Vascular and platelet responses to aspirin in patients with coronary artery disease
Correspondence to: Dr A. D. Blann, Centre for Cardiovascular Sciences, University of Birmingham, City Hospital, Birmingham, B18 7QH, UK. Tel/fax: +44 121 507 5076; e-mail email@example.com
Variability in the response to aspirin (sometimes known as aspirin resistance) in modulating platelet activity is a potentially important clinical issue in coronary artery disease (CAD), but may be also be important in other areas of pathophysiology.
Materials and methods
Testing the hypothesis of a relationship between aspirin resistance and vascular function, inflammation and coagulation, we recruited 175 stable CAD outpatients taking 75 mg aspirin daily. Indices were compared to 58 controls not taking aspirin. Platelet activity was assessed by light transmission aggregometry (LTA) to 0·5 mg/mL arachidonic acid (AA), plasma markers soluble P selectin and thromboxane (ELISA), and resting and AA stimulated membrane P selectin and PAC-1 expression (flow cytometry). Vascular function was assessed by arterial stiffness (Sphygmocor system), von Willebrand factor and soluble E selectin (ELISA), inflammation by high sensitivity CRP and interleukin-6, and coagulation by tissue factor and fibrin d-dimers levels (all immunoassay).
The 5-min LTA response AA was superior to flow cytometry in discriminating the response of platelets to aspirin. Using the cut-off of 20% LTA response to AA, 32·6% of patients were aspirin resistant. The latter had higher soluble P selectin (P = 0·03), CRP (P = 0·029) and fibrin d-dimers (P = 0·01) compared to those who were aspirin sensitive. There was no relationship between aspirin response status and any vascular index.
We conclude that LTA is a more sensitive marker of aspirin resistance than is flow cytometry for P-selectin and PCA-1, and that aspirin response has no influence on vascular function.