High blood pressure High amounts of sugar in the blood due to insulin resistance or diabetes Plaque may begin to build up where the arteries are damaged.
Dietary[ edit ] The relation between dietary fat and Atherosclerosis and age is controversial. Writing in ScienceGary Taubes detailed that political considerations played into the recommendations of government bodies. Laboratory animals fed rancid fats develop atherosclerosis. Rats fed DHA -containing oils experienced marked disruptions to their antioxidant systems, and accumulated significant amounts of phospholipid hydroperoxide in their blood, livers and kidneys.
The health food industry's dietary supplements are self-regulated and outside of FDA regulations. Mechanism[ edit ] Atherogenesis is the developmental process of atheromatous plaques. It is characterized by a remodeling of arteries leading to subendothelial accumulation of fatty substances called plaques.
The buildup of an atheromatous Atherosclerosis and age is a slow process, developed over a period of several years through a complex series of cellular events occurring within the arterial wall and in response to a variety of local vascular circulating factors. One recent hypothesis suggests that, for unknown reasons, leukocytessuch as monocytes or basophilsbegin to attack the endothelium of the artery lumen in cardiac muscle.
The ensuing inflammation leads to formation of atheromatous plaques in the arterial tunica intimaa region of the vessel wall located between the endothelium and the tunica media.
The bulk of these lesions is made of excess fat, collagenand elastin. At first, as the plaques grow, only wall thickening occurs without any narrowing.
Stenosis is a late event, which may never occur and is often the result of repeated plaque rupture and healing responses, not just the atherosclerotic process by itself.
Cellular[ edit ] Micrograph of an artery that supplies the heart showing significant atherosclerosis and marked luminal narrowing. Tissue has been stained using Masson's trichrome.
Early atherogenesis is characterized by the adherence of blood circulating monocytes a type of white blood cell to the vascular bed lining, the endotheliumthen by their migration to the sub-endothelial space, and further activation into monocyte-derived macrophages.
Fatty streaks may appear and disappear. Low-density lipoprotein LDL particles in blood plasma invade the endothelium and become oxidized, creating risk of cardiovascular disease. A complex set of biochemical reactions regulates the oxidation of LDL, involving enzymes such as Lp-LpA2 and free radicals in the endothelium.
Initial damage to the endothelium results in an inflammatory response. Monocytes enter the artery wall from the bloodstream, with platelets adhering to the area of insult. This may be promoted by redox signaling induction of factors such as VCAM-1which recruit circulating monocytes, and M-CSFwhich is selectively required for the differentiation of monocytes to macrophages.
The monocytes differentiate into macrophageswhich proliferate locally,  ingest oxidized LDL, slowly turning into large " foam cells " — so-called because of their changed appearance resulting from the numerous internal cytoplasmic vesicles and resulting high lipid content. Under the microscope, the lesion now appears as a fatty streak.
Foam cells eventually die and further propagate the inflammatory process. In addition to these cellular activities, there is also smooth muscle proliferation and migration from the tunica media into the intima in response to cytokines secreted by damaged endothelial cells.
This causes the formation of a fibrous capsule covering the fatty streak. Intact endothelium can prevent this smooth muscle proliferation by releasing nitric oxide.
Calcification and lipids[ edit ] Calcification forms among vascular smooth muscle cells of the surrounding muscular layer, specifically in the muscle cells adjacent to atheromas and on the surface of atheroma plaques and tissue. With the atheromatous plaque interfering with the regulation of the calcium deposition, it accumulates and crystallizes.
A similar form of an intramural calcification, presenting the picture of an early phase of arteriosclerosis, appears to be induced by a number of drugs that have an antiproliferative mechanism of action Rainer Liedtke Cholesterol is delivered into the vessel wall by cholesterol-containing low-density lipoprotein LDL particles.
To attract and stimulate macrophages, the cholesterol must be released from the LDL particles and oxidized, a key step in the ongoing inflammatory process.
The process is worsened if there is insufficient high-density lipoprotein HDLthe lipoprotein particle that removes cholesterol from tissues and carries it back to the liver. The foam cells and platelets encourage the migration and proliferation of smooth muscle cells, which in turn ingest lipids, become replaced by collagen and transform into foam cells themselves.
A protective fibrous cap normally forms between the fatty deposits and the artery lining the intima.
These capped fatty deposits now called 'atheromas' produce enzymes that 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 with an egg-shaped cross-section, still with a circular opening. If the enlargement is beyond proportion to the atheroma thickness, then an aneurysm is created.
Although arteries are not typically studied microscopically, two plaque types can be distinguished: Beneath the endothelium there is a "fibrous cap" covering the atheromatous "core" of the plaque.
The core consists of lipid-laden cells macrophages and smooth muscle cells with elevated tissue cholesterol and cholesterol ester content, fibrin, proteoglycans, collagen, elastin, and cellular debris.Jan 27, · Although the clinical manifestations of cardiovascular disease (CVD), such as myocardial infarction, stroke, and peripheral vascular disease, appear from middle age, the process of atherosclerosis can begin early in childhood.
The early stage and progression of atherosclerosis in youth are. Atherosclerosis usually doesn’t cause symptoms until middle or older age. But as the narrowing becomes severe, it can choke off blood flow and cause pain.
Blockages can also rupture suddenly. If you have atherosclerosis in the arteries in your arms and legs, you may have symptoms of peripheral artery disease, such as leg pain when walking (claudication).
If you have atherosclerosis in the arteries leading to your kidneys, you develop high blood pressure or .
Atherosclerosis is classed as a disease of aging, such that increasing age is an independent risk factor for the development of atherosclerosis. Atherosclerosis is also associated with premature biological aging, as atherosclerotic plaques show evidence of cellular senescence characterized by reduced cell proliferation, irreversible growth .
Atherosclerosis is a condition where the arteries become narrowed and hardened due to a buildup of plaque around the artery wall. It is also known as arteriosclerotic vascular disease. Your risk for atherosclerosis increases if your father or a brother was diagnosed with heart disease before 55 years of age, or if your mother or a sister was diagnosed with heart disease before 65 years of age.