We have speculated previously that the abrupt conversion from chronic stable to unstable angina and the continuum to acute myocardial infarction may result from myocardial ischemia caused by progressive platelet aggregation and dynamic vasoconstriction themselves caused by local increases in thromboxane and serotonin at sites of coronary artery stenosis and endothelial injury. Platelet aggregation and dynamic coronary artery vasoconstriction probably result from the local accumulation of thromboxane and serotonin and also relative decreases in the local concentrations of endothelially derived vasodilators and inhibitors of platelet aggregation, such as endothelium-derived relaxing factor (EDRF) and prostacyclin. With severe reductions in coronary blood flow caused by these mechanisms, platelet aggregates may increase, and an occlusive thrombus composed of platelets and white and red blood cells in a fibrin mesh may develop. When coronary arteries are occluded or narrowed for a sufficient period of time by these mechanisms, myocardial necrosis, electrical instability, or sudden death may occur. We believe that unstable angina and acute myocardial infarction are a continuum in relation to the process of coronary artery thrombosis and vasoconstriction. When the period of platelet aggregation or dynamic vasoconstriction at sites of endothelial injury and coronary artery stenosis is brief, unstable angina or non-Q wave infarction may occur. However, when the coronary artery obstruction by these mechanisms is prolonged for several hours, Q wave myocardial infarction results. Chronic endothelial injury and coronary artery stenosis are probably associated with the accumulation of platelets, white and red blood cells, and a fibrin mesh at the site of stenosis and endothelial injury.

These results compare favorably with other methods of treating AGI, especially in patients with multilevel occlusive disease. Principle advantages include acceptable perioperative mortality, low amputation rate, superior durability with excellent long-term patency, and freedom from secondary interventions and recurrent infections.

The popliteal artery is a relatively short vascular segment but is affected by a unique set of pathologic conditions. These conditions, which may be common throughout the arterial system or exclusive to the popliteal artery, include atherosclerosis, popliteal artery aneurysm, arterial embolus, trauma, popliteal artery entrapment syndrome, and cystic adventitial disease. The clinical manifestations, imaging appearances, and treatment options associated with these pathologic conditions differ significantly. Consequently, the radiologist should be familiar with these conditions to direct imaging for accurate diagnosis and treatment and to prevent loss of limb.

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The theoretical framework for risk stratification among patients with critical limb ischemia provided by the SVS expert panel appears valid. Further validation of the WIfI classification system with multicenter data is justified.