Cardiovascular disease coronary occlusions

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. 

Compared to normotensives, hypertensive persons develop a marked excess of the major cardiovascular diseases. In the age group 45-74, they develop at least twice as much occlusive peripheral artery disease, about three times as much coronary disease, more than four times as much congestive [heart] failure and over seven times the incidence of brain infarction as normotensives. 

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. 

The natural history of the disease is determined by the onset and extent of chronic diabetic complications. Microangiopathic changes are diabetes-specific, causing retinopathy, nephropathy and alterations in the peripheral and autonomous nervous system. Macroangiopathy, which is more typical for Type-II diabetes, leads predominantly to cardiovascular complications with coronary heart disease, myocardial infarction and peripheral vascular occlusion. 

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