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Hypercholesterolemia is an established risk factor for the development of cardiovascular diseases. The atherosclerotic lesions that result from a sustained elevation in blood cholesterol concentration are associated with an accumulation of inflammatory cells and platelets that facilitate the deposition of lipids in the walls of lesion-prone arteries. However, long before these changes occur in large arteries, inflammatory and prothrombogenic responses are observed in arterioles and venules throughout the vascular system (Figure 1). These responses are manifested as endothelial dysfunction and the binding of leukocytes and platelets to the vessel wall. Although several mechanisms have been proposed to explain the phenotypic changes that occur in the microvas-culature during hypercholesterolemia, oxidative stress and a diminished bioavailability of nitric oxide (NO) have gained much attention in recent years. This chapter describes the responses of the microcirculation to hypercholesterolemia and addresses the mechanism that underlies this systemic inflammatory condition.

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Lower Your Cholesterol In Just 33 Days

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