OCCURRENCE OF A TERMINAL VASCULARIZATION AFTER EXPERIMENTAL MYOCARDIAL-INFARCTION

Physiological data indicate a residual vascularisation within ischemic myocardial regions where necrosis of most cells have been reported to occur after myocardial infarction. We therefore studied, by means of immunohistochemistry, computer-assisted morphometry, and electron micr oscopy, the terminal vascularisation in correlation to cardiomyocytes in ten canine hearts 1 and 3 weeks after occlusion of the left anterio r descending (LAD) coronary artery. In comparison to non-infarcted myo cardium we found the following alterations in infarcted myocardium: (1 ) the area density of cardiomyocytes decreased from 98% (control) to 7 .9% (1 week after occlusion) and to 2.7% (3 weeks after occlusion); (2 ) the number of capillaries was diminished to 11.6% and to 2.6%; respe ctively; (3) smooth muscle alpha-actin was induced in endothelial (EC) cells of the microvessels; and (4) terminal resistance vessels increa sed 11-fold and 20-fold in number, respectively. Our findings confirm the necrosis of the vast majority of cardiomyocytes and capillaries wi thin the first 3 weeks after myocardial infarction. Besides a small nu mber of capillaries, many terminal resistance vessels, however, seem t o persist in the scarring infarcted tissue. The occurrence of these mi crovessels is supposed to be important for the granulation tissue as w ell as for the control and regulation of a residual blood supply durin g scar formation.