[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).

[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.

[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.

[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.