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

Combined hyperlipidemia is increasing in frequency and is the most common lipid disorder associated with obesity, insulin resistance and diabetes mellitus. It is associated with other features of the metabolic syndrome including hypertension, hyperuricemia, hyperinsulinemia and highly atherogenic subfractions of lipoprotein remnant particles including small dense low density lipoprotein-cholesterol. This review examines the mechanisms by which combined hyperlipidemia arises and the various drugs including fibric acid derivatives, hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, and nicotinic acid which can be used either as monotherapy or in combination to manage it and to improve prognosis from atherosclerotic disease in diabetes mellitus, insulin resistant states and primary combined hyperlipidemia. The therapeutic approach to combined hyperlipidemia involves determination of whether the cause is hepatocyte damage or metabolic derangements. Combined hyperlipidemia due to hepatocyte damage should be treated by attention to the primary cause. In the case of metabolic dysfunction because of imbalance in glucose and fat metabolism, therapy of diabetes mellitus and obesity should be optimised prior to commencement of lipid lowering drugs. Both fibric acid derivatives and HMG-CoA reductase inhibitors can be used in the treatment of combined hyperlipidemia with fibric acid derivatives having greater effects on triglycerides and HMG-CoA reductase inhibitors on LDL-C though both have effects on the other cardiovascular risk factors. There is some evidence of benefit with both interventions in mild combined hyperlipidemias and large scale trials are underway. Fibric acid derivatives and HMG-CoA reductase inhibitor therapy can be combined with care, provided that gemfibrozil is avoided, fibric acid derivatives are given in the mornings and shorter half -life HMG-CoA reductase inhibitors are used at night. Combined hyperlipidemia emergencies occur with predominant hypertriglyceridemia in pregnancy or as a cause of pancreatitis. Therapy in the former should aim to reduce chylomicron production by a low fat diet and intervention to suppress VLDL-C secretion using omega-3 fatty acids. In the latter case, fluid therapy alone and medium chain plasma triglyceride infusions usually reduce levels satisfactorily though apheresis may be required. Blood glucose levels also need aggressive management in these conditions. Combined hyperlipidemia is likely to become an increasing problem with the increase in the prevalence of obesity and diabetes mellitus and needs aggressive management to reduce cardiovascular risk.
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PMID:Drug treatment of combined hyperlipidemia. 1472 15

This study examined stroke risk factor profiles, management and outcomes for elderly patients with English-speaking background (ESB) and non-English-speaking background (NESB). This is an observational cohort study with both retrospective and prospective components. In total, 186 consecutive acute stroke patients aged > or =65 years admitted to our hospital were recruited over a 12-month period. Patient characteristics, stroke risk factors and management, in-hospital mortality, functional independence measurement scores before admission and at discharge, and discharge destination were recorded. On admission, NESB patients with atrial fibrillation (AF) were less likely to be taking warfarin than ESB patients (1 out of 19 with NESB vs. 19 out of 41 with ESB, p = 0.001). More NESB patients had a history of diabetes mellitus (DM) than ESB patients (41.4 vs. 10.2%, respectively; p = 0.001). However, ESB and NESB patients were comparable in terms of age, gender, preadmission functional status as well as other stroke risk factors (including smoking and alcohol drinking pattern, prevalence of hypertension and lipid disorder) and their management. In-hospital mortality was similar between ESB and NESB patients (10.2 vs. 8.6%). In conclusion, we found an association with our population of elderly NESB patients and an underutilization of warfarin for AF as well as a higher frequency of DM. Determination of the underlying reasons for such differences may be of value in the primary health care of NESB patients.
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PMID:Comparison of stroke risk factors and outcomes in patients with English-speaking background versus non-English-speaking background. 1545 14

Essential arterial hypertension often predisposes patients to prothrombotic state and increased risk of vascular and organ complications. Vital role in regulation of hemostatic processes is played by genetic factors, renin-angiotensin system and disorders of lipid metabolism. Prime genetic factors involved in the process are 4G/5G polymorphism of promoter region coding tissue plasminogen activator inhibitor-1 (PAI-1) and I/D polymorphism for angiotensin converting enzyme (ACE) gene. The aim of work was the evaluation of alterations within fibrinolysis system (estimation of t-PA and PAI-1 levels), fibrinogen concentration (Fb) and ACE activity with regard to co-existent dyslipidemia and features of left ventricle hypertrophy (LVH). Moreover the analysis of influence of 4G/5G PAI and I/D ACE gene polymorphism on intensification of aforementioned alterations among hypertensive patients was performed. Research was carried out in 170 subjects under 40 years old, in two study groups, HT-- hypertensive group--125 patients with previously untreated hypertension without clinical features of ischaemic heart disease and NT--45 normotensive, healthy subjects. HT group has been further divided into four subgroups: DLP (dyslipidemic, n = 51), NLP (normolipidemic n = 74), LVH+ (with features of left ventricle hypertrophy, n = 35), LVH (-) (without features of left ventricle hypertrophy, n = 90). In a whole HT group significantly higher levels of PAI-1, t-PA and Fb were noted in comparison to NT group, considerably more pronounced within DLP rather than NLP subgroups. Moreover, pronounced increase in ACE activity was recorded in DLP and LVH+ subgroups. It has been proved that 4G/4G homozygous subjects of 4G/5G PAI-1 gene polymorphism from HT group tend to present higher levels of PAI-1 and t-PA if contrasted to 4G/4G genotype of NT group, with more distinct effect within DLP subgroup. Carriers of D allele (genotypes I/D, D/D) of I/D ACE gene polymorphism from HT group characterise with significantly higher activity of ACE in contrast to I/I genotype of HT group, with particularly marked effect in DLP and LVH+ subgroups. Basing on above mentioned results it may be concluded that essential hypertension (especially if complicated with dyslipidemia) impairs fibrinolysis, what might be related to renin-angiotensin system activation in lipid metabolism disorders. Deletion alleles of 4G/5G polymorphism (4G allele) and I/D polymorphism (D allele) in patients with hypertension independently modify fibrinolysis towards prothrombotic state with more distinct effect in dyslipidemia. Increased activity of ACE in D allele carriers may predispose to left ventricle hypertrophy.
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PMID:[Plasminogen activator inhibitor-1 (PAI-1) 4G/5G and angiotensin converting enzyme (ACE) I/D gene polymorphisms and fibrinolytic activity in patients with essential hypertension and dyslipidemia]. 1613 May 96

The prognosis of the patients with the Type II diabetes mellitus without myocardial infarction is as serious as the prognosis of the patients who had experienced myocardial infarction without diabetes mellitus. Consequently there is a big interest of IHD prevention options in diabetic patients, not only by hypertension therapy, but also by hypolipidemic treatment. That is why the results of FIELD study were expected with a great interest. FIELD study randomized 9 795 patients with the Type II diabetes mellitus and initial values of total cholesterol 3.0 to 6.5 mmol/l and in addition with total cholesterol/HDL-cholesterol rate > or = 4.0 or with the values of plasmatic triglycerides between 1.0 and 5.0 mmol/l for treatment with 200 mg of micronized phenophibrate or placebo. As phenophibrate positively influences the typical lipid disorder at diabetic patients, the throughout positive results of phenophibrate had been expected. Study did not fulfil the primary objective of the study of coronary deaths/ non fatal myocardial infarctions (insignificant decrease by 11%). Although phenophibrate significantly decreased non fatal myocardial infarctions and myocardial revascularizations, total mortality and cardiovascular mortality were not positively influenced and they even show non significant aggravating trend. Moreover, the positive effect of phenophibrate on non fatal myocardial infarctions and revascularizations was present only at the persons who had not experienced a cardiovascular disease and only at the persons under 65 years. Phenophibrate positively influenced some diabetic micro vascular complications (nephropathy and retinopathy). Thus, the results of FIELD study present a disappointment and that is why the recommendations of the statin therapy as a priority therapy of dislipidemia stay unchanged also for the patients with Type II diabetes mellitus.
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PMID:[The FIELD study presented and published. Unconvincing results of fenofibrates in diabetic patients]. 1652 3

Data concerning the treatment of lipoprotein disturbances in patients with cerebrovascular disease (CVD) are less robust than those for coronary heart disease (CHD), raising clinical questions as to which is the appropriate therapeutic approach to stroke patients. Although observational cohort studies have failed to demonstrate an association between lipoprotein disorders and stroke incidence, recently completed trials of subjects at risk for CHD have shown that statins reduce not only the risk of myocardial infarction and death, but also that of brain infarction and transient ischemic attacks. At present, it seems reasonable to conclude that stroke patients with undesirable lipid profiles who have a history of CHD should receive specific treatment for the lipid disorder. Recommendations are more problematic for stroke patients with lipid disorder but no history of CHD. Furthermore, many of the risk factors for CVD and vascular dementia (VaD), including serum total cholesterol (TC), lipoprotein(a), diabetes, atrial fibrillation, hypertension, apolipoprotein E levels, and atherosclerosis, have also been shown to increase the risk of Alzheimer's disease (AD). In a recent study, we estimated the prevalence, incidence and rate of progression of Mild Cognitive Impairment (MCI) to dementia, and correlated vascular risk factors with incident MCI and its progression to dementia. We evaluated 2963 individuals from the population-based sample of 5632 subjects 65-84 years old of the Italian Longitudinal Study on Aging, with a 3.5-year follow-up. We found a progression rate to dementia (all causes) of 3.8/100 person-years. Furthermore, age was a risk factor for incident MCI, while education was protective, and serum TC evidenced a non-significant borderline trend for a protective effect. There was a non-significant trend for stroke as a risk factor of progression of MCI to dementia. In conclusion, in our population, among MCI patients who progressed to dementia, 60% progressed to AD and 33% to VaD. Vascular risk factors and CVD may influence the development of MCI and the rate of progression to dementia.
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PMID:Cerebrovascular disease in the elderly: lipoprotein metabolism and cognitive decline. 1670 84

Lipoprotein lipase is a central enzyme in the lipid metabolism, which catalyses the hydrolysis of the triacylglycerol component of chylomicrons and very low density lipoproteins, thereby providing fatty acids and monoacylglycerol for tissue utilisation. LPL gene mutation may affect the activity of LPL, and results in lipid metabolism disorder. It is associated with type 2 diabetes, hypertension, atherosclerosis, obesity and coronary artery disease. Here we review the structure, function, expression regulation of the LPL gene along with its association with complex diseases.
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PMID:[Research progress of lipoprotein lipase gene]. 1728 17

Several studies have shown the occurrence of an independent association between obstructive sleep apnea syndrome (OSAS) and cardiovascular disease, including arterial hypertension, ischemic heart disease, and stroke. The pathogenesis of the cardiovascular complications of OSAS is still poorly understood, however. Several mechanisms are likely to be involved, including sympathetic overactivity, selective activation of inflammatory molecular pathways, endothelial dysfunction, abnormality in the process of coagulation, and metabolic dysregulation. The latter may involve insulin resistance and disorders of lipid metabolism. The aim of this review, which reports the data presented at a workshop jointly endorsed by the European Society of Hypertension and by the European Union COST action on OSAS (COST B26), is to critically summarize the evidence available to support an independent association between OSAS and cardiovascular disease.
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PMID:Sleep apnea: epidemiology, pathophysiology, and relation to cardiovascular risk. 1765 56

Atherosclerosis is considered to be a combined disorder of lipid metabolism and chronic inflammation. Recent studies have reported that liver X receptors (LXRs) are involved in lipid metabolism and inflammation and that LXR agonists inhibit atherogenesis. In contrast, angiotensin II is well known to accelerate atherogenesis through activation of the angiotensin II type 1 receptor (AT1R). To better understand the mechanism of LXR on the prevention of atherogenesis, we examined whether activation of LXR affects AT1R expression in vascular smooth muscle cells. T0901317, a synthetic LXR ligand, decreased AT1R mRNA and protein expression with a peak reduction at 6 hours and 12 hours of incubation, respectively. A well-established ligand of LXR, 22-(R)-hydroxycholesterol, also suppressed AT1R expression. The downregulation of AT1R by T0901317 required de novo protein synthesis. AT1R gene promoter activity measured by luciferase assay revealed that the DNA segment between -61 bp and +25 bp was sufficient for downregulation. Luciferase construct with a mutation in Sp1 binding site located in this segment lost its response to T0901317. T0901317 decreased Sp1 serine phosphorylation. Although preincubation of vascular smooth muscle cells with T0901317 for 30 minutes had no effect on angiotensin II-induced extracellular signal-regulated kinase phosphorylation, phosphorylation of extracellular signal-regulated kinase by angiotensin II was markedly suppressed after 6 hours of preincubation. These results indicate that the suppression of AT1R may be one of the important mechanisms by which LXR ligands exert antiatherogenic effects.
Hypertension 2008 Jun
PMID:Liver X receptor activator downregulates angiotensin II type 1 receptor expression through dephosphorylation of Sp1. 1844 33

Obesity is recognized as a disease when it is associated with current or future health problems. The association of obesity with hypertension, glucose intolerance, and lipid metabolism disorder is diagnosed as metabolic syndrome since it tends to cause arteriosclerotic diseases. Obesity is important since it is pandemic throughout the earth. In this review we explain the concept and classification of obesity. We discuss the disease basis of obesity and metabolic syndrome, especially from the standpoint of adipotoxicity.
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PMID:[Concept and classification of obesity]. 1920 93

The article demonstrates reliably increased risk of arterial hypertension under exposure to general vibration. Lipid metabolism disorders in vibration disease patients were proved to increase risk of atherosclerosis. Recommendations include studies of limbs macrohemodynamics in prophylactic medical examinations among sailing personnel.
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PMID:[Proatherogenic and hemodynamic risk factors of occupational arterial hypertension in sailing personel]. 1994 33


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