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How does the atherosclerosis develop?

Atherosclerosis progresses with a gradual build-up of plaque or thickening of the inside of the walls of the artery, which causes a decrease in the amount of blood flow, and a decrease in the oxygen supply to the vital body organs and extremities. A heart attack may occur if the oxygenated blood supply is reduced to the heart. A stroke may occur if the

oxygenated blood supply is cut off to the brain. Gangrene may occur if the oxygenated blood supply is reduced to the arms and legs.

The resident cells within the artery wall seem to signal an intrusion, "call for help", an inflammation response. Monocytes, one of the 5 main types of white blood cells circulating in the blood, enter the artery wall. Within tissues, monocytes change characteristics and are called macrophages. The macrophages ingest oxidized cholesterol, slowly turning into large "foam cells" – so described because of the appearance numerous vesicles take on to accommodate their high lipid content. The early stages are called fatty streaks. Foam cells eventually die, and further propagate the inflammatory process. Intracellular microcalcification deposits form within vascular smooth muscle cells of the surrounding muscular layer, specifically in the muscle cells adjacent to the atheromas. In time, as cells die, this leads to extracellular calcium deposits between the muscular wall and outer portion of the atheromatous plaques.

Cholesterol is delivered into the wall by LDL particles (low density lipoprotein), especially by the smaller LDL particles, if they are plentiful, because they can pass through the intracellular gaps between the intima lining cells more easily. To attract and stimulate macrophages, the cholesterol must be released from the LDL particles and oxidized, a key step in the ongoing inflammatory process. Additionally, the macrophages must be unable to remove excess cholesterol fast enough, into functioning HDL particles (high density lipoprotein) to avoid becoming foam cells and dying. To date, the only known mechanism by which macrophages can export excess lipid is into HDL particles.

A protective fibrous cap normally forms between the fatty deposits and the artery lining (the intima). These capped fatty deposits (called atheromas) produce enzymes which cause the artery to enlarge over time. As long as the artery enlarges sufficiently to compensate for the extra thickness of the atheroma, then no narrowing, stenosis, of the opening, lumen, occurs. The artery becomes expanded and egg shaped, still with a circular opening. If the enlargement is beyond proportion to the atheroma thickness, then an aneurysm is created.

This process of atheroma formation and progressive artery enlargement, or remodeling, usually starts in childhood and continues for many decades, thereby masking either symptoms or any evidence of the disease by any detection methods, such as angiography, which only evaluate the artery lumen.

In effect, small aneurysms of the muscular portion of the artery wall form aneurysms just large enough to hold the atheroma which are present. The muscular portion of artery walls usually remain strong, even after they have remodeled to compensate for the atheromatous plaques. However, atheromas within the vessel wall are soft and fragile with little elasticity. Arteries constantly expand and contract with each heartbeat, i.e. the pulse. In addition, the calcification deposits between the outer portion of the atheroma and the muscular wall, as they progress, lead to a loss of elasticity, stiffening, of the artery as a whole.

The calcification deposits, after they have become sufficiently advanced, are partially visible by some high resolution X-Ray imaging systems as rings of increased radiographic density forming halos around the outer edges of the atheromatous plaques, within the artery wall. On CT, >130 units on the Hounsfield scale {some argue for 90 units} has been the radiographic density usually accepted as clearly representing tissue calcification within arteries. These deposits demonstrate unequivocal evidence of the disease, relatively advanced, even though the lumen of the artery is often still normal by angiographic or IVUS imaging. Although the disease process tends to be slowly progressive over decades, in later stages, it also becomes unstable with repetitive sudden problems, most without obvious symptoms at the time of occurrence but some producing sudden major debility or death. These problems result from instability of the newer, soft atheromas.

If the fibrous cap separating a soft atheroma from the bloodstream within the artery ruptures, atheroma tissue fragments are exposed and released. Atheroma tissue fragments are very clot promoting; they attract blood platelet accumulation and activate the blood clotting system proteins. This leads to a temporary patch covering and narrowing (stenosis) within the artery lumen. Though this is often a repetitive and progressive process over time, it is typically without symptoms until a severe enough event, in a critical enough area occurs.

Fibrous cap ruptures usually result in only a partial narrowing, stenosis, of the artery lumen, a narrowing which usually partially re-opens with healing and regrowth of the intimal lining. However, sometimes the combination of atheroma material release, bleeding into the atheroma bed, platelet accumulation and accumulation of blood clotting proteins suddenly builds to the point of creating a complete, or near complete obstruction. The obstruction, either at the site of rupture, or as a result of debris sent downstream, prevents adequate blood flow to cells downstream. Cells starved for adequate blood supply are injured and may die.

Areas of severe narrowing, stenosis, detectable by angiography, and to a lesser extent "stress testing" have long been the focus of human diagnostic techniques for heart disease and cardiovascular disease in general. However, these methods focus only on detecting severe narrowing, not the underlying atherosclerosis disease. As demonstrated by human clinical studies, most severe events occur in locations with heavy plaque yet little or no lumen narrowing present before debilitating events suddenly occur. Plaque rupture can lead to artery lumen occlusion within seconds to minutes, and potential permanent debility and sometimes sudden death.

75% lumen stenosis used to be considered by cardiologists as the hallmark of clinically significant disease because it is only at this severity of narrowing of the larger heart arteries that recurring episodes of angina and detectable abnormalities by stress testing methods are seen. However, clinical trials have shown that only about 14% of clinically debilitating events occur at locations with this, or greater severity of narrowing. The majority of events occur due to atheroma plaque rupture at areas without narrowing sufficient enough to produce any angina or stress test abnormalities. Thus, as of the later 1990s, greater attention has been focused on the vulnerable plaque.

Though any artery in the body can be involved, usually only severe narrowing or obstruction of some arteries, those which supply more critically important organs, are recognized. Obstruction of arteries supplying the heart muscle result in a heart attack. Obstruction of arteries supplying the brain result in a stroke. These events are life changing because lost heart muscle and brain cells do not grow back.

The wall of an artery is composed of several layers. The lining or inner layer (endothelium) is usually smooth and unbroken. Atherosclerosis begins when the lining is injured or diseased. Then certain white blood cells called monocytes are activated and move out of the bloodstream and through the lining of an artery into the artery's wall. Inside the lining, they are transformed into foam cells, which are cells that collect fatty materials, mainly cholesterol. In time, smooth muscle cells move from the middle layer into the lining of the artery's wall and multiply there. Connective and elastic tissue materials also accumulate there, as may cell debris, cholesterol crystals, and calcium. This accumulation of fat-laden cells, smooth muscle cells, and other materials forms a patchy deposit called an atheroma or atherosclerotic plaque. As they grow, atheromas thicken the artery's wall and bulge into the channel of the artery. They may narrow or block an artery, reducing or stopping blood flow.

More information on atherosclerosis

What is atherosclerosis? - Atherosclerosis is a stage of arteriosclerosis involving fatty deposits inside the arterial walls. Atherosclerosis can lead to stroke, heart attack, eye problems, and kidney problems.
How does the atherosclerosis develop? - Atherosclerosis is a gradual process that occurs when cholesterol collects under the inner lining of artery walls due to damage from uncontrolled high blood pressure.
What causes atherosclerosis? - Atherosclerosis is caused by a response to damage to the endothelium from high cholesterol, high blood pressure, and cigarette smoking.
What're the risk factors for atherosclerosis? - There are several risk factors that contribute to the development of atherosclerosis, some which can be controlled, and some that cannot.
What're the symptoms of atherosclerosis? - Symptoms of atherosclerosis include the deposition of atheromatous plaques containing cholesterol and lipids on the innermost layer of the walls of large and medium-sized arteries.
How is atherosclerosis diagnosed? - Atherosclerosis is usually diagnosed after other complications have arisen and another conditions has been diagnosed, such as coronary artery disease.
What're the treatments for atherosclerosis? - Medical treatments for atherosclerosis focus on the symptoms. Physical treatments include minimally invasive angioplasty procedures.
How atherosclerosis is prevented? - Prevention of atherosclerosis centers on reducing cholesterol, homocysteine level, keeping triglycerides in check, maintaining a healthful weight.
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