Atherosclerosis - Wikipedia. Atherosclerosis (also known as arteriosclerotic vascular disease or ASVD) is a specific form of arteriosclerosis in which an artery wall thickens as a result of invasion and accumulation of white blood cells (foam cells) and proliferation of intimal- smooth- muscle cell creating an atheromatous (fibrofatty) plaque. These accumulations contain both living, active white blood cells (producing inflammation) and remnants of dead cells, including cholesterol and triglycerides. The remnants eventually include calcium and other crystallized materials within the outermost and oldest plaque. However, they do not affect blood flow for decades because the artery muscular wall enlarges at the locations of plaque. This is promoted by low- density lipoproteins (LDL, plasma proteins that carry cholesterol and triglycerides) without adequate removal of fats and cholesterol from the macrophages by functional high- density lipoproteins (HDL). It is commonly referred to as a . It is caused by the formation of multiple atheromatous plaques within the arteries. On the other hand, unstable plaques are rich in macrophages and foam cells, and the extracellular matrix separating the lesion from the arterial lumen (also known as the fibrous cap) is usually weak and prone to rupture. Upon formation, intraluminal thrombi can occlude arteries outright (e. Apart from thromboembolism, chronically expanding atherosclerotic lesions can cause complete closure of the lumen. Chronically expanding lesions are often asymptomatic until lumen stenosis is so severe (usually over 8. These complications of advanced atherosclerosis are chronic, slowly progressive and cumulative. Most commonly, soft plaque suddenly ruptures (see vulnerable plaque), causing the formation of a thrombus that will rapidly slow or stop blood flow, leading to death of the tissues fed by the artery in approximately five minutes. This catastrophic event is called an infarction. One of the most common recognized scenarios is called coronary thrombosis of a coronary artery, causing myocardial infarction (a heart attack). The same process in an artery to the brain is commonly called stroke. Another common scenario in very advanced disease is claudication from insufficient blood supply to the legs. Atherosclerosis affects the entire artery tree, but mostly larger, high- pressure vessels such as the coronary, renal, femoral, cerebral, and carotid arteries. Introduction. Diet for dogs with liver disease is controversial. I have often seen low protein diets recommended, but recent studies indicate that too little protein. If you aren’t already making bone broth regularly, I’d encourage you to start today! It is an incredibly healthy and very inexpensive addition to any diet and the. For Limited Time Only! Receive a FREE Bottle of Desiccated Heart OR Greenshell Mussel Powder with any order over $75! Atherosclerosis is asymptomatic for decades because the arteries enlarge at all plaque locations, thus there is no effect on blood flow. Even most plaque ruptures do. ![]() These are termed . Arteriosclerosis is a general term describing any hardening (and loss of elasticity) of medium or large arteries (from Greek. ![]() ![]() The term atherogenic is used for substances or processes that cause atherosclerosis. Even most plaque ruptures do not produce symptoms until enough narrowing or closure of an artery, due to clots, occurs. Signs and symptoms only occur after severe narrowing or closure impedes blood flow to different organs enough to induce symptoms. These symptoms, however, still vary depending on which artery or organ is affected. Sub- clinically, the disease begins to appear in childhood, and rarely is already present at birth. Noticeable signs can begin developing at puberty. Though symptoms are rarely exhibited in children, early screening of children for cardiovascular diseases could be beneficial to both the child and his/her relatives. These symptoms are also related to stroke (death of brain cells). Stroke is caused by marked narrowing or closure of arteries going to the brain; lack of adequate blood supply leads to the death of the cells of the affected tissue. Symptoms for the marked narrowing are numbness within the arms or legs, as well as pain. Another significant location for the plaque formation is the renal arteries, which supply blood to the kidneys. Plaque occurrence and accumulation leads to decreased kidney blood flow and chronic kidney disease, which, like all other areas, are typically asymptomatic until late stages. Cardiac stress testing, traditionally the most commonly performed non- invasive testing method for blood flow limitations, in general, detects only lumen narrowing of . A much- cited report involved autopsies of 3. U. S. Although the average age of the men was 2. Theories include high rates of tobacco use and (in the case of the Vietnam soldiers) the advent of processed foods after World War II. Atherosclerosis is initiated by inflammatory processes in the endothelial cells of the vessel wall associated with retained low- density lipoprotein (LDL) particles. Some data suggests that small dense LDL (sd. LDL) particles are more prone to pass between the endothelial cells, going behind the cellular monolayer of endothelium. ![]() LDL particles and their content are susceptible to oxidation by free radicals. However, LDL particles have a half- life of only a couple of days, and their content (LDL particles typically carry 3,0. Once inside the vessel wall, LDL particles can become more prone to oxidation. Endothelial cells respond by attracting monocyte white blood cells, causing them to leave the blood stream, penetrate into the arterial walls and transform into macrophages. The macrophages' ingestion of oxidized LDL particles triggers a cascade of immune responses which over time can produce an atheroma if HDL removal of fats from the macrophages does not keep up. The immune system's specialized white blood cells (macrophages) absorb the oxidized LDL, forming specialized foam cells. If these foam cells are not able to process the oxidized LDL and recruit HDL particles to remove the fats, they grow and eventually rupture, leaving behind cellular membrane remnants, oxidized materials, and fats (including cholesterol) in the artery wall. This attracts more white blood cells, resulting in a snowballing progression that continues the cycle, inflaming the artery. The presence of the plaque induces the muscle cells of the blood vessel to stretch, compensating for the additional bulk, and the endothelial lining thickens, increasing the separation between the plaque and lumen. This somewhat offsets the narrowing caused by the growth of the plaque, but it causes the wall to stiffen and become less compliant to stretching with each heart beat. Chickens, for example, develop atherosclerosis when infected with the Marek's disease herpesvirus. The points labelled '+' in the following list form the core components of metabolic syndrome. Risks multiply, with two factors increasing the risk of atherosclerosis fourfold. In fact, 1. 31- iodine is detectable in autoradiographs of walls of arteries to over 1. The USDA, in its food pyramid, promotes a diet of about 6. The American Heart Association, the American Diabetes Association and the National Cholesterol Education Program make similar recommendations. In contrast, Prof Walter Willett (Harvard School of Public Health, PI of the second Nurses' Health Study) recommends much higher levels of fat, especially of monounsaturated and polyunsaturated fat. Laboratory animals fed rancid fats develop atherosclerosis. Rats fed DHA- containing oils experienced marked disruptions to their antioxidant systems, and accumulated significant amounts of phospholipidhydroperoxide in their blood, livers and kidneys. The health food industry's dietary supplements are self regulated and outside of FDA regulations. Welcome to Our Practice Achieving health through nutrition, natural medicines, movement and right thinking.Chapter One Prana and Pranayama Pranayama is an exact science. It is the fourth Anga or limb of Ashtanga Yoga. It is characterized by a remodeling of arteries leading to subendothelial accumulation of fatty substances called plaques. The buildup of an atheromatous plaque 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, leukocytes, such as monocytes or basophils, begin to attack the endothelium of the artery lumen in cardiac muscle. The ensuing inflammation leads to formation of atheromatous plaques in the arterial tunica intima, a region of the vessel wall located between the endothelium and the tunica media. The bulk of these lesions is made of excess fat, collagen, and 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. 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- Lp. A2) 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- 1, which recruit circulating monocytes, and M- CSF, which is selectively required for the differentiation of monocytes to macrophages. The monocytes differentiate into macrophages, which ingest oxidized LDL, slowly turning into large . 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. 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 2.
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