The major risk of atherosclerotic disease is the occurrence of an acute coronary syndrome. The pathogenesis of instable angina involves the formation of an arterial thrombus as a consequence of the rupture of an atheromatous plaque. This risk of plaque rupture appears to depend on plaque morphology rather than plaque size or severity of stenosis. Ratio of lipid core to fibrous determined by the balance between smooth muscle cells proliferation and extracellular matrix synthesis stabilizing the plaque and macrophages which degrade collagen, determine the plaque vulnerability.

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Unstable angina is one of the main reasons for admission to a cardiology department and the risk of myocardial infarction is high. Non-Q wave myocardial infarction used to be assimilated to unstable angina. Myocardial infarction without prolonged ST segment elevation and with troponin increase is now the category used to describe this condition.

CPK elevation, EKG and clinical parameters are involved in the acute prognosis of patients with unstable coronary syndrome.

The FRISC II trial was the first study to demonstrate the superiority of systematic early angiography followed by a revascularization procedure selected according to the type of lesions to be treated, compared with conventional management. The risks of bleeding complications associated with this therapeutic strategy are minimized by the TIMI classification. This classification no longer corresponds to the current norms of patient safety and comfort. Several methods can be used in order to decrease the risk of bleeding complications; the radial approach is undoubtedly the most efficient one.

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Syndrome de Wellens




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