How do atherosclerosis plaques form

Atherosclerosis is the pathologic process by which cholesterol and calcium plaque accumulate within the arterial wall. When present in the cerebrovascular system, stroke can occur. Atherosclerosis also contributes to peripheral arterial disease, aortic aneurysms, renal artery disease and mesenteric ischemia. The pathophysiologic process by which atherosclerosis occurs is complex and somewhat controversial. The working theory includes four steps:. Back to Healio. Topic Reviews A-Z Save.

The aorta is the large artery that carries blood from the heart to the rest of the body. 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. Atherosclerosis is a process, and there are ways you can slow it down and help lower your risk for heart attack and stroke.

A heart-healthy lifestyle can lower your risk. This includes eating heart-healthy foods, being active, staying at a healthy weight, and not smoking. All of these things have many benefits for your body, your heart, and your blood vessels.

If your risk is high, you might also take medicines that lower your risk. These include medicines to lower cholesterol and blood pressure.

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. Stable and unstable plaque. Plaques are defined based on the risk that they will tear or rupture. Stable plaque is less likely to rupture. These plaques have a thick fibrous cap and are made up of substances that are stable and not likely to rupture.

Unstable plaque is more likely to rupture. These plaques have a thin fibrous cap and are made up of substances like fats that can expand. Inflammation within the plaque can make the fibrous cap unstable and more likely to tear apart. Blocked artery. A blockage in the artery can happen if the plaque tears or ruptures.

This rupture exposes the cholesterol and tissue that was under the fibrous cap. Blood clots form in response to this rupture. The blood clot blocks the blood flow in the artery.

This can cause a heart attack or stroke. The endothelial cells also change shape, and the tight junctions between endothelial cells loosen, increasing the permeability to fluid, lipids, and leukocytes. Lipoprotein particles, and especially low-density lipoprotein LDL , enter the arterial wall and undergo oxidation. Once they have migrated into the intima, monocytes differentiate into macrophages and begin to take up oxidized LDL that has gotten into the intima.

Macrophages retain the lipid they take up, and as they become more lipid-laden, they are referred to as "foam cells. They consist of lipid-containing foam cells in the arterial wall just beneath the endothelium. The image below on the left is a photograph of the inside of an artery; one can see two yellowish fatty streaks beneath the thin endothelial lining of the artery.

These lesions occur in the aorta and coronary arteries of most people by age Over time, they can evolve into atherosclerotic plaques or they can remain stable or even regress.

The cartoon below summarizes the steps by which a fatty streak evolves. Injury to the endothelium triggers monocyte adhesion, a loosening of endothelial cell junctions, and migration of monocytes beneath the endolthelium where they differentiate into macrophages.

The more permeable endothelium also permits LDL to enter the intima of the artery, and macrophages begin engulfing the LDL by phagocytosis. After macrophages become laden with lipid from ingesting LDL, they are referred to as "foam cells," and collections of these create fatty streaks. The cartoon also emphasizes the role of T-lymphocytes, which are also in the intima. They secrete cytokines that eventually induce smooth muscle cells to migrate from the media to the intima.

These smooth muscle cells also begin to proliferate under the influence of growth factors. Over time there is a progressive accumulation of lipid and smooth muscle cells in the intima, and eventually the growing lesion begins to raise the endothelium and encroach on the lumen of the artery.

This is depicted in the image below, which shows a cross-section of an artery at the site of an atherosclerotic plaque.