All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Atherosclerosis
Medical expert of the article
Last reviewed: 05.07.2025
Atherosclerosis is the most common form of the disease; it is the 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 nonatheromatous arteriosclerosis include Mönckeberg's arteriosclerosis and arteriolosclerosis.
Atherosclerosis is the formation of plaques (atheromas) in the intima of medium-sized and large arteries. Plaques contain lipids, inflammatory cells, smooth muscle cells, and connective tissue. Risk factors include dyslipidemia, diabetes, smoking, family history, sedentary lifestyle, obesity, and hypertension. Symptoms occur when plaques enlarge or rupture, reducing or stopping blood flow; manifestations depend on the artery affected. Diagnosis is clinical and confirmed by angiography, ultrasound, or other imaging studies. Treatment includes risk factor management, appropriate diet, physical activity, and antiplatelet agents.
Atherosclerosis can affect all large and medium-sized arteries, including the coronary, carotid, and cerebral arteries, the aorta and its branches, and the great arteries of the extremities. It is a leading cause of morbidity and mortality in the United States and most Western countries. Age-related mortality due to atherosclerosis has decreased in recent years, but in 2001, coronary and cerebrovascular atherosclerosis caused more than 650,000 deaths in the United States (more than cancer and nearly six 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. Atherosclerosis is expected to become the leading cause of death worldwide by 2020.
[ Causes of atherosclerosis
The hallmark of atherosclerosis 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 (such as collagen, glycosaminoglycans, elastic fibers), thrombi, and calcium deposits. All stages of atherosclerosis, from plaque formation and growth to complications, are considered an inflammatory response to injury. Endothelial damage is thought to play a primary role.
Atherosclerosis preferentially affects certain regions of the arteries. Nonlaminar, or turbulent, blood flow (eg, at branching points in the arterial tree) leads to endothelial dysfunction and inhibits endothelial production of nitric oxide, a potent vasodilator and anti-inflammatory factor. Such blood flow also stimulates endothelial cells to produce adhesion molecules, which attract and bind inflammatory cells. Risk factors for atherosclerosis (eg, dyslipidemia, diabetes mellitus, smoking, hypertension), oxidative stressors (eg, superoxide radicals), angiotensin II, and systemic infection also inhibit nitric oxide release and stimulate production of adhesion molecules, proinflammatory cytokines, hemotactic proteins, and vasoconstrictors; the precise mechanisms are unknown. As a result, monocytes and T cells become attached to the endothelium, migrate to the subendothelial space, and initiate and perpetuate the local vascular inflammatory response. Monocytes in the subendothelial space are transformed into macrophages. Blood lipids, especially low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL), also bind to endothelial cells and are oxidized in the subendothelial space. Oxidized lipids and transformed macrophages are transformed into lipid-filled foam cells, which is a typical early atherosclerotic change (so-called fatty streaks). Degradation of red blood cell membranes, which occurs as a result of rupture of the vasa vasorum and hemorrhage into the plaque, may be an important additional source of lipids within the plaque.
Atherosclerosis - Causes and Risk Factors
Symptoms of atherosclerosis
Atherosclerosis initially develops asymptomatically, often over many decades. Signs appear when blood flow is obstructed. Transient ischemic symptoms (eg, stable angina, transient ischemic attacks, intermittent claudication) may develop when stable plaques enlarge and reduce the arterial lumen by more than 70%. Symptoms of unstable angina, MI, ischemic stroke, or resting leg pain may occur when unstable plaques rupture and suddenly obstruct a major artery, with the addition of thrombosis or embolism. Atherosclerosis may also cause sudden death without preceding stable or unstable angina.
Atherosclerotic lesions of the arterial wall can lead to aneurysms and arterial dissection, which manifests itself as pain, pulsating sensations, lack of pulse, or causes sudden death.
What do need to examine?
Who to contact?
Treatment of atherosclerosis
Treatment involves actively addressing risk factors to prevent new plaque formation and reduce existing plaque. Recent studies suggest that LDL levels should be < 70 mg/dL in patients with existing disease or high risk for cardiovascular disease. Lifestyle modifications include diet, smoking cessation, and regular physical activity. Drugs to treat dyslipidemia, hypertension, and diabetes are often needed. These lifestyle modifications and drugs directly or indirectly improve endothelial function, reduce inflammation, and improve clinical outcome. Antiplatelet drugs are effective in all patients.