Relation of Hypoalbuminemia to Response to Aspirin in Patients With Stable Coronary Artery Disease

Abstract

Serum albumin (SA) level is a powerful cardiovascular prognostic marker, suggested to be involved in regulation of platelet function. High on-aspirin platelet reactivity (HAPR) is associated with increased risk for deleterious cardiovascular events. The aim of the present study was to evaluate the association between HAPR and albumin levels in patients with stable coronary artery disease (CAD) treated with aspirin. Patients with known stable CAD, who were taking aspirin (75 to 100 mg qd) regularly for at least 1 month, were screened for the present study. Exclusion criteria: cancer, sepsis or acute infection, active inflammatory/rheumatic disease, recent major surgery, chronic liver failure, the administration of other antiplatelet drugs, nonadherence with aspirin and thrombocytopenia. Blood was drawn from the participants and sent for SA level and platelet function test (VerifyNow). HAPR was defined as aspirin reaction units (ARU) >550. Overall 116 patients were analyzed; age 69 ± 10, 28% women. Twenty (17%) were hypoalbuminemic (≤3.5 g/dl). Hypoalbuminemic patients had similar characteristics to the normal albumin group except mildly higher creatinine in the former. SA levels were significantly lower in the hypoalbuminemic group (3.2 ± 0.2 g/dl vs 4.2 ± 0.4 g/dl, respectively, p <0.001) whereas mean ARU was significantly higher compared with the normal albumin group (548 ± 45 vs 444 ± 66 ARU, respectively, p <0.001). A significant inverse association was observed between SA and ARU with (R2 = 0.67, p <0.001). Multivariate analysis adjusted for potential confounders found that albumin ≤3.5 is the strongest predictor of HAPR in patients with stable CAD (hazards ratio 4.9, 95% confidence interval 2.2 to 32, p = 0.002). In conclusion, hypoalbuminemia is strongly associated with HAPR in patients with stable CAD.