Atherosclerosis Coronary occlusion

Coronary vascular disease Atherosclerosis Hypertension Occlusion of veins... 

In the western countries the most prevalent form of heart disease is coronary heart disease, i.e. the sequelae of atherosclerosis [18] of the coronary arteries. Culmination of coronary arteriosclerosis is manifested by erratic heart activity, arrhythmia or fibrillation, i.e. in drastic cases by coronary occlusion, myocardial infarction and sudden death. Mortality from coronary heart disease varies greatly from one country to the other. The following statistics represent the death rate due to coronary heart disease among the male population between the ages of... 

When drug therapy fails or if extensive coronary atherosclerosis is present, PCI is often performed to restore coronary blood flow, relieve symptoms, and prevent major adverse cardiac events. Patients with one or more critical coronary stenoses (i.e., greater than 70% occlusion of the coronary lumen) detected during coronary angiography may be candidates for PCI. Several catheter-based interventions maybe used during PCI, including ... 

The basic biology of chemokines and their receptors is well covered in Chapters 2 and 3 of this book, and we will focus hereafter upon the roles of individual chemokines and receptors in atherosclerosis. The largest amount of data on the roles of chemokines in cardiovascular disease (C VD) has been obtained from in vitro studies and murine models, which will be discussed in detail. In man, genetic polymorphisms in chemokine and chemokine-receptor genes have pointed to an important role for specific chemokines in various atherosclerotic diseases including coronary artery disease and carotid artery occlusive disease. For properties see Table 1. 

T9. Toth, L., and Koenig, W., Hypoalpha-hyperbeta-lipoproteinemia in a patient with coronary artery disease and occlusive peripheral arterial disease. Atherosclerosis 42,121-124... 

Atherosclerosis is a major cause of death in most industrial societies. The characteristic lesion of this disease, the atherosclerotic plaque, is found in the intima of large- and medium-sized arteries. An additional problem with advanced plaques is that thrombus formation is likely to occur in regions of plaque rupture. The combination of the two events can lead to partial or even total occlusion of major arteries. If this occurs in one or more of the coronary arteries, a serious or even fatal MI may result. A discussion of arteriosclerosis and exogenous agents that can modulate this condition is presented below. 

Atherosclerosis (athero = fatty and sclerosis = scarring or hardening) of the coronary and peripheral vasculature is the leading cause of morbidity and mortality worldwide. Lesions (called plaque) are initiated by an injury to endothelium and thicken the intima of arteries, occlude the lumen, and compromise delivery of nutrients and oxygen to tissue (ischemia). Atherosclerotic lesions primarily occur in large and medium-sized elastic and muscular arteries and progress over decades of life. These lesions cause ischemia, which can result in infarction of the heart (myocardial infarction) or brain (stroke), as well as abnormalities of extremities. The proximate cause of occlusion in these pathological conditions is thrombus formation. 

Aberrant thrombus formation and deposition on blood vessel walls imderlies the pathogenesis of acute cardiovascular disease states which remain the principal cause of morbidity and mortality in the industrialized world [1,2,3]. Plasma proteins, proteases and specific cellular receptors that participate in hemostasis have emerged as important risk considerations in thrombosis and thromboembolic disorders. The clinical manifestations of the above disease states include acute coronary artery and cerebrovascular syndromes, peripheral arterial occlusion, deep vein thrombosis and pulmonary/renal embolism [3]. The most dilabilitating acute events precipitated by these disorders are myocardial infarction and stroke. In addition, the interplay between hemostatic factors and hypertension (4) or atherosclerosis (5) dramatically enhances the manifestation of these pathologic states. 

Most of the cholesterol in plaque results from the ingestion of LDL by the foam cells that line the arteries. High blood plasma LDL therefore promotes atherosclerosis. Because the coronary arteries are narrow, they are especially prone to occlusion by atherosclerotic plaque. 

A EXPERIMENTAL FIGURE 18-21 Atherosclerosis narrows and blocks blood flow through coronary arteries. X-ray multislice computed tomographic image of a human heart reveals a major occlusion (black arrow) of the left anterior descending artery (LAD, arrow) and a narrowing of a nearby vessel (white arrow) as a block in the stream of blood (seen in the arteries as a white tube). [From K. Nieman et al., 2001, Lancet 357 599.]... 

In atherosclerosis, fatty material and cholesterol are deposited inside the lumen of medium- and large-sized blood vessels (arteries). Eventually, the plaque can rupture, triggering the formation of a blood clot. If the blood clot develops in the brain, it can cause a stroke if it develops in a coronary artery, it can cause a vessel occlusion and consequently a heart attack the supply of nutrients and oxygen to the heart muscle is reduced and the contractile muscle cells (cardiomyocytes) die within the blood-deprived myocardium. The tissue becomes necrotic and cardiac performances are impaired. 

Several studies have shown that the extent of coronary artery stenosis due to atherosclerotic plaque formation and expansion into the arterial lumen is not sufficient to explain the incidence of clinical events associated with atherosclerosis [183]. It appears that the generation of clinical events involves plaque mpture, resulting in thrombus formation and arterial occlusion. This mpture is induced by vasomotor disturbances in which oxidized low-density lipoproteins may be involved. Resveratrol is able to regulate vasomotion, which is impaired in atherosclerosis. The key regulators of the vasomotor function are the vasodilator NO and the vasoconstrictor endothelin-1 [167]. A number of in vitro and in vivo studies have shown improved vascular function in response to resveratrol [184, 185]. Resveratrol enhances expression and activity of endothelial nitric oxide synthase [186] and inhibits endothelin-1 secretion and endothelin-1 gene expression in human umbilical vein endothelial cells [187]. Intragastric administration of resveratrol for 12 weeks to hypercholesterolemic rabbits improved the endothelial function, reduced plasma endothelin-1 levels, and induced... 

Qiao, J. H. and Fishbein, M. C. (1991) The severity of coronary atherosclerosis at sites of plaque rupture with occlusive thrombosis, J. Am. Coll. Cardiol., 17,1138-42. 

AH of these are apparently for short durations under normal circumstances. They are examples of the adaptations affecting the structure and function of the body. However, dysfunction occurs when there is either persistence past the point of usefulness, inappropriate activation, a reflex loop pattern or any combination. The activation of any portion can be primary, secondary, or tertiary. The body responds to stress with vasoconstriction of all of the arteries as a means of shunting blood to the muscles. A normal reaction by the coronary vessels is to dilate, not because of an apparent paradoxical effect or receptor difference, but because the sympathetic stimulation increases the inotropic and chronotropic effects on the heart. The increased pressure, because of the rate and force of contraction, typically results in greater capacitance and perfusion of the heart itself. Partial or total occlusion by atherosclerosis or thromboembolic phenomena results in ischemia and possible infarction. The resultant pain and pressure contributes to... 

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