The available evidence demonstrates that the use of clopidogrel plus aspirin in people at high risk of cardiovascular disease and people with established cardiovascular disease without a coronary stent is associated with a reduction in the risk of myocardial infa rct ion and ischaemic stroke , and an increased risk of major and minor bleeding compared with aspirin alone .
According to GRADE criteria , the quality of evidence was moderate for all outcomes except all-cause mortality ( low quality evidence ) and adverse events ( very low quality evidence )
BACKGROUND Aspirin is the prophylactic antiplatelet drug of choice for people with cardiovascular disease .
Adding a second antiplatelet drug to aspirin may produce additional benefit for people at high risk and people with established cardiovascular disease .
This is an up date to a previously published review from 2011 .
OBJECTIVES To review the benefit and harm of adding clopidogrel to aspirin therapy for preventing cardiovascular events in people who have coronary disease , ischaemic cerebrovascular disease , peripheral arterial disease , or were at high risk of atherothrombotic disease , but did not have a coronary stent .
Thrombin formation and platelet activation at the site of vascular injury in patients with coronary artery disease treated with clopidogrel combined with aspirin.
BACKGROUND Data on the effects of oral antiplatelet agents on blood coagulation in vivo are conflicting . The platelet glycoprotein ( GP ) IIIa PlA2 allele has been suggested to modulate antithrombotic actions of clopidogrel . AIM We investigated whether clopidogrel combined with aspirin affects local thrombin formation and platelet activation triggered by vascular injury . METHOD We studied patients with stable coronary artery disease on chronic aspirin therapy r and omised to addition of clopidogrel 75 mg/d ( n = 30 ) or continuation of aspirin 100 mg/d ( n = 30 ) for 4 weeks .  Markers of thrombin generation [ thrombin-antithrombin complexes ( TAT ) and prothrombin 1.2 fragments ( F1.2 ) ] and markers of platelet activation [ soluble CD40 lig and ( sCD40L ) and P-selectin ] were determined in the supernatant of blood sample s obtained from a microvascular injury site . RESULTS Total amounts of thrombin markers produced at the site of injury were similar before and after addition of clopidogrel , whereas platelet release of sCD40L and P-selectin was lower during treatment with aspirin + clopidogrel by 33.8 % and 27.8 % ( p < 0.001 ) , respectively . Patients in the highest tertile of reduction in platelet activation had previous myocardial infa rct ion and peripheral arterial disease and released the highest amounts of sCD40L and P-selectin at baseline . TAT and F1.2 generation as well as sCD40L or P-selectin release were not influenced by the presence of the PlA2 allele . CONCLUSION Our study shows that clopidogrel combined with aspirin does not reduce thrombin formation following vascular injury , but attenuates platelet sCD40L and P-selectin release
The available evidence demonstrates that the use of clopidogrel plus aspirin in people at high risk of cardiovascular disease and people with established cardiovascular disease without a coronary stent is associated with a reduction in the risk of myocardial infa rct ion and ischaemic stroke , and an increased risk of major and minor bleeding compared with aspirin alone .
According to GRADE criteria , the quality of evidence was moderate for all outcomes except all-cause mortality ( low quality evidence ) and adverse events ( very low quality evidence )
BACKGROUND Aspirin is the prophylactic antiplatelet drug of choice for people with cardiovascular disease .
Adding a second antiplatelet drug to aspirin may produce additional benefit for people at high risk and people with established cardiovascular disease .
This is an up date to a previously published review from 2011 .
OBJECTIVES To review the benefit and harm of adding clopidogrel to aspirin therapy for preventing cardiovascular events in people who have coronary disease , ischaemic cerebrovascular disease , peripheral arterial disease , or were at high risk of atherothrombotic disease , but did not have a coronary stent .