Effect of carvedilol on premature ventricular complexes originating from the ventricular outflow tract

Abstract

Abstract Background Carvedilol is one of the most effective beta-blockers in reducing ventricular tachyarrhythmias and mortality in patients with heart failure. One of the possible antiarrhythmic mechanisms of carvedilol is the suppression of store overload-induced Ca2+ release, especially for the triggered activity. Objectives Premature ventricular complex (PVC) originating from the ventricular outflow tract (OT) is the most common form of idiopathic PVC, and its main mechanism is related to triggered activity. We evaluate the efficacy of carvedilol to suppress the OT PVC. Methods The electronic medical records at our hospital were screened to identify OT PVC patients treated with carvedilol. Clinical, electrocardiographic, and Holter monitoring studies were reviewed. Results A total of 25 patients who underwent Holter monitoring before and after carvedilol administration were found and enrolled. The mean age of the patients was 54.9 ± 13.9 years, and the mean dose of carvedilol was 18.2 ± 10.2 mg (sustained release formulation, 8/16/32 mg). The 24-h burden of PVC in 18 (72%) of 25 patients was significantly reduced from 12.2 ± 9.7% to 4.4 ± 6.7% (P = 0.006). In seven patients, the burden of PVC was changed from 7.1 ± 6.1% to 9.8 ± 8.4% (P = 0.061). There was no difference in age, carvedilol dose, duration of treatment, ventricular function, and left atrial size between responding and non-responding groups. Conclusion In this retrospective pilot study, treatment with carvedilol showed PVC suppression in 72% of patients. Now, we are conducting a prospective, randomized, multicenter study to evaluate the effect of carvedilol on OT PVC (Clinical trial registration: FOREVER trial, Clinical-Trials.gov: NCT03587558).

Keywords

• Carvedilol
• Premature ventricular complex
• Ryanodine receptor calcium release
• Triggered activity