Abstract
Two hundred one patients with acute transmural myocardial infarction were studied to determine the relation of heart block and the degree of left ventricular dysfunction. Right bundle branch block occurred in 17, left bundle branch block in 7 and either left anterior or left posterior hemiblock in 8 patients. Hemodynamic studies were carried out before heart block developed. Complete heart block occurred in 9 of 92 patients with diaphragmatic (inferior) myocardial infarction and in 6 of 109 with anterior infarction. In patients with diaphragmatic infarction who experienced complete heart block hemodynamic measurements before block did not differ significantly from those in patients without block. Similarly, in patients who had right bundle branch block or hemiblock the hemodynamic variables did not differ from those in patients without bundle branch block. In patients with anterior infarction who experienced complete heart block, however, stroke index (P < 0.01) and stroke work index (P < 0.05) were significantly lower before block than in patients without block. Similarly, patients with anterior infarction with progression to left bundle branch block had a lower stroke index (P < 0.002) and stroke work index (P < 0.05) than patients without bundle branch block. The data indicate that patients whose anterior infarction is followed by complete heart block or left bundle branch block have a greater degree of left ventricular dysfunction than patients with anterior infarction who do not manifest these conduction defects. The profound hemodynamic derangement in the patients with these defects is probably a result of more extensive myocardial necrosis. Complete heart block after diaphragmatic infarction and right bundle branch block and hemiblock were not associated with significantly different hemodynamic measurements, thus suggesting that these conduction defects are unrelated to the extent of left ventricular dysfunction. Although only a small number of patients with heart block were studied, careful analysis of the clinical and hemodynamic data support the findings.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 961-966 |
| Number of pages | 6 |
| Journal | American Journal of Cardiology |
| Volume | 39 |
| Issue number | 7 |
| DOIs | |
| State | Published - 1977 |
| Externally published | Yes |
Bibliographical note
Funding Information:From the Cardiology Unit, Department of Medicine, University of Rochester School of Medicine and Dentistry and Strong Memorial Hospital, Rochester, New York. This study was supported in part by Contract I HV 81331 and Training Grant HL 05500 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Manuscript received September 20, 1976; revised manuscript received December 13, 1976, accepted December 14, 1976. * Present address: Department of Medicine, University of Minnesota School of Medicine and Hennepin County Medical Center, Fifth and Portland South, Minneapolis, Minnesota 55415.
