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Despite significant medical advances, coronary artery disease (which results from atherosclerosis and causes heart attacks) and atherosclerotic stroke are responsible for more deaths than all other causes combined.
Atherosclerosis begins when white blood cells called monocytes migrate from the bloodstream into the wall of the artery and are transformed into cells that accumulate fatty materials. In time, these fat-laden monocytes accumulate, leading to a patchy thickening in the inner lining of the artery. Each area of thickening (called an atherosclerotic plaque or atheroma) is filled with a soft cheeselike substance consisting of various fatty materials, principally cholesterol, smooth muscle cells, and connective tissue cells. Atheromas may be scattered throughout the medium and large arteries, but usually they form where the arteries branch off "presumably because the constant turbulence at these areas injures the arterial wall, making it more susceptible to atheroma formation. .
Arteries affected with atherosclerosis lose their elasticity, and as the atheromas grow, the arteries narrow. With time, the atheromas collect calcium deposits, may become brittle, and may rupture. Blood may then enter a ruptured atheroma, making it larger, so that it narrows the artery even more. A ruptured atheroma also may spill its fatty contents and trigger the formation of a blood clot (thrombus). The clot may further narrow or even occlude the artery, or it may detach and float downstream where it causes an occlusion (embolism). .
Usually, atherosclerosis doesn't produce symptoms until it severely narrows the artery, or until it causes a sudden obstruction. Symptoms depend on where the atherosclerosis develops; thus, they may reflect problems in the heart, the brain, the legs, or almost anywhere in the body. .
As atherosclerosis severely narrows an artery, the areas of the body it serves may not receive enough blood, which carries oxygen to the tissues.