Author + information
- Received May 30, 1995
- Revision received August 9, 1995
- Accepted August 17, 1995
- Published online January 1, 1996.
- Christoper M. Kramer, MD, FACCa,**,1,
- Victor A. Ferrari, MD, FACC*,
- Walter J. Rogers, MSa,
- Therese M. Theobald, RDCSa,
- Michael L. Nance, MD*,
- Leon Axel, PhD, MD* and
- Nathaniel Reichek, MD, FACCa
- ↵**Address for correspondence: Dr. Christopher M. Kramer, Cardiology Division, Allegheny General Hospital, 320 East North Avenue, Pittsburgh, Pennsylvania 15212.
Objectives. We hypothesized that angiotensin-converting enzyme inhibitors would limit dysfunction in the first 8 weeks after transmural infarction in adjacent noninfarcted regions, as well as attenuate left ventricular remodeling.
Background. Angiotensin-converting enzyme inhibition limits ventricular dilation and hypertrophy and improves survival after anterior infarction, but its effect on regional function during remodeling is not well characterized.
Methods. Thirteen sheep underwent coronary ligation to create an anteroapical infarction. At postinfarction day 2, eight sheep were randomized to therapy with the angiotensin-converting enzyme inhibitor ramipril, and five sheep received no therapy. Animals were studied with magnetic resonance myocardial tagging before and 8 weeks after infarction. Left ventricular volume, mass and ejection fraction were measured, as were changes in percent circumferential shortening within the subendocardium and subepicardium of infarcted and noninfarcted myocardium, both adjacent to and remote from the infarction.
Results. Angiotensin-converting enzyme inhibition limited the increase in end-diastolic volume from a mean (±SD) of +1.5 ± 0.7 ml/kg in control animals to +0.5 ± 0.8 ml/kg in the treated group (p < 0.04). Segmental function within infarcted and remote noninfarcted tissue did not differ between groups. However, angiotensin-converting enzyme inhibition limited the decline in function in the adjacent noninfarcted region 8 weeks after infarction. Percent circumferential shortening in the subendocardium decreased by −13 ± 5% in the control group compared with −5 ± 5% in the treated group (p < 0.03).
Conclusions. In concert with a reduction in left ventricular remodeling after anterior infarction, angiotensin-converting enzyme inhibition limits the decline in function in the adjacent noninfarcted region. Dysfunction in adjacent noninfarcted regions may be an important determinant of left ventricular remodeling after infarction.
↵1 Dr. Kramer was supported in part by Grant F32 HL 08708 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland and by an Allegheny-Singer Research Institute New Investigator's Award, Pittsburgh, Pennsylvania.
This work was also supported in part by Grants HL 42958 and HL 43014 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland and by a grant-in-aid from the American Heart Association (Pennsylvania affiliate).
- Received May 30, 1995.
- Revision received August 9, 1995.
- Accepted August 17, 1995.
- American College of Cardiology