Association between Multiplate-measured aspirin resistance and vitamin D deficiency in stable coronary artery disease

Insufficient inhibition of platelets in patients with atherosclerosis despite antiplatelet therapy leads to important clinical consequences. The present study evaluated the role of vitamin D (VD) deficiency in aspirin resistance (AR) in patients with stable coronary artery disease (CAD) treated with aspirin.

This study included 70 patients with stable CAD who had been using 100 mg aspirin for at least seven days. Serum 25-hydroxyvitamin D [25-(OH)D] concentration was measured and patients with 25-(OH)D level < 20 ng/dl were defined as the VD deficient group. A Multiplate Platelet Function Analyzer (Multiplate) device was used to evaluate AR. Patients were defined as aspirin-sensitive (AS) when their AUC was ≤ 30 U, and aspirin resistant (AR) when their AUC was > 30 U.

AUC was > 30 U in 15 (21%) patients and these patients were considered AR. The mean 25-(OH)D level was 18.7 ±12.2 ng/ml in all patients. Forty-five (64%) patients were VD deficient. The rate of AR was higher in the VD deficient group than the sufficient group (29% vs. 8%, p = 0.041). The mean AUC was higher in the VD deficient group than the sufficient group (30.2 ±29.1 vs. 15.3 ±13.1 U; p = 0.018). In ROC analysis 25-(OH)D level < 19.25 ng/dl predicted AR with 86.7% sensitivity, 61.8% specificity (AUC = 0.696, 95% CI: 0.551-0.840, p = 0.021).

In the current study, an association was found between VD deficiency and AR in patients with stable CAD. VD supplementation may reduce platelet aggregation and overcome AR.