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

The TIMI phase II pilot study enrolled 288 patients with acute myocardial infarction who were treated with recombinant tissue plasminogen activator (rt-PA) within 4 hours of symptom onset and who were assigned to coronary angioplasty of the infarct-related vessel 18 to 48 hours after rt-PA treatment. The patients were followed to ascertain (1) vital status; (2) whether they suffered a recurrent myocardial infarction; (3) whether they received coronary angioplasty or bypass grafting; and (4) whether they were rehospitalized for a cardiac event. Risk factors for these events or combination of these events were identified and reported. The estimated 6-week, 6-month, and 1-year cumulative event rate of death or myocardial infarction was 9.1 +/- 1.7%, 12.9 +/- 2.0%, and 13.6 +/- 2.0%, respectively. With the exception of repeat hospital admissions, most of the above cardiac events occurred early during the patients' follow-up course. Cox proportional hazard analyses revealed that continuing chest pain after rt-PA administration, history of congestive heart failure, low systolic blood pressure at the time of initial evaluation, and history of hypertension increased the risk of death or recurrent myocardial infarction, while a history of chest discomfort at baseline evaluation and older age was predictive of future hospitalization or a revascularization procedure.
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PMID:Tissue plasminogen activator followed by percutaneous transluminal coronary angioplasty: one-year TIMI phase II pilot results. TIMI Investigators. 210 25

An increased platelet-vessel wall interaction plays an important role in most forms of cardiovascular disease. In healthy arteries, the vascular endothelium prevents platelet adhesion and aggregation. As a mediator of this protective function, the endothelium produces prostacyclin, endothelium-derived nitric oxide and tissue plasminogen activator. Cardiovascular risk factors such as hypertension, hyperlipidemia and diabetes are associated with an increased platelet activation and with decreased antithrombotic properties of the blood vessel wall. The available inhibitors of platelet function interfere only with one of various mechanisms of platelet activation and of the platelet-vessel wall interaction. Prostaglandin inhibitors, such as aspirin and newer, more specific inhibitors, prevent the production and/or the effect of thromboxane A2 on platelets and the blood vessel wall. Other drugs interfere with the effect of adenosine diphosphate on platelets, or they increase intracellular concentration of cyclic GMP or AMP in platelets and vascular smooth muscle cells. The protective effects of platelet inhibitors in primary and particularly in secondary prevention of cardiovascular diseases have been documented in numerous studies. The successful clinical use of these substances, however, requires a selective prescription of the drugs in patients with cardiovascular disease.
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PMID:[Thrombocyte inhibitors in cardiovascular therapy]. 221 49

Pulmonary embolism can produce severe cardiopulmonary dysfunction characterized by pulmonary artery hypertension, right ventricular failure, and hypoxemia. The search for the source of a pulmonary embolus, by exploration of the veins of the lower limbs and the inferior vena cava should be systematically carried out in all cases of pulmonary embolus which are not immediately life-threatening to the patient. The treatment of deep vein thrombosis associated with pulmonary embolism with thrombolytic agents has been proposed and utilized for approximately 20 years. Although superior results have been claimed with thrombolytic agents, the use of this type of treatment remains limited to massive or sub-massive pulmonary embolism. Fibrinolytic agents with high specificity for fibrin in the thrombi and little systemic activation of the fibrinolytic system have been developed and tested in preliminary clinical trials of patients with acute pulmonary embolism. The largest published experience available has been with recombinant tissue plasminogen activator (rtPA). The acylated streptokinase-plasminogen complex (APSAC) and pro-urokinase also gave promising results. All these agents were accompanied by unexpectedly high incidence of systemic activation of the fibrinolytic system and by hemorrhagic complications with frequencies similar to those that follows the use of first generation products (urokinase and streptokinase). Hence, their superior clinical efficacy must be clearly proven before they are substituted for a more widely available and less expensive drug, such as streptokinase.
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PMID:Pathogenesis and management of acute pulmonary embolism. 251 49

Smoke inhalation injuries in humans are associated with many uncontrolled variables which impact on the lung and make the cause of the pulmonary response difficult to assess. In this report, an established model of smoke inhalation injury in the dog was used to study the early responses of tissue and serum angiotensin-converting enzyme (ACE), tissue plasminogen activator (PLA), and plasma angiotensin II. Animals were exposed to smoke from burning sawdust and kerosene for five minutes. The hemodynamic and pulmonary mechanical responses were typical with a rise in pulmonary artery pressure, pulmonary vascular resistance, and venous admixture (shunt fraction) while dynamic compliance fell. Within five minutes of smoke exposure, lung ACE declined without any change in serum ACE. Lung PLA dropped one hour after injury. Plasma angiotensin II increased within 30 minutes without evidence for systemic hypertension. These early enzymatic changes substantiate the presence of pulmonary endothelial damage known to occur in this form of chemical injury. These changes may condition the lung's physiologic response to the injury and to additional stresses which are multiple when smoke inhalation occurs in conjunction with a cutaneous burn.
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PMID:Effect of acute smoke inhalation on angiotensin converting enzyme, plasminogen activator, and angiotensin-II in the dog. 255 91

The fibrinolytic system was studied in 43 type I diabetic patients with long duration of the disease, with or without evidence of microangiopathy, and in 26 control subjects. There were positive and independent correlations between tissue plasminogen activator (tPA) activity after venous occlusion and HbA1c, and between triglycerides and plasminogen activator inhibitor (PAI-1) and tPA antigen concentrations before and after venous occlusion. The tPA activities both at rest and after venous occlusion were higher in the patients. There were no differences with regard to sex, hypertension or nephropathy for the levels of fibrinolytic variables in these patients. Subjects with retinopathy did not differ from those without retinopathy. Diabetes duration showed a significant negative association with tPA activity in multivariate regression analysis. Tobacco-smoking diabetics, as compared to non-smoking, had an increased tPA antigen release at venous occlusion, but also higher PAI-1 levels and reduced specific activity of the tPA protein. When assessed with the new specific assays now available, the fibrinolytic parameters appear to be specific indicators of endothelial dysfunction related to smoking and to degree of glycaemic control in type I diabetic subjects.
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PMID:Glycaemic control, smoking habits and diabetes duration affect the extrinsic fibrinolytic system in type I diabetic patients but microangiopathy does not. 313

In diseases associated with thrombotic or thromboembolic complications, a reduction in the fibrinolytic potential may contribute to the risk to develop thrombosis. To investigate whether juvenile cerebral infarction is associated with a permanent defect of the fibrinolytic system we measured the main components of the fibrinolytic system, tissue plasminogen activator (t-PA) and its fast acting inhibitor (PAI) in plasma samples of 21 patients (aged 21-44 years) 3-24 months after the acute event. The data obtained were compared to those from thirteen healthy young volunteers (22-46 years). A direct effect of known risk factors on the fibrinolytic system could be excluded because patients avoided their risk factors immediately after the ischemic cerebral attack. Hypertension and the combination of oral contraceptives and smoking had been the most striking original risk factors. Levels of t-PA antigen and t-PA activity before and after venous occlusion, or PAI activity were not different between patients and controls suggesting that at least a permanent decrease in the activity of the fibrinolytic system does not exist in these patients. However, our findings do not exclude that a temporary defect in fibrinolysis might have contributed to the acute onset of the thrombotic cerebral event possibly induced by the risk factors originally present.
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PMID:[Persistent changes in tissue-type plasminogen activator and plasminogen activator inhibitor fibrinolytic parameters in patients following juvenile ischemic cerebral infarct]. 314 88

Greater understanding of the underlying pathophysiology of acute myocardial infarction (AMI) has led to more aggressive management and lower mortality, both in-hospital and long term. AMI results mainly from thrombotic occlusion of the infarct-related coronary artery. The ensuing necrosis evolves over a 6-12 h period providing a time window for interventions designed to reduce eventual infarct size. The most appropriate interventions are those which restore coronary artery patency and hence myocardial blood flow as soon as possible. Occasionally, disruption of the occluding thrombus and compression of the underlying atheromatous lesion is best achieved by direct percutaneous transluminal coronary angioplasty. For the vast majority however, revascularisation by drug therapy is more appropriate. As soon as possible, all patients without contraindications should be offered oral aspirin and intravenous thrombolysis, usually with streptokinase but occasionally with tissue plasminogen activator. Patients in whom these agents are contraindicated should be considered for intravenous beta-blockade using atenolol or metoprolol to reduce myocardial demand and hence infarct size. Patients with large infarcts, impaired ventricular function, left ventricular failure or hypertension should be considered for early angiotensin-converting enzyme inhibitor therapy. Other agents may be valuable symptomatically, but have no proven role in reducing infarct size or mortality. After the first 24 h, the main aims of management are to assess the likelihood of later ischaemic events or death (risk stratification) and hence to choose appropriate long term secondary prophylaxis.
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PMID:The management of acute myocardial infarction. 876 16

A review of the literature on cerebral vasospasm after aneurysmal subarachnoid haemorrhage (SAH) has shown that angiographic vasospasm occurs in 67.3% of cases when angiography is timed for the highest likelihood, and delayed ischaemic deficit or symptomatic vasospasm in 32.6%. The presence of vasospasm has a marked effect on overall outcome of SAH, and the outcome of delayed ischaemia itself is in about one-third death and in one-third permanent deficit. Management with fluid loading or induced hypertension and with calcium antagonists has been reported widely for both prevention and treatment, and can reduce the incidence and improve the outcome of vasospasm. Other forms of treatment including tissue plasminogen activator, aminosteroids and transluminal angioplasty also appear useful. In spite of these improved therapeutic possibilities, large numbers of patients are still being reported in whom no specific treatment is used.
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PMID:Cerebral arterial spasm--a clinical review. 754 61

Among endothelial secretogogues prostacyclin (PGI2), nitric oxide (NO) and tissue plasminogen activator (t-PA) play a crucial role in maintaining thromboresistance, tone and structure of the vascular wall. Most receptor agonists, such as B2 kinin receptor agonists, or shear force produce a coupled release of all three secretogogues, and therefore interactions between them are to be expected. Essentially, PGI2 is a platelet suppressant, NO a vasodilator and t-PA a fibrinolytic agent. These and other properties of endothelial secretogogues supplement each other in protecting the cardiovascular system from injuries. It is not surprising that disturbances of the secretory function of endothelial cells are associated with atherosclerosis, diabetes, thrombosis or hypertension. Traditionally, PGI2, NO, t-PA or their substitutes are used individually for the treatment of peripheral arterial disease, angina pectoris or acute myocardial infarction. In light of recent findings, their joint administration can be advocated. For instance, NO donors will potentiate platelet-suppressant action of PGI2 analogues, whereas exogenous PGI2 or TXA2 synthase inhibitors (i.e. following increase in endogenous PGI2) will abolish a paradox of prothrombotic action of t-PA or streptokinase. The replacement therapy with PGI2, NO or t-PA should match as closely as possible the physiologically coupled release of these secretogogues.
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PMID:Interactions between endothelial secretogogues. 754 32

Cerebrovascular disease is one of the major causes of morbidity and mortality in the developed world. A number of important risk factors have been identified with the occurrence of stroke, including advancing age, hypertension, smoking and diabetes mellitus, but the mechanisms that link these risk factors to the development of cerebrovascular disease are unclear. The pathogenesis of cerebrovascular disease includes syndromes of atherothrombotic brain infarction and intracerebral hemorrhage. The role of abnormalities of the coagulation and fibrinolytic systems in these processes has not been properly evaluated with regard to clinical outcome, although there is evidence that raised concentrations of fibrinogen are associated with an increased risk of stroke. Smaller studies have identified increases in FVIII/vWF in association with acute stroke and raised levels of tissue plasminogen activator. Although factor VII is considered a risk factor for coronary artery disease, little is known regarding its role in the development of cerebrovascular disease. Improved understanding of the pathogenesis of stroke and the potential to predict patients at risk of stroke should herald the beginning of new approaches in stroke management.
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PMID:Risk factors for cerebrovascular disease and the role of coagulation and fibrinolysis. 757 90


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