Archives of medical sciences. Atherosclerotic diseases · 2021
Association between Multiplate-measured aspirin resistance and vitamin D deficiency in stable coronary artery disease.
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Surmen Semih, Ozer Pelin Karaca, Emet Samim, Govdeli Elif Ayduk, Elitok Ali
Аннотация
INTRODUCTION: 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.
MATERIAL AND METHODS: 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.
RESULTS: 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).
CONCLUSIONS: 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.
MATERIAL AND METHODS: 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.
RESULTS: 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).
CONCLUSIONS: 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.