The cause of premature ventricular contraction (PVC)-mediated cardiomyopathy is unknown. The estimated prevalence of PVCs is high in the general population with reported 40-75% on ambulatory monitoring. PVCs are often considered benign, but may be associated with increased risk of sudden death or associated with chest pain, syncope, or heart failure, especially when structural heart disease is present. A long-term study on patients with relatively low PVC burden showed no difference in survival. However, high PVC burden is associated with lower left ventricular function in patients with and without structural disease. Unfortunately, suppressing PVCs by ablation or antiarrhythmic medications do not always improve ventricular function in patients. Animal models have showed that bigeminy pacing near the apex could induce a cardiomyopathy that is reversible without myocardial structural changes. However, these models do not explain the lack of cardiomyopathy development in some human subjects with frequent PVCs such as bigeminy. We propose that frequent pathologic PVCs lead to PVC- induced cardiomyopathy in normal hearts and PVC-worsened cardiomyopathy in hearts with abnormal tissue characteristics. The pathologic versus benign PVCs can be determined by LV function during PVC, which is quantitatively assessed using advanced real-time cardiac magnetic resonance imaging (MRI) techniques. LV function during PVC is likely a result of a combination of factors including PVC site of origin, coupling interval, and conduction time through the myocardium. Together with tissue characterization of the ventricular myocardium by cardiac MRI and electroanatomic voltage mapping, this proposal seeks to identify hemodynamic and structural features in PVC-induced or worsened cardiomyopathy in order to better select patients for treatment.