Topic Overview

What is atherosclerosis?

Atherosclerosis, sometimes called "hardening of the arteries," occurs when fat (cholesterol) and calcium build up in the inner lining of the arteries, forming a substance called plaque. Over time, the fat and calcium buildup narrows the artery and blocks blood flow through it.

Atherosclerosis can happen in all arteries. If you have atherosclerosis in one of your arteries, there is a good chance that you have atherosclerosis in other blood vessels throughout your body.

What problems does atherosclerosis cause?

Coronary artery disease . When atherosclerosis affects the arteries that supply blood to the heart, the coronary arteries, it can restrict blood flow to the heart muscle.

Heart attack . Plaque, caused by atherosclerosis, is surrounded by a fibrous cap. This fibrous cap may tear or rupture if blood suddenly flows faster or if the artery suddenly narrows. A tear or rupture tells the body to repair the injured artery lining, much as it might heal a cut on the skin, by forming a blood clot to seal the area. A blood clot that forms in an artery can completely block blood flow to the heart muscle and cause a heart attack. See a picture of how atherosclerosis can cause a heart attack.

Stroke or transient ischemic attack (TIA). When atherosclerosis affects the arteries that supply blood to the brain, it may cause a transient ischemic attack (TIA) or stroke.

Peripheral arterial disease . Atherosclerosis can affect arteries in other parts of the body, such as the pelvis and legs, causing poor circulation.

Abdominal aortic aneurysm . Atherosclerosis can make the walls of the aorta weak. The aorta is the large artery that carries blood from the heart to the rest of the body.

How is atherosclerosis treated?

A major part of treating atherosclerosis and coronary artery disease involves lifestyle changes (such as quitting smoking) and medicines to help reduce high cholesterol, control high blood pressure, and manage other things that increase a person's risk of heart attack, stroke, and other complications.

Reversing atherosclerosis

If you think of atherosclerosis as a response to injury, the buildup of fibrous plaque can be reversed by removing the source of injury. In the case of high cholesterol, by reducing the amount of LDL cholesterol in your arteries and increasing the amount of HDL—which removes cholesterol that is already in your artery walls—you can actually reverse atherosclerosis. The ability to reverse atherosclerosis helps explain why treating high cholesterol can reduce the risk of further complications from atherosclerosis.

How does atherosclerosis happen?

Although the exact process is not completely understood, scientists have described three different stages of atherosclerosis that lead to clogged arteries. These stages do not necessarily occur in order, nor is there always a progression from one stage to the next.

The fatty streak. The "fatty streak" appears as a yellow streak running inside the walls of the major arteries, such as the aorta. The streak consists of cholesterol, white blood cells, and other cellular matter. The fatty streak by itself does not cause symptoms of heart disease but can develop into a more advanced form of atherosclerosis, called fibrous plaque.

The plaque. A plaque forms in the inner layer of the artery. Plaque is a buildup of cholesterol, white blood cells, calcium, and other substances in the walls of arteries. Over time, plaque narrows the artery, and the artery hardens.

Plaque sometimes reduces blood flow to the heart muscle, which can cause angina symptoms. Plaque in the large artery in the neck (carotid artery stenosis) may block blood flow to the brain and is a common cause of transient ischemic attack (sometimes called "mini-stroke") and stroke.

Plaques are covered with a fibrous cap, which may rupture if some trigger causes a surge in blood pressure or causes the artery to constrict. A person may have a heart attack if a plaque breaks open, creating a blood clot that completely blocks blood flow through the artery.

Complicated lesion. The last stage of atherosclerosis occurs when the plaque breaks open, exposing the cholesterol and tissue underneath. Blood clots form in response to this rupture and cause symptoms of a heart attack and unstable angina.

Why does atherosclerosis happen?

Response-to-injury. This theory suggests that atherosclerosis develops as a result of repetitive injury to the inner lining of the artery.

Injury may stimulate cells to grow and divide as part of the inflammatory process. This normal, healing response to chronic injury may actually result in the growth of atherosclerotic plaque.

This injury could be caused by any number of things, including:

• Physical stress on the artery lining, such as stress caused by high blood pressure.
• A response to an infection within the artery wall.
• Oxidative damage to the artery lining. Oxidative damage refers to injury caused by unstable molecules called free radicals. Free radicals are formed during reactions between oxygen and LDL ("bad" or low-density lipoprotein) cholesterol.
• Oxidized LDL cholesterol may cause injury to the blood vessel wall and promote an inflammatory reaction that clogs the artery lining with debris. But exactly why high cholesterol levels promote plaque formation is not clear. Cholesterol is found normally in all cell membranes, but it may alter the physical properties of the blood vessel wall, making it more susceptible to damage.

How smoking leads to atherosclerosis

Smoking plays a large role in the development of atherosclerosis. The carbon monoxide and nicotine contained in tobacco smoke affect blood flow through your arteries by:

• Making it easier for cholesterol-carrying lipoproteins to enter the walls of your arteries.
• Promoting the formation of fibrous plaque.
• Promoting the formation of blood clots that can completely block your arteries.

How does atherosclerosis cause an aortic aneurysm?

Atherosclerosis is one of the major causes of abdominal aortic aneurysm.

The wall of the aorta (and all blood vessels) is a dynamic tissue made up of living cells that need nutrients and oxygen. Many of these nutrients seep from the inside of the blood vessel through the walls to nourish the rest of the blood vessel. When the inner lining of the vessel is covered with an atherosclerotic plaque, nutrients can no longer seep through sufficiently. The cells receive no oxygen, and some of them die. As the atherosclerosis progresses and cells continue to die, the walls become weaker and weaker.

At some point, a critical relationship is reached between the pressure experienced in the center of the blood vessel, the wall tension, and the strength of the wall itself. When this point is reached, the wall begins to dilate (grow larger) in the area of the plaque. As the diameter of the vessel grows, the wall tension increases, leading to even more dilation. The end result is an aneurysm.