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Figure 1 Link between cardiovascular (CV) risk factors, endothelial dysfunction, inflammation, and acute coronary syndromes. Endothelial dysfunction can be caused by many pro-inflammatory atherogenic factors (i.e., oxidative stress, low shear stress, glycation end-products, smoking, probably infections). Initially, endothelial nitric oxide synthesis is decreased, leading to impairment of endothelial-dependent vasorelaxation; this represents one of the earliest changes of atherosclerosis. Endothelial cells thereafter increase expression of adhesion molecules (VCAM, ICAM-1, and so forth), which facilitate monocyte and platelet adherence to the vessel wall through their cell-surface integrin receptors. Inflammatory cells are responsible for the release of TF, the major trigger of the coagulation cascade. ACE = angiotensin converting enzyme; CNP = c-type natriuretic peptide; ICAM-1 = intercellular adhesion molecule; MCP-1 = monocyte chemoattractant protein-1; NFk = nuclear factor kappa; PDGF = platelet-derived growth factor; PGI₂ = prostaglandin; TGF = transforming growth factor; VCAM = vascular cell adhesion molecule.