Antiplatelet agents have a beneficial effect in reducing all cause mortality and fatal cardiovascular events in patients with IC .
BACKGROUND Peripheral arterial disease ( PAD ) is common and is a marker of systemic atherosclerosis .
Patients with symptoms of intermittent claudication ( IC ) are at increased risk of cardiovascular events ( myocardial infa rct ion ( MI ) and stroke ) and of both cardiovascular and all cause mortality .
OBJECTIVES To determine the effectiveness of antiplatelet agents in reducing mortality ( all cause and cardiovascular ) and cardiovascular events in patients with intermittent claudication .
Enhanced antiplatelet effect of clopidogrel in patients whose platelets are least inhibited by aspirin: a randomized crossover trial.
OBJECTIVE We aim ed to determine whether adding clopidogrel to aspirin in patients at high risk of future cardiovascular events would suppress laboratory measures of the antiplatelet effects of aspirin ; and have greater platelet inhibitory effects in patients with the least inhibition of platelets by aspirin . METHODS We performed a r and omized , double-blind , placebo-controlled , crossover trial , comparing clopidogrel 75 mg day(-1 ) versus placebo , in 36 aspirin-treated patients with symptomatic objective ly confirmed peripheral arterial disease . RESULTS The addition of clopidogrel to aspirin did not suppress platelet aggregation induced by arachidonic acid , urinary 11 dehydro thromboxane B2 concentrations , or soluble markers of platelet activation markers ( P-selectin , CD40-lig and ) and inflammation ( high sensitivity serum C-reactive protein , interleukin-6 ) . Clopidogrel significantly inhibited platelet aggregation induced by ADP ( reduction 26.2 % ; 95 % CI : 21.3 - 31.1 % , P < 0.0001 ) and collagen ( reduction 6.2 % ; 95 % CI : 3.2 - 9.3 % , P = 0.0003 ) . The greatest inhibition of collagen-induced platelet aggregation by clopidogrel was seen in patients with the least inhibition of arachidonic acid induced aggregation by aspirin [ lower tertile of arachidonic acid-induced platelet aggregation : 2.8 % ( 95 % CI : -0.8 to 6.3 % ) reduction in mean collagen-induced aggregation by clopidogrel ; middle tertile : 4.0 % ( 95 % CI : 0.4 - 7.6 % ) ; upper tertile 12.6 % ( 95 % CI : 4.5 - 20.8 % ) ; P-value for interaction 0.01 ] . CONCLUSIONS The greatest platelet inhibitory effect of clopidogrel occurs in patients with the least inhibition of arachidonic acid-induced platelet aggregation by aspirin . This raises the possibility that the clinical benefits of adding clopidogrel to aspirin may be greatest in patients whose platelets are least inhibited by aspirin . Confirmation in clinical outcome studies may allow these patients to be targeted with antiplatelet drugs that inhibit the ADP receptor , thereby overcoming the problem of laboratory aspirin resistance
Antiplatelet agents have a beneficial effect in reducing all cause mortality and fatal cardiovascular events in patients with IC .
BACKGROUND Peripheral arterial disease ( PAD ) is common and is a marker of systemic atherosclerosis .
Patients with symptoms of intermittent claudication ( IC ) are at increased risk of cardiovascular events ( myocardial infa rct ion ( MI ) and stroke ) and of both cardiovascular and all cause mortality .
OBJECTIVES To determine the effectiveness of antiplatelet agents in reducing mortality ( all cause and cardiovascular ) and cardiovascular events in patients with intermittent claudication .