OBJECTIVE: Increasing evidence suggests a relationship between vitamin D (VD) insufficiency and cardiovascular disease. The present study evaluated the effect of VD insufficiency on epicardial coronary flow rate, subclinical atherosclerosis, and endothelial function. METHODS: The present study was cross-sectional and observational. We enrolled 222 consecutive patients who had undergone coronary angiography for suspected ischemic heart disease and were found to have normal or near-normal coronary arteries. Thereafter, 25(OH)D3 levels were measured and the coronary flow rate was assessed using the thrombolysis in myocardial infarction frame count. Slow coronary flow (SCF) was defined as a thrombolysis in myocardial infarction frame count greater than 27/frame. Endothelial function was assessed by brachial artery flow-mediated dilatation. Carotid intima-media thickness, an indicator of subclinical atherosclerosis, was measured using B-mode ultrasonography. RESULTS: The mean level of 25(OH)D3 was 31.8 ng/ml, and 47% (n=106) of the patients had insufficient 25(OH)D levels (<30 ng/ml). Baseline characteristics were similar between VD-insufficient and VD-sufficient groups. The incidence of SCF was significantly higher in the VD-insufficient group than in patients with sufficient VD (relative risk=3.5, 95% confidence interval=1.1-10.5, P=0.01). After adjusting for cardiovascular disease risk factors, VD insufficiency was independently associated with SCF. The linear regression analysis showed that VD insufficiency was correlated independently with % flow-mediated dilatation (β=0.424, P<0.001) and carotid intima-media thickness (β=0.43, P<0.001). CONCLUSION: A strong association was found between VD insufficiency and the SCF phenomenon. In addition, VD insufficiency was associated with endothelial dysfunction and subclinical atherosclerosis. We believe that further studies are required to clarify the role of VD in patients with SCF.
OBJECTIVE: Increasing evidence suggests a relationship between vitamin D (VD) insufficiency and cardiovascular disease. The present study evaluated the effect of VD insufficiency on epicardial coronary flow rate, subclinical atherosclerosis, and endothelial function. METHODS: The present study was cross-sectional and observational. We enrolled 222 consecutive patients who had undergone coronary angiography for suspected ischemic heart disease and were found to have normal or near-normal coronary arteries. Thereafter, 25(OH)D3 levels were measured and the coronary flow rate was assessed using the thrombolysis in myocardial infarction frame count. Slow coronary flow (SCF) was defined as a thrombolysis in myocardial infarction frame count greater than 27/frame. Endothelial function was assessed by brachial artery flow-mediated dilatation. Carotid intima-media thickness, an indicator of subclinical atherosclerosis, was measured using B-mode ultrasonography. RESULTS: The mean level of 25(OH)D3 was 31.8 ng/ml, and 47% (n=106) of the patients had insufficient 25(OH)D levels (<30 ng/ml). Baseline characteristics were similar between VD-insufficient and VD-sufficient groups. The incidence of SCF was significantly higher in the VD-insufficient group than in patients with sufficient VD (relative risk=3.5, 95% confidence interval=1.1-10.5, P=0.01). After adjusting for cardiovascular disease risk factors, VD insufficiency was independently associated with SCF. The linear regression analysis showed that VD insufficiency was correlated independently with % flow-mediated dilatation (β=0.424, P<0.001) and carotid intima-media thickness (β=0.43, P<0.001). CONCLUSION: A strong association was found between VD insufficiency and the SCF phenomenon. In addition, VD insufficiency was associated with endothelial dysfunction and subclinical atherosclerosis. We believe that further studies are required to clarify the role of VD in patients with SCF.