Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin D is an important prohormone for optimal intestinal calcium absorption for mineralization of bone. Because the vitamin D receptor is present in multiple tissues, there has been interest in evaluating other potential functions of vitamin D, particularly, in cardiovascular diseases (CVD). Cross-sectional studies have reported that vitamin D deficiency is associated with increased risk of CVD, including hypertension, heart failure, and ischemic heart disease. Initial prospective studies have also demonstrated that vitamin D deficiency increases the risk of developing incident hypertension or sudden cardiac death in individuals with preexisting CVD. Very few prospective clinical studies have been conducted to examine the effect of vitamin D supplementation on cardiovascular outcomes. The mechanism for how vitamin D may improve CVD outcomes remains obscure; however, potential hypotheses include the downregulation of the renin-angiotensin-aldosterone system, direct effects on the heart, and vasculature or improvement of glycemic control. This review will examine the epidemiologic and clinical evidence for vitamin D deficiency as a cardiovascular risk factor and explore potential mechanisms for the cardioprotective effect of vitamin D.
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PMID:Vitamin D deficiency and risk for cardiovascular disease. 1959 2

Ischemic heart disease and cerebrovascular ischemia are leading causes of mortality in industrialized countries. The pathogenesis of these diseases involves the formation of atherosclerotic plaques with eventual rupture and superimposed thrombosis. This process is inhibited by high-density lipoprotein (HDL), the main protein component of which is apolipoprotein A-I (apo A-I). Vitamin D3 is a hormone produced by sun-exposed skin but is acquired also in the diet. The Framingham Offspring Study and the Third National Health and Nutritional Examination Survey showed a link between vitamin D3 intake and cardiovascular risk factors. The link between 25-hydroxyvitamin D3 and HDL cholesterol (HDLc) and apo A-I is not as clear. Studies in vitamin D receptor knockout mice demonstrated higher HDLc and hepatic apo A-I messenger RNA expression relative to wild type. Experiments in cultured hepatocytes supported these observations. Human studies evaluating the relationship between vitamin D3 and apo A-I and HDLc have yielded conflicting results, but most suggest a positive link between increasing vitamin D3 levels and plasma apo A-I and HDLc. The purpose of this review is to examine the evidence linking vitamin D status and cardiovascular disease, to determine if there is a relationship between vitamin D levels and development of an atherogenic lipid profile. Our objectives are to determine if plasma vitamin D levels correlate with plasma HDLc and apo A-I and, if so, offer speculation as to how apo A-I in the context of high vitamin D levels provides enhanced atheroprotection.
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PMID:The emerging evidence for vitamin D-mediated regulation of apolipoprotein A-I synthesis. 2211 50

Vitamin D is necessary for bone health but may also have many extra-skeletal effects. The vitamin D endocrine system has major effects on gene and protein expression in many cells and tissues related to the cardiovascular system. In addition, many preclinical studies in animals with vitamin D deficiency or genetically silenced expression of the vitamin D receptor or vitamin D metabolizing enzymes suggest that the absence of vitamin D action may result in cardiovascular events. This includes dysfunctions of endothelial cells, thereby accelerating the process of atherosclerosis, hypertension or abnormal coagulation, ultimately resulting in higher risks for all major cardiovascular or cerebrovascular events. A wealth of observational studies in different parts of the world have fairly consistently found a strong association between a poor vitamin D status and surrogate markers or hard cardiovascular events. A few Mendelian randomization studies did, however, not find a link between genetically lower serum 25OHD concentrations and cardiovascular events. Finally, many RCTs could not demonstrate a consistent effect on surrogate markers, and a limited number of RCTs did so far not find whatever effect on hard cardiovascular endpoints such as myocardial ischemia or infarction, stroke, or cardiovascular death. In conclusion, preclinical data generated a plausible hypothesis of a link between vitamin D status and extra-skeletal events, including cardiovascular endpoints. Whether the vitamin D endocrine system is redundant for the human vascular system or whether the RCTs have not been optimally designed to answer the research question is thus not yet settled.
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PMID:Vitamin D and cardiovascular disorders. 3140 2