- Key People:
- Rudolf Schoenheimer
- Related Topics:
- aging
- old age
- arteriosclerosis
- atherosclerotic plaque
- atheromatous lesion
- On the Web:
- Harvard Health Publishing - Atherosclerosis (Nov. 09, 2026)
atherosclerosis
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What is atherosclerosis?
Atherosclerosis is a chronic disease where fats, cholesterol, calcium, and other substances accumulate in the inner lining of medium and large arteries, causing arterial thickening and stiffness.
Tiny fatty streaks can form in childhood and grow as low-density lipoproteins (LDLs) infiltrate the endothelium. Immune cells engulf these materials, becoming foam cells that accumulate in the lining. Calcium, minerals, smooth muscle cells, and debris also deposit, enlarging lesions into atherosclerotic plaques that narrow blood vessels.
Plaque development can lead to blood clot formation, obstructing blood flow and causing tissue damage. Risk factors include family history of cardiovascular disease, smoking, obesity, high cholesterol, and diabetes.
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Which parts of the body does atherosclerosis affect?
Atherosclerosis is a chronic disease where fats, cholesterol, calcium, and other substances deposit within the arteries' inner lining. This can affect various parts of the body, notably the aorta and its large branches.
When atherosclerosis affects the coronary arteries, it can lead to coronary heart disease, reducing blood supply to the heart muscle and causing chest pain or a heart attack. In cerebral vessels, it can cause blood clots and stroke. Atherosclerosis can also affect arteries throughout the body, potentially leading to aneurysms or reduced blood flow to organs.
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What happens inside blood vessels during atherosclerosis?
During atherosclerosis, fats, cholesterol, calcium, and other substances accumulate in the artery's inner lining. This prompts immune cells (macrophages) to engulf the fatty materials, turning into foam cells that accumulate within the lining.
Over time, these deposits enlarge into atherosclerotic plaques, narrowing the artery and reducing blood flow. Injury to the endothelium may result in the formation of fibrous caps of scar tissue. The plaques can also rupture, leading to blood clot formation that further obstructs the artery, potentially causing tissue damage or blockage elsewhere.
Atherosclerosis can begin early in life with the formation of tiny fatty streaks.2 Britannica SourcesCreated from Britannica articles using AI. AI can make mistakes, so verify using Britannica articles. -
What are plaques and how do they form in atherosclerosis?
Atherosclerotic plaques are deposits of lipids and other materials that build up on the inner walls of arteries, causing them to stiffen and narrow.
Plaque formation begins with fatty streaks in the arteries, which can start in childhood. Low-density lipoproteins (LDLs) infiltrate the endothelium, and immune cells called macrophages are drawn to the site. Macrophages consume the fatty materials and become foam cells, which accumulate in the endothelial lining and die. Other materials, such as calcium salts, minerals, smooth muscle cells, and cellular debris, are also deposited in the lining. This causes the lesions to enlarge and thicken, forming atherosclerotic plaques, which can narrow the vessel channel and interfere with blood flow.
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How can atherosclerosis lead to health problems like heart attacks or strokes?
Atherosclerosis, a chronic disease, occurs when substances like fats and cholesterol deposit within artery walls, leading to thickening and stiffening. This can result in coronary heart disease, decreasing blood supply to the heart and causing chest pain or a heart attack if arteries become completely blocked.
In cerebral vessels, atherosclerosis can lead to blood clot formation and stroke. Atherosclerotic plaques can also rupture, causing acute thrombotic occlusion, leading to heart attack or stroke. Risk factors include family history, smoking, high cholesterol, and diabetes.
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What are some changes seen in the blood vessel walls because of atherosclerosis?
Atherosclerosis, a form of arteriosclerosis, is characterized by changes in the artery walls, including the deposition of fatty substances like cholesterol in the intima, the innermost layer of the artery. Macrophages, or inflammatory white blood cells, attempt to eliminate these lipid deposits, but they eventually become inefficient, die, and accumulate at the site of deposition, forming foam cells.
These deposits enlarge into atherosclerotic plaques, causing the vessel channel to narrow and disrupting blood flow. Endothelial injury and lipid deposition can result in scar tissue formation, reducing the vessel walls' elasticity and increasing blood pressure. In some instances, the aorta and iliac arteries widen, resulting in aneurysms, or they may harden and calcify, which increases flow resistance.
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atherosclerosis, chronic disease caused by the deposition of fats, cholesterol, calcium, and other substances in the innermost layer of endothelium of the large and medium-sized arteries. Atherosclerosis is the most common arterial abnormality characterized as arteriosclerosis, which is defined by the loss of arterial elasticity due to vessel thickening and stiffening.
Atherosclerotic lesions frequently are found in the aorta and in large aortic branches. They are also prevalent in the coronary arteries, where the condition is called coronary heart disease (also called coronary artery disease or ischemic heart disease). When atherosclerosis affects the coronary arteries, which bring oxygen-rich blood to the heart muscle, it can decrease the supply of blood to the heart muscle and result in chest pain known as angina pectoris. The complete occlusion of one or more coronary arteries can cause the death of a section of the heart muscle (myocardial infarction, or heart attack). Atherosclerotic lesions of the cerebral vessels may lead to formation of blood clots and stroke.
Pathophysiology
Evidence indicates that in some persons atherosclerosis can begin in childhood with the formation of tiny “fatty streaks,” or streaks of fat deposition, in the arteries. As the endothelium is infiltrated by more and more fatty materials—primarily low-density lipoproteins (LDLs), protein-lipid complexes that serve as a vehicle for delivering cholesterol to the body—immune cells called macrophages are drawn to the site to scavenge the materials. When filled with lipids, the macrophages become known as “foam cells,” which later die and accumulate in the endothelial lining. Other materials are also deposited in the lining, including salts of calcium and other minerals, smooth muscle cells, and cellular debris of varying composition. This causes the initially tiny lesions to enlarge and thicken to form atheromas, or atherosclerotic plaques. These plaques may narrow the vessel channel, interfering with the flow of blood.
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Endothelial injury, either as a result of lipid deposition or as a result of another cause, may also be accompanied by the formation of fibrous caps of scar tissue. These areas of scar tissue make the vessel walls less elastic, with one consequence being an increase in blood pressure. Thick plaques that severely occlude an artery can significantly decrease the flow of blood to vascular beds in tissues served by the artery, thereby causing severe tissue damage. In addition, a disturbance to the endothelium may result in the formation of a blood clot (thrombus) at the site of a plaque, likewise obstructing the channel or breaking loose from the site and causing a catastrophic blockage elsewhere.
Risk factors
A family history of cardiovascular disease, smoking, stress, obesity, and high blood cholesterol levels, particularly in association with LDLs, are among the factors that contribute to an increased risk of developing atherosclerosis. Men develop atherosclerosis more often than women, and individuals with diabetes mellitus have a significantly higher incidence of the disease.
Treatment
Certain drugs can reduce the risks associated with atherosclerosis. These include statins, which reduce the level of cholesterol and fat in the blood, as well as anticoagulants and other drugs such as aspirin, which prevent formation of blood clots. In large arteries such as the aorta or carotids, sections obstructed by atheromas can be removed surgically and replaced with synthetic materials. Atherosclerotic plaques can also be removed from the carotid circulation by atherectomy, in which the fatty deposits are carefully removed by a tiny knife inserted into the vessel via a catheter.
In the case of occluded coronary arteries, the lives of countless cardiac patients have been saved by coronary bypass surgery, in which sections of blood vessels from other parts of the body are used to route blood flow around the obstructions. Some occlusions can be opened by balloon angioplasty, in which a catheter is inserted to the site of obstruction and a balloon is inflated in order to dilate the artery and flatten the plaque deposits. Passages opened in this way frequently reclose over time, but the chances of this occurring can be reduced significantly by the insertion of expandable wire-mesh stents as part of the angioplasty procedure. Some stents are “drug-eluting”—that is, coated with a drug that inhibits the kind of cell growth that leads to reclosure.
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