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Premature ventricular contractions (PVCs) are ubiquitous. In patients with frequent PVCs (>1000/24 h) 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 haemodynamic impairment, including increased LV end-diastolic dimension (LVEDD), diastolic dysfunction and elevated brain naturetic peptide levels.3–5 Pharmacological suppression6 or catheter ablation7–10 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-recognised, aetiology for non-ischaemic dilated cardiomyopathy, initiated and maintained by the long-term adverse consequences of frequent ventricular ectopy.
There are substantial gaps in our understanding of this process. There are no epidemiological data defining the prevalence of high-frequency PVCs assessed by 24 h monitoring in the general population; the size of the population at risk for developing cardiomyopathy is unknown. Is the risk determined by absolute PVC frequency alone? PVC frequency is at least modestly correlated to the extent of LV dysfunction and ventricular dilation at the time of initial clinical presentation;7 9–11 the vast majority of patients who demonstrated improved ventricular function following ablation had PVC frequencies >10 000/24 h.7–10 …
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