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. 2009 Dec 30;33(2):E1–E7. 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

Toru Kubo 1, Hiroaki Kitaoka 1,, Makoto Okawa 1, Shigeo Yamanaka 2, Takayoshi Hirota 1, Eri Hoshikawa 1, Kayo Hayato 1, Naohito Yamasaki 1, Yoshihisa Matsumura 1, Nobufumi Yasuda 3, Tetsuro Sugiura 2, Yoshinori L Doi 1
PMCID: PMC6653149  PMID: 20043329

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. Copyright © 2010 Wiley Periodicals, Inc.

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