cholecalciferol and Coronary-Disease

The reported low mortality rate from coronary heart disease in Portugal, Spain, Italy, Greece, and France, to a lesser extent, has been attributed in numerous nutritional studies to the consumption of a Mediterranean-type diet. There are still many unresolved issues about the direct causal effect of the Mediterranean dietary regime on low incidence of coronary heart disease. An analysis of coronary heart disease mortality rates in Europe from a latitudinal gradient perspective has shown to have a close correlation to incident solar radiation. It is surmised that the resulting increased in situ biosynthesis of Vitamin D(3) could be the critical missing confounder in the analysis of the beneficial health outcome of the Mediterranean diet.

Topics: Adult; Cholecalciferol; Coronary Disease; Diet, Mediterranean; Europe; Female; Humans; Male; Prevalence; Sunlight; Time Factors

Imbalancing nutritionally adequate diets with an excessive amount of fat calories and cholesterol has obscured the fact that intimal thickening occurs spontaneously in time on low-fat cholesterol-free diets during the aging process, and that intimal thickening can be accelerated by dietary angiotoxic "risk factors." Electron microscopy of arterial tissue from animal models identified degenerated smooth muscle cells in the fetus from sows kept on low-fat cholesterol-free diets. After birth, the degenerated smooth muscle cells increased in number with age. The presence of angiotoxic "risk factors" such as oxidized cholesterol and vitamin D3 (cholecalciferol) in the diet of such animal models increased the frequency of smooth muscle cell death in their arteries. Two types of pathology could be developed in the thoracic aorta by continuous or short term feeding of 12.5 times more vitamin D than normally present in commercial rations: 1) a diffuse fibroelastic intimal thickening in the thoracic aorta (arteriosclerosis) with no evidence of lipid deposition by continuous feeding of vitamin D or 2) an initimal thickening in the thoracic aorta and intimal thickening with foam cells and extracellular lipid deposits (atherosclerosis) in the coronary arteries after a short period of supplemental vitamin D followed by 3 to 4 months of supplement-free diets. These two types of arterial damage were identical to that in the plugs of thoracic aorta obtained as a by-product of elective coronary bypass surgery. Although all of the possible sources of oxidized cholesterol in the diet have as yet not been identified, laboratory studies have identified oxidized cholesterol as an angiotoxic factor. Since population groups that consume less vitamin D-supplemented foods, less deep fat fried cholesterol-containing foods, and less hydrogenated fats have a lower incidence of coronary heart disease than Americans, it seems judicious for food processors to reduce these previously unconsidered risk factors to a minimum. This could be done by eliminating vitamin D2 and D3 from all vitamin supplements, from all food and cereal products and from the diet of livestock 1 month before they were killed so that the intake of vitamin D is no larger than the 400 IU/quart in milk which is necessary to prevent rickets in children. Deep fat fryers, which are kept at almost 200 C for 24 hr/day, could perhaps be replaced with microwave ovens in fast food chain outlets. Processors could hydrogenate ve

Topics: Aging; Animals; Aorta, Thoracic; Aortic Diseases; Arteriosclerosis; Cell Survival; Cholecalciferol; Cholesterol; Cholesterol, Dietary; Coronary Disease; Diet; Dietary Fats; Dietary Proteins; Energy Intake; Fats, Unsaturated; Female; Humans; Lipoproteins, LDL; Myocardium; Oxidation-Reduction; Pregnancy; Risk

As a long-term multisystem disorder, chronic heart failure (CHF) can gravely affect on bone metabolism, prompting a severe bone loss and increasing predisposition to fractures and the development of osteoporosis.. The aim of the study was to investigate whether in patients with CHF a therapy combining calcium and vitamin D3 supplement (Calcemin Advance) and calcitonin (Miacalcic) can help to prevent and treat osteopenia and osteoporosis.. Using dual-energy X-ray absorptiometry, we measured bone mineral density (BMD) in 59 patients with coronary heart disease (CHD) complicated with chronic heart failure.. Our results suggest that following the standard treatment protocol of CHD complicated with CHF resulted in significant BMD loss in the lumbar vertebrae, approaching the level of osteopenia. After taking a calcium and vitamin D3 supplement, patients with this heart disorder had significant increase of BMD in the lumbar vertebrae and in the femoral bone. Patients with CHD complicated with CHF and diagnosed osteoporosis taking Calcemin Advance did not experience osteoprotection outcome, rather their BMD continued to decrease. However, combined therapy with Miacalcic and Calcemin Advance was effective in significantly increasing L1, L2 - L4 BMD in these patients.. We demonstrated effectiveness of using a calcium and vitamin D3 supplement, for patients with CHD complicated with CHF and diagnosed osteopenia. Patients with CHD complicated by CHF and diagnosed osteoporosis did not experience osteoprotective action when using Calcemin Advance. However, in these patients L1 lumbar vertebra BMD significantly increased after the combined therapy.

Topics: Bone Density; Calcitonin; Calcium; Cholecalciferol; Coronary Disease; Heart Failure; Humans; Lumbar Vertebrae

Coronary artery ectasia (CAE) is identified as dilation of one or more segments of coronary arteries that reaches 1.5 times or more, compared with near segments that are normal. Several etiologies like atherosclerosis, autoimmune diseases and congenital anomalies have been proposed for this condition. Vitamin D deficiency activates the renin-angiotensin-aldosterone system, which affects the cardiovascular system. For these reasons, we investigated the serum level of vitamin D in patients with CAE compared with individuals with normal coronary arteries.. The study group included 30 patients (20 males and 10 females, mean age: 57 ± 9 years) with isolated CAE without any stenotic lesions, and the control group consisted of 60 age/gender matched subjects who had normal coronary angiograms (CAG) (40 males and 20 females, mean age: 57 ± 8 years). All participants underwent CAG at Tehran Heart Center between December 2015 and March 2016. Along with routine lab tests, vitamin D, serum albumin, calcium, phosphorus and alkaline phosphatase levels were analyzed and the unadjusted and adjusted effects of vitamin D on CAE were evaluated using logistic regression model.. The median vitamin D level of the patients with CAE was lower than that of the control group (6.5 [3.0, 18.8] ng/mL vs. 17.7 [8.9, 27.1] ng/mL; P = 0.002). The logistic regression model showed that vitamin D deficiency was a predictor for the presence of CEA (P = 0.013). After adjustment for confounding variables, this association remained significant (P = 0.025).. An association between CAE and vitamin D deficiency was found in our study.

Topics: Aged; Biomarkers; Case-Control Studies; Cholecalciferol; Coronary Angiography; Coronary Disease; Coronary Vessels; Dilatation, Pathologic; Female; Humans; Iran; Logistic Models; Male; Middle Aged; Vitamin D Deficiency

Topics: Atherosclerosis; Cholecalciferol; Clinical Trials as Topic; Coronary Disease; Depression; Estrogens; Female; Hormone Replacement Therapy; Hospitals, Community; Humans; Male; Menopause; Mentors; North America

130 young and middle age patients of both sexes with chronic form of coronary heart disease: functional class II-III stable exertional angina pectoris including functional class I-III chronic cardiac insufficiency were studied. In protocol 1 cured 70 patients (48 (68.6%) males and 22 (31.4%) females) 32-59 years of age (medium age was 48.4 +/- 3.25 years) with coronary heart disease. In protocol 2 (with prescription of calcium-D3) cured 60 patients (40 (66.7%) males and 20 (33.3%) females) 34-58 years of age (medium age was 47.8 +/- 3.12 years) with coronary heart disease. The groups were comparable on key parameters of disease. All patients had alimentary calcium deficit and (or) risk factors of osteoporosis, instrumental signs (X-ray filming and densitometry) of initial or evident osteoporosis. Correction of alimentary calcium deficit was realized by prescription of 1-3 tablets of calcium- Ds in different food intakes. Positive dynamics in decrease of functional class of angina pectoris and nitroglycerin requirement in both groups was noticed. Negative influence of calcium- D3 on studied indices of coronary heart disease severity was absent. The thirst and dry mouth in patients, who took furosemide, in group 1 were noticed against the background of body weight decrease (p < 0.05) and increase of diuresis. Decrease of the therapy antiarrhythmic action (p < 0.05) in patients, who took hydrochlorothiazide, was noticed too. It leaded to needs of furosemide and hydrochlorothiatide dose correction in protocol 1. In whole use of calcium- D3 together with anti-ischemic drugs in patients with chronic forms of coronary heart disease did not impair clinical course of angina pectoris and did not decrease efficiency of coronary heart disease therapy.

Topics: Calcium; Cholecalciferol; Coronary Disease; Diuretics; Drug Interactions; Female; Furosemide; Humans; Male; Middle Aged; Osteoporosis; Sodium Chloride Symporter Inhibitors

The effects of five different dietary levels of vitamin D3 on the coronary arteries of groups of 17-60 2-month old weanling Yorkshire swine were studied. Four groups were fed the following levels of vitamin D3 per ton of ration continuously for 4 months: group I--100,000 IU, group II--300,000 IU, group IV--2,000,000, and group V--4,000,000 IU. Swine in group III were fed the diet containing 100,000 IU of vitamin D3 per ton of ration for the first 2 months of the study after which they were fed a diet supplemented with 4,000,000 IU of vitamin D3 per ton of ration for the remaining 2 months of the study. The highest degree of intimal thickening of the coronary arteries was observed among group V. The thickened areas contained numerous lipid-containing cells and degenerate cells without stainable lipid. Electron microscopic examination revealed a greater frequency of degenerate cells without stainable lipid in the coronary arteries of groups III and IV than in groups I and II. These results suggest a possible link between excessive daily intake of vitamin D3 and the development of human coronary atherosclerosis.

Topics: Animals; Cholecalciferol; Coronary Disease; Coronary Vessels; Humans; Lipids; Male; Microscopy, Electron; Muscle, Smooth, Vascular; Swine

The following mechanisms for inactivating excessive Ca++ are found in the vessel wall (e.g. in old age, arteriosclerosis, hypertension, or overdosage with Vitamin D3): 1. The production of Matrix Vesicles, which reduce biologically active extracellular Ca++ by precipitating it during the initial stage of calcification. 2. An increase in the number of muscle cells changed from the "k" to the "m" form. These also possess a mechanism for reducing the intracellular Ca++ level. If in spite of these mechanisms the extracellular Ca++ concentration remains raised, this can result in calcification of the interzellular substance, particularly the elastic material.

Topics: Aged; Animals; Aorta, Thoracic; Calcinosis; Calcium; Cholecalciferol; Coronary Disease; Coronary Vessels; Disease Models, Animal; Elastic Tissue; Humans; Lipids; Microscopy, Electron; Muscle, Smooth, Vascular; Rats; Risk

Coronary atherosclerosis developed in normolipemic swine fed a basal ration supplemented with 125,000 IU, 62,500 IU and 31,250 IU of vitamin D3/kg of diet for 3 months and subsequently only the basal ration for the following 3 months. Lesions consisted of intimal atheromata and calcified internal elastica and caused luminal narrowing. The incidence of atherosclerotic lesions was proportional to the vitamin D3 doses. The present experimentally induced lesions had many morphological features resembling those in coronary arteries from human subjects.

Topics: Adult; Aged; Animals; Arteries; Arteriosclerosis; Calcinosis; Calcium; Cholecalciferol; Cholesterol; Coronary Disease; Coronary Vessels; Disease Models, Animal; Humans; Middle Aged; Swine

Aortic, coronary and cardiac lesions were induced in swine by a hypervitaminosis D3 diet Lipid-free intimal plaques overlying focally calcified medial or internal elastica occured in the thoracic aorta, pulmonary trunk and coronary artery of swine fed a basal ration supplemented with 250,000 IU of vitamin D3/kg of diet for an induction period of 4 months. Cartilage formation with minimal calcification was initiated in the aortic valve during this period. When such animals were subsequently fed only the basal ration free of excessive vitamin D3 for 3 months, intimal plaques regressed in the aorta and pulmonary trunk but progressed in the coronary artery. The calcific deposits in the medial elastica and internal elastica of all three arteries decreased in size. Atherosclerotic intimal thickening occurred in the main coronary arteries. The most severe lesion occupied 75 p.100 of the lumen area. Multiple intimal plaques were noted in the left atrium and aortic and mitral valves. The thickened intima at these coronary and cardiac sites contained calcified elastica and collagen fibers.

Topics: Animals; Aorta, Thoracic; Aortic Diseases; Calcinosis; Cardiovascular Diseases; Cholecalciferol; Coronary Disease; Coronary Vessels; Heart Diseases; Microscopy, Electron; Myocardium

Topics: Arteries; Arteriosclerosis; Cholecalciferol; Cholesterol; Chromatography; Coronary Disease; Desmosterol; Drug Therapy; Lipid Metabolism; Tissue Distribution; Triparanol

Topics: Ascorbic Acid; Cardiomyopathies; Child; Cholecalciferol; Coronary Disease; Heart; Humans; Infant; Vitamins