About Coronary Artery Disease

Coronary Artery Disease

Coronary artery disease, often early in life, coronary arterial fatty streaks and tied in bed later in the process of atherosclerosis in coronary blood flow and myocardial ischemia caused by a pathological process. CV is all over the world are known to be one of the most important causes of morbidity and mortality. CAD, the most important public health problem in developed countries, but in recent years, the frequency is increasing in developing countries. Official data and TARF (in Turkish adults and Risk Factors for Heart Disease) study data were evaluated with the time in our country 45% of all deaths from cardiovascular disease, heart disease, 36%, 32% were the result of coronary heart disease. The prevalence of coronary heart disease in our society, increasing with age and affects about 5% of people over the age of 60. The number of coronary artery disease in 2010, 3.4 million people in our country is expected to arrive. Coronary artery disease is the most important mechanisms underlying atherosclerosis.


A number of hypotheses have been proposed to explain how atherosclerosis occurs. Those which are most of them in the 'injury response' hypothesis. Normal arterial structure consists of three layers. Most of the inside of blood vessel wall with a semi-permeable barrier, the endocrine and paracrine function, as well as a single layer of the intima is lined by endothelial cells. Middle layer of the vessel elasticity

media, which creates a layer composed of smooth muscle. Adventisia located in the outermost layer. The most important step in the hypothesis of recurrent damage to endothelial damage response. Endothelium; vasoactive substances secretion and the regulation of vascular flat muscles contraction and relaxation, coagulation regulation, leukocyte adhesion, solid and liquid substances acts as a barrier. In addition, by inhibiting the adhesion of blood cells, by dilating blood vessels and vascular protective effect by inhibiting the proliferation of vascular smooth muscle. Developed in the presence of proatherogenic factors in this protective function is lost due to endothelial dysfunction and atherosclerosis begins. Endothelial dysfunction as a result of low-density lipoprotein (LDL) and oxidized to cross the endothelium-subintimal is a comfortable distance. Macrophages and oxidized LDL receptors are. Phagocytosis by macrophages and foam cells, composed of lipids. In the early stages of atherosclerosis, lipid, mostly as a cell within the foam cells. As you continue to proatherogenic factors, both circulating LDL is directly connected to the intimal proteoglycans, as well as foam cells mainly because of the fragmentation of the released cholesterol esters in lipid begins to accumulate outside the cell. As a result of the intimal layer of connective tissue, cholesterol and cell breakdown products of lipid-filled core. The age of the lesion progresses, the media layer of smooth muscle cells migration and proliferation of these cells and fibrous connective tissue proteins to produce a title with the atherosclerotic plaque covered above, consists of mature atherosclerotic plaque. Meanwhile, the central part of the plate are starved of oxygen and begins to develop necrosis. A plaque with focal or massive calcifications may occur. However, sometimes fibrous plaque build up in the title fissures and ulcers, and smooth muscle cells, blood circulation is in contact with oil. As a result, an intense thrombogenic reaction begins. Narrowing of the lumen and gradually increases as a result of repeated attacks. As a result of complete occlusion of the coronary artery, myocardial infarction and sudden death may occur if there is such a sufficient. As a result of rupture of the fibrous plaque next to the title of their lipid components in the circulation through the cholesterol plaque can cause embolisms.


Histological, immunohistochemical, and electron microscopy methods, using extremely detailed morphological studies were performed on recordings. American Heart Association, the morphology of plaques dedicated to the 8 type:


Type 1 lesions: That intensive lipid-laden macrophages, the initial lesion.



Type 2 lesions: the number of macrophages was increased, and stratification. Other than macrophages, smooth muscle cells, as well as inside, outside the cell lipid droplets There. If the Type 2 lesion sensitive regions develops fast growing up (type 2a lesion), less-sensitive regions are formed more slowly than the development of Type 2 lesions (lesion Tip2b).


Type 3 lesions: The most important distinguishing feature of type 2 according to the lesion is small lipid deposits. Under this lipid macrophages and T cells, the lesion accumulates in the deepest place. Endothelial dysfunction begins to develop during this period.


Type 4 lesion: Classically defined as atherosclerotic plaque or atheroma. During this period, limited to the intimal intensive lipid available. This is called a lipid core. At this stage in order to protect the actual volume of artery lumen reconstruction begins. However, with the viewing of these lesions is difficult coronary angiography.


Type 5 lesions: the lesions are characterized by an increase of fibrous tissue covering the lipid core. Developing fibrous tissue, proliferating and secreting collagen and proteoglycans, matrix proteins, such as smooth muscle cells are generated. This so called fibroatheroma circuit or Type 5 lesions.


Type 6 lesions: the Type 4 and Type 5 lesions, fissures, hematoma, or thrombus formation occurs with. Clinical symptoms, mortality and morbidity in the most watched type. Type 6 is also called lesions, complicated lesions.


Type 7 lesions: lipid core, or any part of the lesion occurs with the development of calcification.


Lesion type 8: Lipid burden is less fibrotic plaques.