Premature ventricular contractions: pathophysiology, prognostic impact, and management

Premature ventricular contractions (PVCs) arise from an early depolarization originating in either of the cardiac ventricles. They are common in individuals both with and without structural heart disease, although their true prevalence remains uncertain. Several electrophysiological mechanisms can initiate the PVC, with re-entry being the most frequent. The detection of PVCs should prompt a thorough clinical evaluation to identify potential underlying cardiac disease, yet many PVCs ultimately prove to be idiopathic. In individuals with established structural heart disease, PVCs have been associated with a poorer prognosis; however, clinical trials aimed at suppressing PVCs in this population have not demonstrated improved outcomes. In contrast, the prognostic significance of PVCs in patients without structural heart disease remains unclear. Factors such as PVC burden, PVC morphology, and cardiac magnetic resonance findings have been proposed as prognostic markers, although the evidence is still debated. In general, patients without structural heart disease and with a low PVC burden can be reassured regarding their prognosis. Treatment is primarily guided by symptoms, although reducing PVC burden may be considered even in asymptomatic individuals to mitigate the risk of complications such as PVC-induced cardiomyopathy or PVC-triggered sustained ventricular arrhythmias. Antiarrhythmic drugs are commonly used as first-line therapy, and the choice of medication should take into account patient characteristics, suspected pathophysiology, and PVC features. Catheter ablation (CA) is more effective than pharmacologic therapy in reducing or eliminating PVCs and may be considered as a first-line option in specific situations where rapid PVC suppression is desired. As an invasive procedure, CA carries potential risks that must be weighed carefully. Operator experience, PVC origin, anatomical considerations, and patient preference all play important roles in decision-making. Further research is needed to better identify patients at risk and to target specific pathophysiological mechanisms. Advances in device-based, patient-driven arrhythmia monitoring and the integration of artificial intelligence are likely to influence future PVC diagnostics and risk stratification.