LAUSR

Over the past 2 decades, heart failure has become the leading cause of cardiovascular morbidity and mortality. Epidemiological studies show that approximately half of the patients diagnosed with heart failure have a normal ejection fraction.1 The combination of an aging population along with a marked increase in the prevalence of comorbid conditions has resulted in a steady increase in the diagnosis of heart failure with preserved ejection fraction (HFpEF). Compared with patients with left ventricular dysfunction, patients with HFpEF appear to have better survival, although mortality remains significantly higher than that of the healthy population.2 Of equal concern is the high rate of morbidity and frequent hospital admissions associated with HFpEF.3 Despite multiple large-scale clinical trials, no study has identified a treatment that can improve overall survival.4-6 Heart failure with preserved ejection fraction is characterized by broad phenotypic diversity. Recent research has characterized subgroups of patients with different clinical outcomes, with the intent of identifying independent disease processes that will respond to directed therapies.7-9 Proposed classifications have ranged from a model that classifies HFpEF into 4 categories based on pathophysiological mechanisms to a complex analysis using phenomapping. While each model has successfully discriminated HFpEF subgroups based on outcomes, there is no guideline-based consensus on the best means of prognostication. A simple objective biomarker is needed to provide better risk stratification in HFpEF, particularly among patients admitted with decompensated heart failure. The detection of cardiac troponins has been established as one of the strongest biomarkers in ischemic heart disease, as well as heart failure with reduced ejection fraction (HFrEF). In a large study of patients with heart failure in the ADHERE registry, the presence of elevated troponin level was associated with increased in-hospital mortality, from 2.7% to 8.0%.10 Furthermore, a direct correlation was found between the degree of troponin elevation and death. However, evidence supporting the role of troponins in HFpEF is limited.11,12 In this context, the study by Pandey et al13 in this issue of JAMA Cardiology fills a gap in the literature regarding the use of cardiac troponin as a biomarker for risk stratification in HFpEF. The authors analyze all cases of left ventricular ejection fraction of 50% or higher in the Get With the Guidelines– Heart Failure (GWTG-HF) registry. In this large cohort of 96 769 patients, only 35.0% had a troponin evaluation during hospitalization. Of those 34 233 patients, 22.9% had an elevated troponin level, and this group had twice the in-hospital mortality of those with a normal troponin levels (hazard ratio, 2.19; P < .001) as well as a significant increase in length of stay. In a subset of 14 819 patients with follow-up data available, elevated troponin level was also associated with increased 30day mortality, 30-day readmissions, and 1-year mortality. Multiple factors were associated with troponin elevation, including age, male sex, black race, ischemic cause of heart failure, worsened renal function, higher heart rate, and higher B-type natriuretic peptide (BNP) levels. Given the strong evidence of the critical role of troponin level in assessing cardiovascular disease, and the class I recommendation for troponin testing in patients with decompensated heart failure, it was distressing for us to read that only 35% of patients in this registry had a troponin evaluation during their admission. This study highlights the valuable role that troponins play in risk stratifying patients with decompensated HFpEF and supports the current guidelines. We hope that these results will promote the increased use of troponin evaluation in the assessment of HFpEF and adherence with guideline-based recommendations. In addition, this study highlights the critical difference between the prognosis in patients with HFrEF vs HFpEF. Compared with patients with HFpEF and a positive troponin finding in the ADHERE registry, similar patients in the present study had half the in-hospital mortality (8.0% vs 3.95%). Whether these differences relate to differences in the patient population (HFpEF vs a predominantly HFrEF population) or management strategies in different time periods cannot be concluded from the current data. Furthermore, these findings raise the question of whether troponin level is simply a marker of disease severity or whether troponin release is a phenotypic characteristic of a specific subset of patients with HFpEF. Future research should investigate the presence of troponin release among previously identified HFpEF subgroups. What is clear from this study is that the presence of an elevated troponin level identifies a subgroup of patients requiring intensive in-hospital evaluation and treatment followed by more rigorous follow-up after discharge. It is important to emphasize that the prognostic value of troponin in this study was independent of BNP levels. Whether these 2 biomarkers can be used in combination to provide even better risk stratification for patients with HFpEF remains to be answered. Related article Opinion