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Apoptosis and Histopathologic Changes in Diffuse Coronary Atherosclerosis

Ruda Zorc-Pleskovi, DD, PhD

Olga Vraspir-Porenta, MD, PhD

Mateja Legan, MD, PhD

Daniel Petrovi, MD, PhD

The aims of the study were to investigate the histopathologic characteristics of atherosclerotic lesions and to evaluate the role of apoptosis or programmed cell death in diffuse coronary atherosclerosis. The study included 59 patients who underwent coronary artery bypass grafting coupled with coronary endarterectomy because of diffuse coronary atherosclerosis. Histopathologic analysis of endarterectomy sequesters showed atheroma with confluent extracellular lipid core—type IV lesions in 13 cases (22%); atheroma with lipid core and a cap of fibromuscular layers—type V lesions in 9 cases (15.3%); predominantly calcified fibrous tissue—type VII lesions in 13 cases (22%); and predominantly fibrous tissue—type VIII lesions in 24 cases (40.7%). TUNEL-positive cells were observed in 4 endarterectomy sequesters (6.8%) of subjects with diffuse coronary atherosclerosis. TUNEL-positive cells were demon strated in the area of mononuclear infiltrates as well as in the vessel wall. The percentage of TUNEL-positive cells in mononuclear infiltrates was 0.5%. Intense mononuclear infiltrates in tunica intima were found in 50% of sequesters, and they consisted of macrophages (40%), T-lymphocytes (17%), and B-lymphocytes (14%). In the area of infiltrates the proportion of MIB-1-positive cells was 2.7%, which was higher than in the intima outside the area of infil trates (0.5%). In conclusion, apoptosis, which is confined to mononuclear infiltrates, is most likely involved in the development of diffuse coronary atherosclerosis; however, the percentage of apoptotic cells was low (0.5%). A higher proportion of apoptotic cells in the area of infiltrates compared to the rest of the intima was associated with a higher proportion of MIB-1-positive cells. Atherosclerotic lesions in diffuse coronary atherosclerosis were advanced, with a predom inance of type VII to VIII lesions.

Angiology, Vol. 54, No. 1, 81-84 (2003)
DOI: 10.1177/000331970305400110


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