HA, Butler J
Eur J Heart Fail: 31 Jan 2024; epub ahead of print | PMID: 38297972
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<div><h4>Association between secondhand smoke exposure and incident heart failure: The Multi-Ethnic Study of Atherosclerosis (MESA).</h4><i>Lin GM, Lloyd-Jones DM, Colangelo LA, Lima JAC, Szklo M, Liu K</i><br /><b>Aims</b><br />There are no studies on the association between secondhand smoke (SHS) exposure and incident heart failure (HF). This cohort study aimed to examine the associations of self-reported and urinary cotinine-assessed SHS exposure with incident HF.<br /><b>Methods and results</b><br />This study included 5548 non-active smoking participants aged 45-84 years and free of known cardiovascular diseases and HF at baseline who self-reported SHS exposure time in the Multi-Ethnic Study of Atherosclerosis (MESA) at baseline (2000-2002). A cohort subset of 3376 non-active smoking participants underwent urinary cotinine measurements. HF events were verified by medical records or death certificates and ascertained from baseline through 2019. Multivariable Cox proportional hazards regression analysis was used with adjustment for demographic variables, traditional cardiovascular risk factors, physical activity, tobacco pack-years and medications. During a median follow-up of 17.7 years, 353 and 196 HF events were identified in the self-report cohort and cohort subset, respectively. In the self-report cohort, compared with the SHS unexposed group (0 h/week), the highest tertile of the SHS exposed group (7-168 h/week) was not associated with incident HF (hazard ratio [HR] 0.70, 95% confidence interval [CI] 0.49-1.00; p = 0.052). In contrast, in the cohort subset, participants with detectable urinary cotinine >7.07 ng/ml had a higher risk of incident HF than those with undetectable urinary cotinine ≤7.07 ng/ml (HR 1.45, 95% CI 1.03-2.06; p = 0.034). There were no significant heterogeneities in HF risk by age, sex, race/ethnicity, or past smoking status.<br /><b>Conclusion</b><br />Secondhand smoke exposure reflected by modestly increased urinary cotinine (>7.07 ng/ml) rather than self-report in non-active smokers was associated with a 40-50% higher risk of any HF event.<br /><br />© 2024 European Society of Cardiology.<br /><br /><small>Eur J Heart Fail: 30 Jan 2024; epub ahead of print</small></div>
Lin GM, Lloyd-Jones DM, Colangelo LA, Lima JAC, Szklo M, Liu K
Eur J Heart Fail: 30 Jan 2024; epub ahead of print | PMID: 38291555
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<div><h4>Transcatheter aortic valve implantation impact on left ventricular myocardial damage: long term follow-up.</h4><i>Myon F, Marut B, Kosmala W, Auffret V, ... Oger E, Donal E</i><br /><b>Introduction</b><br />Aortic stenosis (AS) is causing myocardial damages and replacement is mainly indicated based on symptoms. Non-invasive estimation of myocardial work (MW) provide a less afterload dependent tool that, we sought to look at the impact of transcatheter aortic valve implantation (TAVI) on the myocardium at long-term follow-up and according to current indications.<br /><b>Methods</b><br />We conducted an observational, cross-sectional, single-center study. Patients were selected based on the validated indication for a TAVI. Standardized echocardiographies were repeated.<br /><b>Results</b><br />102 patients were included. Mean age was 85-year-old, 45% were female, 68% get high-blood pressure and 52% had a coronary disease. One fifth was suffering from low-flow low-gradient aortic stenosis. Follow-up was performed at 22 ± 9.5 months after the TAVI. No TAVI-dysfunction was observed. LVEF was stable (62 ± 8%), and global longitudinal strain get improved (-14.0% ± 3.7 vs -16.0% ± 3.6, p-value <0.0001). No improvement of the MW-parameters was noticed (Global Work Index (LV GWI) 2099 ± 692mmHg% vs 2066 ± 706mmHg%, p=0.8, Global Constructive (LV GCW) 2463 ± 736mmHg% vs 2463 ± 676mmHg%, p=0.8). Global Wasted Work increased (214 [149; 357] mmHg% vs 247 [177; 394] mmHg%, p= 0.0008).<br /><b>Conclusion</b><br />In a population of severe symptomatic AS-patients who had undergone a TAVI, the non-invasive myocardial indices that assess the LV performance at long term follow-up did not improve. These results are questioning the timing of the intervention and the need for a more attention in the pharmacological management of these AS-patients.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Eur Heart J Cardiovasc Imaging: 17 Jan 2024; epub ahead of print</small></div>
Myon F, Marut B, Kosmala W, Auffret V, ... Oger E, Donal E
Eur Heart J Cardiovasc Imaging: 17 Jan 2024; epub ahead of print | PMID: 38236150
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<div><h4>High-Intensity Interval Training Is Associated With Improved 10-Year Survival by Mediating Left Ventricular Remodeling in Patients With Heart Failure With Reduced and Mid-Range Ejection Fraction.</h4><i>Hsu CC, Fu TC, Wang CH, Huang TS, Cherng WJ, Wang JS</i><br /><b>Background</b><br />This study aimed to assess the left ventricular (LV) remodeling response and long-term survival after high-intensity interval training (HIIT) in patients with various heart failure (HF) phenotypes during a 10-year longitudinal follow-up.<br /><b>Methods and results</b><br />Among 214 patients with HF receiving guideline-directed medical therapy, those who underwent an additional 36 sessions of aerobic exercise at alternating intensities of 80% and 40% peak oxygen consumption (<mml:math xmlns:mml=\"http://www.w3.org/1998/Math/MathML\"><mml:semantics><mml:mrow><mml:mover><mml:mi>V</mml:mi><mml:mo>̇</mml:mo></mml:mover></mml:mrow><mml:annotation>$$ \\dot{\\mathrm{V}} $$</mml:annotation></mml:semantics></mml:math>O<sub>2peak</sub>) were considered HIIT participants (n=96). Patients who did not undergo HIIT were considered participants receiving guideline-directed medical therapy (n=118). Participants with LV ejection fraction (EF) <40%, ≥40% and <50%, and ≥50% were considered to have HF with reduced EF, HF with mid-range EF, and HF with preserved EF, respectively. <mml:math xmlns:mml=\"http://www.w3.org/1998/Math/MathML\"><mml:semantics><mml:mrow><mml:mover><mml:mi>V</mml:mi><mml:mo>̇</mml:mo></mml:mover></mml:mrow><mml:annotation>$$ \\dot{\\mathrm{V}} $$</mml:annotation></mml:semantics></mml:math>O<sub>2peak</sub>, serial LV geometry, and time to death were recorded. In all included participants, 10-year survival was better (<i>P</i>=0.015) for participants who underwent HIIT (80.3%) than for participants receiving guideline-directed medical therapy (68.6%). An increased <mml:math xmlns:mml=\"http://www.w3.org/1998/Math/MathML\"><mml:semantics><mml:mrow><mml:mover><mml:mi>V</mml:mi><mml:mo>̇</mml:mo></mml:mover></mml:mrow><mml:annotation>$$ \\dot{\\mathrm{V}} $$</mml:annotation></mml:semantics></mml:math>O<sub>2peak</sub>, decreased minute ventilation carbon dioxide production slope, and reduced LV end-diastolic diameter were protective factors against all-cause mortality. Regarding 138 patients with HF with reduced EF (<i>P</i>=0.044) and 36 patients with HF with mid-range EF (<i>P</i>=0.036), 10-year survival was better for participants who underwent HIIT than for participants on guideline-directed medical therapy. Causal mediation analysis showed a significant mediation path for LV end-diastolic diameter on the association between HIIT and 10-year mortality in all included patients with HF (<i>P</i><0.001) and those with LV ejection fraction <50% (<i>P</i>=0.006). HIIT also had a significant direct association with 10-year mortality in patients with HF with LV ejection fraction <50% (<i>P</i>=0.027) but not in those with LV ejection fraction ≥50% (n=40).<br /><b>Conclusions</b><br />Reversal of LV remodeling after HIIT could be a significant mediating factor for 10-year survival in patients with HF with reduced EF and those with HF with mid-range EF.<br /><br /><br /><br /><small>J Am Heart Assoc: 19 Jan 2024:e031162; epub ahead of print</small></div>
Hsu CC, Fu TC, Wang CH, Huang TS, Cherng WJ, Wang JS
J Am Heart Assoc: 19 Jan 2024:e031162; epub ahead of print | PMID: 38240219
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<div><h4>Temporal Trend in Revascularization for Patients With Ischemic Cardiomyopathy and Multivessel Coronary Artery Disease.</h4><i>Alzahrani AH, Alabbadi S, Itagaki S, Egorova N</i><br /><b>Background</b><br />Current guidelines recommend revascularization in patients with ischemic cardiomyopathy (ICM). However, there is limited information about the trends and outcomes of coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI) in ischemic cardiomyopathy patients with multivessel coronary artery disease.<br /><b>Methods and results</b><br />Using New Jersey state mandatory registries, 8083 patients with ischemic cardiomyopathy with CABG or PCI revascularization for multivessel coronary artery disease from 2007 to 2018 were included in the analysis. Joinpoint regression and multivariable logistic regression analyses were performed to assess the annual percentage change in trends and predictors of the 30-day mortality rate, respectively. A decline in CABG procedures was observed from 2007 to 2011 (annual percentage change, -11.5%; <i>P</i>=0.003), followed by stabilization. The PCI trend remained unchanged from 2007 to 2010 and then increased significantly (annual percentage change, 3.2%; <i>P</i>=0.02). In the subsample of patients with proximal left anterior descending artery plus circumflex and right coronary artery, CABG was a predominant procedure until 2011, and the proportion of both procedures did not differ thereafter. In the subsample of patients with left anterior descending artery and any other artery stenosis, PCI remained dominant from 2007 to 2018, while in patients with left main and any other artery stenosis, CABG remained dominant from 2007 to 2018 (<i>P</i><0.001). The 30-day risk-adjusted mortality rate was higher after PCI versus CABG for each year, but after adjustment for completeness of revascularization, there was no difference between groups.<br /><b>Conclusions</b><br />The patterns of revascularization procedures for patients with ischemic cardiomyopathy with multivessel coronary artery disease have changed over the years, as evidenced by the changes in CABG and PCI trends. CABG and PCI had comparable 30-day risk-adjusted mortality risks.<br /><br /><br /><br /><small>J Am Heart Assoc: 19 Jan 2024:e032212; epub ahead of print</small></div>
Alzahrani AH, Alabbadi S, Itagaki S, Egorova N
J Am Heart Assoc: 19 Jan 2024:e032212; epub ahead of print | PMID: 38240212
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<div><h4>Cholesterol Crystal Dissolution Rate of Serum Predicts Outcomes in Patients With Aortic Stenosis Undergoing Transcatheter Aortic Valve Replacement.</h4><i>Al-Kassou B, Al-Kassou L, Mahn T, Lütjohann D, ... Latz E, Zimmer S</i><br /><b>Background</b><br />Aortic stenosis has pathophysiological similarities with atherosclerosis, including the deposition of cholesterol-containing lipoproteins. The resulting cholesterol crystals activate the NLRP3 (NOD-like receptor protein 3) inflammasome, leading to inflammation and cardiovascular diseases. We aimed to investigate the cholesterol crystal dissolution rate (CCDR) of serum in patients with aortic stenosis and to assess the prognostic value of this biomarker.<br /><b>Methods and results</b><br />The study included 348 patients with aortic stenosis undergoing transcatheter aortic valve replacement. The CCDR was measured using flow cytometry to enumerate cholesterol crystals that were added to a serum solution, at baseline and after 2 hours of incubation. Based on the median CCDR, the cohort was stratified into high and low cholesterol crystal dissolvers. The incidence of the primary end point, a composite of 1-year all-cause mortality and major vascular complication, was significantly lower in the high CCDR group (7.3 per 100 person-years) compared with the low CCDR group (17.0 per 100 person-years, <i>P</i>=0.01). This was mainly driven by a lower 1-year mortality rate in patients with a high CCDR (7.3 versus 15.1 per 100 person-years, <i>P</i>=0.04). Unplanned endovascular interventions were significantly less frequent in high cholesterol crystal dissolvers (12.8 versus 22.6 per 100 person-years, <i>P</i>=0.04). Although low-density lipoprotein cholesterol levels were comparable in both groups (101.8±37.3 mg/dL versus 97.9±37.6 mg/dL, <i>P</i>=0.35), only patients with a low CCDR showed a benefit from statin treatment. In multivariate analysis, low CCDR (hazard ratio, 2.21 [95% CI, 0.99-4.92], <i>P</i>=0.04) was significantly associated with 1-year mortality.<br /><b>Conclusions</b><br />The CCDR is a novel biomarker associated with outcome in patients with aortic stenosis undergoing transcatheter aortic valve replacement. It may provide new insights into patients\' anti-inflammatory capacity and additional prognostic information beyond classic risk assessment.<br /><br /><br /><br /><small>J Am Heart Assoc: 19 Jan 2024:e031997; epub ahead of print</small></div>
Al-Kassou B, Al-Kassou L, Mahn T, Lütjohann D, ... Latz E, Zimmer S
J Am Heart Assoc: 19 Jan 2024:e031997; epub ahead of print | PMID: 38240198
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<div><h4>Identification of Fatigue Subtypes and Their Correlates in Prevalent Heart Failure: A Secondary Analysis of the Atherosclerosis Risk in Communities Study.</h4><i>Pavlovic N, Ndumele CE, Abshire Saylor M, Szanton SL, ... Himmelfarb C, Leoutsakos JM</i><br /><b>Background</b><br />Among patients with heart failure (HF), fatigue is common and linked to quality of life and functional status. Fatigue is hypothesized to manifest as multiple types, with general and exertional components. Unique subtypes of fatigue in HF may require differential assessment and treatment to improve outcomes. We conducted this study to identify fatigue subtypes in persons with prevalent HF in the ARIC study (Atherosclerosis Risk in Communities) and describe the distribution of characteristics across subtypes.<br /><b>Methods</b><br />We performed a cross-sectional analysis of 1065 participants with prevalent HF at ARIC visit 5 (2011-2013). We measured exertional fatigue using the Modified Medical Research Council Breathlessness scale and general fatigue using the Patient Reported Outcomes Measurement Information System fatigue scale. We used latent class analysis to identify subtypes of fatigue. Number of classes was determined using model fit statistics, and classes were interpreted and assigned fatigue severity rating based on the conditional probability of endorsing survey items given class. We compared characteristics across classes using multinomial regression.<br /><b>Results</b><br />Overall, participants were 54% female and 38% Black with a mean age of 77. We identified 4 latent classes (fatigue subtypes): (1) high general/high exertional fatigue (18%), (2) high general/low exertional fatigue (27%), (3) moderate general/moderate exertional fatigue (20%), and (4) low/no general and exertional fatigue (35%). Female sex, Black race, lower education level, higher body mass index, increased depressive symptoms, and higher prevalence of diabetes were associated with higher levels of general and exertional fatigue.<br /><b>Conclusions</b><br />We identified unique subtypes of fatigue in patients with HF who have not been previously described. Within subtype, general and exertional fatigue were mostly concordant in severity, and exertional fatigue only occurred in conjunction with general fatigue, not alone. Further understanding these fatigue types and their relationships to outcomes may enhance our understanding of the symptom experience and inform prognostication and secondary prevention efforts for persons with HF.<br /><br /><br /><br /><small>Circ Cardiovasc Qual Outcomes: 19 Jan 2024:e010115; epub ahead of print</small></div>
Pavlovic N, Ndumele CE, Abshire Saylor M, Szanton SL, ... Himmelfarb C, Leoutsakos JM
Circ Cardiovasc Qual Outcomes: 19 Jan 2024:e010115; epub ahead of print | PMID: 38240158
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<div><h4>Safety and Efficacy of Combining Left Atrial Appendage Occlusion With Another Cardiac Procedure.</h4><i>Ismayl M, Ahmed H, Freeman JV, Alkhouli M, Lakkireddy D, Goldsweig AM</i><br /><b>Background</b><br />Clinical outcomes of left atrial appendage occlusion (LAAO) combined with other cardiac procedures have not been previously examined.<br /><b>Objectives</b><br />This study sought to evaluate the safety and efficacy of combining LAAO with other cardiac procedures vs isolated LAAO.<br /><b>Methods</b><br />We conducted a retrospective cohort study using the 2016 to 2020 National Inpatient Sample database to compare patients undergoing LAAO combined with another cardiac procedure vs isolated LAAO. Outcomes included risk-adjusted major adverse cardiovascular events (MACEs), in-hospital mortality, major complications, length of stay (LOS), and total costs.<br /><b>Results</b><br />The total cohort included 88,910 weighted encounters, of which 1,225 (1.4%) involved concomitant cardiac procedures. After risk adjustment, patients in the concomitant procedure group had similar odds of MACEs (adjusted OR: 1.82; 95% CI: 0.94-2.74); in-hospital mortality; and complications including stroke, acute kidney injury, major bleeding, blood transfusion, and vascular injury. They also had similar LOS (1 day vs 1 day; P = 0.32) and higher costs ($44,723 vs $32,364; P < 0.01) compared with isolated LAAO but shorter LOS (1 day vs 2 days; P < 0.01) and lower costs ($51,552 vs $63,170; P = 0.04) compared with LAAO with sequential procedures. In subgroup analyses, concomitant atrial fibrillation/atrial flutter ablation had higher adjusted odds of heart block (P < 0.01), and concomitant transcatheter aortic valve replacement had higher adjusted odds of stroke (P = 0.02) and vascular injury (P < 0.01).<br /><b>Conclusions</b><br />In this retrospective observational study, combining LAAO with another cardiac intervention appeared to be associated with similar MACEs and LOS. However, certain complications appeared to be more frequent, and the cost was higher with combined procedures.<br /><br />Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.<br /><br /><small>JACC Cardiovasc Interv: 22 Jan 2024; 17:262-273</small></div>
Ismayl M, Ahmed H, Freeman JV, Alkhouli M, Lakkireddy D, Goldsweig AM
JACC Cardiovasc Interv: 22 Jan 2024; 17:262-273 | PMID: 38267141
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<div><h4>The spectrum of post-myocardial infarction care: From acute ischemia to heart failure.</h4><i>Akhtar KH, Khan MS, Baron SJ, Zieroth S, ... Butler J, Fudim M</i><br /><AbstractText>Heart failure (HF) is the leading cause of mortality in patients with acute myocardial infarction (AMI), with incidence ranging from 14% to 36% in patients admitted due to AMI. HF post-MI develops due to complex inter-play between macrovascular obstruction, microvascular dysfunction, myocardial stunning and remodeling, inflammation, and neuro-hormonal activation. Cardiogenic shock is an extreme presentation of HF post-MI and is associated with a high mortality. Early revascularization is the only therapy shown to improve survival in patients with cardiogenic shock. Treatment of HF post-MI requires prompt recognition and timely introduction of guideline-directed therapies to improve mortality and morbidity. This article aims to provide an up-to-date review on the incidence and pathogenesis of HF post-MI, current strategies to prevent and treat onset of HF post-MI, promising therapeutic strategies, and knowledge gaps in the field.</AbstractText><br /><br />Copyright © 2024. Published by Elsevier Inc.<br /><br /><small>Prog Cardiovasc Dis: 17 Jan 2024; epub ahead of print</small></div>
Akhtar KH, Khan MS, Baron SJ, Zieroth S, ... Butler J, Fudim M
Prog Cardiovasc Dis: 17 Jan 2024; epub ahead of print | PMID: 38242191
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<div><h4>Role of Cerebral Embolic Protection Devices in Patients Undergoing Transcatheter Aortic Valve Replacement: An Updated Meta-Analysis.</h4><i>Kaur A, Dhaliwal AS, Sohal S, Gwon Y, ... Basman C, Tamis-Holland J</i><br /><b>Background</b><br />Cerebral embolic protection devices (CEPD) capture embolic material in an attempt to reduce ischemic brain injury during transcatheter aortic valve replacement. Prior reports have indicated mixed results regarding the benefits of these devices. With new data emerging, we performed an updated meta-analysis examining the effect of CEPD during transcatheter aortic valve replacement on various clinical, neurological, and safety parameters.<br /><b>Methods and results</b><br />A comprehensive review of electronic databases was performed comparing CEPD and no-CEPD in transcatheter aortic valve replacement. Primary clinical outcome was all-cause stroke. Secondary clinical outcomes were disabling stroke and all-cause mortality. Neurological outcomes included worsening of the National Institutes of Health Stroke Scale score, Montreal Cognitive Assessment score from baseline at discharge, presence of new ischemic lesions, and total lesion volume on neuroimaging. Safety outcomes included major or minor vascular complications and stage 2 or 3 acute kidney injury. Seven randomized controlled trials with 4016 patients met the inclusion criteria. There was no statistically significant difference in the primary clinical outcome of all-cause stroke; secondary clinical outcomes of disabling stroke, all-cause mortality, neurological outcomes of National Institutes of Health Stroke Scale score worsening, Montreal Cognitive Assessment worsening, presence of new ischemic lesions, or total lesion volume on diffusion-weighted magnetic resonance imaging between CEPD versus control groups. There was no statistically significant difference in major or minor vascular complications or stage 2 or 3 acute kidney injury between the groups.<br /><b>Conclusions</b><br />The use of CEPD in transcatheter aortic valve replacement was not associated with a statistically significant reduction in the risk of clinical, neurological, and safety outcomes.<br /><br /><br /><br /><small>J Am Heart Assoc: 19 Jan 2024:e030587; epub ahead of print</small></div>
Kaur A, Dhaliwal AS, Sohal S, Gwon Y, ... Basman C, Tamis-Holland J
J Am Heart Assoc: 19 Jan 2024:e030587; epub ahead of print | PMID: 38240252
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<div><h4>Administrative Model for Profiling Hospital Performance on Coronary Artery Bypass Graft Surgery: Based on the Chinese Hospital Quality Monitoring System.</h4><i>Su X, Zhang D, Gu D, Rao C, ... Fan J, Zheng Z</i><br /><b>Background</b><br />We aimed to develop an administrative model to profile the performance on the outcomes of coronary artery bypass grafting across hospitals in China.<br /><b>Methods and results</b><br />This retrospective study was based on the Chinese Hospital Quality Monitoring System (HQMS) from 2016 to 2020. The coronary artery bypass grafting cases were identified by procedure code, and those of 2016 to 2017 were randomly divided into modeling and validation cohorts, while those in other years were used to ensure the model stability across years. The outcome was discharge status as \"death or withdrawal,\" and that withdrawal referred to discharge without medical advice when patients were in the terminal stage but reluctant to die in the hospital. Candidate covariates were mainly identified by diagnoses or procedures codes. Patient-level logistic models and hospital-level hierarchical models were established. A total of 203 010 coronary artery bypass grafts in 699 hospitals were included, with 60 704 and 20 233 cases in the modeling and validation cohorts and 40 423, 42 698, and 38 952 in the years 2018, 2019, and 2020, respectively. The death or withdrawal rate was 3.4%. The areas under the curve were 0.746 and 0.729 in the patient-level models of modeling and validation cohorts, respectively, with good calibration and stability across years. Hospital-specific risk-standardized death or withdrawal rates were 2.61% (interquartile range, 1.87%-3.99%) and 2.63% (interquartile range, 1.97%-3.44%) in the modeling and validation cohorts, which were highly correlated (correlation coefficient, 0.96; <i>P</i><0.001). Between-hospital variations were distinguished among hospitals of different volumes and across years.<br /><b>Conclusions</b><br />The administrative model based on Hospital Quality Monitoring System could profile hospital performance on coronary artery bypass grafting in China.<br /><br /><br /><br /><small>J Am Heart Assoc: 19 Jan 2024:e031924; epub ahead of print</small></div>
Su X, Zhang D, Gu D, Rao C, ... Fan J, Zheng Z
J Am Heart Assoc: 19 Jan 2024:e031924; epub ahead of print | PMID: 38240224
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<div><h4>Impact of High Lipoprotein(a) on Long-Term Survival Following Coronary Artery Bypass Grafting.</h4><i>Yuan S, Li F, Zhang H, Zeng J, ... Zhao Y, Zheng Z</i><br /><b>Background</b><br />Lipoprotein(a) is a possible causal risk factor for atherosclerosis and related complications. The distribution and prognostic implication of lipoprotein(a) in patients undergoing coronary artery bypass grafting remain unknown. This study aimed to assess the impact of high lipoprotein(a) on the long-term prognosis of patients undergoing coronary artery bypass grafting.<br /><b>Methods and results</b><br />Consecutive patients with stable coronary artery disease who underwent isolated coronary artery bypass grafting from January 2013 to December 2018 from a single-center cohort were included. The primary outcome was all-cause death. The secondary outcome was a composite of major adverse cardiovascular and cerebrovascular events. Of the 18 544 patients, 4072 (22.0%) were identified as the high-lipoprotein(a) group (≥50 mg/dL). During a median follow-up of 3.2 years, primary outcomes occurred in 587 patients. High lipoprotein(a) was associated with increased risk of all-cause death (high lipoprotein(a) versus low lipoprotein(a): adjusted hazard ratio [aHR], 1.31 [95% CI, 1.09-1.59]; <i>P</i>=0.005; lipoprotein(a) per 1-mg/dL increase: aHR, 1.003 [95% CI, 1.001-1.006]; <i>P</i>=0.011) and major adverse cardiovascular and cerebrovascular events (high lipoprotein(a) versus low lipoprotein(a): aHR, 1.18 [95% CI, 1.06-1.33]; <i>P</i>=0.004; lipoprotein(a) per 1-mg/dL increase: aHR, 1.002 [95% CI, 1.001-1.004]; <i>P</i>=0.002). The lipoprotein(a)-related risk was greater in patients with European System for Cardiac Operative Risk Evaluation <3, and tended to attenuate in patients receiving arterial grafts.<br /><b>Conclusions</b><br />More than 1 in 5 patients with stable coronary artery disease who underwent coronary artery bypass grafting were exposed to high lipoprotein(a), which is associated with higher risks of death and major adverse cardiovascular and cerebrovascular events. The adverse effects of lipoprotein(a) were more pronounced in patients with clinically low-risk profiles or not receiving arterial grafts.<br /><br /><br /><br /><small>J Am Heart Assoc: 19 Jan 2024:e031322; epub ahead of print</small></div>
Yuan S, Li F, Zhang H, Zeng J, ... Zhao Y, Zheng Z
J Am Heart Assoc: 19 Jan 2024:e031322; epub ahead of print | PMID: 38240214
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<div><h4>Long-Term Results Of Atrial Fibrillation Surgery Concomitant With Mitral Valve Surgery: A Propensity Score-Matched Multicenter Study.</h4><i>Kim MS, Kim HJ, Je HG, Cho YH, ... Lee S, Lee SH</i><br /><b>Objective</b><br />The aim of the study was to elucidate the long-term outcomes of atrial fibrillation (AF) surgery in AF patients with mitral valve (MV) disease and AF, by comparing the patients who underwent MV surgery with and without AF surgery.<br /><b>Methods</b><br />Between 2005 and 2017, 2680 patients with AF who underwent MV surgery (MV surgery with AF surgery, n=1841; MV surgery without AF surgery, n=839) at 5 centers were included. After propensity score-matching, 1442 patients were extracted (AF surgery group, n=721; non-AF surgery group, n=721). All-cause mortality, cardiac mortality, major adverse cardiac and cerebrovascular events (MACCE), stroke or transient ischemic attack (TIA), and permanent pacemaker implantation were compared between the AF surgery and non-AF surgery groups.<br /><b>Results</b><br />Overall survival rates at 5 and 10 years postoperatively were 91.0% and 80.7% in the AF surgery group, and 86.5% and 75.9% in the non-AF surgery group, respectively (P=0.013). Cardiac-mortality free survival rates at 5 and 10 years postoperatively were 96.9% and 91.7% in the AF surgery group and 90.9% and 83.7% in the non-AF surgery group, respectively(P<0.001). Cumulative incidence of reoperation, MACCE, and stroke or TIA were lower in the matched AF surgery group compared with the matched non-AF surgery group up to 15 years postoperatively(P=0.010, P<0.001, and P=0.012, respectively). Cumulative incidence of permanent pacemaker implantation was higher in the matched AF surgery group, compared with the matched non-AF surgery group(P<0.001).<br /><b>Conclusions</b><br />In AF patients with MV disease, MV surgery concomitant with AF surgery was associated with lower mortality, cardiac mortality, MACCE, and stroke or TIA up to 15 years after surgery when compared with MV surgery without AF surgery.<br /><br />Copyright © 2024. Published by Elsevier Inc.<br /><br /><small>J Thorac Cardiovasc Surg: 16 Jan 2024; epub ahead of print</small></div>
Kim MS, Kim HJ, Je HG, Cho YH, ... Lee S, Lee SH
J Thorac Cardiovasc Surg: 16 Jan 2024; epub ahead of print | PMID: 38237763
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<div><h4>Mixed aortic valve disease: Association with paravalvular leak and reduced survival after TAVR.</h4><i>Demirel C, Winter MP, Nitsche C, Koschatko S, ... Hengstenberg C, Bartko PE</i><br /><b>Background</b><br />Transcatheter aortic valve replacement (TAVR) revolutionized the therapy of severe aortic stenosis (AS) with rising numbers. Mixed aortic valve disease (MAVD) treated by TAVR is gaining more interest, as those patients represent a more complex cohort as compared to isolated AS. However, concerning long-term outcome for this cohort only limited data is available.<br /><b>Aims</b><br />To assess the prevalence of MAVD in TAVR patients, investigate its association with paravalvular regurgitation (PVR), and analyse its impact on long-term mortality after TAVR.<br /><b>Methods</b><br />We conducted a registry-based cohort study using the Vienna TAVR registry, enrolling patients who underwent TAVR at Medical University of Vienna between 01/2007 and 05/2020 with available TTE before and after TAVR (n=880). Data analysis included PVR incidence and long-term survival outcomes.<br /><b>Results</b><br />647 (73.52%) out of 880 patients had > mild AR next to severe AS. MAVD was associated with PVR compared to isolated AS with an OR of 2.06, 95% CI: 1.51- 2.81; p= <0.001. More than mild PVR after TAVR, (n168 out of 880 = 19.09%) was related to higher mortality compared to absence of PVR with a HR of 1.33, 95% CI: 1.05- 1.67; p= 0.016. MAVD patients developing ≥ mild PVR after TAVR was also associated with higher mortality compared to absence of PVR with HR of 1.30 and 95% CI: 1.04-1.62; p= 0.022.<br /><br /><b>Conclusions:</b><br/>and relevance</b><br />MAVD is prevalent among TAVR patients and presents unique challenges, with increased PVR risk and worse outcomes compared to isolated AS. Long-term survival for MAVD patients, not limited to those developing PVR post TAVR is compromised. Earlier intervention before the occurrence of structural myocardial damage or surgical valve replacement might be a potential workaround to improve outcomes.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Eur Heart J Cardiovasc Imaging: 17 Jan 2024; epub ahead of print</small></div>
Demirel C, Winter MP, Nitsche C, Koschatko S, ... Hengstenberg C, Bartko PE
Eur Heart J Cardiovasc Imaging: 17 Jan 2024; epub ahead of print | PMID: 38236149
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<div><h4>Prioritizing the primary prevention of heart failure: Measuring, modifying and monitoring risk.</h4><i>Patel R, Peesay T, Krishnan V, Wilcox J, Wilsbacher L, Khan SS</i><br /><AbstractText>With the rising incidence of heart failure (HF) and increasing burden of morbidity, mortality, and healthcare expenditures, primary prevention of HF targeting individuals in at-risk HF (Stage A) and pre-HF (Stage B) Stages has become increasingly important with the goal to decrease progression to symptomatic (Stage C) HF. Identification of risk based on traditional risk factors (e.g., cardiovascular health which can be assessed with the American Heart Association\'s Life\'s Essential 8 framework), adverse social determinants of health, inherited risk of cardiomyopathies, and identification of risk-enhancing factors, such as patients with viral disease, exposure to cardiotoxic chemotherapy, and history of adverse pregnancy outcomes should be the first step in evaluation for HF risk. Next, use of guideline-endorsed risk prediction tools such as Pooled Cohort Equations to Prevent Heart Failure provide quantification of absolute risk of HF based in traditional risk factors. Risk reduction through counseling on traditional risk factors is a core focus of implementation of prevention and may include the use of novel therapeutics that target specific pathways to reduce risk of HF, such as mineralocorticoid receptor agonists (e.g., fineronone), angiotensin-receptor/neprolysin inhibitors, and sodium glucose co-transporter-2 inhibitors. These interventions may be limited in at-risk populations who experience adverse social determinants and/or individuals who reside in rural areas. Thus, strategies like telemedicine may improve access to preventive care. Gaps in the current knowledge base for risk-based prevention of HF are highlighted to outline future research that may target approaches for risk assessment and risk-based prevention with the use of artificial intelligence, genomics-enhanced strategies, and pragmatic trials to develop a guideline-directed medical therapy approach to reduce risk among individuals with Stage A and Stage B HF.</AbstractText><br /><br />Copyright © 2024. Published by Elsevier Inc.<br /><br /><small>Prog Cardiovasc Dis: 23 Jan 2024; epub ahead of print</small></div>
Patel R, Peesay T, Krishnan V, Wilcox J, Wilsbacher L, Khan SS
Prog Cardiovasc Dis: 23 Jan 2024; epub ahead of print | PMID: 38272339
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<div><h4>The relationship between triglyceride-glucose index and prospective key clinical outcomes in patients hospitalised for coronary artery disease.</h4><i>Hao B, Lyu L, Xu J, Zhu X, ... Yang Y, Liu H</i><br /><b>Background</b><br />The triglyceride-glucose (TyG) index is regarded as a dependable alternative for assessing insulin resistance (IR), given its simplicity, cost-effectiveness, and strong correlation with IR. The relationship between the TyG index and adverse outcomes in patients with coronary heart disease (CHD) is not well established. This study examines the association of the TyG index with long-term adverse outcomes in hospitalized CHD patients.<br /><b>Methods</b><br />In this single-center prospective cohort study, 3321 patients hospitalized with CHD were included. Multivariate Cox regression models were employed to assess the associations between the TyG index and the incidence of all-cause mortality and major adverse cardiovascular events (MACEs). To examine potential nonlinear associations, restricted cubic splines and threshold analysis were utilized.<br /><b>Results</b><br />During a follow-up period of 9.4 years, 759 patients (22.9%) succumbed to mortality, while 1291 (38.9%) experienced MACEs. Threshold analysis demonstrated a significant \"U\"-shaped nonlinear relationship with MACEs, with different hazard ratios observed below and above a TyG index of 8.62 (below: HR 0.71, 95% CI 0.50-0.99; above: HR 1.28, 95% CI 1.10-1.48). Notably, an increased risk of all-cause mortality was observed only when the TyG index exceeded 8.77 (HR 1.53, 95% CI 1.19-1.96).<br /><b>Conclusions</b><br />This study reveals a nonlinear association between the TyG index and both all-cause mortality and MACEs in hospitalized CHD patients with CHD. Assessing the TyG index, particularly focusing on individuals with extremely low or high TyG index values, may enhance risk stratification for adverse outcomes in this patient population.<br /><br />© 2024. The Author(s).<br /><br /><small>Cardiovasc Diabetol: 22 Jan 2024; 23:40</small></div>
Hao B, Lyu L, Xu J, Zhu X, ... Yang Y, Liu H
Cardiovasc Diabetol: 22 Jan 2024; 23:40 | PMID: 38254088
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<div><h4>Clinical and prognostic implications of left ventricular dilatation in heart failure.</h4><i>Kasa G, Teis A, Juncà G, Aimo A, ... Bayés-Genis A, Delgado V</i><br /><b>Aims</b><br />To assess the agreement between left ventricular end-diastolic diameter index (LVEDDi) and volume index (LVEDVi) to define LV dilatation and to investigate the respective prognostic implications in patients with heart failure (HF).<br /><b>Methods and results</b><br />Patients with HF symptoms and LV ejection fraction (LVEF) < 50% undergoing cardiac magnetic resonance (CMR) were evaluated retrospectively. LV dilatation was defined as LVEDDi or LVEDVi above the upper normal limit according to published reference values. Patients were followed-up for the combined endpoint of cardiovascular death or HF hospitalization during 5 years. A total of 564 patients (median age 64 years; 79% men) were included. LVEDDi had a modest correlation with LVEDVi (r = 0.682, p < 0.001). LV dilatation was noted in 84% of patients using LVEDVi-based definition and in 73% using LVEDDi-based definition, whereas 20% of patients displayed discordant definitions of LV dilatation. During a median follow-up of 2.8 years, patients with both dilated LVEDDi and LVEDVi had the highest cumulative event rate (HR 3.00, 95% CI 1.15-7.81, p = 0.024). Both LVEDDi and LVEDVi were independently associated with the primary outcome (hazard ratio 3.29, 95%, p < 0.001 and 2.8, p = 0.009; respectively).<br /><b>Conclusions</b><br />The majority of patients with HF and LVEF < 50% present both increased LVEDDi and LVEDVi whereas 20% show discordant linear and volumetric definitions of LV dilatation. Patients with increased LVEDDi and LVEDVi have the worst clinical outcomes suggesting that the assessment of these two metrics is needed for better risk stratification.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Eur Heart J Cardiovasc Imaging: 21 Jan 2024; epub ahead of print</small></div>
Kasa G, Teis A, Juncà G, Aimo A, ... Bayés-Genis A, Delgado V
Eur Heart J Cardiovasc Imaging: 21 Jan 2024; epub ahead of print | PMID: 38246859
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<div><h4>Limitations of Apical Sparing Pattern in Cardiac Amyloidosis: A Multicenter Echocardiographic Study.</h4><i>Cotella J, Randazzo M, Maurer MS, Helmke S, ... Slivnick JA, Lang RM</i><br /><b>Background</b><br />Although impaired left ventricular (LV) global longitudinal strain (GLS) with apical sparing is a feature of cardiac amyloidosis (CA), its diagnostic accuracy has varied across studies. We aimed to determine the ability of apical sparing ratio (ASR) and most common echocardiographic parameters to differentiate patients with confirmed CA from those with clinical and/or echocardiographic suspicion of CA, but with this diagnosis ruled out.<br /><b>Methods</b><br />We identified 544 patients with confirmed CA and 200 controls as defined above (CTRL Patients). Measurements from transthoracic echocardiograms (TTE) were performed using artificial intelligence software (Us2.AI, Singapore) and audited by an experienced echocardiographer. Receiver-operating characteristic curve analysis was used to evaluate the diagnostic performance and optimal cutoffs for the differentiation of CA patients from CTRL Patients. Additionally, a group of 174 healthy subjects (Healthy CTRL) was included to provide insight on how Patients and Healthy controls differed echocardiographically.<br /><b>Results</b><br />LV GLS was more impaired (-13.9 ± 4.6% vs -15.9 ± 2.7%, p < 0.0005) and ASR was higher (2.4 ± 1.2 vs 1.7 ± 0.9, p < 0.0005) in the CA group vs. CTRL Patients. Relative wall thickness and ASR were the most accurate parameters for differentiating CA from CTRL Patients (AUC: 0.77 and 0.74, respectively). However, even with the optimal cutoff of 1.67, ASR was only 72% sensitive and 66% specific for CA, indicating presence of apical sparing in 32% of CTRL Patients and even in 6% Healthy CTRLs.<br /><b>Conclusions</b><br />Apical sparing did not prove to be a CA-specific biomarker for accurate identification of CA, when compared to clinically similar controls with no CA.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Eur Heart J Cardiovasc Imaging: 18 Jan 2024; epub ahead of print</small></div>
Cotella J, Randazzo M, Maurer MS, Helmke S, ... Slivnick JA, Lang RM
Eur Heart J Cardiovasc Imaging: 18 Jan 2024; epub ahead of print | PMID: 38243591
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<div><h4>Emerging devices for heart failure management.</h4><i>Chouairi F, Levin A, Biegus J, Fudim M</i><br /><AbstractText>There have been significant advances in the treatment of heart failure (HF) in recent years, driven by significant strides in guideline-directed medical therapy (GDMT). Despite this, HF is still associated with high levels of morbidity and mortality, and most patients do not receive optimal medical therapy. In conjunction with the improvement of GDMT, novel device therapies have been developed to better treat HF. These devices include technology capable of remotely monitoring HF physiology, devices that modulate the autonomic nervous system, and those that structurally change the heart with the ultimate aim of addressing the root causes of HF physiology As these device therapies gradually integrate into the fabric of HF patient care, it becomes increasingly important for modern cardiologists to become familiar with them. Hence, the objective of this review is to shed light on currently emerging devices for the treatment of HF.</AbstractText><br /><br />Copyright © 2024. Published by Elsevier Inc.<br /><br /><small>Prog Cardiovasc Dis: 17 Jan 2024; epub ahead of print</small></div>
Chouairi F, Levin A, Biegus J, Fudim M
Prog Cardiovasc Dis: 17 Jan 2024; epub ahead of print | PMID: 38242194
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Abstract
<div><h4>Primary and Secondary Cardiovascular and Kidney Prevention With Canagliflozin: Insights From the CANVAS Program and CREDENCE Trial.</h4><i>Sharma A, Razaghizad A, Joury A, Levin A, ... Perkovic V, Mahaffey KW</i><br /><b>Background</b><br />This study evaluated the effects of canagliflozin in patients with type 2 diabetes with and without prevalent cardiovascular disease (secondary and primary prevention).<br /><b>Methods and results</b><br />This was a pooled participant-level analysis of the CANVAS (Canagliflozin Cardiovascular Assessment Study) Program and CREDENCE (Canagliflozin and Renal Events in Diabetes With Established Nephropathy Clinical Evaluation) trial. The CANVAS Program included participants with type 2 diabetes at elevated cardiovascular risk, whereas the CREDENCE trial included participants with type 2 diabetes and albuminuric chronic kidney disease. Hazard ratios (HRs) with interaction terms were obtained from Cox regression models to estimate relative risk reduction with canagliflozin versus placebo across the primary and secondary prevention groups. We analyzed 5616 (38.9%) and 8804 (61.1%) individuals in the primary and secondary prevention subgroups, respectively. Primary versus secondary prevention participants were on average younger (62.2 versus 63.8 years of age) and more often women (42% versus 31%). Canagliflozin reduced the risk of major adverse cardiovascular events (HR, 0.84 [95% CI, 0.76-0.94]) consistently across primary and secondary prevention subgroups (<i>P</i><sub>interaction</sub>=0.86). Similarly, no treatment effect heterogeneity was observed with canagliflozin for hospitalization for heart failure, cardiovascular death, end-stage kidney disease, or all-cause mortality (all <i>P</i><sub>interaction</sub>>0.5).<br /><b>Conclusions</b><br />Canagliflozin reduced cardiovascular and kidney outcomes with no statistical evidence of heterogeneity for the treatment effect across the primary and secondary prevention subgroups in the CANVAS Program and CREDENCE trial. Although studies on the optimal implementation of canagliflozin within these populations are warranted, these results reinforce canagliflozin\'s role in cardiorenal prevention and treatment in individuals with type 2 diabetes.<br /><b>Registration</b><br />URL: https://www.clinicaltrials.gov; Unique identifiers: NCT01032629, NCT01989754, NCT02065791.<br /><br /><br /><br /><small>J Am Heart Assoc: 19 Jan 2024:e031586; epub ahead of print</small></div>
Sharma A, Razaghizad A, Joury A, Levin A, ... Perkovic V, Mahaffey KW
J Am Heart Assoc: 19 Jan 2024:e031586; epub ahead of print | PMID: 38240199
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<div><h4>High-Sensitivity C-Reactive Protein Is Associated With Heart Failure Hospitalization in Patients With Metabolic Dysfunction-Associated Fatty Liver Disease and Normal Left Ventricular Ejection Fraction Undergoing Coronary Angiography.</h4><i>Zhou XD, Chen QF, Targher G, Byrne CD, ... Lip GYH, Zheng MH</i><br /><b>Background</b><br />Systemic chronic inflammation plays a role in the pathophysiology of both heart failure with preserved ejection fraction (HFpEF) and metabolic dysfunction-associated fatty liver disease. This study aimed to investigate whether serum hs-CRP (high-sensitivity C-reactive protein) levels were associated with the future risk of heart failure (HF) hospitalization in patients with metabolic dysfunction-associated fatty liver disease and a normal left ventricular ejection fraction.<br /><b>Methods and results</b><br />The study enrolled consecutive individuals with metabolic dysfunction-associated fatty liver disease and normal left ventricular ejection fraction who underwent coronary angiography for suspected coronary heart disease. The study population was subdivided into non-HF, pre-HFpEF, and HFpEF groups at baseline. The study outcome was time to the first hospitalization for HF. In 10 019 middle-aged individuals (mean age, 63.3±10.6 years; 38.5% women), the prevalence rates of HFpEF and pre-HFpEF were 34.2% and 34.5%, with a median serum hs-CRP level of 4.5 mg/L (interquartile range, 1.9-10 mg/L) and 5.0 mg/L (interquartile range, 2.1-10.1 mg/L), respectively. Serum hs-CRP levels were significantly higher in the pre-HFpEF and HFpEF groups than in the non-HF group. HF hospitalizations occurred in 1942 (19.4%) patients over a median of 3.2 years, with rates of 3.7% in non-HF, 20.8% in pre-HFpEF, and 32.1% in HFpEF, respectively. Cox regression analyses showed that patients in the highest hs-CRP quartile had a ≈4.5-fold increased risk of being hospitalized for HF compared with those in the lowest hs-CRP quartile (adjusted-hazard ratio, 4.42 [95% CI, 3.72-5.25]).<br /><b>Conclusions</b><br />There was a high prevalence of baseline pre-HFpEF and HFpEF in patients with metabolic dysfunction-associated fatty liver disease and suspected coronary heart disease. There was an increased risk of HF hospitalization in those with elevated hs-CRP levels.<br /><br /><br /><br /><small>J Am Heart Assoc: 19 Jan 2024:e032997; epub ahead of print</small></div>
Abstract
<div><h4>Association of Dysglycaemia with Persistent Infarct Core Iron in Patients with Acute ST-Segment Elevation Myocardial Infarction.</h4><i>Lechner I, Reindl M, Oberhollenzer F, Tiller C, ... Metzler B, Reinstadler SJ</i><br /><b>Background</b><br />Dysglycaemia increases the risk of myocardial infarction and subsequent recurrent cardiovascular events. However, the role of dysglycaemia in ischemia/reperfusion injury with development of irreversible myocardial tissue alterations remains poorly understood. In this study we aimed to investigate the association of ongoing dysglycaemia with persistence of infarct core iron and their longitudinal changes over time in patients undergoing primary percutaneous coronary intervention (PCI) for acute ST-segment elevation myocardial infarction (STEMI).<br /><b>Methods</b><br />We analyzed 348 STEMI patients treated with primary PCI between 2016 and 2021 that were included in the prospective MARINA-STEMI study (NCT04113356). Peripheral venous blood samples for glucose and glycated hemoglobin (HbA1c) measurements were drawn on admission and 4 months after STEMI. Cardiac magnetic resonance (CMR) imaging including T2* mapping for infarct core iron assessment was performed at both time points. Associations of dysglycaemia with persistent infarct core iron and iron resolution at 4 months were calculated using multivariable regression analysis.<br /><b>Results</b><br />Intramyocardial hemorrhage was observed in 147 (42%) patients at baseline. Of these, 89 (61%) had persistent infarct core iron 4 months after infarction with increasing rates across HbA1c levels (<5.7%: 33%, ≥5.7: 79%). Persistent infarct core iron was independently associated with ongoing dysglycaemia defined by HbA1c at 4 months (OR: 7.87 [95% CI: 2.60-23.78]; p<0.001), after adjustment for patient characteristics and CMR parameters. The independent association was present even after exclusion of patients with diabetes (pre- and newly diagnosed, n=16).<br /><b>Conclusions</b><br />In STEMI patients treated with primary PCI, ongoing dysglycaemia defined by HbA1c is independently associated with persistent infarct core iron and a lower likelihood of iron resolution. These findings suggest a potential association between ongoing dysglycaemia and persistent infarct core iron, which warrants further investigation for therapeutic implications.<br /><br />Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.<br /><br /><small>J Cardiovasc Magn Reson: 16 Jan 2024:100996; epub ahead of print</small></div>
Lechner I, Reindl M, Oberhollenzer F, Tiller C, ... Metzler B, Reinstadler SJ
J Cardiovasc Magn Reson: 16 Jan 2024:100996; epub ahead of print | PMID: 38237898
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<div><h4>Sex-based Differences in the Phenotypic Expression and Prognosis of Idiopathic Non-ischemic Cardiomyopathy: A Cardiovascular Magnetic Resonance Study.</h4><i>Mallabone M, Labib D, Abdelhaleem A, Dykstra S, ... Fine NM, White JA</i><br /><b>Aims</b><br />We sought to characterize sex-related differences in CMR-based cardiovascular phenotypes and prognosis in patients with idiopathic non-ischemic cardiomyopathy (NICM).<br /><b>Methods and results</b><br />Patients with NICM enrolled in the Cardiovascular Imaging Registry of Calgary (CIROC) between 2015 and 2021 were identified. Z-score values for chamber volumes and function were calculated as standard deviation from mean values of 157 sex-matched healthy volunteers, ensuring reported differences were independent of known sex-dependencies. Patients were followed for the composite outcome of all-cause mortality, heart failure admission, or ventricular arrhythmia.A total of 747 patients were studied, 531 (71%) males. By Z-score values, females showed significantly higher left ventricular (LV) ejection fraction (EF; median difference 1 SD) and right ventricular (RV) EF (difference 0.6 SD) with greater LV mass (difference 2.1 SD; p-value<0.01 for all) versus males despite similar chamber volumes. Females had a significantly lower prevalence of mid-wall striae (MWS) fibrosis (23% versus 36%; p-value<0.001). Over a median follow-up of 4.7 years, 173 patients (23%) developed the composite outcome, with equal distribution in males and females. LV EF and MWS were significant independent predictors of the outcome (respective HR [95% CI] 0.97 [0.95-0.99] and 1.6 [1.2-2.3]; p-value=0.003 and 0.005). There was no association of sex with the outcome.<br /><b>Conclusions</b><br />In a large contemporary cohort, NICM was uniquely expressed in females versus males. Despite similar chamber dilation, females demonstrated greater concentric remodelling, lower reductions in bi-ventricular function, and a lower burden of replacement fibrosis. Overall, their prognosis remained similar to male patients with NICM.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Eur Heart J Cardiovasc Imaging: 17 Jan 2024; epub ahead of print</small></div>
Mallabone M, Labib D, Abdelhaleem A, Dykstra S, ... Fine NM, White JA
Eur Heart J Cardiovasc Imaging: 17 Jan 2024; epub ahead of print | PMID: 38236156
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<div><h4>Usage of Older Donors is Associated with Higher Mortality After Heart Transplantation: A UNOS Observational Study.</h4><i>Jaiswal A, Kittleson M, Pillai A, Baran D, Baker WL</i><br /><b>Introduction</b><br />Utilization of heart from older donors is variable across centers with uncertain outcomes of recipients. We sought to utilize a national registry to examine usage and outcomes of heart transplant recipients from older donors. We also explored the impact of current donor heart allocation scheme on outcomes of hearts from older donors.<br /><b>Methods</b><br />This observational study utilized the United Network for Organ Sharing database between 2015 and 2023 with donors categorized into age < 45 years or ≥ 45 years and evaluated organ disposition and geographical variation. 30-day, 1- and 3- year mortality, and graft failure rates were compared amongst recipients as per donor age group. We also evaluated annual trends in HT for each group over the follow-up period.<br /><b>Results</b><br />24,966 adult donors were recovered: 3,742 (15.0%) were ≥ 45 years; 3,349 (15.6%) adults received heart from such donors with significant geographical variation, and a declining utilization in the transplantation rate in current donor allocation system. Donors with age ≥ 45 years had higher comorbidities and were allotted with a significantly shorter ischemic time to recipients who were significantly less likely to receive temporary mechanical circulatory support and more likely female. Unadjusted and adjusted, 30-day mortality were similar but 1- and 3-year mortality and graft failure rates were significantly higher in recipients of such donors. spline analysis suggested a higher 1-year mortality risk at older donor age with risk increasing after age 40 years.<br /><b>Conclusions</b><br />Older donor age was associated with worsened 1- and 3-year mortality and graft failure for heart transplant recipients.<br /><br />Copyright © 2024. Published by Elsevier Inc.<br /><br /><small>J Heart Lung Transplant: 15 Jan 2024; epub ahead of print</small></div>
Jaiswal A, Kittleson M, Pillai A, Baran D, Baker WL
J Heart Lung Transplant: 15 Jan 2024; epub ahead of print | PMID: 38232792
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<div><h4>Acute Response of the Noninfarcted Myocardium and Surrounding Tissue Assessed by T2 Mapping After STEMI.</h4><i>Bergamaschi L, Landi A, Maurizi N, Pizzi C, ... Valgimigli M, Pavon AG</i><br /><b>Background</b><br />ST-segment elevation myocardial infarction (STEMI) is associated with a systemic and local inflammatory response with edema. However, their role at the tissue level is poorly characterized.<br /><b>Objectives</b><br />This study aims to characterize T2 values of the noninfarcted myocardium (NIM) and surrounding tissue and to investigate prognostic relevance of higher NIM T2 values after STEMI.<br /><b>Methods</b><br />A total of 171 consecutive patients with STEMI without prior cardiovascular events who underwent cardiac magnetic resonance after primary percutaneous coronary intervention were analyzed in terms of standard infarct characteristics. Edema of the NIM, liver, spleen, and pectoralis muscle was assessed based on T2 mapping. Follow-up was available for 130 patients. The primary endpoint was major adverse cardiac events (MACE), defined as cardiovascular death, myocardial infarction, unplanned coronary revascularization or rehospitalization for heart failure. The median time from primary percutaneous coronary intervention to cardiac magnetic resonance was 3 days (IQR: 2-5 days).<br /><b>Results</b><br />Higher (above the median value of 45 ms) T2 values in the NIM area were associated with larger infarct size, microvascular obstruction, and left ventricular dysfunction and did not correlate with C-reactive protein, white blood cells, or T2 values of the pectoralis muscle, liver, and spleen. At a median follow-up of 17 months, patients with higher (>45 ms) NIM T2 values had increased risk of MACE (P < 0.001) compared with subjects with NIM T2 values ≤45 ms, mainly caused by a higher rate of myocardial reinfarction (26.3% vs 1.4%; P < 0.001). At multivariable analysis, higher NIM T2 values independently predicted MACE (HR: 2.824 [95% CI: 1.254-6.361]; P = 0.012).<br /><b>Conclusions</b><br />Higher NIM T2 values after STEMI are independently associated with worse cardiovascular outcomes, mainly because of higher risk of myocardial infarction.<br /><br />Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.<br /><br /><small>JACC Cardiovasc Imaging: 24 Jan 2024; epub ahead of print</small></div>
Bergamaschi L, Landi A, Maurizi N, Pizzi C, ... Valgimigli M, Pavon AG
JACC Cardiovasc Imaging: 24 Jan 2024; epub ahead of print | PMID: 38276932
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<div><h4>Transcatheter Pulmonary Valve Replacement With Balloon-Expandable Valves: Utilization and Procedural Outcomes From the IMPACT Registry.</h4><i>Stefanescu Schmidt AC, Armstrong AK, Aboulhosn JA, Kennedy KF, ... McElhinney DB, Bhatt AB</i><br /><b>Background</b><br />Transcatheter pulmonary valve replacement (TPVR) has expanded and evolved since its initial commercial approval in the United States in 2010.<br /><b>Objectives</b><br />This study sought to characterize real-world practice, including patient selection, procedural outcomes, complications, and off-label usage.<br /><b>Methods</b><br />Characteristics and outcomes for patients undergoing balloon-expandable TPVR were collected from the American College of Cardiology National Cardiovascular Data Registry IMPACT (Improving Pediatric and Adult Congenital Treatment) Registry.<br /><b>Results</b><br />Between April 2016 and March 2021, 4,513 TPVR procedures were performed in patients with a median age of 19 years, 57% with a Melody (Medtronic Inc) and 43% with a SAPIEN (Edwards Lifesciences) valve. Most implanting centers performed <10 cases annually. One-third of transcatheter pulmonary valve implants were into homograft conduits, one-third were into bioprosthetic valves (BPVs), 25% were in native or patched right ventricular outflow tracts (RVOTs), and 6% were into Contegra (Medtronic Inc) conduits. Over the course of the study period, SAPIEN valve use grew from ∼25% to 60%, in large part because of implants in patients with a native/patched RVOT. Acute success was achieved in 95% of patients (95.7% in homografts, 96.2% in BPVs, 94.2% in native RVOTs, and 95.4% in Contegra conduits). Major adverse events occurred in 2.4% of procedures, more commonly in patients with a homograft (2.9%) or native RVOT (3.4%) than a prior BPV (1.4%; P = 0.004).<br /><b>Conclusions</b><br />This study describes novel population data on the use and procedural outcomes of TPVR with balloon-expandable valves. Over time, there has been increasing use of TPVR to treat regurgitant native RVOT anatomy, with the SAPIEN valve more commonly used for this application.<br /><br />Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.<br /><br /><small>JACC Cardiovasc Interv: 22 Jan 2024; 17:231-244</small></div>
Stefanescu Schmidt AC, Armstrong AK, Aboulhosn JA, Kennedy KF, ... McElhinney DB, Bhatt AB
JACC Cardiovasc Interv: 22 Jan 2024; 17:231-244 | PMID: 38267137
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<div><h4>Dapagliflozin and Mode of Death in Heart Failure With Improved Ejection Fraction: A Post Hoc Analysis of the DELIVER Trial.</h4><i>Vardeny O, Desai AS, Jhund PS, Fang JC, ... McMurray JJV, Solomon SD</i><br /><b>Importance</b><br />Heart failure with improved ejection fraction (HFimpEF), defined as prior left ventricular ejection fraction (LVEF) 40% or lower that has increased to greater than 40%, is understudied.<br /><b>Objective</b><br />To examine mode of death and the association of dapagliflozin with reductions in cause-specific death in patients with HFimpEF.<br /><b>Design, setting, and participants</b><br />This was a post hoc analysis from the Dapagliflozin Evaluation to Improve the Lives of Patients With Preserved Ejection Fraction Heart Failure (DELIVER) randomized clinical trial, conducted from August 2018 to December 2020. The trial randomly assigned patients with HF with LVEF greater than 40%, New York Heart Association class II to IV symptoms, and elevated natriuretic peptides to treatment with dapagliflozin (10 mg, once daily) or placebo. The presence of HFimpEF was captured through study case report forms. The primary outcome was a composite of worsening HF events (hospitalization or urgent HF visits) or cardiovascular death. Clinical outcomes were adjudicated by a blinded clinical end points committee. Data were analyzed from May 2022 to August 2023.<br /><b>Intervention</b><br />Dapagliflozin vs placebo.<br /><b>Main outcomes and measures</b><br />The mode of death in relation to HFimpEF status was examined, as well as the association of randomized treatment with cause-specific death in Cox regression models.<br /><b>Results</b><br />Of 1151 patients with HFimpEF in DELIVER, 190 (16.5%) died, compared with 833 patients (16.3%) of 5112 with LVEF consistently greater than 40%. The overall distribution of mode of death was similar in those with HFimpEF compared with those with LVEF consistently greater than 40% (noncardiovascular death: 103 of 190 [54%] vs 428 of 833 [51%]; cardiovascular death: 87 of 190 [46%] vs 405 of 833 [49%], respectively). Most deaths in individuals with HFimpEF were noncardiovascular (103 of 180 [54%]). For cardiovascular deaths, sudden deaths were most common (36 of 190 events [19%]), followed by HF-related (29 of 190 events [15%]). Among patients with HFimpEF, treatment with dapagliflozin was associated with lower rates of cardiovascular death relative to placebo, a difference primarily due to lower rates of sudden death (hazard ratio, 0.38; 95% CI, 0.18-0.79; P for interaction = .01).<br /><br /><b>Conclusions:</b><br/>and relevance</b><br />The findings in this study support current guideline recommendations for use of sodium-glucose transport protein 2 inhibitor therapy, and further suggest that the addition of a sodium-glucose transport protein 2 inhibitor therapy to other guideline-directed medical therapies may help reduce cardiovascular mortality in patients with HFimpEF.<br /><b>Trial registration</b><br />ClinicalTrials.gov Identifier: NCT03619213.<br /><br /><br /><br /><small>JAMA Cardiol: 24 Jan 2024; epub ahead of print</small></div>
Vardeny O, Desai AS, Jhund PS, Fang JC, ... McMurray JJV, Solomon SD
JAMA Cardiol: 24 Jan 2024; epub ahead of print | PMID: 38265835
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<div><h4>Streamlining Randomized Clinical Trials for Device Therapies in Heart Failure: Bayesian Borrowing of External Data.</h4><i>Saville BR, Burkhoff D, Abraham WT</i><br /><b>Background</b><br />The Breakthrough Devices Program of the US Food and Drug Administration has accelerated the development and evaluation of medical devices for patients with heart failure. One such device is the Optimizer Smart System, which the US Food and Drug Administration approved in 2019.<br /><b>Methods and results</b><br />The Optimizer device was evaluated in a pivotal randomized clinical trial (FIX-HF-5C [Confirmatory Randomized Trial Evaluating the Optimizer System]) that leveraged Bayesian borrowing of external data to reduce the sample size and determine therapeutic device benefit versus continued medical therapy. Bayesian borrowing is explained in the context of the FIX-HF-5C trial, including an overview of the statistical methodologies, regulatory considerations, and interpretations of trial results.<br /><b>Conclusions</b><br />The US Food and Drug Administration Breakthrough Devices Program and novel Bayesian statistical methodology accelerated the path to regulatory approval and patient access to a potentially lifesaving device and may serve as a model for future clinical trials.<br /><br /><br /><br /><small>J Am Heart Assoc: 23 Jan 2024:e033255; epub ahead of print</small></div>
Saville BR, Burkhoff D, Abraham WT
J Am Heart Assoc: 23 Jan 2024:e033255; epub ahead of print | PMID: 38258663
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<div><h4>RNA in cardiovascular disease: A new frontier of personalized medicine.</h4><i>Abdul-Rahman T, Lizano-Jubert I, Bliss ZSB, Garg N, ... Gupta R, Lavie CJ</i><br /><AbstractText>Personalized medicine has witnessed remarkable progress with the emergence of RNA therapy, offering new possibilities for the treatment of various diseases, and in particular in the context of cardiovascular disease (CVD). The ability to target the human genome through RNA manipulation offers great potential not only in the treatment of cardiac pathologies but also in their diagnosis and prevention, notably in cases of hyperlipidemia and myocardial infarctions. While only a few RNA-based treatments have entered clinical trials or obtained approval from the US Food and Drug Administration, the growing body of research on this subject is promising. However, the development of RNA therapies faces several challenges that must be overcome. These include the efficient delivery of drugs into cells, the potential for immunogenic responses, and safety. Resolving these obstacles is crucial to advance the development of RNA therapies. This review explores the newest developments in medical studies, treatment plans, and results related to RNA therapies for heart disease. Furthermore, it discusses the exciting possibilities and difficulties in this innovative area of research.</AbstractText><br /><br />Copyright © 2024. Published by Elsevier Inc.<br /><br /><small>Prog Cardiovasc Dis: 20 Jan 2024; epub ahead of print</small></div>
Abdul-Rahman T, Lizano-Jubert I, Bliss ZSB, Garg N, ... Gupta R, Lavie CJ
Prog Cardiovasc Dis: 20 Jan 2024; epub ahead of print | PMID: 38253161
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<div><h4>Impact of Pericoronary Adipose Tissue Attenuation on Periprocedural Myocardial Injury in Patients With Chronic Coronary Syndrome.</h4><i>Yamamoto T, Kawamori H, Toba T, Sasaki S, ... Hirata KI, Otake H</i><br /><b>Background</b><br />Perivascular inflammation contributes to the development of atherosclerosis and microcirculatory dysfunction. Pericoronary adipose tissue (PCAT) attenuation, measured by coronary computed tomography angiography, is a potential indicator of coronary inflammation. However, the relationship between PCAT attenuation, microcirculatory dysfunction, and periprocedural myocardial injury (PMI) remains unclear.<br /><b>Methods and results</b><br />Patients with chronic coronary syndrome who underwent coronary computed tomography angiography before percutaneous coronary intervention were retrospectively identified. PCAT attenuation and adverse plaque characteristics were assessed using coronary computed tomography angiography. The extent of microcirculatory dysfunction was evaluated using the angio-based index of microcirculatory resistance before and after percutaneous coronary intervention. Overall, 125 consecutive patients were included, with 50 experiencing PMI (PMI group) and 75 without PMI (non-PMI group). Multivariable analysis showed that older age, higher angio-based index of microcirculatory resistance, presence of adverse plaque characteristics, and higher lesion-based PCAT attenuation were independently associated with PMI occurrence (odds ratio [OR], 1.07 [95% CI, 1.01-1.13]; <i>P</i>=0.02; OR, 1.06 [95% CI, 1.00-1.12]; <i>P</i>=0.04; OR, 6.62 [95% CI, 2.13-20.6]; <i>P</i>=0.001; and OR, 2.89 [95% CI, 1.63-5.11]; <i>P</i><0.001, respectively). High PCAT attenuation was correlated with microcirculatory dysfunction before and after percutaneous coronary intervention and its exacerbation during percutaneous coronary intervention. Adding lesion-based PCAT attenuation to the presence of adverse plaque characteristics improved the discriminatory and reclassification ability in predicting PMI.<br /><b>Conclusions</b><br />Adding PCAT attenuation at the culprit lesion level to coronary computed tomography angiography-derived adverse plaque characteristics may provide incremental benefit in identifying patients at risk of PMI. Our results highlight the importance of microcirculatory dysfunction in PMI development, particularly in the presence of lesions with high PCAT attenuation.<br /><b>Registration</b><br />URL: https://center6.umin.ac.jp/cgi-open-bin/ctr/ctr_view.cgi?recptno=R000057722; Unique identifier: UMIN000050662.<br /><br /><br /><br /><small>J Am Heart Assoc: 19 Jan 2024:e031209; epub ahead of print</small></div>
Yamamoto T, Kawamori H, Toba T, Sasaki S, ... Hirata KI, Otake H
J Am Heart Assoc: 19 Jan 2024:e031209; epub ahead of print | PMID: 38240235
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<div><h4>Efficacy and Safety of Low-Dose Edoxaban by Body Weight in Very Elderly Patients With Atrial Fibrillation: A Subanalysis of the Randomized ELDERCARE-AF Trial.</h4><i>Akao M, Yamashita T, Fukuzawa M, Hayashi T, Okumura K</i><br /><b>Background</b><br />The ELDERCARE-AF trial showed that low-dose edoxaban benefits elderly patients with nonvalvular atrial fibrillation considered ineligible for standard oral anticoagulants due to high bleeding risk, but whether this applied to patients with extremely low body weight was unclear.<br /><b>Methods and results</b><br />This was a prespecified subanalysis by body weight (≤45, >45 kg) of the phase 3, multicenter, randomized, double-blind, placebo-controlled, event-driven ELDERCARE-AF trial, which compared low-dose edoxaban (15 mg once daily) with placebo in Japanese patients considered ineligible for oral anticoagulants at the recommended therapeutic strength or the approved doses. The primary efficacy and safety end points were stroke or systemic embolism and major bleeding (International Society on Thrombosis and Hemostasis definition), respectively. The ≤45-kg weight group included 374/984 patients (38.0%), and the >45-kg group included 610/984 patients (62.0%). The stroke or systemic embolism rate was lower with edoxaban than placebo in both weight groups (≤45 kg: hazard ratio [HR], 0.36 [95% CI, 0.16-0.80]; >45 kg: HR, 0.31 [95% CI, 0.13-0.73]; interaction <i>P</i>=0.82). Major bleeding incidence was numerically higher with edoxaban than placebo (≤45 kg: HR, 3.05 [95% CI, 0.84-11.11]; >45 kg: HR, 1.40 [95% CI, 0.56-3.48), with no interaction with body weight (interaction <i>P</i>=0.33). All-cause mortality was higher in the ≤45-kg group, with no significant difference between treatment groups.<br /><b>Conclusions</b><br />The benefit of edoxaban 15 mg was consistent in elderly patients with atrial fibrillation and extremely low body weight, though clinicians must remain vigilant about the risk of major bleeding, especially gastrointestinal bleeding.<br /><b>Registration information</b><br />ClinicalTrials.gov. Identifier: NCT02801669.<br /><br /><br /><br /><small>J Am Heart Assoc: 19 Jan 2024:e031506; epub ahead of print</small></div>
Akao M, Yamashita T, Fukuzawa M, Hayashi T, Okumura K
J Am Heart Assoc: 19 Jan 2024:e031506; epub ahead of print | PMID: 38240204
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<div><h4>Artificial Intelligence of Arterial Doppler Waveforms to Predict Major Adverse Outcomes Among Patients Evaluated for Peripheral Artery Disease.</h4><i>McBane RD, Murphree DH, Liedl D, Lopez-Jimenez F, ... Bjarnason H, Wennberg PW</i><br /><b>Background</b><br />Patients with peripheral artery disease are at increased risk for major adverse cardiac events, major adverse limb events, and all-cause death. Developing tools capable of identifying those patients with peripheral artery disease at greatest risk for major adverse events is the first step for outcome prevention. This study aimed to determine whether computer-assisted analysis of a resting Doppler waveform using deep neural networks can accurately identify patients with peripheral artery disease at greatest risk for adverse outcome events.<br /><b>Methods and results</b><br />Consecutive patients (April 1, 2015, to December 31, 2020) undergoing ankle-brachial index testing were included. Patients were randomly allocated to training, validation, and testing subsets (60%/20%/20%). Deep neural networks were trained on resting posterior tibial arterial Doppler waveforms to predict major adverse cardiac events, major adverse limb events, and all-cause death at 5 years. Patients were then analyzed in groups based on the quartiles of each prediction score in the training set. Among 11 384 total patients, 10 437 patients met study inclusion criteria (mean age, 65.8±14.8 years; 40.6% women). The test subset included 2084 patients. During 5 years of follow-up, there were 447 deaths, 585 major adverse cardiac events, and 161 MALE events. After adjusting for age, sex, and Charlson comorbidity index, deep neural network analysis of the posterior tibial artery waveform provided independent prediction of death (hazard ratio [HR], 2.44 [95% CI, 1.78-3.34]), major adverse cardiac events (HR, 1.97 [95% CI, 1.49-2.61]), and major adverse limb events (HR, 11.03 [95% CI, 5.43-22.39]) at 5 years.<br /><b>Conclusions</b><br />An artificial intelligence-enabled analysis of Doppler arterial waveforms enables identification of major adverse outcomes among patients with peripheral artery disease, which may promote early adoption and adherence of risk factor modification.<br /><br /><br /><br /><small>J Am Heart Assoc: 19 Jan 2024:e031880; epub ahead of print</small></div>
McBane RD, Murphree DH, Liedl D, Lopez-Jimenez F, ... Bjarnason H, Wennberg PW
J Am Heart Assoc: 19 Jan 2024:e031880; epub ahead of print | PMID: 38240202
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<div><h4>Rapid three-dimensional quantification of high-intensity plaques from coronary atherosclerosis T-weighted characterization to predict periprocedural myocardial injury.</h4><i>Nakazawa M, Matsumoto H, Li D, Slomka PJ, ... Xie Y, Shinke T</i><br /><b>Background</b><br />High-intensity plaque (HIP) on magnetic resonance imaging (MRI) has been documented as a powerful predictor of periprocedural myocardial injury (PMI) following percutaneous coronary intervention (PCI). Despite the recent proposal of three-dimensional HIP quantification to enhance the predictive capability, the conventional pulse sequence, which necessitates the separate acquisition of anatomical reference images, hinders accurate three-dimensional segmentation along the coronary vasculature. Coronary atherosclerosis T<sub>1</sub>-weighted characterization (CATCH) enables the simultaneous acquisition of inherently coregistered dark-blood plaque and bright-blood coronary artery images. We aimed to develop a novel HIP quantification approach using CATCH and to ascertain its superior predictive performance compared to the conventional two-dimensional assessment based on plaque-to-myocardium signal intensity ratio (PMR).<br /><b>Methods</b><br />In this prospective study, CATCH MRI was conducted before elective stent implantation in 137 lesions from 125 patients. On CATCH images, dedicated software automatically generated tubular three-dimensional volumes of interest on the dark-blood plaque images along the coronary vasculature, based on the precisely matched bright-blood coronary artery images, and subsequently computed PMR and HIP volume (HIP<sub>vol</sub>). Specifically, HIP<sub>vol</sub> was calculated as the volume of voxels with signal intensity exceeding that of the myocardium, weighted by their respective signal intensities. PMI was defined as post-PCI cardiac troponin-T >5× the upper reference limit.<br /><b>Results</b><br />The entire analysis process was completed within 3minutes per lesion. PMI occurred in 44 lesions. Based on the receiver operating characteristic curve analysis, HIP<sub>vol</sub> outperformed PMR for predicting PMI (C-statistics, 0.870 [95% CI, 0.805-0.936] vs. 0.787 [95% CI, 0.706-0.868]; p = 0.001). This result was primarily driven by the higher sensitivity HIP<sub>vol</sub> offered: 0.886 (95% CI, 0.754-0.962) vs. 0.750 for PMR (95% CI, 0.597-0.868; p = 0.034). Multivariable analysis identified HIP<sub>vol</sub> as an independent predictor of PMI (odds ratio, 1.15 per 10-μL increase; 95% CI, 1.01-1.30, p = 0.035).<br /><b>Conclusions</b><br />Our semi-automated method of analyzing coronary plaque using CATCH MRI provided rapid HIP quantification. Three-dimensional assessment using this approach had a better ability to predict PMI than conventional two-dimensional assessment.<br /><br />Copyright © 2024. Published by Elsevier Inc.<br /><br /><small>J Cardiovasc Magn Reson: 16 Jan 2024:100999; epub ahead of print</small></div>
Nakazawa M, Matsumoto H, Li D, Slomka PJ, ... Xie Y, Shinke T
J Cardiovasc Magn Reson: 16 Jan 2024:100999; epub ahead of print | PMID: 38237903
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<div><h4>Characterization of Quantitative Susceptibility Mapping in the Left Ventricle of the Myocardium.</h4><i>Tyler A, Huang L, Kunze K, Neji R, ... Masci PG, Roujol S</i><br /><b>Background</b><br />Myocardial quantitative susceptibility mapping (QSM) may offer better specificity to iron than conventional T<sub>2</sub>* imaging in the assessment of cardiac diseases, including intra-myocardial haemorrhage. However, the precision and repeatability of cardiac QSM has not yet been characterized. The aim of this study is to characterize these key metrics in a healthy volunteer cohort and show the feasibility of the method in patients.<br /><b>Methods</b><br />Free breathing respiratory-navigated multi-echo 3D gradient echo (GRE) images were acquired, from which QSM maps were reconstructed using the MEDI toolbox. This technique was first evaluated in a susceptibility phantom containing tubes with known concentrations of gadolinium. In vivo characterization of myocardial QSM were then performed in a cohort of 10 healthy volunteers where each subject was scanned twice. Mean segment susceptibility, precision (standard deviation of voxel magnetic susceptibilities within one segment), and repeatability (absolute difference in segment mean susceptibility between repeats) of QSM were calculated for each AHA myocardial segment. Finally, the feasibility of the method was shown in ten patients, including four with haemorrhagic infarcts.<br /><b>Results</b><br />The phantom experiment showed a strong linear relationship between measured and predicted susceptibility shifts (R<sup>2</sup> > 0.99). For the healthy volunteer cohort, AHA segment analysis showed the mean segment susceptibility was 0.00 ± 0.02 ppm, the mean precision was 0.05 ± 0.04 ppm, and the mean repeatability was 0.02 ± 0.02 ppm. Cardiac QSM was successfully performed in all patients. Focal iron deposits were successfully visualized in the patients with haemorrhagic myocardial infarctions.<br /><b>Conclusion</b><br />The precision and repeatability of cardiac QSM were successfully characterized in phantom and in vivo experiments. The feasibility of the technique was also successfully demonstrated in patients. While challenges still remain, further clinical evaluation of the technique is now warranted.<br /><b>Trial registration</b><br />This work does not report on a health care intervention.<br /><br />Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.<br /><br /><small>J Cardiovasc Magn Reson: 16 Jan 2024:101000; epub ahead of print</small></div>
Tyler A, Huang L, Kunze K, Neji R, ... Masci PG, Roujol S
J Cardiovasc Magn Reson: 16 Jan 2024:101000; epub ahead of print | PMID: 38237902
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<div><h4>Prognostic Value of Mid-term Cardiac Magnetic Resonance Follow-up in Patients with Non-ischemic Dilated Cardiomyopathy: A prospective cohort study.</h4><i>Xu Y, Li Y, Wang S, Wan K, ... Han Y, Chen Y</i><br /><b>Background</b><br />The prognostic value of follow-up cardiac magnetic resonance (CMR) in dilated cardiomyopathy (DCM) patients is unclear. We aimed to investigate the prognostic value of cardiac function, structure, and tissue characteristics at mid-term CMR follow-up.<br /><b>Methods</b><br />The study population was a prospectively enrolled cohort of DCM patients who underwent guideline-directed medical therapy (GDMT) with baseline and follow-up CMR, which included measurement of biventricular volume and ejection fraction, late gadolinium enhancement, native T1, native T2, and extracellular volume. During follow-up, major adverse cardiac events (MACE) were defined as a composite endpoint of cardiovascular death, heart transplantation, and heart-failure readmission.<br /><b>Results</b><br />Among 235 DCM patients (median CMR interval: 15.3 months; interquartile range: 12.5-19.2 months), 54 (23.0%) experienced MACE during follow-up (median: 31.2 months; interquartile range: 20.8-50.0 months). In multivariable Cox regression, follow-up CMR models showed significantly superior predictive value than baseline CMR models. Stepwise multivariate Cox regression showed that follow-up left ventricular ejection fraction (LVEF; hazard ratio [HR], 0.93; 95% confidence interval [CI], 0.91-0.96; P<0.001) and native T1 (HR, 1.01; 95% CI, 1.00-1.01; P=0.030) were independent predictors of MACE. Follow-up LVEF ≥ 40% or stable LVEF < 40% with T1 ≤ 1273 ms indicated low risk (annual event rate < 4%), while stable LVEF < 40% and T1 > 1273 ms or LVEF < 40% with deterioration indicated high risk (annual event rate > 15%).<br /><b>Conclusions</b><br />Follow-up CMR provided better risk stratification than baseline CMR. Improvements in the LVEF and T1 mapping are associated with a lower risk of MACE.<br /><br />Copyright © 2024. Published by Elsevier Inc.<br /><br /><small>J Cardiovasc Magn Reson: 16 Jan 2024:101002; epub ahead of print</small></div>
Xu Y, Li Y, Wang S, Wan K, ... Han Y, Chen Y
J Cardiovasc Magn Reson: 16 Jan 2024:101002; epub ahead of print | PMID: 38237899
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<div><h4>Low-flow in aortic valve stenosis patients with reduced ejection fraction does not depend on left ventricular function.</h4><i>Gersch S, Lange T, Beuthner BE, Elkenani M, ... Schuster A, Toischer K</i><br /><b>Background</b><br />Patients with severe aortic stenosis (AS) and reduced left ventricular ejection fraction (LVEF) can be distinguished into high- (HG) and low-gradient (LG) subgroups. However, less is known about their characteristics and underlying (pathophysiological) hemodynamic mechanisms.<br /><b>Methods</b><br />98 AS patients with reduced LVEF were included. Subgroup characteristics were analyzed by a multimodal approach using clinical and histological data, next-generation sequencing (NGS) and applying echocardiography as well as cardiovascular magnetic resonance (CMR) imaging. Biopsy samples were analyzed with respect to fibrosis and mRNA expression profiles.<br /><b>Results</b><br />40 patients were classified as HG-AS and 58 patients as LG-AS. Severity of AS was comparable between the subgroups. Comparison of both subgroups revealed no differences in LVEF (p = 0.1), LV mass (p = 0.6) or end-diastolic LV diameter (p = 0.12). Neither histological (HG: 23.2% vs. LG: 25.6%, p = 0.73) and circulating biomarker-based assessment (HG: 2.6 ± 2.2% vs. LG: 3.2 ± 3.1%; p = 0.46) of myocardial fibrosis nor global gene expression patterns differed between subgroups. Mitral regurgitation (MR), atrial fibrillation (AF) and impaired right ventricular function (MR: HG: 8% vs. LG: 24%; p < 0.001; AF: HG: 30% vs. LG: 51.7%; p = 0.03; RVSVi: HG 36.7 vs. LG 31.1 ml/m2, p = 0.045; TAPSE: HG 20.2 vs. LG 17.3 mm, p = 0.002) were more frequent in LG-AS patients compared to HG-AS. These pathologies could explain the higher mortality of LG vs. HG-AS patients.<br /><b>Conclusion</b><br />In patients with low-flow severe aortic stenosis, low transaortic gradient and cardiac output are not primarily due to LV dysfunction or global changes in gene expression, but may be attributed to other additional cardiac pathologies like mitral regurgitation, atrial fibrillation or right ventricular dysfunction. These factors should also be considered during planning of aortic valve replacement.<br /><br />© 2024. The Author(s).<br /><br /><small>Clin Res Cardiol: 18 Jan 2024; epub ahead of print</small></div>
Gersch S, Lange T, Beuthner BE, Elkenani M, ... Schuster A, Toischer K
Clin Res Cardiol: 18 Jan 2024; epub ahead of print | PMID: 38236417
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<div><h4>Impact of Bempedoic Acid on Total Cardiovascular Events: A Prespecified Analysis of the CLEAR Outcomes Randomized Clinical Trial.</h4><i>Nicholls SJ, Nelson AJ, Lincoff AM, Brennan D, ... Bloedon L, Nissen SE</i><br /><b>Importance</b><br />The ATP citrate lyase (ACL) inhibitor, bempedoic acid, reduces low-density lipoprotein cholesterol (LDL-C) level and major adverse cardiovascular events (MACE) by 13% in patients at high cardiovascular risk with intolerance of statin and high-intensity statin medications. The effects of bempedoic acid on total cardiovascular events remain unknown.<br /><b>Objective</b><br />To determine the impact of bempedoic acid on the total incidence of MACE.<br /><b>Design, setting, and participants</b><br />Included in this prespecified analysis of the Cholesterol Lowering via Bempedoic Acid, an ACL-Inhibiting Regimen (CLEAR) Outcomes trial were patients with, or at high risk for, cardiovascular disease, with hypercholesterolemia and inability to take guideline-recommended statins. Study data were analyzed from December 2016 to November 2022.<br /><b>Interventions</b><br />Patients were randomly assigned to treatment with bempedoic acid or placebo daily.<br /><b>Main outcomes and measures</b><br />The primary end point was the time to first event for a composite of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or coronary revascularization (MACE-4). The key secondary end point was time to first event for cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke (MACE-3). This prespecified analysis compared the total number of cardiovascular events in the treatment groups.<br /><b>Results</b><br />A total of 13 970 patients (mean [SD] age, 65 [9] years; 7230 male [51.8%]) were included in the study. A total of 9764 participants (69.9%) had prior atherosclerotic cardiovascular disease and a baseline LDL-C level of 139 mg/dL; treatment with bempedoic acid resulted in a 21% reduction in LDL-C level and a 22% reduction in high-sensitivity C-reactive protein (hsCRP) level at 6 months. Median (IQR) follow-up was 3.4 (3.1-3.9) years. A total of 1746 positively adjudicated first MACE-4 events and 915 additional MACE events in 612 patients were recorded, with coronary revascularization representing 32.8% (573 of 1746) of first events and 69.4% (635 of 915) of additional events. For the total incidence of cardiovascular events, treatment with bempedoic acid was associated with a reduction in risk of MACE-4 (hazard ratio [HR], 0.80; 95% CI, 0.72-0.89; P <.001), MACE-3 (HR, 0.83; 95% CI, 0.73-0.93; P = .002), myocardial infarction (HR, 0.69; 95% CI, 0.58-0.83; P < .001), and coronary revascularization (HR, 0.78; 95% CI, 0.68-0.89; P <.001), although no statistically significant difference was observed for stroke (HR, 0.80; 95% CI, 0.63-1.03). A lower HR for protection with bempedoic acid was observed with increasing number of MACE events experienced by patients.<br /><br /><b>Conclusion:</b><br/>and relevance</b><br />Lowering LDL-C level with bempedoic acid reduced the total number of cardiovascular events in patients with high cardiovascular risk, statin therapy intolerance, and elevated LDL-C levels.<br /><br /><br /><br /><small>JAMA Cardiol: 17 Jan 2024; epub ahead of print</small></div>
Nicholls SJ, Nelson AJ, Lincoff AM, Brennan D, ... Bloedon L, Nissen SE
JAMA Cardiol: 17 Jan 2024; epub ahead of print | PMID: 38231501
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<div><h4>The Association of Off-Hour vs. On-Hour ICU Admission Time with Mortality in Patients with Cardiogenic Shock - a Retrospective Multicenter Analysis.</h4><i>Naumann D, Fischer J, Gmeiner J, Lüsebrink E, ... Orban M, Scherer C</i><br /><b>Background</b><br />Studies have shown a so-called off-hour effect for many different diseases, but data are scarce concerning cardiogenic shock. We therefore assessed the association of off-hour vs. on-hour intensive care unit (ICU) admission with 30-day mortality in patients with cardiogenic shock.<br /><b>Methods</b><br />In total, 1720 cardiogenic shock patients (666 admitted during off-hours) from two large university hospitals in Germany were included in retrospect.<br /><b>Results</b><br />An admission during off-hours was associated with an increased 30-day mortality compared to an admission during on-hours (crude mortality 48% vs. 41%, HR 1.17 (1.03-1.33), p = 0.017). This effect remained significant after propensity score matching (p = 0.023). Neither patients with a combined SCAI stage D and E (p = 0.088) or C (p = 0.548) nor those requiring cardiopulmonary resuscitation (p = 0.114) had a higher mortality at off-hour admission. In contrast, those without veno-arterial extracorporeal membrane oxygenation (VA-ECMO) (HR 1.17 (1.00-1.36), p = 0.049), without acute myocardial infarction (HR 1.27 (1.02-1.56), p = 0.029) or a with combined SCAI stage A and B (HR 2.23 (1.08-4.57), p = 0.025) had an increased mortality at off-hour admission.<br /><b>Conclusion</b><br />Our study showed an increased mortality in patients with cardiogenic shock admitted during off-hours especially in those with a milder onset of disease. This stresses the importance of a thorough workup of each patient especially at times of limited resources, the menace of underestimating the severity of cardiogenic shock and the need for an improved twenty-four seven available risk stratification.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.<br /><br /><small>Eur Heart J Acute Cardiovasc Care: 02 Feb 2024; epub ahead of print</small></div>
Naumann D, Fischer J, Gmeiner J, Lüsebrink E, ... Orban M, Scherer C
Eur Heart J Acute Cardiovasc Care: 02 Feb 2024; epub ahead of print | PMID: 38306600
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<div><h4>Genetic Association of Lipid-Lowering Drugs with Aortic Aneurysms: A Mendelian Randomization Study.</h4><i>Gao X, Luo W, Qu L, Yang M, ... Wang Y, Xiu J</i><br /><b>Aims</b><br />The lack of effective pharmacotherapies for aortic aneurysms (AA) is a persistent clinical challenge. Lipid metabolism plays an essential role in AA. However, the impact of lipid-lowering drugs on AA remains controversial. The study aimed to investigate the genetic association between lipid-lowering drugs and AA.<br /><b>Methods</b><br />Our research used publicly available data on genome-wide association studies (GWASs) and expression quantitative trait loci (eQTL) studies. Genetic instruments, specifically eQTLs related to drug-target genes and SNPs (single nucleotide polymorphisms) located near or within the drug-target loci associated with low-density lipoprotein cholesterol (LDL-C), have been served as proxies for lipid-lowering medications. Drug-Target Mendelian Randomization (MR) study is used to determine the causal association between lipid-lowering drugs and different types of AA.<br /><b>Results</b><br />The MR analysis revealed that higher expression of HMGCR (3-hydroxy-3-methylglutaryl coenzyme A reductase) was associated with increased risk of AA (OR = 1.58, 95% CI = 1.20-2.09, p = 1.20 × 10-03) and larger lumen size (aortic maximum area: OR = 1.28, 95% CI = 1.13-1.46, p = 1.48 × 10-04; aortic minimum area: OR = 1.26, 95% CI = 1.21-1.42, p = 1.78 × 10-04). PCSK9 (Proprotein convertase subtilisin/kexin type 9) and CETP (Cholesteryl ester transfer protein) show a suggestive relationship with AA (PCSK9: OR = 1.34, 95% CI = 1.10-1.63, p = 3.07 × 10-03; CETP: OR = 1.38, 95% CI = 1.06-1.80, p = 1.47 × 10-02). No evidence to support genetically mediated NPC1L1 (Niemann-Pick C1-Like 1) and LDLR (low-density lipoprotein cholesterol receptor) are associated with AA.<br /><b>Conclusions</b><br />This study provides causal evidence for the genetic association between lipid-lowering drugs and aortic aneurysms. Higher gene expression of HMGCR, PCSK9, and CETP increases AA risk. Furthermore, HMGCR inhibitors may link with smaller aortic lumen size.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.<br /><br /><small>Eur J Prev Cardiol: 01 Feb 2024; epub ahead of print</small></div>
Gao X, Luo W, Qu L, Yang M, ... Wang Y, Xiu J
Eur J Prev Cardiol: 01 Feb 2024; epub ahead of print | PMID: 38302118
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<div><h4>The Association of Lipoprotein(a) and Coronary Artery Calcium in Asymptomatic Patients: A Systematic Review and Meta-analysis.</h4><i>Martignoni FV, Eduardo J, Marques IR, Gomes C, ... de Vasconcellos HD, Miedema M</i><br /><b>Aims</b><br />Lipoprotein(a) [Lp(a)] is an atherogenic lipid particle associated with increased risk for coronary heart disease (CHD) events. Coronary artery calcium (CAC) score is a tool to diagnose subclinical atherosclerosis and guide clinical decision-making for primary prevention of CHD. Studies show conflicting results concerning the relationship between Lp(a) and CAC in asymptomatic populations. We conducted a meta-analysis to evaluate the association of Lp(a) and CAC in asymptomatic patients.<br /><b>Methods</b><br />We systematically searched PubMed, Embase, and Cochrane until April 2023 for studies evaluating the association between Lp(a) and CAC in asymptomatic patients. We evaluated CAC>0 Agatston units, and CAC>100. Lp(a) was analysed as a continuous or dichotomous variable. We assessed the association between Lp(a) and CAC with pooled odds ratios (OR) adopting a random-effects model.<br /><b>Results</b><br />A total of 23,105 patients from 18 studies were included in the meta-analysis with a mean age of 55.9 years, 46.4% female. Elevated Lp(a) increased the odds of CAC>0 (OR 1.31; 95% CI 1.05 to 1.64; p=0.02), CAC ≥100 (OR 1.29; 95% CI 1.01 to 1.65; p=0.04; ), and CAC progression (OR 1.43; 95% CI 1.20 to 1.70; p<0.01; ). For each increment of 1 mg/dL in Lp(a) there was a 1% in the odds of CAC>0 (OR 1.01; 95% CI 1.01 to 1.01; p<0.01).<br /><b>Conclusions</b><br />Our findings of this meta-analysis suggest that Lp(a) is positively associated with a higher likelihood of CAC. Higher Lp(a) levels increased the odds of CAC >0. These data support the concept that Lp(a) is atherogenic, although with high heterogeneity and a low level of certainty.<br /><b>Protocol registration</b><br />CRD42023422034.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Eur J Prev Cardiol: 01 Feb 2024; epub ahead of print</small></div>
Martignoni FV, Eduardo J, Marques IR, Gomes C, ... de Vasconcellos HD, Miedema M
Eur J Prev Cardiol: 01 Feb 2024; epub ahead of print | PMID: 38300625
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<div><h4>Association Between Cardiovascular disease and Risk of Female Sexual Dysfunction: A Systematic Review and Meta-Analysis.</h4><i>Dilixiati D, Cao R, Mao Y, Li Y, ... Azhati B, Rexiati M</i><br /><b>Aim</b><br />Female sexual dysfunction (FSD) is a considerably underestimated condition. It has been repeatedly reported that patients with cardiovascular diseases (CVD) may suffer from an increased risk of FSD. However, there is still a lack of comprehensive and systematic evaluation of various CVD and FSD. We aimed to elucidate the association between CVD and FSD through a comprehensive literature review and meta-analysis.<br /><b>Methods and result</b><br />The PubMed, Scopus, Embase, and Cochrane Library databases were systematically searched from inception to February 28, 2023. We identified all relevant studies reporting the risk of FSD in subjects with or without CVD. The associations between CVD and the risk of FSD were assessed by calculating pooled ORs (cross-sectional studies) and RRs (longitudinal studies) with 95% CIs. We employed random-effects models to account for potential heterogeneity, and the quality of the included studies was assessed using the Newcastle-Ottawa Scale (NOS). Fifty-four articles with 148,946 individuals were included in our meta-analysis. Compared with control subjects, subjects with CVD had a 1.51-fold increased risk of FSD (OR 1.51 95% CI, 1.34-1.69, P < .001, heterogeneity I2 = 91.4%, P < .001). Subgroup analyses indicated that the association between CVD and FSD remained significant in longitudinal studies (RR 1.50 95% CI, 1.21-1.86, P < .001, heterogeneity I2 = 86.7%, P < .001). Particularly, hypertension (OR 1.41 95% CI, 1.23-1.62, P < .001, heterogeneity I2 = 82.7%, P < .001), stroke (OR 1.81 95% CI, 1.54-2.12, P < .001, heterogeneity I2 = 0%, P < .423), and myocardial infarction (OR 2.07 95% CI, 1.60-2.67, P < .001 heterogeneity I2 = 82.4%, P < .001) were significantly associated with FSD. Meta-regression revealed that the primary sources of heterogeneity in FSD are attributable to adjustments for covariates, study design, and study population.<br /><b>Conclusion</b><br />Our meta-analysis indicated that patients with CVD suffer from a greater risk of developing FSD. Meanwhile, we validated these findings in longitudinal queues. Notably, conditions such as hypertension, stroke, and myocardial infarction demonstrated a significant association with the incidence of FSD.<br /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.<br /><br /><small>Eur J Prev Cardiol: 31 Jan 2024; epub ahead of print</small></div>
Dilixiati D, Cao R, Mao Y, Li Y, ... Azhati B, Rexiati M
Eur J Prev Cardiol: 31 Jan 2024; epub ahead of print | PMID: 38297501
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<div><h4>Long-Term Autograft Dilation and Durability After the Ross Procedure are Similar Among Infants, Children, and Adolescents with Primary Aortic Stenosis.</h4><i>Nguyen SN, Bouhout I, Singh S, Vinogradsky AV, ... Bacha EA, Goldstone AB</i><br /><b>Objective</b><br />Autograft durability and remodeling are thought to be superior in younger pediatric patients after the Ross operation. We sought to delineate the fate of the autograft across the pediatric age spectrum in patients with primary aortic stenosis (AS).<br /><b>Methods</b><br />We retrospectively reviewed patients aged ≤18 years with primary AS who underwent the Ross operation from 1993 to 2020. Patients were categorized by age. The primary endpoint was autograft dimensional change. Secondary endpoints were severe neo-aortic insufficiency (AI) and autograft reintervention.<br /><b>Results</b><br />One hundred and nineteen patients underwent the Ross operation, including 37 (31.1%) in group I (<18 months), 24 (20.2%) in group II (18 months-8 years), and 58 (48.7%) in group III (8-18 years). All groups exhibited similar annular growth rates within the first 5 postoperative years, followed by a collective decrease in annulus growth rates from years 5-10. Group III experienced rapid sinus dilation in the first 5 years, followed by stabilization of the sinus z-score from years 5-10; groups I and II demonstrated stable sinus z-scores over 10 years. There were 4 (3.4%) early and 2 (1.7%) late mortalities at a median follow-up of 8.1 years [range: 0.01-26.3]. At 15 years, there was a similar incidence of severe neo-AI (0.0%±0.0% vs. 0.0%±0.0% vs. 3.9%±3.9%, p=0.52) and autograft reintervention (8.4%±6.0% vs. 0.0%±0.0% vs. 2.4%±2.4%, p=0.47) in all groups.<br /><b>Conclusions</b><br />Age at the Ross operation for primary AS does not influence long-term autograft remodeling or durability. Other physiologic or technical factors are likely greater determinants of autograft fate.<br /><br />Copyright © 2024. Published by Elsevier Inc.<br /><br /><small>J Thorac Cardiovasc Surg: 22 Jan 2024; epub ahead of print</small></div>
Nguyen SN, Bouhout I, Singh S, Vinogradsky AV, ... Bacha EA, Goldstone AB
J Thorac Cardiovasc Surg: 22 Jan 2024; epub ahead of print | PMID: 38266984
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<div><h4>Classification Algorithm to Distinguish Between Type 1 and Type 2 Myocardial Infarction in Administrative Claims Data.</h4><i>Wasfy JH, Price M, Normand ST, Januzzi JL, McCarthy CP, Hsu J</i><br /><b>Background</b><br />Type 2 myocardial infarction (T2MI) and type 1 myocardial infarction (T1MI) differ with respect to demographics, comorbidities, treatments, and clinical outcomes. Reliable quality and outcomes assessment depends on the ability to distinguish between T1MI and T2MI in administrative claims data. As such, we aimed to develop a classification algorithm to distinguish between T1MI and T2MI that could be applied to claims data.<br /><b>Methods</b><br />Using data for beneficiaries in a Medicare accountable care organization contract in a large health care system in New England, we examined the distribution of MI diagnosis codes between 2018 to 2021 and the patterns of care and coding for beneficiaries with a hospital discharge diagnosis <i>International Classification of Diseases</i>, <i>Tenth Revision</i> code for T2MI, compared with those for T1MI. We then assessed the probability that each hospitalization was for a T2MI versus T1MI and examined care occurring in 2017 before the introduction of the T2MI code.<br /><b>Results</b><br />After application of inclusion and exclusion criteria, 7759 hospitalizations for myocardial infarction remained (46.5% T1MI and 53.5% T2MI; mean age, 79±10.3 years; 47% female). In the classification algorithm, female gender (odds ratio, 1.26 [95% CI, 1.11-1.44]), Black race relative to White race (odds ratio, 2.48 [95% CI, 1.76-3.48]), and diagnoses of COVID-19 (odds ratio, 1.74 [95% CI, 1.11-2.71]) or hypertensive emergency (odds ratio, 1.46 [95% CI, 1.00-2.14]) were associated with higher odds of the hospitalization being for T2MI versus T1MI. When applied to the testing sample, the C-statistic of the full model was 0.83. Comparison of classified T2MI and observed T2MI suggest the possibility of substantial misclassification both before and after the T2MI code.<br /><b>Conclusions</b><br />A simple classification algorithm appears to be able to differentiate between hospitalizations for T1MI and T2MI before and after the T2MI code was introduced. This could facilitate more accurate longitudinal assessments of acute myocardial infarction quality and outcomes.<br /><br /><br /><br /><small>Circ Cardiovasc Qual Outcomes: 19 Jan 2024:e009986; epub ahead of print</small></div>
Wasfy JH, Price M, Normand ST, Januzzi JL, McCarthy CP, Hsu J
Circ Cardiovasc Qual Outcomes: 19 Jan 2024:e009986; epub ahead of print | PMID: 38240159
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<div><h4>Association of plasma proteomics with incident coronary heart disease in individuals with and without type 2 diabetes: results from the population-based KORA study.</h4><i>Luo H, Huemer MT, Petrera A, Hauck SM, ... Peters A, Thorand B</i><br /><b>Background</b><br />Coronary heart disease (CHD) is a major global health concern, especially among individuals with type 2 diabetes (T2D). Given the crucial role of proteins in various biological processes, this study aimed to elucidate the aetiological role and predictive performance of protein biomarkers on incident CHD in individuals with and without T2D.<br /><b>Methods</b><br />The discovery cohort included 1492 participants from the Cooperative Health Research in the Region of Augsburg (KORA) S4 study with 147 incident CHD cases (45 vs. 102 cases in the group with T2D and without T2D, respectively) during 15.6 years of follow-up. The validation cohort included 888 participants from the KORA-Age1 study with 70 incident CHD cases (19 vs. 51 cases in the group with T2D and without T2D, respectively) during 6.9 years of follow-up. We measured 233 plasma proteins related to cardiovascular disease and inflammation using proximity extension assay technology. Associations of proteins with incident CHD were assessed using Cox regression and Mendelian randomization (MR) analysis. Predictive models were developed using priority-Lasso and were evaluated on top of Framingham risk score variables using the C-index, category-free net reclassification index (cfNRI), and relative integrated discrimination improvement (IDI).<br /><b>Results</b><br />We identified two proteins associated with incident CHD in individuals with and 29 in those without baseline T2D, respectively. Six of these proteins are novel candidates for incident CHD. MR suggested a potential causal role for hepatocyte growth factor in CHD development. The developed four-protein-enriched model for individuals with baseline T2D (ΔC-index: 0.017; cfNRI: 0.253; IDI: 0.051) and the 12-protein-enriched model for individuals without baseline T2D (ΔC-index: 0.054; cfNRI: 0.462; IDI: 0.024) consistently improved CHD prediction in the discovery cohort, while in the validation cohort, significant improvements were only observed for selected performance measures (with T2D: cfNRI: 0.633; without T2D: ΔC-index: 0.038; cfNRI: 0.465).<br /><b>Conclusions</b><br />This study identified novel protein biomarkers associated with incident CHD in individuals with and without T2D and reaffirmed previously reported protein candidates. These findings enhance our understanding of CHD pathophysiology and provide potential targets for prevention and treatment.<br /><br />© 2024. The Author(s).<br /><br /><small>Cardiovasc Diabetol: 03 Feb 2024; 23:53</small></div>
Luo H, Huemer MT, Petrera A, Hauck SM, ... Peters A, Thorand B
Cardiovasc Diabetol: 03 Feb 2024; 23:53 | PMID: 38310303
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<div><h4>Sirolimus-coated balloon in all-comer population of coronary artery disease patients: the EASTBOURNE DIABETES prospective registry.</h4><i>Caiazzo G, Oliva A, Testa L, Heang TM, ... Cortese B, EASTBOURNE investigators</i><br /><b>Background</b><br />The outcomes of percutaneous coronary intervention (PCI) in diabetic patients are still suboptimal, and it is unclear if diabetic patients might derive a benefit from the use of drug-coated balloons.<br /><b>Aims</b><br />To evaluate the impact of diabetes mellitus on the outcomes of patients undergoing PCI with sirolimus-coated balloon (SCB) MagicTouch (Concept Medical, India).<br /><b>Methods</b><br />We conducted a subgroup analysis of the prospective, multicenter, investigator-initiated EASTBOURNE registry, evaluating the performance of MagicTouch SCB in patients with and without diabetes. The study primary endpoint was target lesion revascularization (TLR) at 12-month follow-up. Secondary clinical endpoints were major adverse clinical events (MACE), death, myocardial infarction (MI), and BARC 2-5 bleedings.<br /><b>Results</b><br />Among 2,083 enrolled patients, a total of 864 suffered from diabetes (41.5%). Patients with diabetes had a numerically higher occurrence of TLR (6.5% vs. 4.7% HR 1.38, 95%CI 0.91-2.08), all-cause death (3.8% vs. 2.6%, HR 1.81, 95%CI 0.95-3.46), and MACE (12.2% vs. 8.9%; HR 1.26 95%CI 0.92-1.74). The incidence of spontaneous MI was significantly higher among diabetic patients (3.4% vs. 1.5%, HR 2.15 95%CI 1.09-4.25); bleeding events did not significantly differ. The overall incidence of TLR was higher among in-stent restenosis (ISR) as compared to de-novo coronary lesions, irrespectively from diabetes status.<br /><b>Conclusions</b><br />In the EASTBOURNE DIABETES registry, diabetic patients treated with the MagicTouch SCB did not have a significant increase in TLR when compared to non-diabetic patients; moreover, diabetic status did not affect the study device performance in terms of TLR, in both de-novo lesions and ISR.<br /><br />© 2024. The Author(s).<br /><br /><small>Cardiovasc Diabetol: 03 Feb 2024; 23:52</small></div>
Caiazzo G, Oliva A, Testa L, Heang TM, ... Cortese B, EASTBOURNE investigators
Cardiovasc Diabetol: 03 Feb 2024; 23:52 | PMID: 38310281
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<div><h4>Tricuspid Regurgitation and Clinical Outcomes in Heart Failure With Reduced Ejection Fraction.</h4><i>Adamo M, Metra M, Claggett BL, Miao ZM, ... Teerlink JR, GALACTIC-HF Investigators and Patients</i><br /><b>Background</b><br />Tricuspid regurgitation (TR) is common and is associated with poor outcomes in patients with heart failure (HF). However, data with adjudicated events from fully characterized patients with heart failure with reduced ejection fraction (HFrEF) are lacking.<br /><b>Objectives</b><br />This study sought to explore the association between mild or moderate/severe TR and clinical outcomes of patients with HFrEF.<br /><b>Methods</b><br />GALACTIC-HF (Global Approach to Lowering Adverse Cardiac Outcomes Through Improving Contractility in Heart Failure) was a double-blind, placebo-controlled randomized trial comparing omecamtiv mecarbil vs placebo in patients with symptomatic HFrEF.<br /><b>Results</b><br />Among the 8,232 patients analyzed in the GALACTIC-HF trial, 8,180 (99%) had data regarding baseline TR (none: n = 6,476 [79%], mild: n = 919 [11%], and moderate/severe: n = 785 [10%]). The primary composite outcome of a first HF event or cardiovascular death occurred in 2,368 (36.6%) patients with no TR, 353 (38.4%) patients with mild TR, and 389 (49.6%) patients with moderate/severe TR. Moderate/severe TR was independently associated with a higher relative risk of the primary composite outcome compared with either no TR (adjusted HR: 1.12 [95% CI: 1.01-1.26]; P = 0.046) or no/mild TR (adjusted HR: 1.14 [95% CI: 1.02-1.27]; P = 0.025) driven predominantly by HF events. The association between moderate/severe TR and clinical outcomes was more pronounced in outpatients with worse renal function, higher left ventricular ejection fraction, and lower N-terminal pro-B-type natriuretic peptide and bilirubin levels. The beneficial treatment effect of omecamtiv mecarbil vs placebo on clinical outcomes was not modified by TR.<br /><b>Conclusions</b><br />In symptomatic patients with HFrEF, baseline moderate/severe TR was independently associated with cardiovascular death or HF events driven predominantly by HF events. The beneficial treatment effect of omecamtiv mecarbil on the primary outcome was not modified by TR.<br /><br />Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.<br /><br /><small>JACC Heart Fail: 19 Jan 2024; epub ahead of print</small></div>
Adamo M, Metra M, Claggett BL, Miao ZM, ... Teerlink JR, GALACTIC-HF Investigators and Patients
JACC Heart Fail: 19 Jan 2024; epub ahead of print | PMID: 38300212
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<div><h4>Increasing Utilization of Extended Criteria Donor Hearts for Transplantation: The OCS Heart EXPAND Trial.</h4><i>Schroder JN, Patel CB, DeVore AD, Casalinova S, ... Milano CA, Smith JW</i><br /><b>Background</b><br />Extended criteria donor (ECD) hearts available with donation after brain death (DBD) are underutilized for transplantation due to limitations of cold storage.<br /><b>Objectives</b><br />This study evaluated use of an extracorporeal perfusion system on donor heart utilization and post-transplant outcomes in ECD DBD hearts.<br /><b>Methods</b><br />In this prospective, single-arm, multicenter study, adult heart transplant recipients received ECD hearts using an extracorporeal perfusion system if hearts met study criteria. The primary outcome was a composite of 30-day survival and absence of severe primary graft dysfunction (PGD). Secondary outcomes were donor heart utilization rate, 30-day survival, and incidence of severe PGD. The safety outcome was the mean number of heart graft-related serious adverse events within 30 days. Additional outcomes included survival through 2 years benchmarked to concurrent nonrandomized control subjects.<br /><b>Results</b><br />A total of 173 ECD DBD hearts were perfused; 150 (87%) were successfully transplanted; 23 (13%) did not meet study transplantation criteria. At 30 days, 92% of patients had survived and had no severe PGD. The 30-day survival was 97%, and the incidence of severe PGD was 6.7%. The mean number of heart graft-related serious adverse events within 30 days was 0.17 (95% CI: 0.11-0.23). Patient survival was 93%, 89%, and 86% at 6, 12, and 24 months, respectively, and was comparable with concurrent nonrandomized control subjects.<br /><b>Conclusions</b><br />Use of an extracorporeal perfusion system resulted in successfully transplanting 87% of donor hearts with excellent patient survival to 2 years post-transplant and low rates of severe PGD. The ability to safely use ECD DBD hearts could substantially increase the number of heart transplants and expand access to patients in need. (International EXPAND Heart Pivotal Trial [EXPANDHeart]; NCT02323321; Heart EXPAND Continued Access Protocol; NCT03835754).<br /><br />Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.<br /><br /><small>JACC Heart Fail: 13 Jan 2024; epub ahead of print</small></div>
Schroder JN, Patel CB, DeVore AD, Casalinova S, ... Milano CA, Smith JW
JACC Heart Fail: 13 Jan 2024; epub ahead of print | PMID: 38276933
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<div><h4>Recruiting a Diverse Cardiology Physician Workforce.</h4><i>Snow SC, Alhanti B, Douglas PS</i><br /><b>Importance</b><br />Understanding trends in the representation of women and individuals from underrepresented racial and ethnic populations in cardiovascular disease and cardiovascular subspecialty fellowships is essential to improving the diversity of the cardiology workforce.<br /><b>Objective</b><br />To examine changes in the representation of women and underrepresented individuals in cardiovascular disease and cardiovascular subspecialty fellowships over time.<br /><b>Design, setting, and participants</b><br />This cross-sectional study of trainee sex and race and ethnicity in various training programs from 2008 to 2022 used data from the Accreditation Council for Graduate Medical Education\'s publicly available online source. Participants included all residents, internal medicine residents, general surgery residents, and fellows in cardiovascular disease and cardiovascular subspecialty fellowships.<br /><b>Main outcomes and measures</b><br />Percentages of women and Black and Hispanic trainees in these programs were calculated for each year. Mann-Kendall tests were used to determine if changes over the years represented a significant trend.<br /><b>Results</b><br />Among the 3320 cardiovascular disease trainees in 2022, 848 (25.5%) were women, and 459 (13.8%) were Black or Hispanic, less than the representation among internal medicine trainees at 43.8% and 15.6%, respectively. However, the percentage of women trainees in cardiovascular disease significantly increased from 17.6% in 2008 (P = .001 for time trend) and also increased for interventional cardiology fellowships (from 6.3% in 2008 to 20.1% in 2022; P = .002). Over the same period, the proportion of women in general surgery increased from 27.4% to 45.2% (P < .001). The percentage of Black and Hispanic trainees in internal medicine significantly increased from 8.6% in 2012 (P < .001) while increases in general surgery were not statistically significant (9.7% to 16.1%; P = .35). There were also important increases in the percentages of Black and Hispanic trainees in cardiovascular disease (from 8.3% in 2012; P = .09) and interventional cardiology (3.8% to 13.4%; P = .12).<br /><br /><b>Conclusions:</b><br/>and relevance</b><br />In this study, the representation of women in cardiovascular fellowships, including interventional cardiology, increased over recent years. While representation of Black and Hispanic individuals is low in all residencies, including cardiovascular fellowships, recent positive trends are important to recognize and provide hope to drive future efforts.<br /><br /><br /><br /><small>JAMA Cardiol: 24 Jan 2024; epub ahead of print</small></div>
Snow SC, Alhanti B, Douglas PS
JAMA Cardiol: 24 Jan 2024; epub ahead of print | PMID: 38265823
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<div><h4>Advances in the diagnosis and treatment of transthyretin amyloid cardiomyopathy.</h4><i>Vaishnav J, Brown E, Sharma K</i><br /><AbstractText>Transthyretin amyloid cardiomyopathy (ATTR-CM) is an underrecognized cause of heart failure (HF). ATTR-CM can lead to a number of cardiovascular manifestations including HF, rhythm disturbances, and valvular disease that ultimately limit quality of life and prognosis. Due to advances in diagnostic modalities and therapeutic options, the prevalence of ATTR-CM is rising. There are several classes of medications under active investigation, though most therapies are most efficacious if instituted early on in the disease course. As such, early clinical recognition and prompt diagnosis are crucial to improving disease related outcomes. In this review, we highlight clinical manifestations of ATTR-CM as well as contemporary diagnostic and treatment approaches to the disease.</AbstractText><br /><br />Copyright © 2024. Published by Elsevier Inc.<br /><br /><small>Prog Cardiovasc Dis: 19 Jan 2024; epub ahead of print</small></div>
Vaishnav J, Brown E, Sharma K
Prog Cardiovasc Dis: 19 Jan 2024; epub ahead of print | PMID: 38246305
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This program is still in alpha version.