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• W1434200712 abstract "There are actually no strict criteria for the evaluation of the risk of acute coronary syndrome (ACS) development. Many clinical studies showed absence of dependence between severity of the coronary arteries stenosis and ischemic heart disease (IHD) clinical course, including possibility of the develop ment of its acute forms, and more than in 50 % cases acute myocardial infarction (MI) develops on the background of stenosis less than 50 %. Approximately in half or even 2/3 patients that died because of acute MI, IHD was not diagnosed vitally and sudden coronary death was the first and last of its manifestations. During recent years it became obvious that the reason of ACS development is neither the severity of stenosis nor the dimension of atherosclerotic plaque; the features of its structure and composi tion predict its instability. The propensity of the plaque to disruption is not directly related to the severity of the traditional risk factors, first of all – hypercholesterolemia (HCE) and increased low density lipoprotein cholesterol (LDL CH). It becomes more obvious that the most clear factor of both initiation and progression of atherosclerosis is inflammation, and the plaque destabilization is determined by high intensity of the chronic inflammatory process occurring in the damaged vascular wall. It is indicated in particular by the significant gradient of temperature between normal and damaged vascular segments which is more than one Celsius degree and reflects highintensity local inflammation. The similar temperature gradient was noted between stable and unstable, disrupting plaques [26]. Distinct differences in the structure of the plaque prone to disruption were also shown. It is characterized by the presence of a big necrotic lipid core, great amount of invaded macrophages and T-cells determining initiation and maintenance of the chronic inflammation. It coincides with less amount of vascular smooth muscle cells (SMC) capable to produce collagen and other components of extracellular matrix that increase the stability of atherosclerotic plaque. Transferring animals to diet with low lipid content or use of lipid-lowering treatment normalize plaque temperature along with decrease of lipids and macrophages content, though increased collagen doesn’t change plaque dimension and its propensity to disruption [26]." @default.
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• W1434200712 date "2015-03-01" @default.
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• W1434200712 title "Role of the acquired immune response in the development of acute coronary syndrome" @default.
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