Pathophysiology of unstable angina. Role of plaque rupture and thrombosis

If excess influx of lipids predominates over the proliferative response, th e atherosclerotic process progresses into the formation of vulnerable lesio ns. This type of lesions are the most clinically relevant since they are th e pathogenic basis for plaque rupture and coronary thrombus formation. Plaq ue rupture is a mechanical event mainly determined by the fibrous cap thick ness and the lipid core size. In addition, biological factors such as infla mmatory infiltration may contribute to weakening and fracture of the fibrou s cap. Exposure of plaque components to flowing blood following rupture is the key event to initiate thrombosis within coronary arteries. Local factor s such as quantity (fissure size), quality (plaque composition) and rheolog y at the site of rupture, together with systemic factors inducing hypercoag ulable or thombogenic states modulate thrombosis at the time of plaque rupt ure. The natural history of acute coronary syndromes probably mirrors that of the underlying plaque rupture and thrombus formation. Angina stabilizati on would correspond to resealing of a rupture, accentuation of symptoms to development of labile thrombosis, non-Q wave infarction to development of t ransient thrombotic occlusion, and Q-wave infarction to establishment of a persistent occlusive thrombosis. Furthermore, this natural history may be m odified by vascular tone and presence of collateral circulation.