Serum albumin predicts platelet reactivity during aspirin medication in CAD

Low albumin levels are linked to high on-aspirin platelet reactivity (HAPR) among patients with stable coronary artery disease (CAD), a new study has found.

The study included 116 patients (mean age, 69±10 years; 28 percent female) with stable CAD who were taking aspirin at 75–100 mg/day for at least 1 month. Serum albumin levels were measured from drawn blood samples. Those who had cancer, sepsis or acute infection, active inflammatory disease, chronic liver failure, were on other antiplatelet drugs and had had recent major surgery were ineligible for analysis.

Twenty patients were found to be hypoalbuminemic and showed significantly lower serum albumin levels (3.2±0.2 vs 4.2±0.4 g/dL; p<0.001). On the other hand, mean aspirin reaction units (ARU), used as a measure of platelet aggregation, were significantly elevated in the hypoalbuminemic group (548±45 vs 444±66 ARU; p<0.001).

Notably, 83 percent of all patients with abnormal ARU were hypoalbuminemic and all had serum albumin levels <4 g/dL. Conversely, more than half of those with hypoalbuminemia had an abnormal ARU.

Multivariate analysis further confirmed these findings. An albumin level ≤3.5 emerged as the strongest predictor of HAPR (hazard ratio, 4.9, 95 percent confidence interval, 2.2–32; p=0.002).

“[T]he current study reports, for the first time, the significant association between serum albumin level and HAPR among patients with stable coronary artery disease treated with aspirin,” said researchers.

“Hypoalbuminemia confers an almost fivefold greater risk for HAPR compared with patients with normal albumin levels. These findings may support the hypothesis that increased platelet activation is one of the mechanisms mediating hypoalbuminemia and worse cardiovascular outcomes,” they added.