A recent study published in Circulation sought to examine the frequency and cause of aspirin resistance. Aspirin, an antiplatelet, is indicated to reduce combined risk of death and nonfatal stroke after ischemic stroke or TIA. It is also indicated to reduce risk of vascular mortality in suspected acute MI, to reduce combined risk of death and nonfatal MI after MI or unstable angina pectoris, to reduce combined risk of MI and sudden death in chronic stable angina, and for revascularization procedures.
A total of 400 healthy volunteers were evaluated for their response to a single oral dose of 325mg immediate-release or enteric-coated aspirin. Patient responses reflected that of aspirin’s mechanism as a cyclooxygenase-1 inhibitor. Patients who appeared “aspirin resistant” underwent repeat testing and if still found “resistant,” were exposed to low-dose enteric coated aspirin (81mg) and clopidogrel (75mg) for one week each.
Data showed resistance to a single dose of 325mg enteric-coated aspirin (up to 49%) but not to immediate-release aspirin (0%) due to inconsistent absorption levels. All patients responded to aspirin after repeated exposure, an extended post-dosing interval, or addition of aspirin to their platelets ex vivo.
Study authors concluded that pharmacological resistance to aspirin is rare. Pseudoresistance, referring to delayed and reduced drug absorption, seems to complicate the enteric-coated formulation but not immediate-release administration.
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