A Review of the Potential Pathogenicity and Management of Frequent Premature Ventricular Contractions

Very frequent premature ventricular complexes (PVCs) may be a reversible cause of dilated cardiomyopathy. Literature on this largely unrecognized entity has increased in the last 15 years. This paper reviews the literature on the consequences of frequent PVCs on myocardial function and management of PVC-associated cardiomyopathy. The authors reviewed articles published in English before June 2015 describing pathophysiology, risk factors, symptoms, time course, treatment, and outcome of cardiomyopathy associated with PVCs. The search was conducted using Medline and Embase. Keywords included: cardiomyopathy, catheter ablation, antiarrhythmic drug (AAD), pathophysiology, and ventricular premature contractions or synonyms. PVC-associated cardiomyopathy is associated with a high burden of PVC (over 20% of heartbeats). Other risk factors include electrophysiological characteristics, such as PVC QRS width, presence of ventricular tachycardia, retrograde P waves, interpolation, polymorphic PVCs, and longer coupling intervals. Symptoms include palpitations, light-headedness, dyspnea, cough, and dysphagia. The systolic dysfunction and chamber dilatation progress over a few years. Once the PVCs are suppressed by radiofrequency ablation or AADs, the cardiomyopathy usually resolves within 6 months. The pathophysiology remains unknown, but hypotheses mainly include ventricular dyssynchrony resulting in hemodynamic disturbances and abnormalities in calcium handling and oxygen consumption. PVC-associated cardiomyopathy remains a largely unrecognized entity. It is a reversible cause of dilated cardiomyopathy that results from abnormal calcium and oxygen handling within the myocyte, dyssynchrony, and hemodynamic compromise from inefficient heartbeats. Suppression of the PVCs improves myocardial function, cardiac chamber sizes, and patient's symptoms.