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. 2010 Feb;33(2):E1-7.
doi: 10.1002/clc.20622.

Serum cardiac troponin I is related to increased left ventricular wall thickness, left ventricular dysfunction, and male gender in hypertrophic cardiomyopathy

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Serum cardiac troponin I is related to increased left ventricular wall thickness, left ventricular dysfunction, and male gender in hypertrophic cardiomyopathy

Toru Kubo et al. Clin Cardiol. 2010 Feb.

Abstract

Background: Serum cardiac troponin I (cTnI) is a sensitive and specific marker of myocardial injury. However, a systematic evaluation of cTnI in hypertrophic cardiomyopathy (HCM) patients has not been performed.

Hypothesis: The purpose of this study is to evaluate cTnI and determine its relationship to clinical features in HCM.

Methods: We studied serum cTnI in 162 consecutive HCM patients.

Results: Serum cTnI ranged from 0.01 to 0.83 ng/mL (mean, 0.068 +/- 0.100 ng/mL) and was higher in male patients (P < .001), those with atrial fibrillation (P = .033), and left ventricular (LV) systolic dysfunction (P = .046). Serum cTnI values were also correlated with maximum LV wall thickness (r = 0.30, P < .001), LV end-systolic diameter (r = 0.20, P = .012), and E/Ea (peak early transmitral filling velocity/early diastolic mitral annulus velocity; r = 0.24, P = .004). Serum cTnI levels were not significantly different among New York Heart Association (NYHA) functional class and there was no difference between patients with or without LV outflow tract obstruction; although B-type natriuretic peptide (BNP) levels showed significant difference in those variables. Serum cTnI had very weak correlation with BNP values (r = 0.18, P = .023). Multivariate analysis revealed an independent relationship between cTnI and maximum LV wall thickness, E/Ea, and male gender.

Conclusions: In patients with HCM, serum cTnI was associated with important clinical indices such as maximum LV wall thickness, LV dysfunction, and male gender. Serum cTnI seemed to have clinical significance different from that of BNP and may not be reflecting cardiac load but the LV remodeling process in HCM.

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