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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperhomocysteinemia has been recognized as one of the risk factors for atherosclerosis and premature vascular disease. Patients on dialysis and end-stage renal disease also manifest high plasma concentrations of homocysteine. We performed this study to evaluate the effects of folic acid supplementation on hyperhomocysteinemia in CAPD patients. Twenty-three CAPD patients (8 males, 15 females, 49.1 +/- 14.2-years-old) dialyzed for 22.7 +/- 19.2 months participated in the study. Daily 5-mg doses of folic acid supplementation for 4 weeks significantly reduced plasma concentrations of total homocysteine (p < 0.01) and serine (p < 0.001). This observation suggests that the reduction of plasma concentrations of total homocysteine results from activation of homocysteine remethylation to methionine. On the other hand, folic acid supplementation also revealed significant correlations between changes in serum concentrations of both dihomo-gamma-linolenic acid and arachidonic acid and changes in plasma concentrations of total homocysteine (r = -0.517, p < 0.05, r = -0.451, p < 0.05, respectively). In addition, serum concentrations of both dihomo-gamma-linolenic acid and arachidonic acid in 11 CAPD patients with hyperhomocysteinemia (> or = 35 micromol/litter) were significantly lower than those of 12 CAPD patients with normohomocysteinemia (< 35 micromol/litter) (p < 0.05, p < 0.05, respectively). Serum concentrations of both dihomo-gamma-linolenic acid and arachidonic acid in CAPD patients with hyperhomocysteinemia increased significantly (p < 0.01, p < 0.05, respectively) and reached similar levels of CAPD patients with normohomocysteinemia, while plasma concentrations of total homocysteine decreased after folic acid supplementation. These findings suggest that correction of hyperhomocysteinemia in patients on dialysis produces an increase in unsaturated fatty acids.
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PMID:[Effects of folic acid supplementation on hyperhomocysteinemia in CAPD patients: effects on unsaturated fatty acids]. 951 77

The prevention of coronary artery disease is based on the control of several factors associated with a disease or clinical condition and suspected to play a pathogenetic role, defined as 'risk factors'. Smoking is a powerful risk factor for coronary artery disease, with risk of events increasing in relation to the number of cigarettes smoked daily. Smoking cessation is associated within 3-4 years, with a significant reduction in cardiovascular risk. Hyperlipidaemia is a powerful predictor of coronary disease with a strong, independent, continuous and graded positive association between cholesterol levels and risk of coronary events. Several large studies have shown the benefit of cholesterol reduction, and there is clear evidence of the efficacy of statins in the reduction of events in primary and secondary prevention. Hypertension is a significant, strong and independent risk factor for coronary artery disease morbidity and mortality and the reduction of events and mortality by antihypertensive treatment is well documented. Obesity is associated with an increase in all-cause mortality and cardiovascular mortality, with a particularly high risk for subjects with central obesity. Central obesity is also part of the so-called 'metabolic X syndrome' including insulin resistance, which appears to be associated with a particularly high risk of coronary artery disease. Type 1 and type 2 diabetes mellitus are associated with an increased risk of cardiovascular disease, especially in women. Several studies have shown that good metabolic control and multifactorial risk factor reduction significantly lower the coronary risk in these patients. Recent evidence is accumulating that some clotting factors (fibrinogen, factor VII, von Willebrand factor) and fibrinolytic factors (t-PA and PAI-1) are associated with an increased risk of coronary artery disease. The European Concerted Action on Thrombosis (ECAT) showed that the levels of fibrinogen, von Willebrand factor antigen, and t-PA antigen are independent predictors of subsequent coronary syndromes in patients with angina pectoris, and that low fibrinogen is associated with a low risk of events despite high cholesterol levels. Post-menopausal status is associated with increased risk of coronary artery disease, particularly when menopause is premature (before the age of 45) or abrupt (surgical). There is strong, thought not yet completely definite evidence that post-menopausal hormone replacement therapy may significantly reduce the risk of events and improve survival. Hyperhomocysteinaemia is an emerging risk factor independently associated with an increased risk of coronary artery disease, cerebral vascular disease, and peripheral vascular disease. The administration of vitamin B6, B12 or folate seems to be useful and is currently under further evaluation. Recently, attention has been focused on the correlation between coronary artery disease and genetic factors, such as ACE gene polymorphism or the gene polymorphism for the IIIa-moiety of the platelet fibrinogen receptor IIb-IIIa. In primary prevention, control of the major risk factors mainly in patients with clustered factors will substantially reduce the risk of ischaemic events. Secondary prevention of CHD is based on: aggressive behavioural advice, blood pressure reduction in hypertensives, good metabolic control of diabetes, and cholesterol reduction. Aspirin, beta-blockers, ACE inhibitors, and oral anticoagulants, may be useful in selected patients.
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PMID:Classical risk factors and emerging elements in the risk profile for coronary artery disease. 951 44

A case is presented of a woman who had an occlusive stroke at age 29. She was seen in a rehabilitation medicine clinic for central nervous system-mediated pain that had developed soon after a cerebrovascular event. After an extensive workup to find the cause of her cerebrovascular occlusion, it was discovered that she had a markedly elevated fasting plasma homocysteine level of 59 micromol/L. A discussion of premature vascular disease in the rehabilitation patient is followed by a short review of the clinical detection of, and potential therapy for, hyperhomocysteinemia.
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PMID:Hyperhomocysteinemia as a cause of premature stroke in a young patient. 952 90

Hyperhomocysteinemia has recently been identified as an independent risk factor for arterial and venous occlusive disease. In particular, hyperhomocysteinemia has been associated with premature vascular disease, and may act synergistically with other risk factors. Two young patients with severe premature vascular disease, one venous and one arterial, have significantly elevated homocysteine levels. In addition to appropriate anti-coagulant therapy, these patients receive B6 and folate vitamin therapy which normalizes the homocysteine levels. While this course of therapy is prudent, no prospective clinical trials have yet demonstrated that reduction of homocysteine levels correlates with a decreased cardiovascular risk.
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PMID:Hyperhomocysteinemia and premature vascular occlusive disease. 953 44

Mild hyperhomocysteinemia was found to be related to venous thrombosis, cerebrovascular and coronary artery disease (CAD). Some recent studies suggested that a mutation in the gene encoding for 5-10 methylenetetrahydrofolate reductase (MTHFR), due to a transition C-->T at nucleotide 677, is a genetic risk factor for vascular disease. However, several further studies could not confirm this association. We investigated 84 patients with CAD who underwent percutaneous transluminal coronary angioplasty (PTCA) and 106 healthy subjects. The prevalence of the mutated homozygous genotype was much higher than in other Italian populations, Europeans or other major human groups, but no excess of the Val/Val homozygotes was found in patients (28.5%) with respect to healthy subjects (30.2%). Mutated homozygous MTHFR genotype (+/+) was not found to be related to the clinical manifestations of CAD, to the prevalence of the common risk factors and to the rate of restenosis. In conclusion, thermolabile MTHFR does not appear to be associated "per se" with the risk for CAD or for restenosis after PTCA. The high frequency of the +/+ genotype in our Italian population (from Tuscany) confirms a wide macroheterogeneity and suggests a microheterogeneity in the genotype frequencies of the different ethnic populations.
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PMID:The high prevalence of thermolabile 5-10 methylenetetrahydrofolate reductase (MTHFR) in Italians is not associated to an increased risk for coronary artery disease (CAD). 956 81

Vascular disease associated with increased blood concentrations of homocysteine has been known for many years. However, the pathobiochemical mechanisms leading to vasculopathy are still unknown. Several attempts have been made to establish in vitro model systems for the evaluation of homocysteine specific effects in cultured cells. It was concluded from these experiments, that hyperhomocysteinemia has to be considered as a risk factor for atherosclerosis exerting its effects mainly by mechanisms involving oxidative damage. Here, we summarize the homocysteine induced cellular effects which may be due to alterations of the redox thiol status. Effects specific for homocysteine are demonstrated working on different levels of cellular processes involving protein folding and regulation of nuclear factor kappaB (NF-kappaB) controlled gene transcription, the latter opening a new perspective for a novel pathway by which homocysteine might enhance chronic inflammation of the endothelium and possibly contributes to the development of atherosclerosis.
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PMID:The redox status of aminothiols as a clue to homocysteine-induced vascular damage? 958 35

In this valedictory address the research of the Nijmegen homocysteine team on birth defects and vascular disease is presented. Hyperhomocysteinemia was found in women with neural tube defect (NTD) offspring, other birth defects and vascular disease. Raised homocysteine levels in the blood plasma can be explained by lack of B-vitamins (folic acid), mutation of the 5,10-methylenetetrahydrofolate reductase genes or both. Genetic mutations were found on the first chromosome (677 C-->T and 1298 A-C) and can explain up to 50% of the NTD protective effect of folic acid. The inborn error of methionine-homocysteine metabolism was also found in cases with recurrent early pregnancy loss, schisis, congenital heart defects and vascular problems like placental abruption, infarcts and fetal growth retardation. One of the most exciting medical findings of the last years is that folic acid can prevent NTD defects. This might also hold for other birth defects and vascular disease.
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PMID:From birth to conception. Open or closed. 962 14

An association between hyperhomocysteinemia and premature atherosclerosis in patients with non-insulin-dependent diabetes mellitus (NIDDM) has recently been described. Little is known about the role of insulin in homocysteine [H(e)] metabolism. We measured plasma H(e) concentrations in the fasting state and during a hyperinsulinemic-euglycemic clamp in normal subjects and patients with NIDDM. Plasma H(e) decreased significantly from 7.2 +/- 2.6 to 6.0 +/- 2.7 mmol/L (P < .01) in normal subjects, but did not change in patients with NIDDM (6.0 +/- 2.7 to 5.9 +/- 2.5 mmol/L, respectively). These data suggest that plasma H(e) concentrations are regulated by acute hyperinsulinemia in normal subjects, but not in insulin-resistant NIDDM subjects. These abnormalities may have implications for the pathogenesis of premature vascular disease associated with NIDDM.
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PMID:Plasma homocysteine concentrations are regulated by acute hyperinsulinemia in nondiabetic but not type 2 diabetic subjects. 962 67

Hyperhomocysteinemia has recently been identified as an important risk factor for atherosclerotic vascular disease. This article reviews homocysteine metabolism, causes of hyperhomocysteinemia, the pathophysiological findings of this disorder, and epidemiological studies of homocysteine and vascular disease. Screening for hyperhomocysteinemia should be considered for patients at high risk for vascular disease or abnormalities of homocysteine metabolism. For primary prevention of vascular disease, treatment of patients with homocysteine levels of 14 micromol/L or higher should be considered. For secondary prevention, treatment of patients with homocysteine levels of 11 micromol/L or higher should be considered. Treatment is most conveniently administered as a folic acid supplement (400-1000 microg) and a high-potency multivitamin that contains at least 400 microg of folate. Higher doses of folic acid and cyanocobalamin supplements may be required in some patients. Until prospective clinical trial data become available, these conservative recommendations provide a safe, effective, and evidence-based approach to the diagnosis, evaluation, and management of patients with hyperhomocysteinemia.
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PMID:Hyperhomocysteinemia and atherosclerotic vascular disease: pathophysiology, screening, and treatment. off. 964 23

In non-transplant patients mild hyperhomocysteinemia is an independent risk factor for vascular disease. The aim of this study was to determine whether hyperhomocysteinemia is associated with graft vascular disease. Fasting total plasma homocysteine was assessed in 18 patients with graft vasculopathy and 18 transplanted patients without graft vasculopathy matched for age, sex and the time since transplant. All were on cyclosporin. Graft vasculopathy was defined at coronary angiography as stenoses > or = 25%, or aneurysms. We found that hyperhomocysteinemia ( > or = 15 micromol/l) is common among transplanted heart recipients and significantly more frequent in the patients with graft vasculopathy (17/18 versus 11/18). Accordingly, the mean homocysteinemia was significantly higher in the group with graft vasculopathy (23.6+/-7.8 versus 16.9+/-7.1 micromol/l, P=0.01). The elevation of homocysteine plasma levels in the heart transplant recipients has probably multiple causes. The main cause seems to be renal failure. Additional causes could be azathioprine treatment or genetic polymorphisms. These results suggest that besides the immunological factors, homocysteine can play an additional role in the pathogenesis of graft vascular disease.
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PMID:Association of mild hyperhomocysteinemia with cardiac graft vascular disease. 969 Sep 18


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