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Non-ST segment elevation acute coronary syndromes: better results with triple antiplatelet pre-treatment


Aspirin and Clopidogrel ( Plavix ) are platelet antiaggregant drugs widely used and proven to be effective in the treatment of an acute coronary syndrome ( ACS ).
High-risk patients with non-ST segment elevation acute coronary syndrome ( NSTE ACS ) benefit from the addition of glycoprotein ( GP ) IIb/IIIa inhibitor.
In low-risk patients undergoing elective percutanous coronary intervention ( PCI ), receiving Aspirin and high dose ( 600 mg ) Clopidogrel, the addition of a GP IIb/IIIa inhibitor had no additional beneficial effect.
However, no study has been performed examining the value of IIb/IIIa inhibitor in patients with NSTE ACS undergoing PCI.

The ELISA II trial was designed to compare dual antiplatelet, Aspirin and Clopidogrel 600 mg, with triple antiplatelet, Aspirin, Clopidogrel 300 mg and Tirofiban ( Aggrastat, a GP IIb/IIIa inhibitor ) in patients with NSTE ACS, undergoing coronary angiography.

A total of 328 patients with NST ACS were included.
The primary end point was enzymatic infarct size; the secondary end point was the epicardial coronary artery flow ( TIMI flow ) at initial angiogram of the culprit vessel.
The patients were randomised to pre-treatment with dual ( n=166, Aspirin, Clopidogrel 600 mg ) or triple antiplatelet therapy ( n=162, Aspirin, Clopidogrel 300 mg and Tirofiban.

Coronary angiography was performed in 98% of the patients. Enzymatic infarct size could be assessed in 89% of patients.

No significant difference in infarct size was found between the groups.
Initial TIMI 3 flow of the culprit lesion was significantly more often present in patients who received triple antiplatelet therapy ( 67% vs. 47%, p=0.001 ).
There was a strong trend toward better event ( myocardial infarction and death ) free survival both at 96 hours and 30 days after randomization in the triple antiplatelet group.

The ELISA II trial has showed that in patients with NSTE ACS, triple antiplatelet pre-treatment tended to decrease enzymatic infarct size and was associated with a significantly better perfusion of the culprit vessel at initial angiography.
Enzymatic infarct size was smaller than expected and therefore a larger trial might be needed to evaluate whether the observed difference in infarct size is real or based on chance.

Source: European Society of Cardiology ( ESC ) Congress, 2005


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