Premature ventricular contractions (PVCs) are ubiquitous. In patients with frequent PVCs (>1000/24 hr) but no evidence of cardiac disease, longitudinal studies in small populations suggest that the risk of new cardiovascular events or death over the subsequent 10 years differed little from the general population (1,2). These findings helped generate the concept of the “benign” PVC. However, despite a normal left ventricular ejection fraction (LVEF), many patients have evidence of more subtle hemodynamic impairment, including increased LV end diastolic dimension (LVEDD), diastolic dysfunction, and elevated brain naturetic peptide levels (3-5). Pharmacologic suppression (6) or catheter ablation (7-10) of very frequent PVCs in selected patients with reduced LVEF but no other cardiac abnormalities can restore normal ventricular function and dimensions. Collectively, these data define an important, if under-recognized, etiology for nonischemic dilated cardiomyopathy, initiated and maintained by the long-term adverse consequences of frequent ventricular ectopy.
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