Are antiarrhythmic agents indicated in premature ventricular complex-induced cardiomyopathy and when?

INTRODUCTION: Premature ventricular complexes (PVCs) are the most common ventricular arrhythmia that are encountered in the clinical practice. Recent data suggests that high PVC burden may lead to the development of PVC-induced cardiomyopathy (PVC-CM) even in patients without structural heart disease. Treatment for effective suppression of PVCs, can reverse PVC-CM. Both antiarrhythmic drugs (AADs) and catheter ablation (CA) are recognized treatment modalities for any cardiac arrhythmias. However, with increasing preference of CA, the role of AADs needs further defining regarding their efficacy, safety, indications and patient selection to treat PVC-CM. METHODS: To ascertain the role of AADs to treat PVC-CM; whether they are indicated to treat PVC-CM, and if so, when, we interrogated PubMed and other search engines for English language publications with key words premature ventricular complexes (PVCs), cardiomyopathy, anti-arrhythmic drugs, catheter ablation, and pharmacological agents. All publications were carefully reviewed and scrutinized by the authors for their inclusion in the review paper. For illustration of cases, ethical standard was observed as per the 1975 Declaration of Helsinki, and the patient was treated as per the prevailing standard of care. Informed consent was obtained from the patient for conducting the ablation procedure. RESULTS: Our literature search specifically the pharmacological treatment of PVC-CM with AADs revealed significant paradigm shift in treatment approach for PVCs and PVC-induced cardiomyopathy. No major large, randomized control trials of AADs versus CA for PVC-CM were found. We found that beta-blockers and calcium channel blockers are particularly effective in the treatment of PVCs originating from right ventricular outflow tract. For Class Ic AADs - flecainide and propafenone, small clinical studies showed Class Ic AADs to be effective in PVC suppression, but their usage was not recommended in patients with significant coronary artery disease. Mexiletine was found to have modest effect on PVC suppression. Studies showed sotalol to significantly reduce PVCs frequency in patients receiving both low and high doses. Studies also showed amiodarone to have higher successful PVC suppression, but not recommended as a first-line treatment for patients with idiopathic PVCs in the absence of symptoms and left ventricular dysfunction. For dronedarone, no major clinical data were available. CONCLUSIONS: Based on the available data in the literature, we conclude that AADs play important role in the treatment of PVC-induced cardiomyopathy. However, appropriate patient selection criteria are vitally important, and in general terms AADs are indicated or polymorphic PVCs, epicardial PVCs; and when CA procedure is contraindicated, or not feasible or failed.

Premature ventricular contraction diurnal profiles predict distinct clinical characteristics and beta-blocker responses.

INTRODUCTION: Frequent premature ventricular complexes (PVCs) can lead to symptoms, such as cardiomyopathy and increased mortality. Beta-blockers are recommended as first-line therapy to reduce PVC burden; however, the response is unpredictable. The objective of this study is to determine whether PVC diurnal-variability patterns are associated with different clinical profiles and predict drug response. METHODS: Consecutive patients with frequent PVCs (burden ≥ 1%), referred for Holter monitoring between 2014 and 2016, were included. Follow-up Holters, when available, were assessed after beta-blocker initiation to assess response (≥50% reduction). Patients were divided into three groups on the basis of relationship between hourly PVC count and mean HR during each of the 24 Holter hours: (1) fast-HR-dependent-PVC (F-HR-PVC) for positive correlation (Pearson, P < 0.05), (2) slow-HR-dependent-PVC (S-HR-PVC) for a negative, and (3) independent-HR-PVC (I-HR-PVC) when no correlation was found. RESULTS: Of the 416 patients included, 50.2% had F-HR-PVC, 35.6% I-HR-PVC, and 14.2% S-HR-PVC with distinct clinical profiles. Beta-blocker therapy was successful in 34.0% patients overall: patients with F-HR-PVC had a decrease in PVC burden (18.8 ± 10.4% to 9.3 ± 6.6%, P < 0.0001; 62% success), I-HR-PVC had no change (18.4 ± 17.9% to 20.6 ± 17.9%, P = 0.175; 0% success), whereas S-HR-PVC had an increase in burden (14.6 ± 15.3% to 20.8 ± 13.8%, P = 0.016; 0% success). The correlation coefficient was the only predictor of beta-blocker success (AUC = 0.84, sensitivity = 100%, specificity = 67.7%; r ≥ 0.4). CONCLUSIONS: A simple analysis of Holter PVC diurnal variability may provide incremental value to guide clinical PVC management. Only patients displaying a F-HR-PVC profile benefited from beta-blockers. An alternative strategy should be considered for others, as beta-blockers may have no effect or can even be harmful.