High-Sensitivity Cardiac Troponin in Hypertrophic Cardiomyopathy: Diagnostic Insights and Future Directions

Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disorder, yet challenges remain in assessing disease severity and phenotypic heterogeneity. High-sensitivity cardiac troponin (hs-cTn) has emerged as a potential biomarker of myocardial stress in nonischemic cardiomyopathies. Through an evaluation of observational cohort, mechanistic, and longitudinal studies, this narrative review synthesizes the current evidence on the role of cardiac troponin in HCM, including its pathophysiological basis, patterns of elevation, associations with imaging and clinical outcomes, and potential clinical applications. Across multiple cohorts, approximately one-quarter to one-half of patients with HCM demonstrated elevated hs-cTn concentrations at rest, even in the absence of acute coronary syndromes, consistent with chronic low-grade myocardial injury. Troponin elevation consistently correlated with markers of disease severity, including greater left ventricular hypertrophy, myocardial fibrosis on cardiac magnetic resonance imaging, elevated filling pressures, reduced exercise capacity, and arrhythmic burden. Exercise- or stress-related troponin rises have also been reported, particularly in higher-risk phenotypes and in the presence of myocardial edema. Recent trials of cardiac myosin inhibitors show troponin levels decline with disease-modifying therapy, supporting hs-cTn as a biologically responsive marker of active myocardial injury. Although hs-cTn lacks disease specificity and is not a standalone diagnostic or prognostic tool, it may provide useful adjunctive information when interpreted alongside imaging and clinical findings. Prospective studies with serial measurement, standardized assays, and integration with risk models are needed to define its role in risk stratification and clinical management.