Compared with aspirin , thienopyridines significantly reduced gastrointestinal adverse effects .
However , thienopyridines increased the odds of skin rash and diarrhoea , ticlopidine more than clopidogrel .
Allocation to ticlopidine , but not clopidogrel , significantly increased the odds of neutropenia .
The thienopyridine derivatives are at least as effective as aspirin in preventing serious vascular events in patients at high risk , and possibly somewhat more so .
However , the size of any additional benefit is uncertain and could be negligible .
Clopidogrel has a more favourable adverse effects profile than ticlopidine and so is the thienopyridine of choice .
BACKGROUND Aspirin is the most widely studied and prescribed antiplatelet agent for preventing serious vascular events , reducing the odds of such events among high vascular risk patients by about a quarter .
Thienopyridine derivatives inhibit platelet activation by a different mechanism and so may be more effective .
OBJECTIVES To determine the effectiveness and safety of thienopyridine derivatives ( ticlopidine and clopidogrel ) versus aspirin for preventing serious vascular events ( stroke , myocardial infa rct ion ( MI ) or vascular death ) in patients at high risk , and specifically in patients with a previous TIA or ischaemic stroke .
Effect of platelet antigen polymorphism on platelet inhibition by aspirin, clopidogrel, or their combination.
OBJECTIVES We studied the modifier effect of platelet antigen polymorphism ( PlA2 ) on platelet inhibition by acetylsalicylic acid ( ASA , i.e. , aspirin ) , clopidogrel , or their combination in patients with coronary heart disease . BACKGROUND Clopidogrel , when administered with ASA , was shown to significantly improve the outcome of patients with acute coronary syndromes compared with patients receiving only ASA . We have shown previously that the effect of ASA on platelets is modified by the glycoprotein IIIa single nucleotide polymorphism PlA2 . Hence , an important pharmacogenetic question remains whether the antiplatelet effect of clopidogrel is uniform for all patients or , like acetylsalicylic acid , more selective . METHODS Thirty PlA1/A1 and 30 PlA1/A2 patients were assigned r and omly to ASA 325 mg/day , clopidogrel 75 mg/day , or both . After 10 days , platelet function was studied . RESULTS Clopidogrel provided stronger platelet inhibition than ASA with adenosine diphosphate as the agonist , and combination therapy result ed in greater inhibition than either inhibitor used alone ( p < 0.0001 ) . The use of ASA result ed in greater inhibition compared with clopidogrel with epinephrine ( p < 0.0001 ) and collagen as agonists ( p < 0.0001 ) . With collagen as the agonist , platelets from PlA1/A2 donors were markedly and significantly less inhibited by ASA ( p = 0.005 ) . In contrast , with clopidogrel , no significant difference could be detected between inhibition of Pl(A1/A1 ) and Pl(A1/A2 ) platelets . CONCLUSIONS The combination of ASA and clopidogrel appears superior to either agent alone in inhibiting platelet function . Pl(A2 ) functions as an important modifier for platelet responsiveness to ASA but not to clopidogrel . These findings could have significant impact on the future design of pharmacogenetic antithrombotic strategies for patients with coronary heart disease
Compared with aspirin , thienopyridines significantly reduced gastrointestinal adverse effects .
However , thienopyridines increased the odds of skin rash and diarrhoea , ticlopidine more than clopidogrel .
Allocation to ticlopidine , but not clopidogrel , significantly increased the odds of neutropenia .
The thienopyridine derivatives are at least as effective as aspirin in preventing serious vascular events in patients at high risk , and possibly somewhat more so .
However , the size of any additional benefit is uncertain and could be negligible .
Clopidogrel has a more favourable adverse effects profile than ticlopidine and so is the thienopyridine of choice .
BACKGROUND Aspirin is the most widely studied and prescribed antiplatelet agent for preventing serious vascular events , reducing the odds of such events among high vascular risk patients by about a quarter .
Thienopyridine derivatives inhibit platelet activation by a different mechanism and so may be more effective .
OBJECTIVES To determine the effectiveness and safety of thienopyridine derivatives ( ticlopidine and clopidogrel ) versus aspirin for preventing serious vascular events ( stroke , myocardial infa rct ion ( MI ) or vascular death ) in patients at high risk , and specifically in patients with a previous TIA or ischaemic stroke .