title: Effects of angiotensin-converting enzyme inhibitor therapy on presence of late potentials detected using signal-averaged electrocardiography in patients with congestive heart failure.
abstract: BACKGROUND
  Angiotensin-converting enzyme (ACE) inhibitors have been shown to improve the mortality rate in patients with congestive heart failure. The exact mechanism of this effect is uncertain. Signal-averaged electrocardiography has been used to evaluate the presence of late potentials as a marker for sudden cardiac death. We examined prospectively the effects of ACE inhibitor therapy on signal-averaged ECGs and ventricular arrhythmia frequency in 20 patients with moderate to severe left ventricular dysfunction and symptomatic congestive heart failure.
  
  
  METHODS
  A signal-averaged ECG and 24 h Holter monitor were performed immediately before and both 1 week and 6 weeks after captopril initiation. The mean dose of captopril at 6 weeks was 38 +/- 31 mg. The patients (19 men and one woman, mean age 63 +/- 12 years) had a baseline ejection fraction of 22 +/- 7% and mean functional class of 2.6 +/- 0.5. The cause of congestive heart failure was coronary artery disease in 18 patients, idiopathic cardiomyopathy in one, and valvular disease in one.
  
  
  RESULTS
  All three signal-averaged ECG time-domain parameters tended to improve over the course of the study (study 1, 2, 3: QRS duration (ms) = 108 +/- 11, 106 +/- 12, 105 +/- 11; low-amplitude signal duration (ms) = 30 +/- 8, 31 +/- 10, 28 +/- 10; root mean voltage (microV) = 33 +/- 20, 37 +/- 24, 40 +/- 2, respectively). These changes were not statistically significant, although the improvement in QRS duration was nearly so with P = 0.06. The occurrence and complexity of ventricular ectopy did not appear to be consistently altered.
  
  
  CONCLUSIONS
  ACE inhibitor therapy with captopril did not appear to alter ventricular ectopy over the course of this study. However, the trends toward improvement of signal-averaged ECG parameters deserve further evaluation in a larger and longer-term study.
authors.affiliation: Mid-America Heart Institute, St Luke's Hospital, Kansas City, Missouri.
authors.forename: J L
authors.initials: JL
authors.lastname: Vacek
authors.forename: L R
authors.initials: LR
authors.lastname: Handlin
authors.forename: C J
authors.initials: CJ
authors.lastname: Beaufort
authors.forename: C A
authors.initials: CA
authors.lastname: Koenig
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000328:Adult; D000368:Aged; D002216:Captopril / Q000494:pharmacology / Q000627:therapeutic use*; D002312:Cardiomyopathy, Hypertrophic / Q000150:complications; D003327:Coronary Disease / Q000150:complications; D015716:Electrocardiography, Ambulatory / Q000187:drug effects*; D005260:Female; D006333:Heart Failure / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology*; D006349:Heart Valve Diseases / Q000150:complications; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D013318:Stroke Volume / Q000187:drug effects*; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D002216:Captopril