Background: Both detectable serum cardiac troponin I (cTnI) and ventricular dysrhythmias are common in patients with chronic heart failure (CHF) and are paralleled with the severity of the CHF. However, the relationship between serum cTnI and ventricular arrhythmia severity in patients with CHF remains unknown; the mechanism of the ventricular arrhythmia in the CHF patients also remains unclear.
Materials and methods: The study group included 218 patients with CHF who had cTnI assay drawn at the time of initial presentation. Patients with acute myocardial infarction or myocarditis were excluded from the analysis. The patients were divided into two groups: cTnI-positive with serum cTnI > 0.5 ng mL(-1) (n = 98) and cTnI-negative with serum cTnI < or = 0.5 ng mL(-1) (n = 120). The severity of ventricular dysrhythmias was assessed by 24-h Holter monitoring, using prospectively defined measures of ventricular arrhythmic burden.
Results: Prevalence of risk factors for ventricular dysrhythmias was equal in both groups. All measures of ventricular ectopy were much higher in patients of the cTnI-positive groups. Mean hourly ventricular pairs (13.59 +/- 10.3 vs. 11.1 +/- 6.01, P = 0.027), mean hourly repetitive ventricular beats (26.01 +/- 13.67 vs. 22.01 +/- 13.56, P = 0.032), and the frequency of ventricular tachycardia episodes per 24 h (12.54 +/- 16.68 vs. 7.68 +/- 11.54, P = 0.012) were higher in patients with detectable cTnI levels. After inclusion of clinical variables and drug therapies in a multivariate analysis, the positive relationship between cTnI and the frequency of ventricular pairs (P = 0.03), repetitive ventricular beats (P = 0.037), and ventricular tachycardia (P = 0.03) remained independent. In multivariate logistic regression, the risk of developing ventricular tachycardia was higher in patients with detectable cTnI levels with an adjusted odds ratio (OR) of 2.31 (95% CI, 1.22-2.65, P = 0.003).
Conclusions: In patients with CHF, serum cTnI is closely related to increased occurrence of ventricular dysrhythmias and could identify a subgroup of patients with ventricular tachycardia. The minimal myocardial injury detected by serum cTnI might be the abnormal substrate for ventricular dysrhythmias.