Author + information
- Received May 13, 1992
- Revision received August 4, 1992
- Accepted August 13, 1992
- Published online March 1, 1993.
- John A. Rumberger, PhD, MD, FACC∗,1,
- Thomas Behrenbeck, MD, PhD,
- Jerome R. Breen, MD,
- Judd E. Reed, BS and
- Bernard J. Gersh, MB, ChB, DPhil, FACC
- ↵∗Address for correspondence: John A. Rumberger, PhD, MD, Department of Cardiovascular Diseases and Internal Medicine, Mayo Clinic and Foundation, 200 First Street SW, Rochester, Minnesota 55905.
Objectives. This study was designed to serially assess time-dependent changes in both chamber volume and myocardial muscle mass after infarction in humans.
Background. Dilation of the left ventricular chamber has been previously described after transmural myocardial infarction.
Methods. Global left ventricular chamber volumes and muscle mass were quantified by using cine computed tomographic scanning in 18 patients at hospital discharge and 6 weeks, 6 months and 1 year after an initial transmural myocardial infarction (12 anterior and 6 inferior). No patient had heart failure during the initial hospital stay or on any subsequent follow-up visit.
Results. The patients with anterior myocardial infarction (estimated infarct extent 27 ± 2% of left ventricle) demonstrated a progressive increase in left ventricular end-diastolic volume from 148 ± 9 ml (mean ± SEM) at hospital discharge to 180 ± 9 ml at 1 year after infarction (p < 0.001). However, global left ventricular muscle mass decreased significantly during the 1st 6 weeks after infarction but returned by 1 year to nearly the value determined at hospital discharge (177 ± 13 vs. 165 ± 10 g, p = NS). The changes in global muscle mass did not parallel the steady and progressive increases in chamber end-diastolic volume. The end-diastolic chamber volume to muscle mass ratio, an index of global left ventricular wall tension, increased steadily after hospital discharge but remained level by 1 year after infarction. The time course of changes in global end-systolic chamber volume was roughly proportional to the concomitant changes in end-diastolic volume. During this same time period, left ventricular stroke volume remained constant or improved from that determined at baseline. Global left ventricular end-diastolic and end-systolic volumes remained relatively static daring the 1st year in the patient subgroup with inferior wall myocardial infarction (estimated infarct extent 10 ± 1% of left ventricle), but global muscle (myocardial) mass initially decreased and then increased in a pattern similar, although of smaller magnitude, to that observed in patients with anterior wall myocardial infarction.
Conclusions. Overall, left ventricular end-diastolic and eadsystolic chamber volumes increase progressively from hospital discharge to 1 year after an initial transmural myocardial infarction in patients with a moderately large anterior wall infarction hut remain stable in patients with a small inferior wall infarction. Concurrently, total left ventricular muscle mass decreases significantly during the initial 6 weeks after infarction (presumed largely secondary to changes in the necrotic segments) but then returns to the hospital discharge baseline values by 1 year. These data are consistent with the late development of, at most, limited ventricular hypertrophy in the noninfarcted myocardium that occurs well after the early and progressive left ventricular chamber dilation observed in patients with a moderate to large myocardial infarction. These data, in particular as applied to patients with anterior infarction, suggest that ventricular wall tension is significantly elevated at least during the 1st year after an initial transmural myocardial infarction. These observations nay explain the potential utility of agents aimed at reducing afterload or ventricular wall tension during the early convalescent phase after myocardial infarction.
↵1 Dr. Rumberger is supported by an Established Investigator Award from the American Heart Association, Dallas, Texas; Grant 34508 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, and the Mayo Foundation, Rochester.
☆ This study was presented in part at the 64th Annual Scientific Sessions of the American Heart Association, Anaheim, California, November 1991.
- Received May 13, 1992.
- Revision received August 4, 1992.
- Accepted August 13, 1992.