Premature ventricular contractions (PVCs) are frequently encountered in patients with or without structural heart disease. Even though PVCs in healthy subjects are considered to be a benign arrhythmia. There is also evidence for the risk of a reversible cardiomyopathy due to the PVC-induced inter- and intraventricular dyssynchrony. Data show that elimination of PVCs by catheter ablation leads to an improvement of left ventricular dysfunction. In one-half of the heart failure patients frequent PVCs occur with more than 1000/24 h. In patients with structural heart disease premature ventricular contractions (PVCs) lead to an increased mortality risk with only a burden of 10 PVC per hour. Further decreasing of left ventricular function and worsening of heart failure are described. Therefore, therapy of frequent monomorphic PVCs is recommended in these subjects. Beta-blockers as part of standard therapy often remain ineffective or may lead to a paradoxic effect in patients with bradycardia. A limiting factor for selection of antiarrhythmic drug due to increasing mortality is the presence of structural heart disease. So in the most cases amiodarone is indicated. There are data showing improvement of LV function after suppression of PVCs by amiodarone with a significant reduction of the PVC burden in comparison to baseline. However, the adverse effects of amiodarone are well-known especially in long-term therapy. On the other hand, radiofrequency catheter ablation is a widely applied and safe treatment option for PVCs with a high acute success rate of up to 90% PVC reduction in various circumstances like pre-existing heart failure and post myocardial infarction subjects. Some small-sample studies show the benefit of catheter ablation in subjects with depressed LV function. To date, there are no randomized data for comparison of catheter ablation and amiodarone for therapy of PVCs in patients with structural heart disease.