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Cardiac troponin I and ventricular arrhythmia in patients with chronic heart failure
1Shandong University, Shandong Provincial Hospital, 324 Jingwu Weiqi Road, Jinan 250021, China. liuzunqi69@sina.com
Insights
Detectable serum cardiac troponin I (cTnI) in chronic heart failure (CHF) patients is linked to more frequent ventricular dysrhythmias. This finding may help identify patients at higher risk for ventricular tachycardia.
Area of Science:
- Cardiology
- Biomarkers
- Electrophysiology
Background:
- Ventricular dysrhythmias and elevated cardiac troponin I (cTnI) are common in chronic heart failure (CHF).
- The direct relationship between serum cTnI levels and the severity of ventricular arrhythmias in CHF patients was previously unclear.
- The underlying mechanisms driving ventricular arrhythmias in CHF patients remain incompletely understood.
Purpose of the Study:
- To investigate the association between detectable serum cTnI and the severity of ventricular dysrhythmias in patients with CHF.
- To determine if serum cTnI can identify a subgroup of CHF patients at increased risk for ventricular arrhythmias, particularly ventricular tachycardia.
Main Methods:
- A cohort of 218 patients with CHF was analyzed, excluding those with acute myocardial infarction or myocarditis.
- Patients were stratified into cTnI-positive (>0.5 ng mL(-1)) and cTnI-negative (<=0.5 ng mL(-1)) groups.
- Ventricular dysrhythmia severity was quantified using 24-hour Holter monitoring, assessing measures like hourly ventricular pairs, repetitive ventricular beats, and ventricular tachycardia frequency.
Main Results:
- Patients with detectable cTnI levels exhibited significantly higher mean hourly ventricular pairs, repetitive ventricular beats, and 24-hour ventricular tachycardia episodes.
- Multivariate analysis confirmed an independent positive relationship between cTnI levels and the frequency of ventricular pairs, repetitive beats, and ventricular tachycardia.
- Detectable cTnI was independently associated with a 2.31-fold increased risk of developing ventricular tachycardia (adjusted OR: 2.31; 95% CI, 1.22-2.65; P = 0.003).
Conclusions:
- Detectable serum cTnI is closely associated with an increased occurrence of ventricular dysrhythmias in patients with CHF.
- Serum cTnI can identify a subgroup of CHF patients with a higher burden of ventricular arrhythmias, including ventricular tachycardia.
- Minimal myocardial injury, indicated by detectable serum cTnI, may represent an abnormal substrate contributing to ventricular dysrhythmias in CHF.
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.
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