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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular disease is the leading cause of mortality in Mexico, as well as in other Western countries. Conventional risk factors for atherosclerosis, such as cigarette smoking, systemic hypertension, diabetes mellitus, and hypercholesterolemia, do not explain this association completely. Recently, it has been recognized that hyperhomocysteinemia contributes to the atherosclerotic process, promoting endothelial damage and oxidative stress in the vascular wall. Homocysteine, an amino acid generated under physiologic conditions after ingestion of protein-rich foods, is used in a variety of metabolic pathways. Elevated plasma levels of this amino acid (higher than 15 mmol/L or lower in the presence of other cardiovascular risk factors) promote the development of atherosclerosis. Folic acid and vitamin B6 and B12 supplements decrease plasma levels of homocysteine effectively and may play an important role in the prevention and treatment of atherosclerotic vascular disease.
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PMID:[Hyperhomocysteinemia. A new coronary risk factor]. 1151 57

Cardiovascular disease mortality is high in children on maintenance dialysis, accounting for about 25% of patient deaths. Cardiovascular-related mortality rates for children on dialysis are higher than for children with successful kidney transplants. Data on the long-term consequences of risk factors for cardiovascular disease are lacking for pediatric end-stage renal disease patients. This article reviews pediatric data pertaining to the following risk factors: anemia, hypertension, hyperlipidemia, left ventricular hypertrophy, abnormal calcium-phosphorus metabolism, and hyperhomocysteinemia. The potential relationship of end-stage renal disease to the etiology of several functional disorders of the cardiovascular system is discussed. Clinical studies are needed to assess the prevalence of cardiovascular disease and of cardiovascular disease risk factors in the pediatric end-stage renal disease population. Possible preventive and therapeutic guidelines need to be developed for at-risk children on maintenance dialysis.
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PMID:Risk factors for cardiovascular disease in children on maintenance dialysis. 1153 19

The endothelium, a continuous cellular monolayer lining the blood vessels, has an enormous range of important homeostatic roles. It serves and participates in highly active metabolic and regulatory functions including control of primary hemostasis, blood coagulation and fibrinolysis, platelet and leukocyte interactions with the vessel wall, interaction with lipoprotein metabolism, presentation of histocompatibility antigens, regulation of vascular tone and growth and further of blood pressure. Many crucial vasoactive endogenous compounds like prostacyclin, thromboxane, nitric oxide, endothelin, angiotensin, endothelium derived hyperpolarizing factor, free radicals and bradykinin are formed in the endothelial cells to control the functions of vascular smooth muscle cells and of circulating blood cells. These versatile and complex systems and cellular interactions are extremely vulnerable. The balances may be disturbed by numerous endogenous and exogenous factors including psychological and physical stress, disease states characterized by vasospasm, inflammation, leukocyte and platelet adhesion and aggregation, thrombosis, abnormal vascular proliferation, atherosclerosis and hypertension. The endothelial cells are also the site of action of many drugs and exogenous toxic substances (e.g. smoking, alcohol). As markers and assays for endothelial dysfunction, direct measurement of nitric oxide, its metabolites from plasma and urine, functional measurement of vascular nitric oxide dependent responses and assay of different circulating markers have been used. In numerous pathological conditions (e.g. atherosclerosis, hypertension, congestive heart failure, hyperhomocysteinemia, diabetes, renal failure, transplantation, liver cirrhosis) endothelial dysfunction has been described to exist. Some of them, as well as hormonal and nutritional factors and drug treatment will be discussed in this short review.
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PMID:Clinically important factors influencing endothelial function. 1153 60

Cardiovascular disease is the leading cause of morbidity and mortality in end-stage renal disease. Causes include those usually found in the general population, those related to the uremic status, and those related to dialytic treatment. Hypertension, hypotension, anemia, hypoalbuminemia, malnutrition, dyslipidemia, reactive C protein, calcium-phosphate product, dialysis modalities, and hyperhomocysteinemia are discussed extensively. Special emphasis is put on hyperparathyroidism as a traditional toxin. The emergent role of sleep apnea has been confirmed in animal models as well as in humans studied using polysomnography. There are difficulties in diagnosing coronary disease, because angiography is not risk-free, is expensive, and should be reserved for patients having symptoms of heart failure and/or patients having diabetes mellitus, and/or patients entering a transplantation list. This allows patients with coronary disease to undergo coronary artery bypass (preferably) or percutaneous transluminal angioplasty. Patients for whom surgery is not appropriate should be treated using more traditional medical procedures.
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PMID:The heart in uremia: role of hypertension, hypotension, and sleep apnea. 1157 20

Few and contrasting data are available on the prevalence of hemostatic risk factors in patients with central retinal vein occlusion (CRVO). Aim of this study was to investigate the metabolic and inherited risk factors for venous thrombosis in 100 CRVO patients (age: 59 yrs; range 18-77) and in 100 controls (age: 56 yrs; range 18-84). In patients homocysteine (Hcy) levels were significantly higher than in controls and were affected by the C677T methylenetetrahydrofolate reductase (MTHFR) polymorphism (p < 0.001). The prevalences of activated protein C resistance (APCR), factor V Leiden positivity, elevated PAI-1 and Lp(a) levels were significantly higher in patients with respect to controls. At multivariate analysis, only hyperhomocysteinemia (OR 11, 95% CI 3.6-36.2; p < 0.0001) and elevated PAI-1 levels (OR 8.9, 95% CI 3.5-41.3; p < 0.01), in addition to hypertension (OR 40.5, 95% CI 8.6-188.8; p < 0.00001) and hypercholesterolemia (OR 3.1, 95% CI 1.6-20.5; p < 0.05), were independent risk factors for CRVO. These data demonstrate a potential role of hemostatic risk factors in the pathophysiology of CRVO.
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PMID:Thrombophilic risk factors in patients with central retinal vein occlusion. 1208 91

The high incidence of cardiovascular disease after renal transplantation is related to a high prevalence and accumulation of risk factors before and after transplantation. Hypertension, posttransplantation diabetes, and hyperlipidemia are well-recognized risk factors for the development of cardiovascular events after renal transplantation and are strongly associated with immunosuppressive therapy. Hyperhomocysteinemia is a potential risk factor for cardiovascular disease in renal transplant recipients, but although a growing matter of study, a direct association with immunosuppressive agents is not yet proven. In addition to treatment intervention, risk management should also involve tailoring the immunosuppressive regimen to minimize the more indirect cardiovascular risk factors such as renal dysfunction and acute rejection.
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PMID:Graft function and other risk factors as predictors of cardiovascular disease outcome. 1158 39

Hyperhomocysteinemia is a risk factor for obstructive large-vessel disease. Here, we studied plasma concentrations of homocysteine and vitamins in patients suffering from subcortical vascular encephalopathy (SVE), a cerebral small-vessel disease leading to dementia. These results were compared to the homocysteine and vitamin plasma concentrations from patients with cerebral large vessel disease and healthy control subjects. Plasma concentrations of homocysteine, vascular risk factors and vitamin status (B6, B12, folate) were determined in 82 patients with subcortical vascular encephalopathy, in 144 patients with cerebral large-vessel disease and in 102 control subjects. Patients with SVE, but not those with cerebral large-vessel disease, exhibited pathologically increased homocysteine concentrations in comparison with control subjects without cerebrovascular disease. Patients with SVE also showed lower vitamin B6 values in comparison to subjects without cerebrovascular disease. Logistic regression analysis showed that homocysteine is associated with the highest risk for SVE (odds ratio 5.7; CI 2.5-12.9) in comparison to other vascular risk factors such as hypertension, age and smoking. These observations indicate that hyperhomocysteinemia is a strong independent risk factor for SVE.
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PMID:Homocysteine in cerebrovascular disease: an independent risk factor for subcortical vascular encephalopathy. 1159 41

Numerous clinical and epidemiological studies have identified elevated homocysteine levels in plasma as a risk factor for atherosclerotic vascular disease and thromboembolism. Hyperhomocysteinemia may develop as a consequence of defects in homocysteine-metabolizing genes; nutritional conditions leading to vitamin B(6), B(12), or folate deficiencies; or chronic alcohol consumption. Homocysteine is an intermediate in methionine metabolism, which takes place mainly in the liver. Impaired liver function leads to altered methionine and homocysteine metabolism; however, the molecular basis for such alterations is not completely understood. In addition, the mechanisms behind homocysteine-induced cellular toxicity are not fully defined. In the present work, we have examined the expression of the main enzymes involved in methionine and homocysteine metabolism, along with the plasma levels of methionine and homocysteine, in the liver of 26 cirrhotic patients and 10 control subjects. To gain more insight into the cellular effects of elevated homocysteine levels, we have searched for changes in gene expression induced by this amino acid in cultured human vascular smooth muscle cells. We have observed a marked reduction in the expression of the main genes involved in homocysteine metabolism in liver cirrhosis. In addition, we have identified the tissue inhibitor of metalloproteinases-1 and alpha1(I)procollagen to be upregulated in vascular smooth muscle cells and liver stellate cells exposed to pathological concentrations of homocysteine. Taken together, our observations suggest (1) impaired liver function could be a novel determinant in the development of hyperhomocysteinemia and (2) a role for elevated homocysteine levels in the development of liver fibrosis.
Hypertension 2001 Nov
PMID:Hyperhomocysteinemia in liver cirrhosis: mechanisms and role in vascular and hepatic fibrosis. 1171 26

Hyperhomocysteinemia (hHcys) has been recognized as a new risk factor for cardiovascular diseases independent of plasma lipid levels or other factors. However, it remains unknown whether hHcys is implicated in the target organ damages associated with hypertension. The present study first examined the possible role of hHcys in the development of glomerulosclerosis in Dahl salt-sensitive (DS) hypertensive rats. High-performance liquid chromatography showed that plasma total homocysteine (tHcys) concentration was 7.64 +/- 0.29 micromol/L in conscious DS rats on a low salt (0.4% NaCl) diet, which was higher than 5.23 +/- 0.25 micromol/L in Dahl salt-resistant normotensive rats. When these rats were exposed to a high salt (4% NaCl) diet, plasma tHcys markedly increased in DS rats (14.7 +/-1.31 micromol/L) but not in Dahl salt-resistant rats (5.34 +/- 0.54 micromol/L). An iron chelater, desferrioxamine (0.3 mg/kg IV per day), completely normalized high salt--induced elevations of plasma tHcys and significantly attenuated the sclerotic changes in the glomeruli in DS rats. To further determine whether hHcys has an independent effect in the development of glomerulosclerosis, Sprague-Dawley rats were fed drinking water containing methionine (1 g/kg per day) for 6 weeks to produce hHcys. In these rats, plasma tHcys increased to 12.5 +/- 1.9 micromol/L (versus 6.1 +/- 2.6 micromol/L in control rats), and the aorta exhibited typical sclerotic changes, but arterial pressure was not altered. Urinary protein excretion increased to 52 +/- 2 mg/24 hours (versus 17 +/- 2 mg/24 hours in control rats), and the glomerular mesangium was expanded with glomerular hypercellularity, capillary collapse, and fibrous deposition in the rats with hHcys. These results suggest that elevated plasma homocysteine may be an important pathogenic factor for glomerular damage in hypertension independent of arterial pressure.
Hypertension 2002 Feb
PMID:Implications of hyperhomocysteinemia in glomerular sclerosis in hypertension. 1188 87

Hyperhomocysteinemia is recognised as a risk factor of ischaemic heart disease and vascular complications of arterial hypertension. Methylenetetrahydrofolate reductase (MTHFR) gene C677T polymorphism is associated with hyperhomocysteinaemia. The aim of the study was the assessment of an association of the above polymorphism with type 2 diabetes with special attention to myocardial infarction and arterial hypertension accompanying diabetes. The study group consisted of 172 type 2 diabetics. 172 control subjects with normal glucose tolerance were age and sex matched to patients with diabetes. C677T polymorphism in MTHFR gene locus was detected using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) method. CT and TT genotypes were found more often among diabetics (OR 1.83, 95% CI 1.16-2.89; p < 0.01). This finding may be secondary to the excess of T allele bearers among diabetics with myocardial infarction when compared to diabetics without infarction and to control group. Upon obtained results the potential role of genotypes CT and TT as risk factors of myocardial infarction among patients with type 2 diabetes could not be excluded (OR 2.33, 95% CI 0.93-5.8; p = 0.07). Genotypes containing T allele are not associated with diabetes type 2 and concomitant arterial hypertension (OR 1.45, 95% CI 0.89-2.57; p = 0.14). A confirmation in further studies is needed for the presented findings.
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PMID:[Methylenetetrahydrofolate reductase gene polymorphism in patients with type 2 diabetes]. 1192 64


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