These syndromes usually occur when an acute thrombus forms in an atherosclerotic coronary artery. Atheromatous plaque sometimes becomes unstable or inflamed, causing it to rupture or split, exposing thrombogenic material, which activates platelets and the coagulation cascade and produces an acute thrombus. Platelet activation involves a conformational change in membrane glycoprotein (GP) IIb/IIIa receptors, allowing cross-linking (and thus aggregation) of platelets. Even atheromas causing minimal obstruction can rupture and result in thrombosis; in > 50% of cases, pre-event stenosis is < 40%. Thus, although the severity of stenosis helps predict symptoms, it does not always predict acute thrombotic events. The resultant thrombus abruptly interferes with blood flow to parts of the myocardium. Spontaneous thrombolysis occurs in about two thirds of patients; 24 h later, thrombotic obstruction is found in only about 30%. However, in virtually all cases, obstruction lasts long enough to cause tissue necrosis.