Abstract
Antiplatelet agents are mainly used in the prevention and management of atherothrombotic complications. Dual antiplatelet therapy, combining aspirin and clopidogrel, is the standard care for patients having acute coronary syndromes or undergoing percutaneous coronary intervention according to the current ACC/AHA and ESC guidelines. But in spite of administration of dual antiplatelet therapy, some patients develop recurrent cardiovascular ischemic events especially stent thrombosis which is a serious clinical problem. Antiplatelet response to clopidogrel varies widely among patients based on ex vivo platelet function measurements. Clopidogrel is an effective inhibitor of platelet activation and aggregation due to its selective and irreversible blockade of the P2Y12 receptor. Patients who display little attenuation of platelet reactivity with clopidogrel therapy are labeled as low or nonresponders or clopidogrel resistant. The mechanism of clopidogrel resistance remains incompletely defined but there are certain clinical, cellular and genetic factors including polymorphisms responsible for therapeutic failure. Currently there is no standardized or widely accepted definition of clopidogrel resistance. The future may soon be realised in the routine measurement of platelet activity in the same way that blood pressure, cholesterol and blood sugar are followed to help guide the therapy, thus improving the care for millions of people. This review focuses on the methods used to identify patients with clopidogrel resistance, the underlying mechanisms, metabolism, clinical significance and current therapeutic strategies to overcome clopidogrel resistance.J Enam Med Col 2016; 6(1): 38-46
Highlights
Oral antiplatelet agents are the cornerstone of modern pharmacotherapy in the prevention and management of cardiovascular atherothrombotic diseases according to the current ACC/AHA and ESC guidelines.[1,2] It is well-established that the antiplatelet response to clopidogrel is not uniform and it varies widely among patients[3,4] and it reflects failure of clopidogrel to achieve its anti-aggregatory effect
Clopidogrel is the gold standard for the prevention of subacute stent thrombosis (SAT) in subjects undergoing PCI and reducing major adverse cardiovascular events in patients with non-ST segment elevation acute coronary syndromes.[5]
The use of clopidogrel has tremendously increased over the last few years, following its effectiveness together with aspirin in greatly reducing clinical adverse events in patients having acute coronary syndrome or undergoing PCI
Summary
Oral antiplatelet agents are the cornerstone of modern pharmacotherapy in the prevention and management of cardiovascular atherothrombotic diseases according to the current ACC/AHA and ESC guidelines.[1,2] It is well-established that the antiplatelet response to clopidogrel is not uniform and it varies widely among patients[3,4] and it reflects failure of clopidogrel to achieve its anti-aggregatory effect. Clopidogrel is the gold standard for the prevention of subacute stent thrombosis (SAT) in subjects undergoing PCI and reducing major adverse cardiovascular events in patients with non-ST segment elevation acute coronary syndromes.[5] This article discusses the definition, detection, risk factors and clinical consequences of clopidogrel resistance and role of current therapeutic strategies to overcome clopidogrel resistance. Platelets adhere to the sites of vascular injury.
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