Troponin T, Left Ventricular Ejection Fraction, and Tricuspid Regurgitation Velocity for Biomarker- and
Hasan Burak Isleyen1, Sevil Tugrul Yavuz2, Sercan Bulut3
1Department of Cardiology, İstanbul Nişantaşı Üniversitesi, Istanbul 34475, Turkey.
Insights
Troponin T, left ventricular ejection fraction (LVEF), and tricuspid regurgitation velocity (TRV) are linked to mortality in critically ill heart failure patients. These markers offer risk enrichment within clinical severity, not standalone rules.
Area of Science:
- Cardiology
- Critical Care Medicine
- Biomarkers
Background:
- Troponin T indicates cardiomyocyte injury.
- Left ventricular ejection fraction (LVEF) and tricuspid regurgitation velocity (TRV) assess ventricular and cardiopulmonary function.
- Identifying mortality risk in critically ill heart failure patients requires integrated biomarker and hemodynamic data.
Purpose of the Study:
- To evaluate if synchronized troponin T and echocardiographic data can identify mortality risk in critically ill heart failure patients.
- To differentiate statistical association from clinically meaningful incremental discrimination of these markers.
- To assess the prognostic value of troponin T, LVEF, and TRV in intensive care unit (ICU) heart failure admissions.
Main Methods:
- Utilized MIMIC-IV and MIMIC-IV-ECHO databases for adult ICU admissions with heart failure.
- Employed multivariable Cox models adjusted for demographics, comorbidities, illness severity, and organ support.
- Performed sensitivity analyses including complete-case and multiple imputation methods.
Main Results:
- Higher troponin T levels were associated with increased 28-day mortality (HR, 1.09; p=0.003).
- Higher LVEF was associated with decreased 28-day mortality (HR per percentage point, 0.99; p=0.004).
- Measurable TRV was associated with mortality (HR, 1.28; p=0.005); troponin T and LVEF showed small incremental discrimination after covariate adjustment.
Conclusions:
- Troponin T, LVEF, and TRV are associated with mortality in ICU heart failure patients.
- These markers provide risk enrichment within a clinical severity framework.
- Their utility is best as supplementary information rather than independent decision-making tools.
Abstract:
Troponin T is a molecular marker of cardiomyocyte injury, whereas left ventricular ejection fraction (LVEF) and tricuspid regurgitation velocity (TRV) reflect downstream ventricular and cardiopulmonary measures. This study evaluated whether synchronized troponin T and echocardiographic data can identify mortality risk in critically ill patients with heart failure, while separating statistical association from clinically meaningful incremental discrimination. Adult intensive care unit admissions with heart failure diagnoses were identified from MIMIC-IV and MIMIC-IV-ECHO. The primary endpoint was 28-day all-cause mortality; one-year mortality was secondary. Multivariable Cox models were adjusted for demographics, comorbidity, illness severity, organ support, and laboratory covariates. Restricted cubic splines, proportional hazards diagnostics, variance inflation factors, prespecified subgroup interaction tests, complete-case analyses, and multiple imputation sensitivity analyses were performed. The final cohort included 4362 patients, and 1072 patients (24.6%) died within 28 days. In the primary complete-case Cox model (n = 2087; 659 deaths), higher log-transformed troponin T was associated with higher 28-day mortality (hazard ratio [HR], 1.09; 95% confidence interval [CI], 1.03-1.15; p = 0.003), and higher LVEF was associated with lower mortality (HR per percentage point, 0.99; 95% CI, 0.99-1.00; p = 0.004). After severity and organ-support covariates were entered, troponin T and LVEF produced statistically detectable but very small C-statistic gains. Measurable TRV was available in 1546 patients and was associated with mortality in that subset (HR, 1.28; 95% CI, 1.08-1.52; p = 0.005). Troponin T, LVEF, and TRV were associated with mortality in ICU heart failure. Their contribution was best interpreted as risk enrichment within a clinical severity framework rather than a stand-alone decision rule.
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