[Clinical assessment of major artery vasomotor endothelial function: methodology and importance for evaluating aging as a cardiovascular risk factor]

Abstract

AGING AS A CARDIOVASCULAR RISK FACTOR: Atherosclerosis is the major cause of mortality in the Western world (>50%) as well as in Serbia and Montenegro (>60%). Atherosclerosis/arteriosclerosis functional and structural vascular changes as a consequence of angina pectoris, myocardial infarction, transient ischemic cerebrovascular attacks, stroke, ischaemic attacks in peripheral circulation and/or thromboembolic complications. Aging, lipids (oxidized LDL), infective agents, inflammation, increased glucose level, hypertension, smoking, increased homocysteine level, oxidative stress etc. are recognized as factors which lead to endothelial dysfunction and cause atherosclerosis. Thus, in response to such attacks endothelium releases different substances like: nitric oxide, prostacyclin, endothelium-derived hyperpolarizing factor (EDHF), endothelin, bradykinin, angiotensin II, free oxygen radicals etc. which could be involved in the pathogenesis of atherosclerosis. Atherosclerosis/arteriosclerosis begins with endothelial vasomotor and anti-thrombotic dysfunction and it is of strategic importance to discover this condition earlier. In regard aging, both higher thickness and stiffness of arterial blood vessels appear following an incidence of cardiovascular diseases.

Diagnostic methods: Over the last decade non-invasive, echosonographic method for visualization of carotid intima-media thickness (indicator of arteriosclerosis/atherosclerosis) was introduced in clinical practice. However, it is also used to compare brachial artery diameter changes, linear velocity and bloodflow which are estimated during basal conditions, during ischemia, during reactive hyperemia (endothelium/independent phase) as well as with left ventricular mass index.

Discussion and conclusion: Due to aging there is a decreased response to reactive hyperemia, increased carotid intima-media thickness and increased left ventricular mass, but there is a lack of time-dependent correlation. First endothelial dysfunction occur twenty years before any manifestations appear--as typical vascular and ventricular remodeling. During this period certain markers, for example homocysteine, and diagnostic procedures are important parts of primary prevention.