(Circulation. 1999;99:135-142.)
© 1999 American Heart Association, Inc.
Basic Science Reports |
From the Departments of Surgery and Medicine, School of Medicine and Department of Bioengineering, University of Pennsylvania, Philadelphia, Pa.
Correspondence to Dr L. Henry Edmunds, Jr, Department of Surgery, 6 Silverstein, Hospital of the University of Pennsylvania, Philadelphia, PA 19104. E-mail hedmunds{at}mail.med.upenn.edu
BackgroundExpansion of an acute myocardial infarction predicts progressive left ventricular (LV) dilatation, functional deterioration, and early death. This study tests the hypothesis that restraining expansion of an acute infarction preserves LV geometry and resting function.
Methods and ResultsIn 23 sheep, snares were placed around the distal left anterior descending and second diagonal coronary arteries. In 12 sheep, infarct deformation was prevented by Marlex mesh placed over the anticipated myocardial infarct. Snared arteries were occluded 10 to 14 days later. Serial hemodynamic measurements and transdiaphragmatic quantitative echocardiograms were obtained up to 8 weeks after anteroapical infarction of 0.23 of LV mass. In sheep with mesh, circulatory hemodynamics, stroke work, and end-systolic elastance return to preinfarction values 1 week after infarction and do not change subsequently. Ventricular volumes and ejection fraction do not change after the first week postinfarction. Control animals develop large anteroapical ventricular aneurysms, increasing LV dilatation, and progressive deterioration in circulatory hemodynamics and ventricular function. At week 8, differences in LV end-diastolic pressure, cardiac output, end-diastolic and end-systolic volumes, ejection fraction, stroke work, and end-systolic elastance are significant (P<0.01) between groups.
ConclusionsPreventing expansion of acute myocardial infarctions preserves LV geometry and function.
Key Words: ventricles remodeling myocardial infarction
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