Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Folic acid, a water-soluble vitamin, has been used since the 1940s to treat some cases of macrocytic anemia without neurologic disease. Folate deficiency is best diagnosed with red blood cell folate levels along with macrocytosis and/or megaloblastic anemia. In addition to reversing overt deficiency, the vitamin may reduce the incidence of neural tube defects by 45% in women who receive 400 micrograms per day. It is recommended that all women of childbearing age take 400 micrograms of folate per day. Elevations in homocysteine levels, a metabolite intimately associated with folate, are also being found with increasing regularity in those with cardiovascular diseases. Homocysteine levels are reduced by folic acid administration. Therefore, there is some biologic plausibility, but not currently direct proof, for the assumption that folate supplements may prevent heart disease, stroke, and peripheral arterial disease. Controlled trials should take place before widespread food supplementation with folate is carried out on a large scale because of the possibility of outbreaks of permanent B12-related neurologic damage in those with undiagnosed pernicious anemia. However, if a patient has a premature cardiovascular event and has minimal risk factors, ordering a test to determine homocysteine level may be advisable, and if elevated, treating with folic acid supplement as long as B12 deficiency does not coexist.
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PMID:The role of folic acid in deficiency states and prevention of disease. 904 May 15

The French paradox relates to the paradoxical association of a diet high in saturated fat and cholesterol with low coronary heart disease mortality and is contrary to the 'lipid hypothesis'. France and other regions with low heart disease mortality have a high consumption of fruit and vegetables. Epidemiologic studies show fruit and vegetable consumption is inversely related to coronary heart disease mortality, but recent intervention studies do not support the theory that protection is due to antioxidant vitamins. Fruit and vegetables, however, are rich sources of folate. Folate lowers plasma homocysteine levels. Even mild to moderate elevation in plasma homocysteine level is a strong risk factor for arteriosclerosis of the coronary, cerebral, and peripheral arteries. This should explain not only the French paradox but also why known risk factors may explain as little as 25% of the risk for coronary heart disease.
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PMID:The French paradox unmasked: the role of folate. 935 1

Occlusive coronary artery disease is an important factor of cardiovascular morbidity and mortality. The rupture of the thin fibrous cap of the atheroma may be one of the causes of acute coronary syndrome, however, the mechanism of formation of fibrous plaque are poorly understood. Elevation of plasma homocysteine, hyperhomocystinemia, H(e), has emerged as an independent risk factor for hypertension and fibrotic heart disease. The extracellular matrix (ECM) components, particularly fibrillar collagen, are elevated in the atherosclerotic lesions and are the essential integral element in holding the oxidized low density lipoproteins (LDL), homocystine, macrophage and foam cells in milieu, constituting the primary atherosclerotic and secondary restenotic lesions. In vivo and in vitro physiological, morphological, cellular, biochemical and molecular experiments have suggested the role of tissue homocystine in cardiovascular fibrosis and adverse ECM remodeling following H(e). The tissue homocystine induces cardiovascular fibrosis and may lead to heart failure via the redox-receptor pathway. The underlying cause and mechanism of cardiovascular fibrosis associated with arteriosclerosis, atherosclerosis, hypertension and coronary heart disease, involve changes in the levels of tissue redox state.
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PMID:Homocyst(e)ine and heart disease: pathophysiology of extracellular matrix. 1022 75

Homocysteine is an amino acid that has been strongly associated with vascular disease. Plasma homocysteine concentrations are known to vary with dietary patterns and to decrease with exogenous estrogen use, but no other behavioral factors have been examined as potential modifiers of this risk factor. Because psychological stress has also been implicated in the development of cardiovascular disease, the purpose of this study was to test the hypothesis that acute psychological stress induces elevations in plasma homocysteine concentrations. A secondary aim was to test potential differences in response between premenopausal and postmenopausal women. Thirty-four healthy women, one-half of whom were naturally postmenopausal with no hormone replacement, participated in this study. The psychological stressors included standard mental arithmetic and speech stressors. Blood samples were taken prior to, during, and after the stressors, and heart rate and blood pressure were also monitored. Results indicated significant elevations in plasma homocysteine during acute psychological stress, with a return to baseline concentrations during recovery. The pattern of findings for blood pressure and heart rate was similar, suggesting that the rise in homocysteine concentrations may have been sympathetically-mediated. No effects of menopausal status or endogenous estrogens were found. The findings provide preliminary evidence that plasma homocysteine may be an important factor in the relationship between psychological stress and risk for heart disease.
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PMID:Plasma homocysteine levels increase in women during psychological stress. 1037 99

In our review (Law & Morris, 1998), we presented analyses of data from 10 cohort studies yielding the summary estimate that the risk of ischaemic heart disease was 15% lower at the 90th than at the 10th centile of fruit and vegetable consumption. This 10th-90th centile difference in consumption is a realistic increase for an individual (Zino et al, 1997). The estimate of a 15% difference in heart disease mortality was similar to the expected difference in risk from the increase in potassium consumption (given the corresponding decrease in blood pressure) and the increase in folate consumption (given the corresponding decrease in plasma homocysteine) that would result from this specified increase in fruit and vegetable consumption. Ness and colleagues' own approach to such a review was to tabulate the studies with their methodological details and list the result of each study as showing 'no association' or 'protective effect' (Ness & Powles, 1997), when the evidence did not justify the implicit dichotomy. Associations were reproduced as published, in different formats for different studies, and confidence intervals commonly not reported. This left the reader with little impression of the average size of the association nor the degree of consistency between studies. Ness and colleagues express disapproval of our quantitative approach but provide no sound basis for rejecting it. We believe that our results are valid, and that the quantification of the effect is useful in establishing for the first time the moderate but important reduction in heart disease risk that results from a realistic increase in fruit and vegetable consumption. The main argument of Ness and colleagues is that estimates of effect derived from cohort studies are unreliable. We respond to this first, and then to four methodological issues that they raise.
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PMID:By how much does fruit and vegetable consumption reduce the risk of ischaemic heart disease: response to commentary 1055 6

Nineteen people without prior history of documented heart disease were studied for 8 months to determine the effect of treatment based on an immunologic unified theory of vascular disease. Subjects underwent myocardial perfusion imaging to quantify the extent and severity of coronary artery disease, along with assessment of wall motion abnormalities and ejection fraction by both nuclear and echocardiographic methods. These tests were repeated at the end of the study. Treatment consisted of dietary changes, treatment of cholesterol, triglycerides, homocysteine, lipoprotein (a), fibrinogen, C-reactive protein, and infection. Patients who followed the dietary recommendations demonstrated statistically reduced disease in all three major coronary arteries, whereas those individuals who followed high-protein diets demonstrated statistically greater levels of disease.
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PMID:Reversing heart disease in the new millennium--the Fleming unified theory. 1095 14

Plasma homocysteine levels are lowered by insulin and can be elevated in insulin-resistant states. However, it is uncertain whether homocysteine and insulin resistance or components of the metabolic (insulin resistance) syndrome are related in healthy individuals. Total homocysteine concentrations were measured by gas chromatography-mass spectrometry in samples from 100 male participants in the second follow-up cohort of the Heart Disease and Diabetes Risk Indicators in a Screened Cohort Study. Members of this cohort have each undergone an iv glucose tolerance test with measurement of insulin sensitivity by minimal model analysis. Age ranged from 31--62 yr (mean, 46.8), body mass index from 20.6--36.5 kg/m(2) (mean, 26.3), insulin sensitivity from 0.0--9.6 min/mU.L (mean, 2.32), and homocysteine concentrations from 7.5--30.6 micromol/L (mean, 12.2). In univariate correlation, homocysteine concentrations were unrelated to insulin sensitivity or to components of the metabolic syndrome, including fasting serum triglycerides, high density lipoprotein cholesterol, high density lipoprotein subfraction 2 cholesterol, blood pressure, uric acid, systolic blood pressure, or body mass index. These measures were, nevertheless, highly intercorrelated. These findings strengthen the possibility that in healthy humans, homocysteine metabolism is not substantially affected by insulin action.
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PMID:Plasma total homocysteine concentrations are unrelated to insulin sensitivity and components of the metabolic syndrome in healthy men. 1115 36

Hyperhomocysteinemia (HH) has been associated with cardiovascular and autoimmune diseases and oxidative cell damage. Myelodysplastic syndromes (MDS) are associated with autoimmunity (AI) and increased oxidative stress. We tested the association of HH and oxidative stress in 33 MDS patients, by measuring plasma homocysteine and malondialdehyde (MDA). HH was found in 42% of cases, (4/5) cases with associated cardiovascular events (CVE)(80%), and 9/15 cases with associated AI (60%). Thus in MDS, HH was significantly associated with AI/CVE (chi(2) : p=0.0011), and this association seems to be specific, as demonstrated by the comparison of MDS presenting AI/CVE with the ischemic cardiopathy/rheumatoid arthritis control group (13/20, 65% vs 19/69, 27%; chi(2) : p=0.0021). The levels of MDA indicated increased oxidative stress. Our data may suggest that in a subset of MDS, HH may simultaneously contribute to bone marrow myelodysplasia, CVE and AI pathogenesis, possibly through oxidative cell damage.
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PMID:Hyperhomocysteinemia in myelodysplastic syndromes: specific association with autoimmunity and cardiovascular disease. 1134 66

Homocysteinemia, first identified as a genetic disease in children in the 1960s, is associated with severe widespread atherosclerosis which causes death (in untreated cases) before the age of 10 years. Elevated blood homocysteine is now recognized as a risk factor for heart disease in the general population. The mechanism by which homocysteine induces atherosclerosis is still unknown despite intensive investigation. It is proposed here that the mechanism involves sulfane sulfur formed in the catabolism of homocysteine. This unstable and reactive form of sulfur is formed through the action of several enzymes which are known to use homocysteine, its disulfide (homocystine), or its mixed disulfide with cysteine as substrates. Sulfane sulfur has physiological effects which are consistent with a role in atherogenesis. At very low concentrations, it induces proliferation of many cell types, an effect which is consistent with the fibrosis and hyperplasia, which are prominent features of atherosclerotic lesions. At higher concentrations, it is toxic. Also, it modulates the activity of many enzymes and, through this effect on enzymes of lipid metabolism, it could be responsible for the lipid accumulation seen in atherosclerotic lesions.
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PMID:Possible involvement of sulfane sulfur in homocysteine-induced atherosclerosis. 1142

The use of nutritional supplements in the treatment of cardiovascular disease is rapidly growing in the United States. Many substances are marketed with anecdotal claims of efficacy. Most have not been scientifically studied. Excitement exists in the lay press about the homocysteine hypothesis of coronary artery disease and vitamin cures. A MEDLINE search and review of papers covering the study of popular nutritional supplements were undertaken. The papers were limited to peer-review journals using patient series reports, double-blinded prospective studies, and population studies. A compendium of the available data was obtained and an analysis of each paper's methodology was done. A review of the most popular and most studied oral nutritional supplements for the treatment of heart disease demonstrated relatively few well-founded indications for the widespread application of substances with the exception of the bioflavonoids. Some modest effects for endothelial dysfunction were noted for vitamins C and E. Red wines and beers were also noted to be beneficial. The majority of substances either had no effect or were deleterious.
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PMID:Oral nutritional supplements and heart disease: a review. 1144 26


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