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.
Highlights
IntroductionHC.[1,2] In that regard, it is surprising that the role of cardiac troponin (cTn) in HC patients has not been extensively studied.[4,5,6,7] Elevated cTn is a common finding and associated with adverse disease characteristics, such as wall thickness and late gadolinium enhancement (LGE).[4,5,6,7,8] In 2013, the first report was published that demonstrated an association between elevated cTnT, assessed with a high-sensitivity assay (hs-cTnT) and adverse long-term outcome in HC.[6] Ever since, there is a paucity of confirmatory prospective data.[3,8,9,10] we aimed to validate the association between elevated hs-cTnT and adverse outcomes in a prospective HC cohort with 5 years of clinical follow-up
HC.[1,2] In that regard, it is surprising that the role of cardiac troponin in HC patients has not been extensively studied.[4,5,6,7] Elevated cTn is a common finding and associated with adverse disease characteristics, such as wall thickness and late gadolinium enhancement (LGE).[4,5,6,7,8] In 2013, the first report was published that demonstrated an association between elevated cTnT, assessed with a high-sensitivity assay and adverse long-term outcome in HC.[6]
In multivariate analysis, elevated hs-cTnT remained independently associated with the primary endpoint; together with non-sustained ventricular tachycardia (VT) on Holter monitoring (Figure 1 and Table 2)
Summary
HC.[1,2] In that regard, it is surprising that the role of cardiac troponin (cTn) in HC patients has not been extensively studied.[4,5,6,7] Elevated cTn is a common finding and associated with adverse disease characteristics, such as wall thickness and late gadolinium enhancement (LGE).[4,5,6,7,8] In 2013, the first report was published that demonstrated an association between elevated cTnT, assessed with a high-sensitivity assay (hs-cTnT) and adverse long-term outcome in HC.[6] Ever since, there is a paucity of confirmatory prospective data.[3,8,9,10] we aimed to validate the association between elevated hs-cTnT and adverse outcomes in a prospective HC cohort with 5 years of clinical follow-up
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