Relationship between serum 25-hydroxyvitamin D levels and the SYNTAX score in patients with acute coronary syndrome

OBJECTIVE: The extent of severity and complexity of coronary artery disease (CAD) in patients presenting with ST-segment elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI) and possible correlations between serum 25-hydroxyvitamin D (25(OH)D) have not yet been adequately studied. We evaluated the relationship between 25(OH)D levels and the burden of CAD as assessed by the SYNTAX score (SXscore) in patients with acute coronary syndrome (ACS) including STEMI and NSTEMI. METHODS: After exclusion, a total of 113 patients who were admitted to our hospital due to ACS and who were referred for undergoing coronary angiography were prospectively included. Their mean age was 63.3±18.5 years, and 80.5% of them were men. In total, 44.2% of the patients had NSTEMI and the remaining had STEMI. Blood samples were drawn at admission to evaluate serum 25(OH)D levels. CAD severity was assessed using the SXscore. Patients were classified as having low (SXscore ≤22) or high (SXscore >22) SXscores. Pearson’s and Spearman’s correlation coefficients were used to examine the relationship between serum 25(OH)D levels and the SXscore. RESULTS: 25(OH)D levels were significantly lower in the group with a high SXscore than in the group with a low SXscore (21.0±8.0 vs. 16.7±6.8, p=0.005). Correlation analysis showed a significant correlation between 25(OH)D levels and the SXscore. Multiple linear regression (MLR) analysis was used to determine the significance of the relationship between the SXscore and 25(OH)D, parathyroid hormone, and C-reactive protein levels and eGFR. MLR analysis revealed that only 25(OH)D levels (coefficient beta, -0.217, p=0.029) was significantly associated with the severity of CAD. CONCLUSION: The present study showed that serum 25(OH)D levels were significantly lower in patients with STEMI/NSTEMI and that low serum 25(OH)D levels were significantly correlated with CAD severity and extent. (Anatol J Cardiol 2017; 17: 293-7)