Topic: General Cardiology

Abstract
<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>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>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: 07 Feb 2024; 45:419-438</small></div>
Montone RA, Camilli M, Calvieri C, Magnani G, ... Crea F, Niccoli G
Eur Heart J: 07 Feb 2024; 45:419-438 | PMID: 38238478
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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: 21 Feb 2024; 45:601-609</small></div>
Hamilton DE, Albright J, Seth M, Painter I, ... Sukul D, Gurm HS
Eur Heart J: 21 Feb 2024; 45:601-609 | PMID: 38233027
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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: 07 Mar 2024; 45:778-790</small></div>
Ahn HJ, An HY, Ryu G, Lim J, ... Koh Y, Choi EK
Eur Heart J: 07 Mar 2024; 45:778-790 | PMID: 38231881
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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: 21 Feb 2024; 45:572-585</small></div>
Capranzano P, Moliterno D, Capodanno D
Eur Heart J: 21 Feb 2024; 45:572-585 | PMID: 38240716
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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: 14 Mar 2024; 45:922-936</small></div>
Hausleiter J, Lachmann M, Stolz L, Bedogni F, ... Rudolph V, EuroSMR Investigators
Eur Heart J: 14 Mar 2024; 45:922-936 | PMID: 38243773
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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 NFκB 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: 01 Apr 2024; 81:776-786</small></div>
Costa RM, Cerqueira DM, Bruder-Nascimento A, Alves JV, ... Ho J, Bruder-Nascimento T
Hypertension: 01 Apr 2024; 81:776-786 | PMID: 38240165
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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: 01 Apr 2024; 81:787-800</small></div>
Sun X, Wu J, Zhang X, Xie C, ... Cheng J, Xu Q
Hypertension: 01 Apr 2024; 81:787-800 | PMID: 38240164
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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>Hypertrophic cardiomyopathy dysfunction mimicked in human engineered heart tissue and improved by sodium-glucose cotransporter 2 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 an HCM sarcomere mutation.<br /><b>Methods and results</b><br />Contractility was measured of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) harbouring an 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 the 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\'s 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>Conclusion</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 /><br />© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.<br /><br /><small>Cardiovasc Res: 14 Mar 2024; 120:301-317</small></div>
Wijnker PJM, Dinani R, van der Laan NC, Algül S, ... Kuster DWD, van der Velden J
Cardiovasc Res: 14 Mar 2024; 120:301-317 | PMID: 38240646
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<div><h4>Renalase mediates macrophage-to-fibroblast crosstalk to attenuate pressure overload-induced pathological myocardial fibrosis.</h4><i>Fu R, You N, Li R, Zhao X, ... Li X, Jiang W</i><br /><AbstractText>A potential antifibrotic mechanism in pathological myocardial remodeling is the recruitment of beneficial functional subpopulations of macrophages or the transformation of their phenotype. Macrophages are required to activate molecular cascades that regulate fibroblast behavior. Identifying mediators that activate the antifibrotic macrophage phenotype is tantamount to identifying the button that retards pathological remodeling of the myocardium; however, relevant studies are inadequate. Circulating renalase (RNLS) is mainly of renal origin, and cardiac myocytes also secrete it autonomously. Our previous studies revealed that RNLS delivers cell signaling to exert multiple cardiovascular protective effects, including the improvement of myocardial ischemia, and heart failure. Here, we further investigated the potential mechanism by which macrophage phenotypic transformation is targeted by RNLS to mediate stress load-induced myocardial fibrosis. Mice subjected to transverse aortic constriction (TAC) were used as a model of myocardial fibrosis. The co-incubation of macrophages and cardiac fibroblasts was used to study intercellular signaling. The results showed that RNLS co-localized with macrophages and reduced protein expression after cardiac pressure overload. TAC mice exhibited improved cardiac function and alleviated left ventricular fibrosis when exogenous RNLS was administered. Flow sorting showed that RNLS is essential for macrophage polarization towards a restorative phenotype (M2-like), thereby inhibiting myofibroblast activation, as proven by both mouse RAW264.7 and bone marrow-derived macrophage models. Mechanistically, we found that activated protein kinase B is a major pathway by which RNLS promotes M2 polarization in macrophages. RNLS may serve as a prognostic biomarker and a potential clinical candidate for the treatment of myocardial fibrosis.</AbstractText><br /><br />Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.<br /><br /><small>J Hypertens: 01 Apr 2024; 42:629-643</small></div>
Fu R, You N, Li R, Zhao X, ... Li X, Jiang W
J Hypertens: 01 Apr 2024; 42:629-643 | PMID: 38230609
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<div><h4>Incidences, risk factors, and clinical correlates of severe QT prolongation after the use of quetiapine or haloperidol.</h4><i>Wang CL, Wu VC, Lee CH, Wu CL, ... Huang YT, Chang SH</i><br /><b>Background</b><br />Case reports suggest that quetiapine or haloperidol use is associated with severe QT prolongation (SQTP) and torsades de pointes.<br /><b>Objective</b><br />The purpose of this study was to examine the incidences, risk factors, and outcomes of SQTP in quetiapine and haloperidol users.<br /><b>Methods</b><br />This study accessed electronic medical records from a multicenter health-care hospital system in Taiwan and included patients who received quetiapine or haloperidol therapy and had both baseline and follow-up electrocardiograms. SQTP was defined as a posttreatment corrected QT (QTc) interval exceeding 500 ms or an increase in QTc interval of >60 ms compared with the baseline value. We analyzed the risk factors and outcomes of SQTP using multivariate logistic regression.<br /><b>Results</b><br />Mean increases in QTc interval were +8.3 ± 51.8 and +8.9 ± 44.0 ms after the administration of quetiapine (n = 8832) and haloperidol (n = 2341). Among these users, 1149 (13.0%) and 333 (14.2%) developed SQTP, respectively. Common risk factors for SQTP included old age, heart failure, hypokalemia, amiodarone use, and baseline QTc interval. SQTP in quetiapine users was significantly associated with ventricular arrhythmias (odds ratio 2.84; 95% confidence interval 1.95-4.13) and sudden cardiac death (odds ratio 2.29; 95% confidence interval 1.44-3.66).<br /><b>Conclusion</b><br />More than 10% of patients receiving quetiapine or haloperidol therapy developed SQTP, and many of them were exposed to risk factors for SQTP. SQTP in quetiapine users was significantly associated with increased risks of ventricular arrhythmias and sudden cardiac death. Clinicians should be vigilant for ventricular arrhythmias in quetiapine users who have risk factors for SQTP.<br /><br />Copyright © 2023 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.<br /><br /><small>Heart Rhythm: 01 Mar 2024; 21:321-328</small></div>
Wang CL, Wu VC, Lee CH, Wu CL, ... Huang YT, Chang SH
Heart Rhythm: 01 Mar 2024; 21:321-328 | PMID: 38231170
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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 hemodynamic conditions that are responsible for coronary microvasculature impairment. Relief of AS by transcatheter aortic valve implantation (TAVI) is expected to improve the coronary artery hemodynamic. We aimed to assess the midterm effects of TAVI in coronary flow reserve (CFR) and myocardial resistance reserve (MRR) by a continuous intracoronary thermodilution technique. At-rest and hyperemic coronary flow was measured by a continuous thermodilution technique in 23 patients with AS and compared with that in 17 matched controls, and repeated 6 ± 3 months after TAVI in 11 of the patients with AS. In patients with AS, absolute coronary flow at rest was significantly greater, and absolute resistance at rest was significantly less, than in controls (p <0.01 for both), causing less CFR and MRR (1.73 ± 0.4 vs 2.85 ± 1.1, p <0.01 and 1.95 ± 0.4 vs 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 absolute coronary flow at rest reduction (p = 0.03). In patients with AS, CFR and MRR determined by continuous thermodilution are significantly impaired. At 6-month follow-up, TAVI improves these indexes and partially relieves the pathophysiologic alterations, leading to a partial restoration of CFR and MRR.</AbstractText><br /><br />Copyright © 2024 Elsevier Inc. All rights reserved.<br /><br /><small>Am J Cardiol: 01 Mar 2024; 214:109-114</small></div>
Gutiérrez-Barrios A, Cañadas-Pruaño D, Alfaro LM, Gheorghe L, ... Vázquez-García R, Toro-Cebada R
Am J Cardiol: 01 Mar 2024; 214:109-114 | PMID: 38232809
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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>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>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>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>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>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: 01 Apr 2024; 400:131786</small></div>
Kang DW, Kang SH, Lee K, Nam K, ... Yoon JC, Park SK
Int J Cardiol: 01 Apr 2024; 400:131786 | 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 Elsevier B.V. All rights reserved.<br /><br /><small>Int J Cardiol: 01 Apr 2024; 400:131784</small></div>
Musumeci B, Tini G, Biagini E, Merlo M, ... Boni L, Autore C
Int J Cardiol: 01 Apr 2024; 400:131784 | PMID: 38242504
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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, ... Guo B, Shen Z</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 B.V. All rights reserved.<br /><br /><small>Int J Cardiol: 15 Apr 2024; 401:131782</small></div>
Xia B, Lu Y, Liang J, Li F, ... Guo B, Shen Z
Int J Cardiol: 15 Apr 2024; 401:131782 | PMID: 38246423
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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>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>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: 01 Feb 2024; 17:e009986</small></div>
Wasfy JH, Price M, Normand ST, Januzzi JL, McCarthy CP, Hsu J
Circ Cardiovasc Qual Outcomes: 01 Feb 2024; 17:e009986 | PMID: 38240159
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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: 01 Mar 2024; 12:438-447</small></div>
Schroder JN, Patel CB, DeVore AD, Casalinova S, ... Milano CA, Smith JW
JACC Heart Fail: 01 Mar 2024; 12:438-447 | PMID: 38276933
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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: 06 Feb 2024; 13:e030587</small></div>
Kaur A, Dhaliwal AS, Sohal S, Gwon Y, ... Basman C, Tamis-Holland J
J Am Heart Assoc: 06 Feb 2024; 13:e030587 | PMID: 38240252
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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: 06 Feb 2024; 13:e031209</small></div>
Yamamoto T, Kawamori H, Toba T, Sasaki S, ... Hirata KI, Otake H
J Am Heart Assoc: 06 Feb 2024; 13:e031209 | PMID: 38240235
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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: 06 Feb 2024; 13:e031162</small></div>
Abstract
<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: 06 Feb 2024; 13:e031880</small></div>
McBane RD, Murphree DH, Liedl D, Lopez-Jimenez F, ... Bjarnason H, Wennberg PW
J Am Heart Assoc: 06 Feb 2024; 13:e031880 | PMID: 38240202
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<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: 06 Feb 2024; 13:e031586</small></div>
Sharma A, Razaghizad A, Joury A, Levin A, ... Perkovic V, Mahaffey KW
J Am Heart Assoc: 06 Feb 2024; 13:e031586 | PMID: 38240199
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Abstract
<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: 01 Mar 2024; 9:245-253</small></div>
Nicholls SJ, Nelson AJ, Lincoff AM, Brennan D, ... Bloedon L, Nissen SE
JAMA Cardiol: 01 Mar 2024; 9:245-253 | PMID: 38231501
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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: 01 Mar 2024; 12:552-563</small></div>
Adamo M, Metra M, Claggett BL, Miao ZM, ... Teerlink JR, GALACTIC-HF Investigators and Patients
JACC Heart Fail: 01 Mar 2024; 12:552-563 | PMID: 38300212
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Abstract
<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: 06 Feb 2024; 13:e031924</small></div>
Su X, Zhang D, Gu D, Rao C, ... Fan J, Zheng Z
J Am Heart Assoc: 06 Feb 2024; 13:e031924 | PMID: 38240224
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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: 06 Feb 2024; 13:e031506</small></div>
Akao M, Yamashita T, Fukuzawa M, Hayashi T, Okumura K
J Am Heart Assoc: 06 Feb 2024; 13:e031506 | PMID: 38240204
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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: 06 Feb 2024; 13:e031997</small></div>
Al-Kassou B, Al-Kassou L, Mahn T, Lütjohann D, ... Latz E, Zimmer S
J Am Heart Assoc: 06 Feb 2024; 13:e031997 | PMID: 38240198
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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: 06 Feb 2024; 13:e032997</small></div>
Abstract
<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: 01 Feb 2024; 17:e010115</small></div>
Pavlovic N, Ndumele CE, Abshire Saylor M, Szanton SL, ... Himmelfarb C, Leoutsakos JM
Circ Cardiovasc Qual Outcomes: 01 Feb 2024; 17:e010115 | PMID: 38240158
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This program is still in alpha version.