The Relationship between Vitamin D and Coronary Artery Ectasia in Subjects with a Normal C-Reactive Protein Level

BACKGROUND AND OBJECTIVES Vitamin D is generally known to be closely related to inflammation. The effects of vitamin D on coronary artery disease (CAD) are not fully explained. Nowadays, coronary artery ectasia (CAE) cases are common and are regarded as being a kind of CAD. We aimed to investigate, in a case-control study, the relationship between vitamin D and CAE without an associated inflammatory process. SUBJECTS AND METHODS This study population included 201 patients (CAE group, 121 males; mean age, 61.2±6.4 years) with isolated CAE; and 197 healthy individuals (control group, 119 males; mean age, 62.4±5.8 years), comprising the control group, who had normal coronary arteries. These participants concurrently underwent routine biochemical tests, tests for inflammatory markers, and tests for 25-OH vitamin D in whole-blood draws. These parameters were compared. RESULTS There are no statistical significance differences among the groups for basic clinical characteristics (p>0.05). Inflammatory markers were recorded and compared to exclude any inflammatory process. All of them were similar, and no statistical significance difference was found. The average parathyroid hormone (PTH) level of patients was higher than the average PTH level in controls (41.8±15.1 pg/mL vs. 19.1±5.81 pg/mL; p<0.001). Also, the average 25-OH vitamin D level of patients was lower than the average 25-OH vitamin D level of controls (14.5±6.3 ng/mL vs. 24.6±9.3 ng/mL; p<0.001). In receiver operating characteristic curve analysis, the observed cut-off value for vitamin D between the control group and patients was 10.8 and 85.6% sensitivity and 75.2% specificity (area under the curve: 0.854, 95% confidence interval: 0.678-0.863). CONCLUSION We found that there is an association between vitamin D and CAE in patients who had no inflammatory processes. Our study may provide evidence for the role of vitamin D as a non-inflammatory factor in the pathophysiology of CAE.