Author + information
- Received August 4, 1995
- Revision received October 4, 1995
- Accepted October 11, 1995
- Published online March 1, 1996.
- James J. Milavetz, MD,
- Thomas E. Raya, MD,
- Cynthia S. Johnson, BS,
- Eugene Morkin, MD and
- Steven Goldman, MD, FACC∗
- ↵∗Address for correspondenceDr. Steven Goldman, Cardiology Section. 111 C, Tucson Veterans Affairs Medical Center, Tucson, Arizona 85723, USA
Objectives. This study sought to compare the effects of angiotension-converting enzyme inhibition versus angiotensin II receptor blockade on survival in rats with myocardial infarction.
Background. The effects of speciifc nonpeptide angiotensin receptor blocking agents on survival after myocardial infarction are unknown.
Methods. Rats with a moderate to large myocardial infarction were treated with captpril (2 g/liter drinking water, n= 87) or losartan (2 g/liter drinking water, n= 96). Therapy was initiated immediately after coronary artery ligation and continued for 1 years.
Results. Uncensored median survival in captopril-treated rats that survived at least 48 h was 201.5 days versus 236.0 days for losartan-treated rats (p = 0.066). Median survival censored for rats with lung infections was 201.5 days in captopril-treated rats versus 243.0 days for losartan-treated rats (p = 0.028). Conscious hemodynamic measurements and remodeling data obtained at 1 year in the surviving rats (n = 5 for captopril; n = 9 for losartan) revealed no differences in heart weight, left ventricular pressure, dP/dt, cardiac index, time constant of relaxation or any variable of left ventricular remodeling. The only differences (mean ± SD) were an increase in heart rate (293 ± 19 vs. 260 ± 15 beats/min, p < 0.05) and a decrease in peak developed pressure (153 ± 21 vs. 180 ± 16 mm Hg, p < 0.05) in the losartan-treated rats.
Conclusions. We conclude that in this experimental model of heatr failure, there was no difference between survival after angiotensin II receptor blockade with losartan and with angiotensin-converting enzyme inhibition with captopril.
☆ This study was supported by grants from the Department of Veterans Affairs, Washington, D.C.; National Heart, Lung, and Blood Institute (Program Project) HL-20984 and RO1 HL-48163), National Institutes of Health, Bethesda, Maryland; Arizona Disease Control Research Commission (Grant 82-0697); American Heart Heart Association, Arizona Affiliate; and Du Pont Merck Pharmaceutical Company
- Received August 4, 1995.
- Revision received October 4, 1995.
- Accepted October 11, 1995.