CORONARY-THROMBOSIS IN CHRONIC MYOCARDIAL -ISCHEMIA

Apart from the relevance of disorders of lipid metabolism for the clin ical and morphological progression of coronary artery disease, coronar y thrombosis has received increasing attention in recent years. It is undoubtedly the decisive factor in the pathogenesis of acute coronary syndromes, which is underlined by the therapeutic success of various a ntithrombotic interventions. Furthermore coronary thrombosis is regard ed to be a key factor for morphological disease progression also in st able coronary syndromes, which eventually may lead to critical limitat ion of myocardial perfusion. This is caused by the formation of subcli nical coronary thrombi, which either undergo endogenous lysis or becom e morphologically fixed as they are incorporated into the plaque. Besi des local factors, systemic disturbances of hemostasis and endogenous thrombolysis are of relevance. The concept of thrombotic progression o f coronary thrombosis is supported by data on the reduction of morphol ogical disease progression or antiischemic effectiveness of antithromb otic interventions like aspirin, low-molecular weight heparin and low- dose intermittent urokinase therapy. Percutaneous transluminal coronar y angioplasty results in deep mechanical injury of the vessel wall, wh ich is accompanied by secondary coronary thrombosis in the majority of the cases, not neccessarily leading to abrupt vessel closure. Particu larly, dilatation of primary thrombus as it has been described as the substrate of the culprit lesion in unstable coronary syndromes, promot es release of thrombin and activation of platelets, which in turn furt hers the proliferative processes in the pathogenesis of restenosis. Ev en though data on the reduction of the rate of restenosis by the use o f platelet aggregation inhibitors Like aspirin, ticlopidin and dipyrid amole have not consistently supported this concept, the EPIC Study has shown that even in patients with stable angina pectoris clinical rest enosis rate may be reduced by a platelet-IIb/lIIa-antagonist.