Usefulness of High-Sensitivity Cardiac Troponin T to Predict Long-Term Outcome in Patients with Hypertrophic
D H Frank Gommans1, G Etienne Cramer2, Michael A Fouraux3
1Department of Cardiology , Radboud University Medical Center; Department of Cardiology, Rijnstate Ziekenhuis Arnhem.
Insights
Elevated high-sensitivity cardiac troponin T (hs-cTnT) in hypertrophic cardiomyopathy (HCM) patients is linked to adverse outcomes. This 5-year study prospectively confirms hs-cTnT as a key biomarker for predicting risk in HCM.
Area of Science:
- Cardiology
- Biomarkers
- Cardiovascular Imaging
Background:
- Hypertrophic cardiomyopathy (HCM) is a genetic heart disease with variable clinical outcomes.
- Previous reports suggested an association between cardiac troponin (cTn) and adverse events in HCM, but confirmatory data were limited.
- Risk stratification in HCM relies on clinical factors, imaging, and biomarkers, with a need for improved predictive tools.
Purpose of the Study:
- To prospectively investigate the association between elevated high-sensitivity cardiac troponin T (hs-cTnT) and adverse clinical outcomes in a cohort of hypertrophic cardiomyopathy patients over a 5-year follow-up period.
- To assess the independent predictive value of hs-cTnT for major adverse cardiovascular events in HCM.
- To explore the role of hs-cTnT as a potential biomarker for risk stratification in HCM.
Main Methods:
- A prospective, 5-year follow-up cohort study involving 135 HCM patients.
- Comprehensive evaluation including clinical assessment, cardiac MRI (cine, LGE, T2-weighted imaging), and multi-biomarker assessment (including hs-cTnT).
- Primary endpoint comprised a composite of sudden cardiac death, heart failure related death, stroke-related death, heart failure hospitalization, stroke hospitalization, sustained ventricular tachycardia, appropriate ICD discharge, or progression to NYHA class III-IV.
Main Results:
- Elevated hs-cTnT (≥14ng/L) was identified in 24% (33/135) of HCM patients.
- During a median follow-up of 5.0 years, 18 patients experienced the primary endpoint.
- Univariate analysis showed elevated hs-cTnT was associated with the primary endpoint (HR: 3.4; p=0.009).
- Multivariable analysis revealed that elevated hs-cTnT remained independently associated with adverse outcomes (aHR: 4.7; p=0.002).
- Other factors associated with the primary endpoint included female sex, previous syncope, non-sustained VT, reduced LVEF, and CICP.
Conclusions:
- This prospective 5-year follow-up study provides the first confirmation of an association between elevated hs-cTnT and adverse outcomes in hypertrophic cardiomyopathy.
- hs-cTnT emerges as a significant biomarker for risk prediction in HCM, complementing established clinical variables.
- Further evaluation of hs-cTnT in larger prospective registries is warranted to refine risk stratification strategies in HCM.
Abstract:
Since the first report of an association between cardiac troponin (cTn) and adverse outcome in hypertrophic cardiomyopathy (HD), there is a paucity in confirmative data. We performed a prospective, prespecified 5-year follow-up cohort study of 135 HC patients who participated in a national multicenter project and underwent clinical evaluation, MRI (cine, LGE and T2-weighted imaging) and biomarker assessment (high-sensitivity cTnT (hs-cTnT), N-terminal pro-B-type natriuretic peptide, soluble tumorgenicity suppressor-2, Galectin-3, Growth differentiation factor-15, C-terminal Propeptide of Type I Collagen (CICP)). An elevated hs-cTnT concentration was defined as ≥14ng/L. Follow-up was systematically performed for the primary endpoint: a composite of sudden cardiac death, heart failure related death, stroke-related death, heart failure hospitalization, hospitalization for stroke, spontaneous sustained ventricular tachycardia (VT) or appropriate ICD discharge, and progression to NYHA class III-IV. Elevated hs-cTnT was present in 33 of 135 (24%) HC patients. During a median follow-up of 5.0 years (IQR: 4.9-5.1) 18 patients reached the primary endpoint. Using Cox regression analysis, elevated hs-cTnT was univariately associated with the primary endpoint (HR: 3.4 (95%CI: 1.4-8.7, p=0.009). Also female sex, previous syncope, previous non-sustained VT, reduced LV ejection fraction (<50%) and CICP were associated with the primary endpoint. In multivariable analysis, elevated hs-cTnT remained independently associated with outcome (aHR: 4.7 (95%CI: 1.8-12.6, p = 0.002). In conclusion, this 5-year follow-up study is the first to prospectively confirm the association of elevated hs-cTnT and adverse outcomes. In addition to established clinical variables, cTn seems the biomarker of interest to further improve risk prediction in HC, which should be evaluated in larger prospective registries.
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