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

Statins have pleiotrophic effects related to the pathogenesis of atherosclerosis and thrombogenicity of the vessel wall beyond lipid lowering. The aim of the present study was to examine the effect of atorvastatin treatment on the fibrinolytic system in patients with dyslipidemia. The investigation was carried out on 41 dyslipidemic patients (21 males and 20 females) with a mean age of 53.8 years (range, 30-76). The patients were divided into subgroups according to their cholesterol and triglyceride levels as hypercholesterolemic (n = 26) and mixed-type hyperlipidemic (n = 15) and their risk factors for coronary heart disease including age, sex, hypertension, obesity, smoking, and family history. The patients were started on atorvastatin 10 mg/day, and evaluated within 6-12 weeks to assess the changes in fibrinolytic parameters including global fibrinolytic capacity, plasminogen activator inhibitor type-1 and tissue plasminogen activator, and lipids. After successful lipid-lowering therapy, global fibrinolytic capacity (P = 0.003) and tissue plasminogen activator levels (P = 0.04) were found to be increased and plasminogen activator inhibitor type-1 levels (P = 0.02) decreased in dyslipidemic patients. Global fibrinolytic capacity levels increased (P < 0.001) and plasminogen activator inhibitor type-1 levels decreased (P = 0.01) in patients with hypercholesterolemia (n = 26). However, no significant changes were observed in fibrinolytic parameters in patients with mixed-type hyperlipidemia (n = 15). When the patients were separately evaluated according to risk factors, significant beneficial effects on the fibrinolytic system were observed, especially in patients without obesity and hypertension as well as in older patients and males. These findings suggest that atorvastatin treatment has a beneficial effect on the fibrinolytic system in patients with hypercholesterolemia, but not in patients with mixed-type hyperlipidemia. Further studies are needed to show whether higher doses and longer periods of lipid lowering treatment have beneficial effects in patients with mixed type hyperlipidemia and some risk factors.
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PMID:The effects of atorvastatin treatment on the fibrinolytic system in dyslipidemic patients. 1565 73

In order to maintain an anticoagulant nature, the healthy endothelium secretes factors such as tissue plasminogen activator, ADPase, and expresses membrane thrombomodulin. However, when damaged, it releases increased amounts of pro-coagulants such as von Willebrand factor. Similarly, the healthy endothelium uses nitric oxide, prostacyclin and other molecules to help maintain normal blood pressure, and these molecules also inhibit platelet activity. But a dysfunctional endothelium fails to produce these vasodilators so that vasospasm and hypertension can result. Thus the (damaged/dysfunctional) endothelium can contribute to Virchow's triad by failing to maintain an anticoagulant surface and in failing to correctly regulate blood pressure, factors that are likely to promote thrombosis and hypertension.
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PMID:How a damaged blood vessel wall contibutes to thrombosis and hypertenasion. 1569 58

Due to excessive salt and water retention, hypertension often becomes refractory in patients undergoing peritoneal dialysis (PD). Management of high blood pressure (BP) appears to be of particular importance in such patients because of its substantial impact on the patients' prognosis. However, attempts to control hypertension in PD patients have not been successful in most cases. In this regard, the present study aimed to address the adequacy of current antihypertensive therapy for PD patients. A new antihypertensive strategy expected to improve the outcome was tested on the assumption that treatment with either angiotensin converting enzyme inhibitor (ACE-I) or angiotensin receptor blocker (ARB) in the evening together with alpha1-blocker at bed time and long-acting Ca channel blocker (CCB) in the morning might ameliorate BP control associated with morning hypertension. Enrolled in the present study were 40 patients whose BP was evaluated by both office and home measurement. Due to an emerging concern about morning hypertension, home BP measured early in the morning was used for the analysis. Each patient was categorized into the following four groups in accordance with office and home BP: well-controlled, poorly-controlled, white-coat and masked (opposite to white-coat), hypertension. After the observation period, 28 patients with refractory hypertension were allocated to intensive antihypertensive therapy in which ARB or ACE-I previously prescribed in the morning or daytime was shifted to the night. In addition, alpha1-blocker was given at bed time. Furthermore, long-acting CCB and diuretics were shifted to the morning. The patients were then followed up for 4-6 months. The results were as follows: 1) Of the total number of 40 PD patients, systolic hypertension was noted in 50% of cases by office BP and in 80% by home BP. The former was less frequent than the latter (p=0.0047, n=40). Similarly, diastolic hypertension was noted in 20% by office BP and in 45% by home BP. The former was less frequent than the latter (p=0.0045, n=40 by McNemar's analysis). The distribution of BP control categories was well-controlled in 11%, poorly-controlled in 42%, masked hypertension in 39% and white-coat hypertension in 8% when determined by systolic BP. The distribution was well-controlled in 45%, poorly-controlled in 13%, masked hypertension in 34% and white-coat hypertension in 8% of cases when determined by diastolic BP. 2) In 28 patients subjected to the intensive therapy, the control category of systolic BP was changed from 11 to 37% in well-controlled cases, from 42 to 30% in poorly-controlled cases, from 39 to 26% in masked hypertension cases and from 8 to 7% in white-coat hypertension cases. The shift in categories in both poorly-controlled and masked hypertension cases to the better category (well-controlled), was statistically significant (p=0.001, by Wilcoxon's signed rank test). Similarly, the control category of diastolic BP was changed from 45 to 43% in well-controlled cases, from 13 to 15% in poorly-controlled cases, from 34 to 32% in masked hypertension cases and from 8 to 10% in white-coat hypertension cases. There was a tendency for the prevalence of poorly-controlled and masked hypertension to improve to the well-controlled category in response to intensive therapy (p=0.0625, by Wilcoxon's signed rank test). 3) The plasma concentration of plasminogen activator inhibitor (PAI-1)/tissue plasminogen activator (t-PA) complex (total PAI-1 complex) was significantly decreased after intensive therapy (17.3+/-7.8 ng/ml vs. 13.5+/-4.6 ng/ml, n=28, p<0.01 by paired t-test). In contrast, the plasma concentration of t-PA was unchanged even after intensive therapy (4.8+/-3.9 ng/ml vs. 6.2+/-2.9 ng/ml, n=28, ns). These data suggest that home BP obtained in the morning is a useful measure for evaluating morning hypertension in PD patients, most of whom have refractory hypertension categorized as either poorly-controlled or masked hypertension. Intensive treatment with ACE-I/ARB given in the evening along with alpha1-blocker at bed time combined with a diuretic and/or long-acting CCB in the morning is efficacious in controlling the BP of patients with refractory hypertension in PD patients. The link between the reduction in plasma total PAI-1 levels and the intensive therapy may suggest that this therapeutic strategy could prevent thrombotic events associated with morning hypertension in patients on PD.
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PMID:[Antihypertensive therapy for refractory morning hypertension in patients on peritoneal dialysis]. 1575 62

Carotid stenosis is an important cause of transient ischaemic attacks and stroke. The cause of carotid stenosis is most often atherosclerosis; contributing to the pathogenesis of the lesion are endothelial injury, inflammation, lipid deposition, plaque formation, fibrin, platelets and thrombin. Carotid stenosis accounts for 10-20% of cases of brain infarction, depending on the population studied. Despite successful treatment of selected patients who have had an acute ischaemic stroke with tissue plasminogen activator and the promise of other experimental therapies, prevention remains the best approach to reducing the impact of ischaemic stroke. High-risk or stroke-prone patients can be identified and targeted for specific interventions. At this juncture, treatment of carotid stenosis is a well established therapeutic target and a pillar of stroke prevention. There are two main strategies for the treatment of carotid stenosis. The first approach is to stabilise or halt the progression of the carotid plaque through risk factor modification and medication. Hypertension, diabetes mellitus, smoking, obesity and high cholesterol levels are closely associated with carotid stenosis and stroke; control of these factors may decrease the risk of plaque formation and progression. The second approach is to eliminate or reduce carotid stenosis through carotid endarterectomy or carotid angioplasty and stenting. Carotid endarterectomy, which is the mainstay of therapy for severe carotid stenosis, is beyond the scope of this review. Anticoagulants seem to play little role (if any) in the medical (i.e. non-surgical) treatment of carotid stenosis. Adoption of a healthy lifestyle combined with the reduction of risk factors has been shown to lead to a reduction in the extent of carotid stenosis. The medical treatment of carotid stenosis should be based on the triad of the reduction of risk factors, patient education, and use of antiplatelet agents.
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PMID:Place of drug therapy in the treatment of carotid stenosis. 1598 96

Hypertension is associated with decreased fibrinolytic potential, mainly expressed as elevated plasma plasminogen activator inhibitor type 1 (PAI-1) levels, and increased platelet aggregability, which may account in part for the increased risk of atherosclerosis and its clinical complications in hypertensive patients. The effects of antihypertensive drugs on this prothrombotic state have been investigated and controversial findings have been reported, possibly because of differences in study designs, patients selected, and methodology used. Scarce and conflicting data exist about the effects of diuretics and beta-adrenoceptor antagonists on the fibrinolytic system, whereas ACE inhibitors have generally been reported to improve the fibrinolytic balance by decreasing plasma PAI-1 levels, calcium channel antagonists have been shown to increase tissue plasminogen activator (tPA) activity, and angiotensin II type 1 (AT(1)) receptor antagonists seem to exert neutral effects. beta-Adrenoceptor antagonists, calcium channel antagonists, and AT(1)-receptor antagonists have been reported to exert anti-aggregatory effects on platelets, while contrasting data exist about the influence of ACE inhibitors. Clinical implications of the changes induced by antihypertensive drugs on the fibrinolytic balance and platelet function are still debated. In particular, the question of whether these changes may translate into different degrees of cardiovascular protection in hypertensive patients remains unanswered. While awaiting more information from clinical trials, the choice of antihypertensive drugs, particularly in high-risk patients, should take into account effects beyond their BP-lowering efficacy. Selected agents should have a favorable, or at least neutral, impact on fibrinolytic function and platelet activity.
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PMID:Is the effect of antihypertensive drugs on platelet aggregability and fibrinolysis clinically relevant? 1598 4

Recurrent stress is clinically associated with early onset hypertension and coronary artery disease. A mechanism linking emotion to pathogenic remodeling of the artery wall has not been identified. Stress stimulates acute regulated release of tissue plasminogen activator (t-PA) into the circulation, which is presently attributed to the vascular endothelium. Sympathetic neurons also synthesize t-PA and axonally transport it to the arterial smooth muscle. Unlike release by the endothelium, a stress-stimulated sympathetic discharge would potentially accelerate degradation of the wall matrix by plasmin. To assess whether sympathetic axons are the principal source of acute stress-induced arterial release of t-PA, we compared the output from small densely innervated and large sparsely innervated isolated artery segments before and after sympathetic stimulation, and after ablations. Following phenylephrine infusion densely-innervated microvessels in uveal eyecups were released over 60-fold greater amounts of active t-PA per milligram than the sparsely innervated aorta; and ten-fold more than carotid artery segments. Mesenteric artery release was 4.8-fold greater than release by the carotid artery. In vivo, uveal release of t-PA increased more than three-fold within one minute following superior cervical sympathetic ganglion electrical stimulation, and after phenylephrine, or nicotine infusions of the anterior chamber. Circulating levels of t-PA fell 70% following chemical sympathectomy. We propose that sympathetic nerves are the primary source of stress-induced release of t-PA into and from the densely innervated resistance arteries and arterioles, where dysregulated plasmin-induced proteolysis could damage the wall matrix.
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PMID:Stimulated release of tissue plasminogen activator from artery wall sympathetic nerves: implications for stress-associated wall damage. 1601 5

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 HIV lipodystrophy syndrome, a condition characterized by subcutaneous fat loss sometimes associated with relative or absolute accumulation of central fat, has a high prevalence in the treatment of HIV infection. Associated metabolic alterations include peripheral and hepatic insulin resistance, impaired glucose tolerance, type 2 diabetes, hypertriglyceridemia, hypercholesterolemia, increased free fatty acids, and decreased HDL. Often, these metabolic abnormalities appear or deteriorate before the manifestation of fat redistribution. Hypertriglyceridemia is the leading lipid abnormality after initiation of HIV therapy frequently observed together with low HDL cholesterol. Raised levels of tissue plasminogen activator and plasminogen activator inhibitor-1 have been found in these patients, and there are reports about hypertension associated with antiretroviral therapy. Thus, the lipodystrophy syndrome in HIV therapy resembles a clinical situation that is known as the "metabolic syndrome" in HIV-negative patients. There is now good evidence that the metabolic abnormalities of HIV-infected patients harbor a significant risk for cardiovascular disease with as yet unknown consequences. In addition, several studies report a reduced quality of life in patients with body habitus changes leading to reduced therapy adherence. Current data indicate a rather multifactorial pathogenesis where HIV infection, its therapy, and patient-related factors are major contributors. Therapeutic and preventive strategies have, so far, been of only limited or no success. For reduction of the cardiovascular risk, recommendations proposed for non-HIV-infected patients like the National Cholesterol Education Program (NECP) have been adapted for HIV-infected patients. These should be regarded as rather preliminary and need to be evaluated in further clinical trials. General recommendations include dietary changes and physical activity, switch of antiretroviral drugs (replacement of protease inhibitors), and, finally, use of metabolically active drugs. Lipid-lowering agents can be considered for the treatment of severe hypertriglyceridemia, elevated LDL, or a combination of both. Some HMG-CoA reductase inhibitors, however, share common hepatic metabolization pathways with protease inhibitors (cytochrome P450 3A4 system), thereby potentially leading to additional liver and muscle toxicity. Although clinicians should assess cardiovascular risk factors and target risk reduction in HIV-infected patients, the primary goal in HIV therapy remains to be the effective suppression of viral replication leading to reduced morbidity and mortality.
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PMID:[Metabolic syndrome and hyperlipidemia in HIV-positive patients]. 1617 Jun 75

Excessive hypertension can challenge the brain's capacity to autoregulate cerebral blood flow, and can aggravate increased intracranial pressure (ICP) and cerebral edema. Hypotension may worsen ischemic damage in marginally perfused tissue, and in some cases can trigger cerebral vasodilation and ICP plateau waves. There is a lack of high-quality data regarding optimal BP management in these conditions. Existing guidelines for target BP levels are based largely on class III evidence. Class I data only exist for enteral candesartan and nimodipine use in acute ischemic stroke and aneurismal subarachnoid hemorrhage (SAH), respectively, and for parenteral magnesium use in eclampsia. Class II data exist for reducing BP to <180/105 mmHg in patients with ischemic stroke who are treated with intravenous tissue plasminogen activator, for elevating systolic BP to 180-220 mmHg in SAH patients with symptomatic vasospasm, and for maintaining cerebral perfusion pressure (CPP)>60 mmHg in traumatic brain injury. Short-acting continuous-infusion agents with a reliable dose-response relationship and favorable safety profile are desirable. To reduce BP, labetalol, esmolol, and nicardipine best meet these criteria. Sodium nitroprusside should be avoided in most neurological emergencies because of its tendency to raise ICP and cause toxicity with prolonged infusion. To elevate BP, the preferred agents are phenylephrine, dopamine, and norepinephrine.
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PMID:Optimizing blood pressure in neurological emergencies. 2751 96

An 81 year old man with a history of hypertension received intravenous recombinant tissue plasminogen activator (tPA) for right middle cerebral artery (MCA) infarction. He had not had stroke or arrhythmia previously. The initial National Institute of Health Stroke Scale (NIHSS) score was 8. However, a left MCA territory infarction developed 2 minutes after the full course of tPA therapy was completed, and 24 hours after tPA infusion, NIHSS score was 17. The subsequent magnetic resonance imaging scan confirmed an extensive left MCA territory infarction and a small right MCA territory infarction. Although the intracerebral haemorrhage after tPA therapy is relatively more common, tPA infusion may result in an ischaemic cerebral stroke in rare cases.
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PMID:A left MCA territory infarction during intravenous recombinant tissue plasminogen activator therapy for right MCA territory ischaemic stroke. 1643 25


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