Mechanisms of Occlusion
Most MIs are caused by a disruption in the vascular endothelium associated with an unstable atherosclerotic plaque that stimulates the formation of an intracoronary thrombus, which results in coronary artery blood flow occlusion. If such an occlusion persists long enough (20 to 40 min), irreversible myocardial cell damage and cell death will occur.5
The development of atherosclerotic plaque occurs over a period of years to decades. The initial vascular lesion leading to the development of atherosclerotic plaque is not known with certainty. The two primary characteristics of the clinically symptomatic atherosclerotic plaque are a fibromuscular cap and an underlying lipid-rich core. Plaque erosion may occur due to the actions of metalloproteases and the release of other collagenases and proteases in the plaque, which result in thinning of the overlying fibromuscular cap. The action of proteases, in addition to hemodynamic forces applied to the arterial segment, can lead to a disruption of the endothelium and fissuring or rupture of the fibromuscular cap. The degree of disruption of the overlying endothelium can range from minor erosion to extensive fissuring that results in an ulceration of the plaque. The loss of structural stability of a plaque often occurs at the juncture of the fibromuscular cap and the vessel wall—a site otherwise known as the plaque's "shoulder region." Any amount of disruption of the endothelial surface can cause the formation of thrombus via platelet-mediated activation of the coagulation cascade. If a thrombus is large enough to completely occlude coronary blood flow for a sufficient time period, MI can result.
Mechanisms of Myocardial Damage
The severity of an MI is dependent on three factors: the level of the occlusion in the coronary artery, the length of time of the occlusion, and the presence or absence of collateral circulation. Generally speaking, the more... [continues]
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