الفهرس 
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Abstract
For many years, unstable angina has been considered as an” intermediate syndrome” between chronic stable angina and acute myocardial infarction.
In recent years, its physiopathology has been clarified and there have been major advances in management.
Pathological, angioscopic and biological observations have
demonstrated that unstable angina and myocardial infarction are different clinical presentations that result from a common underlying pathophysiological mechanism, namely, atherosclerotic plaque rupture or erosion, with differing degrees of superimposed thrombosis and distal embolization.
Clopidogrel inhibits platelet aggregation through binding selectively and noncompetitively to platelet ADP receptor in an irreversible manner preventing activation of glycoprotein lib/Ilia receptor which mediates the final common pathway of platelet aggregation.
Atorvastatin is a (HMG-CoA) reductase inhibitor widely used to treat hypercholesteremia .it is metabolized by CYP3a4.patients with atherosclerotic disease are frequently treated with c1opidogrel and atorvastatin or another statin.
Pravastatin is administered as monosodium salt and is present in the systemic circulation as the acid form which accounts for 75% of its activity .It undergoes extensive first-pass metabolism by non-CYP3A4mechanisms.So it will not be involved in interactions with drugs metabolized by CYP450. (Michael 1999).so coadministration of pravastatin with clopidogrel did not influence platelet aggregation.
This study was carried out in the coronary care unit, EI-Minia University Hospital during the period from December 2003 through December 2004.
The purpose of this study to clarify the Influence of Atorvastatin , Pravastatin , and Fluvastatin on the ability of Clopidogrel to inhibit platelet aggregation in patients with unstable angina.
To address this issue 60 patients suffering from unstable angina with platelet count more than 100,000 received aspirin150mg/d and naDROParinNa