Elsevier

Progress in Cardiovascular Diseases

Volume 67, July–August 2021, Pages 80-88
Progress in Cardiovascular Diseases

Prognostic value of troponin I in atrial fibrillation

https://doi.org/10.1016/j.pcad.2021.02.012Get rights and content

Abstract

Objective

To evaluate whether circulating cardiac troponin I (cTnI) levels are associated with worst outcomes in patients with atrial fibrillation (AF).

Methods

Consecutive patients visiting the emergency room (ER) with a new episode of a previously diagnosed AF or a new diagnosis of AF during ER admission between January 1st, 2010 and December 31st, 2015, were enrolled in the study (n = 2617). After applying exclusion criteria and eliminating repeated episodes, 2013 patients were finally included. Of these, 1080 patients with at least one cTnI measurement in the ER were selected and classified into 4 groups according to cTnI quartiles: Q1 (n = 147) cTnI <10 ng/L (Group 1); Q2 (n = 254): 10–19 ng/L (Group 2); Q3 (n = 409): 20–40 ng/L (Group 3); and Q4 (n = 270): cTnI >40 ng/L (Group 4). The median follow-up period was 47.8 ± 32.8 months. The primary endpoint was all-cause death during the follow-up.

Results

A higher mortality was found in group 4 compared with the other groups (58.9% vs. 28.5%, respectively, p < 0.001), along with, hospitalizations (40.4% vs. 30.7%, p = 0.004), and readmissions due to decompensated heart failure (26.7% vs. 2.5%, p = 0.002). The probability of survival without AF recurrences was lower in the Q4 (p = 0.045). Moreover, cTnI levels >40 ng/L (Q4) were an independent risk factor of death (HR, 2.03; 95% CI, 1.64–2.51; p < 0.001).

Conclusion

The assessment of cTnI at ER admission could be a useful strategy for risk stratification of patients diagnosed with AF by identifying a subgroup with medium-term to long-term increased risk of adverse events and mortality.

Introduction

Atrial fibrillation (AF) is one of the most common forms of cardiac arrhythmia worldwide, being also a major risk factor for ischemic stroke.1 AF is an arrhythmia that is also frequently encountered in the emergency room (ER),2 and produces a significant economic burden, increasing long-term disability and mortality.3

According to an Olmstead county cohort, one in every four patients with AF will be diagnosed with heart failure (HF) within six years from the diagnosis4; HF also increases the risk of AF by 4.5-fold in men and 5.9-fold in woman, respectively.5 This risk increases gradually in parallel with impairment of left ventricular systolic function (LVSF) and New York Heart Association (NYHA) Functional Classification class,6 as mirrored by the evidence that AF is an independent predictor of all-cause mortality.7,8

The precise mechanisms involved in AF generation are still largely unknown. Several pathways and risk factors, such as inflammation, autonomic tone, atrial pressure, wall stress and genetics have been previously proposed,9 converging to trigger cardiac remodeling and structural changes in myocardial tissue caused by myocytes death and their replacement with fibrotic tissue, ultimately leading to permanent scars.10 All these circumstances may also promote an increase of the circulating levels of some sensitive and specific biomarkers of myocardiocyte injury, such as cardiac troponins I (cTnI) and T (cTnT). Although the risk stratification in patients with AF is currently performed with clinical and echocardiographic criteria, and cTn elevation are more frequently associated with acute coronary syndromes (ACS), an increase of cTn over their conventional thresholds have been occasionally observed also in patients who suffered prolonged episodes of supraventricular arrhythmias. Shortening of diastole is one of the more probable causes, with ensuing subendocardial ischemia. cTnI release mostly occurs from viable cardiomyocytes, by stimulation of integrins in response to enhanced blood pressure.11

The use of biomarkers in the management of AF, especially cTn, has gained much popularity during the past decade, though the reasons underlying their elevation in AF require further scrutiny. Higher ventricular rate is a possible explanation, since this will then produce an increased oxygen demand that triggers myocardial ischemia, pressure and volume overload, changes in microvascular flow, acute thrombotic events with preexisting AF, altered calcium loading, oxidative stress or structural cardiac tissue alterations, especially when coexisting with coronary artery disease (CAD).12,13 This current evidence, coupled with the relatively easy, fast and accurate measurement of circulating cTn levels would, hence, make them useful biomarkers for improving the prognostic assessment in AF patients.12

Despite recent evidence,14, 15, 16 the implementation of cTn in AF monitoring has not been widely introduced within the major clinical practice guidelines published by the American Heart Association (AHA), the American College of Cardiology (ACC) and the Heart Rhythm Society (HRS) in 2014, and by the 2016 document of the European Society of Cardiology (ESC).17,18 Therefore, the aim of this study is evaluating whether circulating cTnI levels predict the prognosis of patients with AF (i.e., after a first episode). To this end, we analyzed the relationship between cTnI levels in patients with AF and its medium-long term clinical evolution in terms of new AF episodes, adverse events, morbidity and mortality.

Section snippets

Study design and population

We conducted a single-center retrospective observational study. The initial study population consisted of all consecutive patients attending the ER of Valencia General University Hospital Consortium with a new episode of a previously diagnosed AF or a new diagnosis of AF between January 1, 2010 and December 31, 2015 (n = 2617). After applying the exclusion criteria, and eliminating patients with a repeated episode, the sample size decreased to 2013 patients. Of these, all those with at least

Baseline characteristics

The final study population consisted of 1080 patients admitted to ER with a new diagnosis or episode of AF. Mean age was 74 ± 13 years, and 60.1% were women. We found statistically significant differences between cTnI quartiles for age and CHA2DS2-VASc score, as well as for other comorbidities, such as CKD, AMI, stroke, aortic valvulopathy, and ICM. Differences were larger when the Q4 group was compared with those in the other quartiles (Table 1). No significant differences were found for sex,

Discussion

The results of this study support the existence of a convincing association between cTnI levels and risk of mortality in patients with AF. A cTnI value >40 ng/L is an independent risk factor for all-cause mortality in patients with AF and, even more importantly, the higher mortality in Q4 group was not only justified by differences in baseline characteristics. Our study was conducted in poorly controlled conditions, more closely resembling routine clinical practice, and thus representative of

Conclusion

To our knowledge, this is the largest and longest study which has explored the potential association between cTn and mortality in patients presenting to the ER with a new episode of a previously known AF and/or newly diagnosed with AF. Finding new biomarkers directly associated with mortality and other adverse events may improve our precision in estimating risk in patients with AF. To this end, we used real-world clinical data in a significant number of patients and have confirmed that cTnI

Sources of funding

None.

Declaration of Competing Interest

The authors have no association with commercial entities that could be viewed as having an interest in the general area of the submitted manuscript.

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