ATHEROSCLEROSIS OF CORONARY BLOOD VESSELS - LOCAL OR SYSTEMIC INFLAMATION?

The presence of atherosclerotic lesions in the blood vessels is a predisposition for the development and occurrence of acute ischaemic attacks. Bigger atherosclerotic lesions in the coronary blood vessels cause lumen occlusion, which is a cause of acute myocardial infarction. Endothelial dysfunction is defined as an ability of the endothelium to produce vasorelaxing nitric oxide (NO), or deregulation of the other vasoactive substances, such as angiotensin II and endothelin [13]. This definition describes endothelial dysfunction as an improper vasomotor constriction of the vessel, that leads to lumen occlusion of the already existing atherosclerotic lesions. According to the modern model, the development of atherosclerotic plaque and inappropriate endothelial NO production have a synergistic role in patho-physiological and molecular processes in the blood vessels [14]. Lesions in the coronary arteries are deposits of huge quantities of foamy cells and fibrous plaques. The thin fibrous plaques are 10–20% of the total plaque population and are the cause of 80–90% of clinical cases due to their ability to rupture [48]. According to all the results from published studies by far, it has been pointed out that the plaque stability, not the absolute size influences the rupture potential. Elucidating the risk factors that may modify in the atherogenesis and the consequent atherothrombic effect is the first step to this goal.