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Atherosclerosis
Last reviewed: 23.04.2024
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Atherosclerosis is the most frequent variant of pathology; he is most serious, because it causes damage to the coronary arteries, cerebral vessels and cerebrovascular insufficiency. Arteriosclerosis is a general term for several diseases that cause thickening and loss of elasticity of the arterial wall. Forms of non-atheromatous arteriosclerosis include arteriosclerosis of Menkeberg and arteriolosclerosis.
Atherosclerosis is the formation of plaques (atter) in the intima of medium and large arteries. Plaques contain lipids, inflammatory cells, smooth muscle cells and connective tissue. Risk factors include dyslipidemia, diabetes mellitus, smoking, family predisposition, sedentary lifestyle, obesity and hypertension. Symptoms appear when the size or rupture of the plaque increases, which reduces or stops the blood flow; manifestations depend on the affected artery. The diagnosis is established clinically and is confirmed by angiography, ultrasound or other imaging studies. Treatment includes the elimination of risk factors, appropriate diet, physical activity and the appointment of antiplatelet agents.
Atherosclerosis can affect all large and medium-sized arteries, including coronary, carotid and cerebral arteries, the aorta, its branches and trunk arteries of the extremities. This disease is the leading cause of morbidity and mortality in the US and most Western countries. In recent years, mortality due to atherosclerosis has decreased, but in 2001, atherosclerosis of the coronary arteries and cerebral vessels caused more than 650,000 deaths in the US (more than cancer, and almost 6 times more than accidents). The prevalence of atherosclerosis is rapidly increasing in developing countries, and as people in developed countries live longer, the incidence will increase. It is expected that by 2020, atherosclerosis will become the leading cause of death in the world.
[Causes of atherosclerosis
The atherosclerosis feature is an atherosclerotic plaque that contains lipids (intracellular and extracellular cholesterol and phospholipids), inflammatory cells (such as macrophages, T cells), smooth muscle cells, connective tissue (eg, collagen, glycosaminoglycans, elastic fibers), thrombi and calcium deposits . All stages of atherosclerosis - from the formation and growth of plaques to complications - are considered an inflammatory response to damage. It is believed that the primary role is played by endothelial damage.
Atherosclerosis mainly affects certain areas of the arteries. Non-laminar, or turbulent, blood flow (for example, in arterial tree branches) leads to endothelial dysfunction and suppresses endothelial formation of nitric oxide, a potent vasodilator and an anti-inflammatory factor. This blood flow also stimulates endothelial cells to produce adhesion molecules that attract and bind inflammatory cells. Risk factors for atherosclerosis (such as dyslipidemia, diabetes mellitus, smoking, hypertension), oxidative stress factors (eg, superoxide radicals), angiotensin II and systemic infection also inhibit the release of nitric oxide and stimulate the formation of adhesion molecules, pro-inflammatory cytokines, hemotaxis proteins and vasoconstrictors substances; more precise mechanisms are unknown. As a result, monocytes and T-cells are fixed in the endothelium, these cells move to the subendothelial space, initiation and fixation of the local vascular inflammatory response. Monocytes in the subendothelium are transformed into macrophages. Blood lipids, especially low-density lipoproteins (LDL) and very low density (VLDL), also bind to endothelial cells and are oxidized in the subendothelial space. Oxidized lipids and transformed macrophages are converted into lipid filled foam cells, which is a typical early atherosclerotic change (the so-called fatty strips). Degradation of erythrocyte membranes, which occurs due to rupture of vasa vasorum and hemorrhage into the plaque, may be an important additional source of lipids within the plaques.
Atherosclerosis - Causes and risk factors
Symptoms of atherosclerosis
Atherosclerosis first develops asymptomatically, often for many decades. Signs appear when there are obstructions to the blood flow. Transient ischemic symptoms (eg, stable exertional angina, transient ischemic attacks, intermittent claudication) can develop when stable plaques grow and decrease the arterial lumen by more than 70%. Symptoms of unstable angina, myocardial infarction, ischemic stroke, or leg pain at rest can occur when unstable plaques burst and suddenly close a large artery, with the addition of thrombosis or embolism. Atherosclerosis can also cause sudden death without previous stable or unstable angina.
Atherosclerotic lesion of the arterial wall can lead to aneurysms and stratification of the arteries, which is manifested by pain, pulsating sensations, lack of pulse or sudden death.
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Treatment of atherosclerosis
Treatment involves active elimination of risk factors for preventing the formation of new plaques and reducing existing ones. Recent studies indicate that LDL should be <70 mg / dL for an existing disease or a high risk of cardiovascular disease. Changes in lifestyle include diet, cessation of smoking and regular physical activity. Often, drugs are needed to treat dyslipidemia, AH and diabetes mellitus. These lifestyle changes and medicines directly or indirectly improve endothelial function, reduce inflammation and improve the clinical outcome. Antiplatelets are effective in all patients.