Apoptosis as a Mechanism for the Elimination of Cardiomyocytes After Acute Myocardial Infarction

Apoptosis is recognized as a mechanism of cell loss in the setting of acute myocardial infarction (AMI). Whether it contributes to myocyte elimination late after AMI has not yet been confirmed. We attempted to identify the features of apoptosis in myocytes that survived AMI. A search for ongoing apoptosis was performed in samples obtained from 38 human hearts: group I (n = 10), noncardiac death (control); and group II (n = 28), left ventricular aneurysm (in 20 patients, the samples were collected during aneurysmectomy and from 8 at autopsy). The morphometric evaluation included the degree of cellular hypertrophy, density of the capillary network, extent of myocytolysis, and features of apoptosis. Immunohistochemistry for caspase-3 and Bcl-2 was used as a prerequisite for transmission electron microscopy. Slides showing the strongest reaction for caspase-3 and negative for Bcl-2 were selected for transmission electron microscopy. CD-34 immunohistochemistry was used to quantify the capillary density. A significant reduction in capillary density was observed compared to the control group (1,085.6 ± 205.0/mm2 vs 2,968.7 ± 457.3/mm2; p <0.001). Myocytes that survived the acute phase of AMI were significantly hypertrophied (24.5 ± 4.7 μm vs 14.5 ± 1.6 μm; p <0.001) and showed a moderate to severe degree of myocytolysis. The average intensity score of the immunohistochemistry reactions for caspase-3 was 8.2 ± 3.8. Using transmission electron microscopy, apoptotic bodies were found in caspase-3–positive samples. In conclusion, the expression of caspase-3 and the presence of apoptotic bodies confirmed apoptosis as a common pathway of cardiomyocyte death in the setting of a limited blood supply after AMI.