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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Available data indicate that cardiovascular disease has become the leading cause of death in American Indians. However, limited information is available on cardiovascular disease incidence, prevalence, and risk factors in this population. Reported cardiovascular disease rates vary greatly among groups in different geographic areas. These rates have been obtained from studies of varying sizes and different methodologies. The Strong Heart Study, which uses standardized methodology, is designed to estimate cardiovascular disease mortality and morbidity rates and the prevalence of known and suspected cardiovascular disease risk factors in American Indians. The study population consists of 12 tribes in three geographic areas: an area near Phoenix, Arizona, the southwestern area of Oklahoma, and the Aberdeen area of North and South Dakota. The study includes three components. The first is a mortality survey to estimate cardiovascular disease mortality rates for 1984-1988 among tribal members aged 35-74 years, and the second is a morbidity survey to estimate incidence of both first and first or recurrent hospitalized myocardial infarction and stroke (cerebrovascular disease) among tribal members aged 45-74 years in 1984-1988, and the third is a clinical examination of 4,500 tribal members aged 45-74 years in order to estimate the prevalence of cardiovascular disease and its associations with risk factors. Family history, diet, alcohol and tobacco consumption, physical activity, degree of acculturation, and socioeconomic status are assessed in personal interviews. The physical examination includes measurements of body fat, body circumferences, and blood pressure, an examination of the heart and lungs, an evaluation of peripheral vascular disease, and a 12-lead electrocardiogram. Laboratory measurements include fasting and postload glucose, insulin, fasting lipids, apoproteins, fibrinogen, and glycated hemoglobin. Also measured are serum and urine creatinine and urinary albumin. DNA from lymphocytes is isolated and stored for future genetic studies.
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PMID:The Strong Heart Study. A study of cardiovascular disease in American Indians: design and methods. 226 May 46

Evidence has accumulated over the past ten years to implicate elevated plasma fibrinogen levels in cardiovascular disorders such as ischaemic heart disease, stroke and peripheral vascular disease. At a cellular level, insight has been gained into the molecular regulation of fibrinogen biosynthesis and the mechanisms through which fibrinogen may be involved in these disease processes. Here, Nigel Cook and David Ubben summarize this evidence and consider the possibilities for novel therapies targeted at fibrinogen. A variety of structurally diverse pharmacological agents, many of which were developed for their effects on plasma lipids, have serendipitously been found to lower plasma fibrinogen levels.
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PMID:Fibrinogen as a major risk factor in cardiovascular disease. 226 68

Sixty-two patients were examined with the purpose of investigating the relationship between atherosclerotic and nonatherosclerotic risk factors and blood viscosity parameters. It was established that particularly large increases of hematocrit, hemoglobin and fibrinogen were observed in association of such risk factors as smoking and alcohol abuse. The importance of these factors for the development of ischemic stroke is discussed.
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PMID:[Relation of risk factors for the development of ischemic stroke and indices of blood viscosity]. 236 63

This double-blind pilot study observed the effects of a twenty-one day oral ticlopidine treatment (250 mg/twice daily) on the neurologic outcome and the hemorheologic pattern of 15 patients and 15 placebo-treated controls. Patients and controls (age range sixty-six to eighty-six years) were included in the study within twelve hours of the onset of ischemic stroke, confirmed clinically and by computerized tomography. Scores on Hachinski's Scale and the following hemorheologic parameters were monitored weekly for twenty-one days: fibrinogen levels, the whole blood, unfractionated white and red blood cell filterability rates (through 5-micron-pore-diameter filters using a constant-flow positive-pressure system), and the leukocyte count and activation (by microscopic observation). The results showed treatment with ticlopidine improved the neurologic outcome (Hachinski's Score +36%, p less than 0.03) slightly but significantly (p less than 0.001) increased the average values of the whole blood (+19%) and red cell (+17%) filterability rates and decreased fibrinogen levels (-17%).
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PMID:Effects of ticlopidine on the neurologic outcome and the hemorheologic pattern in the postacute phase of ischemic stroke: a pilot study. 238 31

The author studied the diagnostic possibilities of determination of the cerebral blood flow by means of blood viscosity parameters (fibrinogen and hematocrit) in 46 patients with ischemic stroke. It was found that this method allows to reveal the direction of hemodynamic changes in the cerebral vessels but it does not allow to assess the amount of blood entering the brain hemispheres.
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PMID:[The significance of the fibrinogen level and hematocrit for the quantitative determination of cerebral blood flow]. 239 89

Epidemiological observations indicate that high plasma fibrinogen levels are strongly correlated with the frequency of two major thrombotic complications of atherosclerosis, stroke and myocardial infarction. Thrombosis is increasingly recognized as a central mechanism in stroke and myocardial infarction, and fibrinogen is involved in events thought to play a major role in thrombosis. Therefore, elucidation of the relationship between fibrinogen and thrombosis may strengthen the predictive value of this protein and suggest new treatment to prevent stroke and myocardial infarction. The current data relating fibrinogen to thrombosis are not easy to reconcile with the available epidemiological observations. In addition, advances in understanding the atherogenic potential of several risk factors for coronary heart disease have used information on the measurement of the risk factors in population-based studies. Thus, measuring plasma fibrinogen to predict stroke and myocardial infarction may be important in gaining insight into the thrombogenic potential of this protein and in inspiring new strategies against the thrombotic complications of atherosclerosis.
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PMID:Measuring plasma fibrinogen to predict stroke and myocardial infarction. 240 90

Blood proteins could play a critical role in the pathogenesis of cerebral vasospasm in subarachnoid hemorrhage (SAH) as agonists and as antagonists of vasoconstriction. The present study was designed primarily to quantify the inhibition produced by antithrombin III of the phasic responses elicited by cumulative doses of KCl, serotonin (5-HT), uridine triphosphate (UTP), and thrombin in isolated canine basilar arteries, and to ascertain whether other proteins might act similarly. Antithrombin III (1 unit/ml and 3 units/ml) given 2 min beforehand inhibited all agonists. The inhibition was not dependent on a functional endothelium nor due to stimulation of the electrogenic sodium pump. Alpha2-macroglobulin (0.1 mg/ml and 0.4 mg/ml) inhibited the contractile responses to high K+, 5-HT and thrombin. Kallikrein (1 and 4 units/ml) did not inhibit UTP but inhibited high K+ and 5-HT through an effect on the endothelium. Kallikrein (1 unit/ml) irreversibly blocked the responses to thrombin. Globulins (3 mg/ml) and fibrinogen (0.3 mg/ml) were not inhibitory. The results demonstrate that anticoagulant proteins are very effective nonspecific inhibitors of the vasoconstriction, whereas the serine protease kallikrein selectively blocks thrombin. The remarkable potency of antithrombin III suggests that it may protect cerebral arteries from exhibiting vasospasm in SAH.
Stroke
PMID:Vasodilator proteins: role in delayed cerebral vasospasm. 242 60

Acute vascular events, and also chronic atherosclerotic vascular disease, are associated with a rise in blood level of several acute-phase reactants. Of these, fibrinogen is of particular rheological importance since hyperfibrinogenaemia causes hyperviscosity of plasma and whole blood and is an adverse prognostic factor in intermittent claudication, coronary artery disease, and stroke. Activation of the monocyte-macrophage system by fibrinogen degradation products, with release of interleukin-1 and secondary stimulation of liver and bone marrow, may be of pathogenic importance in the stress responses of acute and chronic vascular disease.
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PMID:Rheological importance of acute-phase reactants. 242 64

In a prospective study of the incidence of deep vein thrombosis (DVT) after stroke, and the prophylactic effect of dextran, 50 patients, admitted with a diagnosis of cerebral infarction with paresis of the lower extremity within the first 48 hours, were randomly allocated to treatment or non-treatment groups. The treatment group received 500 ml of dextran 40 on admission and on days 1 and 2, and 250 ml on days 4 and 6. Venesection was performed on admission and if necessary on day 1. The control group received no dextran or venesection. DVT was diagnosed with the 125I-fibrinogen test during the first ten days. The incidence of DVT was 54% in the treatment group and 50% in the control group. There were no statistically significant differences between the groups regarding number of DVTs needing treatment, number of positive scanning points or number of days for scan to become positive. Lethal pulmonary emboli occurred in one treated and in three control patients, respectively. Age and progress of neurologic symptoms predisposed for the development of DVT. The high incidence of DVT in stroke patients indicates the need for prophylactic routines.
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PMID:Venous thromboembolism after cerebral infarction and the prophylactic effect of dextran 40. 243 1

In a double-blind, randomised trial Org 10172 low-molecular-weight (LMW) heparinoid was compared with placebo in the prevention of deep-vein thrombosis in patients with acute thrombotic stroke. Prophylaxis was started within 7 days of the onset of stroke with a loading dose of 1000 anti-factor-Xa units intravenously followed by a fixed dose of 750 anti-factor-Xa units twice a day subcutaneously; it was continued for 14 days or until hospital discharge, if earlier. 50 patients were randomised to receive Org 10172 and 25 to receive placebo. All patients underwent surveillance with I125-fibrinogen leg scanning and impedance plethysmography. Venography was carried out if either test became positive. Venous thrombosis occurred in 2 of 50 patients (4.0%) given Org 10172 and 7 of 25 patients (28.0%) given placebo (p = 0.005); the corresponding rates of proximal-vein thrombosis were 0% and 16%, respectively (p = 0.01). There was one major haemorrhage in the Org 10172 group and one minor bleed in the placebo group.
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PMID:Double-blind randomised trial of Org 10172 low-molecular-weight heparinoid in prevention of deep-vein thrombosis in thrombotic stroke. 243 15


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