This is the development of a new site of depolarization in non-nodal ventricular tissue, which can lead to VPBs. Most of the information is derived from animal studies, from which three common mechanisms have been reported 2,11:Īutomaticity. Very few studies have evaluated the pathophysiology of VPBs in humans. 7 VPBs are increased in patients with dilated cardiomyopathy and heart failure, regardless of the etiology, 8,9 as well as in patients with congenital heart disease, in whom VPBs can result from the primary defect or operative repair. They are infrequently seen on an ECG by comparison, they can be detected in approximately 90% of such patients on a 24-hour ambulatory monitor. 6 The prevalence of VPBs in patients with coronary heart disease (CHD) varies considerably based upon the method of detection. 5 VPBs are common in patients after an acute myocardial infarction (MI), with a reported incidence as high as 93%. 4 Patients with hypertension are more likely to experience VPBs as seen in the ARIC study, hypertensive patients had a 23% increase in the prevalence of VPBs.
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