Keywords: Atherosclerosis, coronary artery disease, Vitamin D deficiency . inflammatory factors are centrally involved in the process of atherosclerosis and plaque rupture.  of longitudinal studies examining the relationship of Vitamin D. The Link between Vitamin D and Coronary Artery Disease of accumulating fat and cholesterol in the walls of the arteries, called an atheromatous plaque. Relation of vitamin D deficiency to cardiovascular risk factors, disease status, and plaque in human carotid artery visualised by scanning electron microscope.
Another reason for the growing epidemic of vitamin D deficiency is the aging population, as has been shown in the effectiveness of skin synthesis which weakens with body ageing; in people over 70 years of age it is four times lower than in young people with the same exposure to the sun [ 78 ].
Lower levels of vitamin D have also been reported within women [ 910 ] and patients with chronic kidney disease who are considered to be patients with a high cardiovascular risk. Another factor increasing the risk of inadequate levels of vitamin D is living in northern regions, the autumn and winter period, low physical activity, being in a nursing home, black skin colour, smoking, obesity, gastrointestinal malabsorption disorders, liver disease, use of glycocorticosteroids, immunosuppressants and also anti-retroviral therapy [ 11 ].
The essence of atherosclerosis is the inflammation of the artery walls as a response to the damage of the vascular endothelium [ 12 ]. It has been shown that chronic treatment with the hydroxycholecalciferol has a positive influence on endothelial cells by reducing the production of reactive oxygen compounds, stimulating production of superoxide dismutase [ 13 ],increasing the endothelial activity of nitric oxide synthase [ 1314 ], as well as protection against the glycosylation end product effects [ 15 ].
Anti-inflammatory effects are exerted through the inhibition of prostaglandin and cyclooxygenase-2 synthesis, and by stimulating the synthesis of cytokines with anti-inflammatory activity [ 16 - 19 ].
Vitamin D and Osteogenic Differentiation in the Artery Wall
Further research is required for the yet unexplained effect of vitamin D on the process of calcification of the vascular wall. It has been shown that at low concentrations, it reduces the calcification of the middle and inner membrane of coronary arteries [ 2021 ] and in high concentrations it stimulates the conversion of mesenchymal cells into osteoblasts and thereby contributes to the formation of calcifications in the central membrane of the artery [ 22 ] which leads to the stabilization of existing atherosclerotic plaques.
In the process of destabilization of the atherosclerotic plaque, the decisive role is played by a thin connective tissue cover, large lipid core, high activity of inflammatory cells and increased neovascularization [ 12 ].
In addition to the anti-inflammatory effect, vitamin D inhibits the conversion of macrophages into foam cells [ 23 ], reduces the neovascularization process by inhibiting the vascular endothelial growth factor and stimulating the apoptosis of epithelial cells, decreases the metalloproteinase activity responsible for the remodelling of the vascular wall and the cardiac muscle leading to the destabilization of atherosclerotic plaques [ 24 - 26 ].
The atherosclerotic plaque rupture is followed by the release of its lipid content, which initiates blood clotting [ 12 ]. The anticoagulant effect of vitamin D exerts by reducing the expression of the procoagulant tissue factor, increasing the anticoagulant production of thrombomodulin [ 27 ], and inhibition of platelet adhesion to vascular endothelial cells [ 28 ].
Vitamin D and Osteogenic Differentiation in the Artery Wall
In addition, the results of recent years show an independent compound of low vitamin D levels and documented risk factors for the cardiovascular system such as hypertension [ 29 ], atherogenic lipid profile [ 30 ], diabetes [ 31 ] and obesity [ 32 ]. As shown, the deficiency of vitamin D leads to the activation of the renin-angiotensin-aldosterone system RAASwhile high levels of vitamin D reduces the plasma renin activity, leading to a reduction of angiotensin II concentration.
This leads to a reduction in blood pressure and control of inflammatory processes in the vascular endothelium, which also reduces the progression of atherosclerosis [ 29 ].
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- Coronary artery disease and its association with Vitamin D deficiency
Particularly noteworthy is the effect of vitamin D on the lipid profile. A compound of high levels of total cholesterol and LDL-C with coronary atherosclerosis is clearly documented. It was further found that the reduction in total cholesterol and low density lipoprotein below recommended levels significantly reduces the cardiovascular risk [ 3334 ].
Many studies show a 25 OH D inverse relationship in serum and different cholesterol fractions [ 30 ]. The explanation for these results may be a common metabolic pathway for vitamin D and cholesterol. Both of these are formed from a single precursor - 7dehydrocholesterol. In addition, the hydroxycholecalciferol can inhibit CYP51A1, which also participates in the synthesis of cholesterol.
Is Vitamin D a New Therapeutic Option in Coronary Artery Disease? Overview Data
Early detection of coronary artery disease CAD in young patients is necessary because young patients with myocardial infarction should have more favorable early and late prognosis than their older counterparts. To our knowledge, there is no published data on the relationship between serum 25 OH D levels and CAD detected by coronary computed tomography angiography CCTA in young adult population.
We hypothesized that low 25 OH D may be associated with subclinical coronary atherosclerosis and coronary plaque burden and composition in young adults. Of those, 98 patients study group diagnosed with coronary atherosclerosis on CCTA, and age- and gender-matched subjects with normal CCTA control groupwere included. The indications for CCTA included: The exclusion criteria were: Demographic and clinical properties were recorded, and blood samples were obtained for biochemical and 25 OH D analyzes.
Written informed consent was obtained from all study participants and the local ethics committee approved the study protocol. The tube current for the protocol was set at mAs. Slice collimation of 0. The bolus tracking technique was used, and images were obtained during a single breath-hold of 6 seconds.
Image analysis Two experienced radiologists blinded to clinical information evaluated all scans with a 3-dimensional workstation Syngo.
Consensus interpretation was performed to obtain a final CCTA diagnosis. The characteristics of the stenoses, plaques and the number of plaques to per-segment were analyzed according to the modified American Heart Association classification [ 11 ].
Plaques were defined as structures that were 1 mm2 and within or adjacent to the vessel lumen and that could be clearly distinguished from the lumen and the surrounding pericardial tissue. Coronary atherosclerosis was defined as the presence of any plaques on a CCTA.
A large number of studies conducted in the past have provided the basic scientific framework and this article attempts to explore the role of Vitamin D deficiency in the pathogenesis of CAD and stresses the need for further research to fill up gap in our knowledge.
Vitamin D deficiency accelerates hardening of the arteries
Like many high-income countries during the last century, low- and middle-income countries are witnessing an alarming increase in the rates of CAD and this change is accelerating. CAD affects people at younger ages in low- and middle-income countries like India compared to high-income countries, thereby having a greater economic impact on low- and middle-income countries except Sub-Saharan African countries where it leads causes of death in those older than 45 years.
The situation in India is especially gruesome with limited resources for setting up an effective screening program and evaluation or management for that matter and statistics projecting India to be the leader in the world for CAD-associated mortality in the next 15—20 years. Besides, there are traditional risk factors for CAD such as tobacco, diet, physical inactivity, dyslipidemia, obesity, hypertension, and diabetes mellitus.
There has been increasing evidence from animal and human studies to suggest that Vitamin D deficiency may be an important risk factor in the pathogenesis of CAD.
VITAMIN D Vitamin D is one of the fat-soluble vitamins also known as sunshine vitamin due to its synthesis in the body following exposure to ultraviolet UV B rays, however it is unique in a way that it acts as a prohormone and mediates its functions by binding to a member of nuclear receptor superfamily, the Vitamin D receptor. Vitamin D can also be obtained through the diet which is referred to as Vitamin D2 ergocalciferol whereas the form of vitamin that is endogenously synthesized by UV-B rays and also occurs in small quantity in the food of animal origin, which is referred to as Vitamin D3 cholecalciferol.
Both of these forms are activated equally efficiently by the hydroxylases in humans, of which the first step of 25 hydroxylation is mediated by cytochrome P like enzyme present in mitochondria and microsomes of hepatocytes. The level of 25 OH D is not tightly regulated, therefore it represents the most accurate measure of Vitamin D level in the circulation, also its long half-life of 3 weeks[ 4 ] makes it the preferred form to be measured to determine the Vitamin D level of an individual.
Small amount of 1 hydroxylase was also found in keratinocyte, trophoblast of placenta, and macrophages associated with granulomata and lymphomas.