Arterial plaque

Platelet adhesion to vessel walls and the subsequent release of adenosine diphosphate (ADP) initiates the formation of the arterial (white) thrombus. The arterial thrombus grows as platelets aggregate. As the thrombus occludes blood flow, it is surrounded by a "red" clot, composed of fibrin, platelets and erythrocytes. Like atherosclerotic plaques, arterial thrombi occlude blood vessels, causing tissue ischemia. 

Cholesterol is the central compound m any discussion of steroids Its name is a combination of the Greek words for bile (chole) and solid (stereos) preceding the characteristic alcohol suffix ol It is the most abundant steroid present m humans and the most important one as well because all other steroids arise from it An average adult has over 200 g of cholesterol it is found m almost all body tissues with relatively large amounts present m the brain and spinal cord and m gallstones Cholesterol is the chief constituent of the plaque that builds up on the walls of arteries m atherosclerosis... 

The state of knowledge in the early 1990s of the effects of fat on health lacks clarity and general agreement. There is great support for the thesis that fully saturated fats are associated with problems of atherosclerosis and arterial fatty deposit, but there is evidence that stearates, which are saturates, are only poorly utilized in human digestion. Another body of work has estabUshed a connection between unsaturated fatty acids and a better state of arterial health and lowered fat body attachment to the arterial wall (23) contrary evidence exists that highly unsaturated fats polymerize more readily and thus contribute to arterial plaque formation. 

Diseases. Liquid crystals have been impHcated in a number of disease conditions in the human body. A complex cholesterol—phosphoHpid—Hpoprotein Hquid crystal phase has been identified in the initiation and maintenance of atheromatous deposits on the aortic intima in dissected human and rabbit arteries (40). The paracrystalHne nature of this precursor to plaque buildup with the resultant loss of arterial elasticity... 

Laser ablation systems hold considerable promise if restenosis (reblocking of the arteries) rates are reduced. The rate as of 1995 is 30%, typically within six months. Mechanical or atherectomy devices to cut, shave, or pulverize plaque have been tested extensively in coronary arteries. Some of these have also been approved for peripheral use. The future of angioplasty, beyond the tremendous success of conventional balloon catheters, depends on approaches that can reduce restenosis rates. For example, if appHcation of a dmg to the lesion site turns out to be the solution to restenosis, balloon catheters would be used for both dilating the vessel and deUvering the dmg. An understanding of what happens to the arterial walls, at the cellular level, when these walls are subjected to the various types of angioplasty may need to come first. 

Vascular grafts are tubular devices implanted throughout the body to replace blood vessels which have become obstmcted by plaque, atherosclerosis, or otherwise weakened by an aneurysm. Grafts are used most often in peripheral bypass surgery to restore arterial blood flow in the legs. 

A number of rare genetic diseases involve collagen abnormalities, including Marfan s syndrome and the Ehlers-Danlos syndromes, which result in hyperextensible joints and skin. The formation of atheroselerotie plaques, which cause arterial blockages in advanced stages, is due in part to the abnormal formation of collagenous structures in blood vessels. 

Coumarin/warfarin, given at a typical dosage of 4 to 5 mg/day, prevents the deleterious formation in the bloodstream of small blood clots and thus reduces the risk of heart attacks and strokes for individuals whose arteries contain sclerotic plaques. Taken in much larger doses, as for example in rodent poisons, Coumarin/warfarin can cause massive hemorrhages and death. 

HDL and VLDL are assembled primarily in the endoplasmic reticulum of the liver (with smaller amounts produced in the intestine), whereas chylomicrons form in the intestine. LDL is not synthesized directly, but is made from VLDL. LDL appears to be the major circulatory complex for cholesterol and cholesterol esters. The primary task of chylomicrons is to transport triacylglycerols. Despite all this, it is extremely important to note that each of these lipoprotein classes contains some of each type of lipid. The relative amounts of HDL and LDL are important in the disposition of cholesterol in the body and in the development of arterial plaques (Figure 25.36). The structures of the various... 

Atherosclerosis. Hardening of the arteries. The formation of obstructive plaques in the arteries. 

LDL, or "bad," cholesterol builds up as a plaque-like deposit on the interior walls of arteries. This process used to be called hardening of the arteries today it is referred to as atherosclerosis. It can lead to cardiovascular diseases, including strokes and heart attacks. In contrast, HDL or "good" cholesterol retards or even reduces arterial deposits. 

Attempting to flow past thin sections to fill wider sections is difficult or may be impossible, because the flow thickens enroute acts like plaque forming along walls of a human artery. Even if both of these ills are avoided, the final result may still contain areas of high shear stresses invisible to the eye but waiting in ambush to cause failure later under extreme conditions previously thought to be well within the material s specifications. 

In general, arterial thrombi are platelet-rich ( white clots ) and form at ruptured atherosclerotic plaques, leading to intraluminal occlusion of arteries that can result in end-organ injury (e.g., myocardial infarction, stroke). In contrast, venous thrombi consist mainly of fibrin and red blood cells ( red clots ), and usually form in low-flow veins of the limbs, producing deep vein thrombosis (DVT) the major threat to life results when lower extremity (and, occasionally, upper extremity) venous thrombi embolize via the right heart chambers into the pulmonary arteries, i.e., pulmonary embolism (PE). 

Atherosclerotic plaques are lesions in the arterial vessels which arise during the process of atherogenesis. Most cases of acute heart attacks are caused by rupture of an atherosclerotic plaque. 

The innermost layer of an artery, which consists of loose connective tissue covered by a monolayer of endothelium that resides on a basement membrane. In human arteries, the intima often contains resident smooth muscle cells even early in life. Atherosclerotic plaques form in the intima. 

Atherosclerosis is a disease characterized by deposits of fatty plaques on the inner wall of arteries. These deposits result in a narrowing of the lumen (inside diameter) of die artery and a decrease in blood supply to the area served by die artery. 

An increase in serum lipids is believed to contribute to or cause atherosclerosis, a disease characterized by deposits of fatty plaques on the inner walls of arteries. These deposits result in a narrowing of the lumen (inside diameter) of the artery and a decrease in blood supply to the area served by the artery. When these fatty deposits occur in the coronary arteries, the patient experiences coronary artery disease. Lowering blood cholesterol levels can arrest or reverse atherosclerosis in the vessels and can significantly decrease the incidence of heart disease. 

The intima of the arterial wall contains hyaluronic acid and chondroitin sulfate, dermatan sulfate, and heparan sulfate proteoglycans. Of these proteoglycans, dermatan sulfate binds plasma low-density lipoproteins. In addition, dermatan sulfate appears to be the major GAG synthesized by arterial smooth muscle cells. Because it is these cells that profiferate in atherosclerotic lesions in arteries, dermatan sulfate may play an important role in development of the atherosclerotic plaque. 

CEA involves exposure of the carotid bifurcation in the neck to a point along the internal carotid artery (ICA) beyond which the atherosclerotic plaque terminates. 

The relationship between LAA and early recurrence is likely to be largely mediated by arterial embolism from atherosclerotic plaque, although recurrent low-flow stroke may also occur due to severe vessel stenosis or occlusion. In recently symptomatic individuals with moderate-or-severe ICA stenosis, platelet-fibrin embolic signals (ES) are commonly detected in the MCA using transcranial Doppler (TCD) ultrasound and have been reported to independently predict a fivefold increase in 90-day recurrence. " ... 

Carotid artery disease is one of the major causes of ischemic stroke. The predominant mechanisms by which it causes stroke are (a) arterial embolism from atherosclerotic plaques (b) hemodynamic changes, leading to watershed infarcts and (c) distal propagation of thrombus originating from acute carotid occlusion. ... 

Pan XM, Saloner D, Reilly LM, Bowersox JC, Murray SP, Anderson CM, Gooding GA, Rapp JH. Assessment of carotid artery stenosis by ultrasonography, conventional angiography, and magnetic resonance angiography correlation with ex vivo measurement of plaque stenosis. J Vase Surg 1995 21(l) 82-88 [discussion 88-89]. 

Carotenoids and cardiovascular diseases — Numerous epidemiological studies aimed to study the relationship of carotenoids and cardiovascular diseases (CVDs) including coronary accident risk and stroke. It appeared then that observational studies, namely prospective and case-control studies, pointed to a protective effect of carotenoids on myocardial infarct and stroke, but also on some atherosclerosis markers such as intima media thickness (IMT) of the common carotid artery (CCA) and atheromatous plaque formation. 

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