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.
The purpose of this study is to evaluate cTnI and determine its relationship to clinical features in HCM.
We studied serum cTnI in 162 consecutive HCM patients.
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.
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.
"Cardiac troponin assays have been previously established to be associated with degree of hypertrophy in patients with known HCM . CTnI is correlated with maximal LV wall thickness in patients with hypertrophic cardiomyopathy . Moreno et al. described an outpatient population with HCM, in who 42% had an elevated hsTnT level, and patients with higher hsTnT levels were more likely to have symptoms of dyspnoea and/or fibrosis on cardiac MRI evaluation . "
[Show abstract][Hide abstract] ABSTRACT: Hypertrophic cardiomyopathy (HCM) is a genetic condition, and relatives of affected persons may be at risk. Cardiac troponin biomarkers have previously been shown to be elevated in HCM. This study examines the new highly-sensitive cardiac troponin I (hsTnI) assay in a HCM screening population.
Nested case--control study of consecutive HCM sufferers and their relatives recruited from May 2010 to September 2011. After informed consent, participants provided venous blood samples and clinical and echocardiographic features were recorded. Associations between the natural log (ln) of the contemporary troponin I (cTnI) and hsTnI assays and markers of cardiac hypertrophy were examined. Multiple regression models were fitted to examine the predictive ability of hsTnI for borderline or definite HCM.
Of 107 patients, 24 had borderline and 19 had definite changes of HCM. Both TnI assays showed significant, positive correlations with measures of cardiac muscle mass. After age and sex adjustment, the area under the receiver operator characteristic (AUROC) curve for the outcome of HCM was 0.78, 95% CI [0.65, 0.90], for ln(hsTnI), and 0.66, 95% CI [0.51, 0.82], for ln(cTnI) (p=0.11). Including the hsTnI assay in a multiple-adjusted "screening" model for HCM resulted in a non-significant improvement in both the AUROC and integrated discrimination index.
Both cTnI and hsTnI show a graded, positive association with measures of cardiac muscle mass in persons at risk of HCM. Further studies will be required to evaluate the utility of these assays in ECG- and symptom-based identification of HCM in at-risk families.
"Several echocardiogram parameters have been reported as predictors of AF occurrence. Kubo et al.  reported a relationship between cTnI serum levels and important echocardiograph indices such as maximum left ventricle wall thickness and left ventricle dysfunction in 162 consecutive patients with hypertrophic cardiomyopathy. They suggest that the relationship between cTnI, left ventricle wall thickness and left ventricle dysfunction is due to myocyte injury, resulting in replacement fibrosis that leads to left ventricle dysfunction. "
[Show abstract][Hide abstract] ABSTRACT: Atrial fibrillation (AF) remains a frequent complication after coronary artery bypass graft surgery (CABG). We evaluate the association of AF occurrence and serum cardiac troponin I (cTnI) levels in the early postoperative period after CABG. Between April 2009 and January 2010, 95 consecutive patients with sinus rhythm who underwent CABG were evaluated. The patients were divided into two groups according to their postoperative rhythms: sinus rhythm group (SR) and AF group (AF). Demographic, clinical variables, and troponin I were evaluated at the pre- and postoperative times. There were no clinical or demographic differences between the two groups. The postoperative troponin I in the SR group was lower than that in the AF group (0.66 ± 1.62 vs. 2.07 ± 5.01 ng/ml; P = 0.029). Using the receiver operating characteristic curves was found as the best cut-off value to predict AF occurrence at the value of 0.901 ng/ml. Using this value of cTnI, a sensitivity of 60% and a specificity of 87% for AF onset prediction were observed. The cTnI serum levels at the postoperative period after CABG were higher in patients who subsequently developed AF. The cut-off value of 0.901 ng/ml is useful for prediction and preventive therapeutic actions.
Interactive Cardiovascular and Thoracic Surgery 11/2011; 14(1):22-5. DOI:10.1093/icvts/ivr019 · 1.16 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Hypertrophic cardiomyopathy (HCM) is characterized by inappropriate hypertrophy, small-vessel coronary artery disease, myocyte disarray, and increased interstitial fibrosis. High-sensitivity troponin T (hs-TnT) could be a reliable indicator of myocardial remodeling, a proposed prognostic marker in HCM. Therefore we hypothesized that increased hs-TnT levels are related to different variables associated with myocardial remodeling, such as the presence of fibrosis assessed with cardiac magnetic resonance imaging (MRI).
We included 95 hemodynamically stable HCM patients, 72 male, aged 45.7 ± 14.2 years, and 45 healthy control subjects with similar age and gender. A complete history and clinical examination was performed, including 12-lead electrocardiogram (ECG), echocardiography, 24-hour ECG-Holter monitoring, symptom-limited treadmill exercise test, and late gadolinium enhancement in cardiac MRI. Risk factors for sudden death were evaluated. A blinded cardiac MRI was performed with late gadolinium enhancement study. Serum hs-TnT levels were assayed. A high proportion (42%) of hemodynamically stable patients studied showed increased levels of hs-TnT. The hs-TnT levels were raised in patients with severe dyspnea: New York Heart Association (NYHA) functional class ≥3 (P = .020), outflow obstruction (P = .013), systolic dysfunction (P = .037), abnormal blood pressure response (P = .036), and presence of gadolinium enhancement (P = .021). The hs-TnT levels correlated positively with the maximum left ventricular wall thickness (r = 0.47; P < .001), left atrial diameter (r = 0.36, P = .014), and outflow gradient (r = 0.28; P = .008).
A high proportion of hemodynamically stable patients show increased levels of hs-TnT. We observed that raised hs-TnT serum levels are associated with different conditions related to the severity of the disease.
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