Aspirin Resistance in Coronary Artery Disease
This trial is active, not recruiting.
|Condition||coronary artery disease|
|Start date||June 2006|
|End date||March 2011|
|Trial size||160 participants|
|Trial identifier||NCT00753935, 040065, 5P50HL081009-03|
The purpose of this study is to evaluate possible mechanisms of aspirin resistance at a molecular level in aspirin-treated patients with coronary artery disease. We hypothesize that certain patient characteristics associate with aspirin resistance. In addition, we will compare the effects of enteric-coated aspirin and chewable aspirin.
|Endpoint classification||pharmacodynamics study|
|Intervention model||parallel assignment|
|Masking||single blind (investigator)|
Serum thromboxane B2
time frame: after 2 weeks of aspirin
Male or female participants at least 40 years old.
Inclusion Criteria: - On aspirin 81-325mg daily at time of enrollment - Documented stable coronary artery disease or > 6 months after CABG or interventional cardiac procedure - Written informed consent Exclusion Criteria: - Pre-menopausal female - Renal disease (creatinine >= 2 mg/dl) - Anemia (Hematocrit < 30%) - Thrombocytopenia (platelet count < 135,000/ul) - Use of NSAIDs or coxibs within the previous 2 weeks - Concurrent use of other anti-platelet agents - Uncontrolled hypertension (systolic BP > 180 mmHg) - Decompensated congestive heart failure - Recent coronary syndrome (< 6 months) - History of significant GI bleeding
|Official title||Evaluation of Aspirin Resistance at a Molecular Level in Aspirin-Treated Patients With Coronary Artery Disease|
|Principal investigator||Mary B Taylor, MD, MSCI|
|Description||Aspirin is commonly used for its antithrombotic effects in patients at risk for cardiovascular events. Its primary mechanism of action is the irreversible acetylation of platelet cyclooxygenase-1, thereby inhibiting platelet production of thromboxane A2, a potent vasoconstrictor and activator of platelets. Previous studies have demonstrated that many patients have recurrent events despite treatment with aspirin, which has been termed "aspirin resistance" or "aspirin nonresponse." This study addresses some of the possible mechanisms for aspirin nonresponse; specifically, we will test the hypothesis that aspirin nonresponse results from states that produce high peroxide concentrations ("oxidative stress") in platelets. In addition, we will evaluate the effect of enteric coating on the pharmacologic efficacy of aspirin in patients with coronary artery disease.|
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