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Published on: December 11, 2017
Concomitant beta-blocker therapy is associated with a lower occurrence of ventricular arrhythmias in patients with
Doron Aronson1, Andrew J Burger
1Division of Cardiology, Rambam Medical Center, Haifa, Israel.
Insights
Beta-blocker therapy significantly reduces ventricular arrhythmias in patients with decompensated heart failure. This finding suggests beta-blockers may prevent sudden cardiac death by suppressing dangerous heart rhythms.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Ventricular arrhythmias are common in advanced heart failure (CHF) and contribute to mortality.
- Beta-blockers are hypothesized to reduce sudden death in CHF by suppressing these arrhythmias.
- Data supporting this in decompensated CHF with neurohumoral activation is limited.
Purpose of the Study:
- To investigate the effect of beta-blocker therapy on ventricular arrhythmias in patients hospitalized for decompensated congestive heart failure.
Main Methods:
- Studied 236 patients with decompensated CHF, 50 on beta-blockers.
- Assessed ventricular ectopy using 24-hour Holter monitoring.
- Analyzed measures including premature ventricular beats (PVCs), couplets, and ventricular tachycardia.
Main Results:
- Patients on beta-blockers showed significantly lower rates of ventricular ectopy.
- Reductions observed: 15% in hourly PVCs, 75% in couplets, 72% in repetitive PVCs, 87% in ventricular tachycardia.
- These reductions remained significant and independent in multivariate analysis.
Conclusions:
- Concomitant beta-blocker use during heart failure decompensation is linked to reduced complex ventricular ectopy and ventricular tachycardia.
- This anti-arrhythmic effect may offer protection against serious arrhythmias during heightened sympathetic activity in CHF.
Background:
Ventricular arrhythmias are nearly universally present in patients with advanced congestive heart failure (CHF) and represent an important cause of mortality in these patients. One of the putative mechanisms for the salutary effects of beta-blockers on sudden death mortality in heart failure is their ability to suppress ventricular arrhythmias. However, supporting data in patients with CHF are sparse, especially in the setting of excessive neurohumoral activation associated with symptomatic decompensated heart failure.
Methods And Results:
We studied 236 patients (159 men; mean age, 61 +/- 14 years) admitted for decompensated CHF. Fifty patients were receiving beta-blockers at the time of the study. The severity of ventricular arrhythmia was assessed by 24-hour Holter recordings by using several prospectively defined measures of ventricular ectopy. All measures of ventricular ectopy were lower in patients receiving beta-blockers. The average hourly total premature ventricular beats (PVCs), hourly ventricular couplets, repetitive PVCs, and frequency of ventricular tachycardia episodes were 15% (P =.02), 75% (P <.05), 72% (P <.05), and 87% (P =.01) lower in patient receiving beta-blockers, respectively. In a multivariate regression analysis, the negative relationship between beta-blockers and the average hourly PVCs (P =.03), the frequency of ventricular pairs (P =.03), repetitive PVCs (P <.05), and ventricular tachycardia episodes (P =.01) remained significant and independent.
Conclusions:
Concomitant beta-blocker therapy during heart failure decompensation is associated with a marked reduction in complex ventricular ectopy and episodes of ventricular tachycardia. This effect of beta-blockers may play an important protective role by preventing serious ventricular arrhythmias during transient increases in sympathetic activity.
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