Acute myocardial infarction occurring while on chronic clopidogrel therapy (‘clopidogrel failure’) is associated with high incidence of clopidogrel poor responsiveness and stent thrombosis

Abstract

ObjectivesThe clinical significance of the laboratory-based phenomenon of clopidogrel hypo-responsiveness and platelet reactivity associated with acute myocardial infarction, despite chronic clopidogrel therapy, is largely unknown. We aimed to determine platelet reactivity and clinical and angiographic features in 29 consecutive patients sustaining an acute myocardial infarction despite chronic (≥1 month) clopidogrel therapy.MethodsPlatelet reactivity was determined on admission using conventional aggregometry. All patients underwent coronary angiography within 24 hours of admission. Patients were matched with clopidogrel-naïve acute myocardial infarction patients. Clopidogrel-naïve patients received a 600 mg clopidogrel loading dose and 75 mg/day thereafter.ResultsOf the 29 study patients, 19 (66%) presented with ST-elevation myocardial infarction, and in 25% the infarction was related to angiographically-proved definite stent thrombosis. Two-thirds of these patients were poor responders to clopidogrel (adenosine diphosphate-induced platelet aggregation >50%) and dual antiplatelet poor responsiveness was found in 57% in the chronic clopidogrel therapy group. Compared with clopidogrel-naïve patients, chronic clopidogrel therapy patients were more likely to demonstrate clopidogrel poor responsiveness (66% versus 38%, p = 0.02), to be diabetic (52% versus 33%, p = 0.1) and to have multi-vessel coronary disease (79% versus 55%, p = 0.03).ConclusionsPatients sustaining acute coronary syndrome despite chronic clopidogrel therapy are more likely to exhibit inadequate platelet inhibition with clopidogrel.

Effect analysis of kinetic energy progressive exercise in patients with acute myocardial infarction after percutaneous coronary intervention: a randomized trial

“…These findings further showed that PEKE could effectively improve the QoL of patients with AMI after PCI and improve their prognosis. The reason may be that PEKE can help regulate vascular tension, reduce peripheral vascular tension, and improve aortic compliance, so as to achieve the purpose of relieving microvasospasm, restoring normal blood pressure, and ultimately improving the patient's exercise endurance, which encompasses prerequisites for optimizing the QoL (22,23).…”

Prior Myocardial Infarction and Treatment Effect of Ticagrelor Versus Prasugrel in Patients With Acute Coronary Syndromes ‐ A Post‐hoc Analysis of the ISAR‐REACT 5 Trial

“… 24 The observation of recurrence of ischemic events despite ongoing antiplatelet therapy highlights the failure of pharmacological secondary prevention strategies and is likely attributable to an ineffective antithrombotic protection owing to drug hyporesponsiveness or adherence issues. 25 , 26 , 27 Currently, aspirin represents the drug of choice for secondary prevention in patients with established CAD, particularly in those with prior MI and revascularization, whereas clopidogrel serves as an alternative in patients with aspirin intolerance or high risk of bleeding. Efforts to either replace aspirin with newer P2Y 12 inhibitors 28 or improve on its efficacy by intensifying or prolonging dual antiplatelet therapy regimens 29 or by adding a low‐dose anticoagulant 30 have not produced convincing results to change current practice.…”