Renal function and aspirin resistance in patients with coronary artery disease

Aspirin resistance and chronic renal failure are both potentially important clinical issues in coronary artery disease. To test the hypothesis of a relationship between the two, we recruited 169 stable outpatients with proven coronary artery disease (myocardial infarction, coronary artery bypass grafting, intra-coronary stents) taking 75 mg aspirin daily. Blood was taken for light transmission aggregometry to agonists arachidonic acid (0.5 mg/mL) and adenosine diphosphate (10 μmol/L), for platelet marker soluble P selectin (enzyme linked immunosorbent assay), resting and stimulated expression of CD62P (flow cytometry) and for renal function (estimated glomerular filtration rate). The estimated glomerular filtration rate was lower when aspirin resistance was defined by response to arachidonic acid after 3, 5 and 7 minutes (approximately 30% of patients) (p < 0.021), and when defined by response to adenosine diphosphate after 3 minutes (approximately 17% of patients)(p = 0.015) compared to those who were sensitive to aspirin. Mean [standard deviation] soluble P selectin levels were 57 [23] ng/mL in 49 patients with aspirin resistance, and 50 [15] ng/mL in the 119 aspirin sensitive patients (p = 0.02). Estimated glomerular filtration rate correlated inversely with platelet CD62P expression at rest (r = − 0.22, p = 0.004), and when stimulated by arachidonic acid (r = − 0.21, p = 0.007) and by adenosine diphosphate (r = − 0.17, p = 0.023). Aspirin resistance was more than twice as prevalent in those with the greatest renal disease (50% of patients) compared to those with the best renal function (21.4%). Our data point to a weak relationship between worsening glomerular filtration rate and aspirin resistance. Nevertheless, we suspect that failure of patients to be fully responsive to aspirin may be important in the pathophysiology of thrombosis in renal dysfunction.