Relation of multi-vessel coronary artery disease to response to aspirin

Background Multi-vessel coronary artery disease (MV-CAD) is correlated with worse outcomes compared with single-vessel CAD (SV-CAD), potentially attributed to more advanced atherosclerotic disease in other vascular beds, greater endothelial dysfunction, thrombin activation and possibly greater platelet reactivity. Objectives The aim of the current study was to evaluate the association between MV-CAD and high on-aspirin platelet reactivity (HAPR) in patients with stable CAD treated with aspirin. Methods Patients with known stable CAD, who were taking aspirin (75–100 mg qd) regularly for at least one month, and had undergone coronary angiography at least 3 months prior to the test, were enrolled. Blood was drawn from the participants and sent for platelet function testing. MV-CAD was defined as >50% stenosis in ≥2 separate major coronary territories per coronary angiography. HAPR was defined as aspirin reaction units (ARU) >550. Results Overall 507 patients were analyzed; age 66.7±11.2, 17.9% women, 223 (44%) had MV-CAD. Mean ARU was significantly higher among patients with MV-CAD vs. SV-CAD (460±68 vs. 440±55, p<0.001, respectively). Furthermore, the rate of HAPR was significantly higher among patients with MV-CAD (figure 1). In a multivariate analysis adjusted for potential confounders, MV-CAD was found to be a strong independent predictor of HAPR [OR=1.8 (95% CI1.05–4.7), p=0.014]. In a reverse analysis, HAPR was associated with a higher number of coronary vessels involved (1.95±0.65 vs. 1.45±0.57, p<0.01) and a strong independent predictor of MVD (OR-2.44, CI 1.83–25.6, p=0.015). Conclusions MV-CAD is significantly associated with HAPR. This could potentially explain, in part, the increased risk and/or worse outcomes in patients with MV-CAD and implies considering intensive anti-thrombotic therapy among these patients. Funding Acknowledgement Type of funding source: None