Premature ventricular complex (PVC) is characterized by the premature occurrence of a QRS complex that is bizarre in shape and lasts longer than 120 msec. The T wave is large and usually of opposite polarity to the QRS complex. A PVC is usually followed by a full compensatory pause. PVCs are commonly encountered in apparently healthy individuals with a reported incidence of approximately 1% on standard 12-lead electrocardiograms (ECG) and 40% to 75% on routine 24 hour to 48 hour Holter monitoring. The clinical presentation may range from asymptomatic to left ventricular (LV) dysfunction with congestive heart failure. In many patients, ectopic ventricular events manifest as asymptomatic, isolated PVCs that have a benign prognosis in those without structural heart disease. In others, PVCs may be frequent and highly symptomatic, presenting as palpitations, chest discomfort, or presyncope. Clinical evidence suggests that frequent PVCs (variably defined in the literature) are more strongly associated with concomitant cardiac disease. The decision to suppress PVCs is largely based on the presence of symptoms, interference with other therapy (e.g., cardiac resynchronization therapy), or suspicion of PVC-mediated cardiomyopathy. When necessary, treatment for PVCs involves beta-blockers, calcium channel blockers, or other antiarrhythmic drugs and catheter ablation in selected cases. Catheter ablation of frequent PVCs has been demonstrated to be effective at PVC suppression and is associated with improvement or normalization of ventricular function.
