[Adhesion molecules and mononuclear cell subpopulations in the coronary and pulmonary arteries of patients with coronary heart disease].

UNLABELLED: Atherosclerosis is a multifactor disease, in which dysfunction of the endothelium leads to the emergence of its adhesion molecules. OBJECTIVE: to investigate the expression of the endothelial adhesion molecules PECAM (CD31), ICAM, and VCAM, as well as adherent endothelial T cells and monocytes. The material examined was en face pulmonary and coronary artery samples taken during autopsies (10 men), and en face specimens obtained from the coronary artery fragments taken from coronary heart disease patients during endarterectomy (37 men). This investigation used antibodies to the adhesion molecules ICAM-1, VCAM-1, and PECAM and those to CD3, CD4, CD8 T-cells and CD68 monocytes. RESULTS: The endothelial cells in the atherosclerotically intact coronary arteries had an elongated shape and were aligned along the blood flow. Those located above atheromas and fibroatheromas changed their shape from elongated to polygonal. Above the fatty streaks and atheromas, the reaction with antibodies to CD31 antigens became weaker at the edge of endothelial cells and disappeared in places. While the atherosclerotic process progressed, the reaction with the CD31 antigen at the edge of endothelial cells was similar in intensity to that on the surface of the endothelium. Adhesion of T cells and monocytes to the endothelium of coronary arteries increased as the atherosclerotic vascular process progressed. T cells and monocytes more often adhered to the endothelium at the sites where the endothelial cells contacted each other. CONCLUSION: Heterogeneity was found in the endothelial cells: their shape, the expression of adhesion molecules, and the adhesion of lymphocytes and monocytes to them changed during the progression of the atherosclerotic process.

[T-cell subpopulations and macrophages in stable and unstable coronary atherosclerotic plaques].

Unstable atherosclerotic plaques are a cause of acute myocardium infarction. Because peripheral blood mononuclear cells are often present in atherosclerotic plaques, we've examined T-cells (CD4, CD8) and macrophages (CD68) in the different areas of atherosclerotic plaques. The cells were counted individually in the center, shoulder at the bottom and in the cap of plaque. All types of studied cells prevailed in the unstable plaque cap than in the stable one (p < 0.05). CD4 and CD68 cells dominated in the shoulder of atherosclerotic plaque (p < 0.05). The difference between the numbers of macrophages at the bottom or in the center of stable and unstable plaques was statistically insignificant (p > 0.05). Prevalence of peripheral blood mononuclears in the cap and at the periphery of unstable plaques points their participation in the development of atherosclerotic plaque instability.

[Anti-inflammatory properties of statins in the study of atherosclerotic plaques in the endartectomized coronary arteries].

Statin therapy reduces blood cholesterol and lipids and exerts an anti-inflammatory effect. Certain statins bind adhesion molecules, including functional leukocytic antigen-1, and therefore block their interaction with T lymphocytes and macrophages expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1). Quantitation of endothelium-adherent T cells and macrophages revealed much smaller numbers of these cells in patients receiving statins. The authors consider that the lower count of T lymphocytes and macrophages in the upper layers of the intima and atherosclerotic plaques may facilitate the conversion of unstable to stable plaques, which reduces the risk of atherosclerotic plaque rupture and resultant vascular thrombosis.

[Immunomorphological study of angiotensin-converting enzyme in coronary shunts].

Coronary bypass surgery is the operation of choice in patients with coronary atherosclerosis. However, some time later, venous shunts frequently stop functioning after successful surgery. The reasons for this include intimal hyperplasia occurring in response to release of cytokines, angiotensin II in particular. In man, the latter is formed by angiotensin-converting enzyme or chimase. The findings show that elevated ATF concentrations are found in some cells in the area of intimal hyperplasia, in macrophages and smooth muscle cells of the shunt hyperplastic intima. The increased ATF concentration in the aorto-coronary shunt cells results in the elevated levels of angiotensin II, the migration of smooth muscle cells, their hypertrophy and hyperplasia, the formation of atherosclerotic plaques, thrombosis, and circulatory disorders.

[Antibodies to Chlamydia pneumoniae in blood serum of patients with ischemic heart disease and presence of complicated lesions in coronary arteries].

Levels of IgM, IgG and IgA antibodies to Chlamydia pneumoniae were measured in 107 patients (age 33-75 years) with documented coronary atherosclerosis and 39 subjects with intact coronary arteries. Rates of seropositivity to C. pneumoniae were 77.6 and 25.6% in patients and "healthy" subjects, respectively (p<0.05). Seropositive (n=83) compared with seronegative (n=24) patients had higher prevalence of complicated lesions (p<0.05).