TY - JOUR
T1 - Physical working capacity after acute myocardial infarction in patients with low ejection fraction and effect of captopril
AU - Hartley, L. Howard
AU - Flaker, Greg
AU - Basta, Lofty
AU - Menapace, Frank
AU - Goldman, Steven
AU - Davis, Barry
AU - Hamm, Peggy
AU - Lamas, Gervasio
AU - Moye, Lemuel
AU - Wun, Chuan Chuan
AU - Pfeffer, Marc
N1 - Funding Information:
From Bri ham and Women’s Hospital, Boston, Massachusetts; University o P.M rssoun Medical Center, Columbia, Missouri; Tulsa Heart Institute, Tulsa, Oklahoma; Geisinger Medical Center, Danville, Pennsylvania; Veterans Administration Medical Center and University of Arizona, Tucson, Arizona; University of Texas School of Public Health, Houston, Texas; and the Sinai Medical Center, Miami Beach, Florida. This study was supported by a grant from Bristol-Myers S uibb Princeton, New Jersey, as an ancillary trial of the Survival an l Vei tricular Enlargement (SAVE) study. Manuscri t received April 6, 1995; revised manuscript received and accept e&uly 24, 1995.
PY - 1995/11/1
Y1 - 1995/11/1
N2 - Previous studies after acute myocardial infarction (AMI) have reported conflicting results on the effects of angiotensin-converring enzyme inhibition on physical working capacity. In an effort to provide more insight into this subject, we examined the effects of captopril on working capacity of patients who had low ejection fractions but no congestive heart failure after AMI. One hundred sixty-six participants were recruited from 5 centers after randomization to either captopril or placebo for the Survival and Ventricular Enlargement study. Upright cycle ergometer tests were performed with continuous measurements of respiratory gases at 4, 12, and 24 months after AMI. Our study concurs with 2 of 3 previous post-AMI studies and supports the conclusion that working capacity is not affected by angio-tensin-converring enzyme inhibition at 4 or 12 months after AMI in patients without congestive heart failure. In addition, no significant effect of captopril was noted at 24 months after AMI. Peak oxygen uptake tended to decrease between 12 and 24 months in the placebo group by an average (± SD) of -22 ± 322 ml/min (n = 66), but to increase in the captopril group (+62 ± 289, n = 57), a difference that was significant (Mann-Whitney chi-square, p = 0.02). This post-hoc observation suggests that a late beneficial effect may have been masked by inadequate study duration. Known benefits of captopril appear not to include an increase in working capacity within the first 24 months after AMI.
AB - Previous studies after acute myocardial infarction (AMI) have reported conflicting results on the effects of angiotensin-converring enzyme inhibition on physical working capacity. In an effort to provide more insight into this subject, we examined the effects of captopril on working capacity of patients who had low ejection fractions but no congestive heart failure after AMI. One hundred sixty-six participants were recruited from 5 centers after randomization to either captopril or placebo for the Survival and Ventricular Enlargement study. Upright cycle ergometer tests were performed with continuous measurements of respiratory gases at 4, 12, and 24 months after AMI. Our study concurs with 2 of 3 previous post-AMI studies and supports the conclusion that working capacity is not affected by angio-tensin-converring enzyme inhibition at 4 or 12 months after AMI in patients without congestive heart failure. In addition, no significant effect of captopril was noted at 24 months after AMI. Peak oxygen uptake tended to decrease between 12 and 24 months in the placebo group by an average (± SD) of -22 ± 322 ml/min (n = 66), but to increase in the captopril group (+62 ± 289, n = 57), a difference that was significant (Mann-Whitney chi-square, p = 0.02). This post-hoc observation suggests that a late beneficial effect may have been masked by inadequate study duration. Known benefits of captopril appear not to include an increase in working capacity within the first 24 months after AMI.
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U2 - 10.1016/S0002-9149(99)80249-5
DO - 10.1016/S0002-9149(99)80249-5
M3 - Article
C2 - 7484820
AN - SCOPUS:0028889261
SN - 0002-9149
VL - 76
SP - 857
EP - 860
JO - The American Journal of Cardiology
JF - The American Journal of Cardiology
IS - 12
ER -