Premature ventricular contractions (PVCs) occur in up to 75% of healthy persons.
Symptoms include palpitations or the perception of skipped beats. Forceful beats are caused by increased cardiac filling during the pause following the PVC. PVCs are more common in patients with hypertension, left ventricular hypertrophy, previous myocardial infarction, and other forms of structural heart disease, such as nonischemic cardiomyopathy.
In the absence of high-risk features (syncope, a family history of premature SCD, structural heart disease), reassurance is appropriate management. PVCs require treatment when symptoms are bothersome or frequent (>10% of all beats or 10,000 PVCs per day). Tachycardia-induced cardiomyopathy may result from frequent PVCs.
First-line treatment for PVC suppression is β-blocker or calcium channel blocker therapy. β-Blockers are preferred in patients with ventricular dysfunction. If PVCs persist despite β-blockade or calcium channel blockade, antiarrhythmic drug therapy may be used. The selection of an antiarrhythmic medication for PVC suppression depends on many factors, including kidney function and comorbid conditions. In young healthy patients without structural heart disease, class IC drugs are usually effective. Amiodarone is most commonly used in patients with structural heat disease, particularly heart failure. Catheter ablation should be considered in patients with continued frequent PVCs despite medical therapy, those who cannot tolerate medical therapy, and patients who develop PVC-related left ventricular dysfunction.