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Volume 19 - Issue 2, March-April 2017
ORIGINAL
THE RELEVANCE OF PLATELET GLYCOPROTEIN GP IIB/IIIA POLYMORPHISM TO ANTI-PLATELETS RESPONSE IN ACUTE CORONARY SYNDROME
NAYEL OMNYA, SOBHY MOHAMMED, BARAKA AZZA, EL-SAMAK MOHAMMED, ABDEL-KADER CHERINE


The potential implication of PlA gene variants of GPIIIa of platelet GP IIb/IIIa as a genetic risk factor provocateur and/or a therapeutic outcome modulator to anti-platelet therapy in acute coronary syndrome (ACS) was probed. Study enrolled 22 controls and 44 ACS patients [non-ST segment elevation myocardial
infarction (NSTEMI) vs ST segment elevation myocardial infarction (STEMI)]. They were risk stratified (TIMI score), sampled for genotyping and estimation of platelet aggregation, then subdivided according to add-on anti-platelet therapy into: clopidogrel or tirofiban subgroups. After 48 hours, the therapeutic outcome
was assessed; clinically; pain relief or complication prevalence (symptomatic, electrocardiographic or hemorrhagic) and the investigational estimates were re-assessed. Intra-procedural evaluation of chest pain,ECG tracing and angiographic findings (number of culprit vessels, thrombus extent, TIMI flow, and myocardial blush) was reported in patients who underwent PCI. Frequency of PlA2 vs PlA1 allele was higher in ACS patients (significant in ≤60 years/doubled in STEMI vs NSTEMI). TIMI score, stratification permitted considering PlA2 variant as independent risk factor in UA/NSTEMI subsets. This was fostered by intra-procedural finding of more stenotic and thrombotic lesions in PlA2 carriers. A lack of significant association between PlA variants and changes in platelet aggregation, debate its causal relation to PlA2 variant being an ACS risk factor. A positive correlation was observed between PlA variants and the therapeutic response
outcome to both clopidogrel and tirofiban regarding platelet aggregation and relief of chest pain. Thus, PlA2 variant could be considered a genetic risk factor contributor rather than an anti-platelet therapeutic response modulator, when speaking of ACS. This awaits larger scale pharmacogenomic studies before a final statement is declared so as to individualize anti-platelet therapy to the best of its therapeutic outcome in ACS settings.

ACUTE CORONARY SYNDROME – GLYCOPROTEIN GP IIB/IIIA – PHARMACOGENOMICS – POLYMORPHISM



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