Comparison of frequency of late potentials in idiopathic dilated cardiomyopathy and ischemic cardiomyopathy with advanced congestive heart failure and their usefulness in predicting sudden death

Holly R. Middlekauff, William G. Stevenson, Mary A. Woo, Debra K. Moser, Lynne Warner Stevenson

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60 Scopus citations

Abstract

Signal-averaged electrocardiograms were obtained in 62 consecutive patients with advanced congestive heart failure (CHF) undergoing evaluation for possible heart transplantation to determine if late potentials: (1) provide unique information compared to assessment of ventricular ectopic activity on ambulatory electrocardiogram, and (2) identify a subgroup of CHF patients with higher sudden death risk. Patients with a history of cardiac arrest or sustained ventricular tachycardia were excluded. CHF was due to old myocardial infarction in 40 patients and idiopathic dilated cardiomyopathy in 22 patients. Late potentials were present in 16 of 40 (40%) patients with old infarction but in only 3 of 22 (14%) patients with nonischemic CHF (p = 0.03). Twenty-four-hour ambulatory electrocardiograms were obtained in 34 patients (55%). Total ventricular ectopic activity and repetitive forms of ectopy were similar in patients with and without late potentials. Nine patients died suddenly, 9 had nonsudden death, 15 underwent heart transplantation and 29 were alive and well after a mean follow-up of 218 ± 154 days. At 1 year, the actuarial risk of death was 37% and of sudden death was 20%. Sudden death risk was 12% in patients with late potentials versus 21% in those without (p = 0.73). Thus, the incidence of the arrhythmia substrate producing late potentials depends on the CHF etiology. The signal-averaged electrocardiogram and ambulatory electrocardiogram provide independent information for possible risk assessment in CHF. However, late potentials are poor predictors of sudden death risk when CHF is advanced, possibly due to the heterogeneity of causes of sudden death-ventricular tachycardia being only 1 of many possible mechanisms.

Original languageEnglish
Pages (from-to)1113-1117
Number of pages5
JournalAmerican Journal of Cardiology
Volume66
Issue number15
DOIs
StatePublished - Nov 1 1990

Bibliographical note

Funding Information:
From The Division of Cardiology, Department of Medicine, University of California at Los Angeles School of Medicine, Los Angeles, California 90024. Dr. Middlekauff is supported by National Research Service Award Institutional Training Grant 2-T32HL07412 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland. Manuscript received March 22, 1990; revised manuscript received June 22, 1990, and accepted June 24.

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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