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High‐Sensitivity Troponin I in Hospitalized and Ambulatory Patients With Heart Failure With Preserved Ejection Fraction: Insights From the Heart Failure Clinical Research Network
Abstract
Background: We sought to study the prevalence of high‐sensitivity troponin and its association with cardiac structure and outcomes in ambulatory and hospitalized patients with heart failure with a preserved ejection fraction ( HF p EF ). Methods and Results: A post hoc analysis utilized data from HF p EF patients: DOSE (Diuretic Optimization Strategies Evaluation) and CARRESS ‐ HF (Cardiorenal Rescue Study in Acute Decompensated Heart Failure) enrolled patients hospitalized with acute HF p EF , and RELAX (Phosphodiesterase‐5 Inhibition to Improve Clinical Status and Exercise Capacity in Heart Failure With Preserved Ejection Fraction) enrolled ambulatory patients with HF p EF . High‐sensitivity troponin I (hs‐TnI) was measured in hospitalized patients at baseline, at 72 to 96 hours, on day 7, and on day 60. In ambulatory patients hs‐TnI was measured at baseline and at week 24. In the ambulatory cohort, correlations between hs‐TnI and cardiac structure and function were assessed. The association between hs‐TnI and a 60‐day composite of emergency room visits, readmissions, and death was assessed for hospitalized patients using multivariable Cox proportional hazard models. The study population included 139 hospitalized and 212 ambulatory patients with HF p EF and hs‐TnI measured at baseline. The median (25th, 75th percentiles) baseline troponin was 17.6 (11.1, 41.0) ng/L in hospitalized patients and 9.5 (5.3, 19.7) ng/L in ambulatory patients ( P <0.001). The prevalence of elevated hs‐TnI (>99% percentile upper reference limit was 86% in hospitalized patients and 53% among ambulatory patients, with stable elevation in ambulatory patients during follow‐up. HF p EF patients with a hs‐TnI above the median were older with worse left ventricular hypertrophy and diastolic dysfunction. Continuously valued hs‐TnI (per doubling) was associated with increased risk of composite end point (adjusted hazard ratio 1.20, 95% confidence interval 1.00‐1.43; P =0.042). Conclusions: Hs‐TnI is commonly elevated among both hospitalized and ambulatory patients with HF p EF . Increased hs‐TnI levels are associated with worse cardiac structure and increased risk of adverse events.
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Patients with HFpEF frequently display chronic low-grade myocardial injury as reflected by elevated levels of troponin, and this degree of myocardial injury is correlated with severity of cardiac dysfunction, hemodynamic congestion, impairment in functional capacity and risk for HF hospitalization.
“Patients with HFpEF also frequently display chronic low-grade myocardial injury as reflected by elevated levels of troponin13,14, and like albuminuria, this degree of myocardial injury in HFpEF is correlated with the severity of cardiac dysfunction, hemodynamic congestion, impairment in functional capacity and risk for HF hospitalization13,14.”
From Effects of tirzepatide on circulatory overload and end-organ damage in heart failure with preserved ejection fraction and obesity: a secondary analysis of the SUMMIT trial (2025) · cites this paper as [14]
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Experimental — accuracy not yet measuredCirculating troponin levels are commonly elevated in HFpEF, where they are associated with greater risk for HF hospitalization or death.
“Circulating troponin levels are commonly elevated in HFpEF, where they are associated with greater risk for HF hospitalization or death14.”
From Effects of tirzepatide on circulatory overload and end-organ damage in heart failure with preserved ejection fraction and obesity: a secondary analysis of the SUMMIT trial (2025) · cites this paper as [14]
The Conclusions report that high-sensitivity troponin I was elevated in a large majority of hospitalized HFpEF patients and more than half of ambulatory patients. The Results (Outcomes in Initially Hospitalized HFpEF; page not provided) associate higher levels with a 60-day composite of emergency-room visits, readmissions, and death. That supports an association with adverse outcomes, but the paper does not establish a separate association with HF hospitalization or death, and it assessed clinical outcomes only in the initially hospitalized cohort. (LLM, conf=0.84)
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Mohammed, S. F., Hussain, S., Mirzoyev, S. A., Edwards, W. D., Maleszewski, J. J., & Redfield, M. M. (2015) · Circulation · doi:10.1161/circulationaha.114.009625 · Cited by 874
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Borlaug, B. A., Zile, M. R., Kramer, C. M., Baum, S. J., Hurt, K., Litwin, S. E., Murakami, M., Ou, Y., Upadhyay, N., & Packer, M. (2025) · Nature Medicine · doi:10.1038/s41591-024-03374-z · Cited by 166
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Metadata
- Authors
- Fudim, M., Ambrosy, A. P., Sun, J., Anstrom, K. J., Bart, B. A., Butler, J., AbouEzzeddine, O., Greene, S. J., Mentz, R. J., Redfield, M. M., Reddy, Y. N. V., Vaduganathan, M., Braunwald, E., Hernandez, A. F., Borlaug, B. A., & Felker, G. M.
- Venue
- Journal of the American Heart Association
- Published
- 2018-12-18
- Volume
- 7
- Issue
- 24
- ISSN
- 2047-9980
- PMC
- PMC6405612
- Cited by
- 25
- References
- 1
- Language
- en
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