Abstract

Premature ventricular contractions (PVCs) are early depolarizations of the myocardium originating in the ventricle. They are often seen in association with structural heart disease and represent increased risk of sudden death,1 yet they are ubiquitous, even in the absence of identifiable heart disease.1,2 They may cause troubling and sometimes incapacitating symptoms such as palpitations, chest pain, presyncope, syncope, and heart failure.3 Traditionally, they have been thought to be relatively benign in the absence of structural heart disease.4,5 Over the last decade, however, PVC-induced cardiomyopathy has been a subject of great interest and the evidence for this entity is rapidly emerging. ### Epidemiology PVCs are common with an estimated prevalence of 1% to 4% in the general population.5 In a normal healthy population, PVCs have been detected in 1% of subjects on standard 12-lead electrocardiography and between 40% and 75% of subjects on 24- to 48-hour Holter monitoring.6 Their prevalence is generally age-dependent,1 ranging from 75 years.8 Commonly thought to be a benign entity,4,5 the concept of PVC-induced cardiomyopathy was proposed by Duffee et al9 in 1998 when pharmacological suppression of PVCs in patients with presumed idiopathic dilated cardiomyopathy subsequently improved left ventricular (LV) systolic dysfunction. Many of these patients often have no underlying structural heart disease and subsequently develop LV dysfunction and dilated cardiomyopathy; in cases of those with an already impaired LV function from underlying structural heart disease, worsening of LV function may occur.10,11 The exact prevalence of PVC-induced cardiomyopathy is not known; it is an underappreciated cause of LV dysfunction, and it is primarily observed in older patients.12 This observation could be due to the fact that the prevalence of …

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