There is extensive literature supporting the role of inflammation in CAD. Hemodynamic forces from hypertension and oxidative stressors, such as tobacco and hyperglycemia, result in vascular endothelial injury. The attachment of leukocytes, transformation of monocytes into macrophages, and subsequent uptake of cholesterol lipoproteins initiate the fatty streak. Cytokine release from the fatty streak recruits further inflammatory cells (macrophages, mast cells, activated T cells), with resulting uptake and oxidation of low-density lipoprotein (LDL). These cytokines also stimulate smooth muscle cell proliferation and development of a collagenous fibrous cap that covers this inflammatory mixture to form the mature atherosclerotic plaque .
Recent data show that the risk for an acute coronary event has less to do with the degree of angiographic luminal stenosis than with the underlying pathology of the atherosclerotic plaque that makes it susceptible to rupture . Activated T cells within the atheromatous core secrete interferon gamma that decreases smooth muscle cell production of collagen . Inflammatory cyto-kine-activated macrophages secrete matrix metal-loproteinases that degrade the extracellular matrix, further weakening the fibrous cap and making it prone to rupture [5,6]. Disruption of
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cardiology.theclinics.com the cap exposes the atheronecrotic core to blood, after which further inflammatory reactions lead to platelet activation, coagulation cascade, further vasomotor dysfunction [7,8], and ultimately luminal occlusion.
Thus, all stages of atherothrombosis implicate inflammation as a key pathogenic mechanism. Several clinical studies have therefore targeted inflammatory factors as potential markers for cardiovascular risk assessment.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...