The continuous growth of aging population and the changes in genetic and environmental factors and social lifestyles have led to an increase in the incidence of coronary heart disease (CHD) (1). The latest survey data have shown that mortality rate of CHD now is higher than that of malignant tumor, making it a life-threatening disease (2). The continuous improvement of scientific research and clinical practices, have led to improvement of treatment of CHD. However, pathogenesis of this disease remains unclear, and common causes of CHD include hypertension, diabetes and smoking (3).

Correlations between serum 25-hydroxyvitamin D3, vitamin B12 and C levels and CHD have attracted increasing attention (4). Vitamin D is a fat-soluble vitamin that plays an important role in the body to regulate calcium and phosphorus metabolism. The lack of vitamin D in the human body can cause a variety of diseases, such as osteoporosis, and diabetes (5). Vitamin C can prevent the oxidation of lipid cells and eliminate oxygen-free radicals to further prevent CHD (6). Serum homocysteine (Hcy) levels were higher but nitric oxide (NO) levels were lower in CHD patients than in normal controls.

Results showed t hat high Hcy levels can lead to CHD. NO levels are closely related to vascular endothelial injury, and NO level is reduced after vascular endothelial injury (7). Hcy metabolism requires the involvement of vitamin B, C and other substances. Lack of vitamins can lead to hyperhomocysteinemia, thereby causing vascular endothelial dysfunction. Supplementation of vitamins provides a new method for the treatment of vascular endothelial injury in patients with CHD (8).

The main pathogenesis of coronary atherosclerotic heart disease is atherosclerosis caused by varying degrees of stenosis and damage, which results in increased blood flow resistance. Under this condition, oxygen and blood supply to myocardial cells is reduced, leading to necrosis or even death (9). Advances in clinical research have shown that Hcy, NO and other substances can reflect impaired coronary vascular endothelial function (10). Hcy is an intermediate product of the metabolism of methionine and cysteine and cannot be synthesized in human body. Hcy has to be formed after methylation of methionine in food by ingesting food (11). After demethylation, methionine in the food is converted to Hcy (11). Therefore, abnormal metabolic process may lead to the accumulation of Hcy, and excessive Hcy can also enter blood circulation (12) to damage vascular endothelial cells, resulting in the excessive growth of vascular smooth muscle cells and over-reaction of the inflammatory system, thereby obstructing lipid metabolism, and inducing vascular endothelial dysfunction and atherosclerosis (13). Vascular endothelial cells, on the other hand, can also synthesize and release NO by catalyzing the conversion of L-arginine to NO via eNOS (14). Thus, with the inhibitory effects on atherosclerosis, NO levels can reflect endothelial cell function and low NO level indicates impaired vascular endothelial function (15).

Vitamins play critical roles in the human body, for example, vitamin D can be synthesized with the involvement of sunlight and play its functions through 25-hydroxy vitamin D3 receptors (16). Vitamin D receptor generally exists in vascular smooth muscle cells and intestinal mucosal cells. Low vitamin D content can cause pathological diseases, such as diabetes and osteoporosis (17). An increasing number of studies have shown that low levels of vitamin D can cause increased incidence and mortality of cardiovascular diseases (18). This study found that 25-hydroxyvitamin D3 level was significantly lower in patients with CHD than in healthy individuals, and 25-hydroxyvitamin D3 and NO levels were positively correlated with each other. Hcy synthesis in the human body requires the involvement of coenzyme such as vitamin B12, and low vitamin B12 levels can lead to homocysteinemia (19). Studies have shown that vitamin B12 is an independent risk factor for CHD, and increasing the level of vitamin B12 can reduce Hcy level and relieve the impaired vascular endothelial function (19). In this study, vitamin B12 levels were significantly lower in patients with CHD than in control group, and vitamin B12 levels were positively correlated with NO levels. In addition, other vitamins, such as vitamin C, an important antioxidant, can effectively prevent CHD and protect vascular endothelial function by removing oxygen free radicals and decreasing peroxidation of serum lipids (20). Therefore, supplementation of vitamin has important clinical value in preventing CHD and improving prognosis of vascular endothelial dysfunction.