Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

AT III activity and concentration were measured in 36 patients (mean age 65.5 yrs, range 43-77 yrs) with ischaemic stroke within maximally 48 h of the acute event. In 12 patients (= 33%) AT III activity was reduced below 18.4 IU/ml: 50% of these patients showed normal and 50% reduced AT III concentration of less than 22 mg/dl. In 15 patients AT III activity and concentration were measured in the acute phase on admission to hospital and 12 months later. In the acute phase, AT III activity was reduced when compared with AT III concentration (y = 0.19 chi + 15.5) and did not correlate with the latter. 12 months later, however, AT III activity and concentration correlated significantly (r = 0.92; p less than 0.001) and the regression line was steeper (y = 0.8 chi). During the acute phase of ischaemic stroke, intravascular coagulation is evidently increased and inactive AT III-thrombin complexes are formed, whereby the concentration of active AT III decreases. A patient with progressive stroke and reduced AT III activity of 14.2 IU/ml was therefore substituted with AT III concentrate. The further neurological course was favourable.
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PMID:Antithrombin III deficiency in ischaemic stroke. 687 91

Purified human and bovine thrombin produced comparable tonic contractions in isolated canine basilar arteries. The magnitude of the contractions was closely related to the number of thrombin Units studied rather than to the amount of protein added to the isolation bath. Thrombin had a much slower onset of action, but was more potent in generating sustained contractions than either serotonin or prostaglandin F2 alpha. Moreover, in contrast to serotonin and prostaglandin F2 alpha, the contractions caused by thrombin were not terminated by equivalent washing. The thrombin-induced contractions were significantly inhibited by prostacyclin, meclofenamic acid, phenoxybenzamine and glycerol. Prostacyclin was the most potent of these inhibitors. The results suggest that thrombin in a "free" form may cause vasoconstriction, in addition to platelet aggregation, in hemostasis and could contribute to the genesis of cerebral vasospasm associated with subarachnoid hemorrhage.
Stroke
PMID:Cerebral arterial contractions induced by human and bovine thrombin. 699 61

The purpose of this study was to clarify differences in coagulation and fibrinolytic activation between the various subtypes and phases of ischaemic stroke. Haemostatic activation markers were measured in 52 patients with cardioembolic stroke, 32 with atherothrombotic stroke and 54 with lacunar stroke and compared with 23 age-matched controls. Data were obtained in the acute (< or = 7 days after onset), subacute (8-28 days) and chronic (> or = 29 days) phases of stroke. In patients with cardioembolic stroke, D-dimer and alpha 2-antiplasmin-plasmin complex levels were higher during the acute and subacute phases, while thrombin-antithrombin III complex levels were higher during the acute phase than in patients with lacunar stroke and controls. In cardioembolic stroke, fibrinopeptide A was increased during the acute and subacute phases, thrombin-antithrombin III complexes were higher during the subacute phase and D-dimer levels were higher during the chronic phase. Protein C activity was lower during the acute phase than in atherothrombotic stroke, lacunar stroke and controls. Protein C antigen was lower during the acute phase than in lacunar stroke and controls and during the chronic phase than in lacunar stroke. In contrast, only D-dimer levels were higher in atherothrombotic stroke patients than controls during the acute and chronic phases and no significant alterations in these markers were observed in the patients with lacunar stroke. These findings suggest that measurement of molecular markers of coagulation and fibrinolysis may be useful for detecting intracardiac thrombin and plasmin generation in patients with cardioembolic stroke.
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PMID:Alterations of haemostatic markers in various subtypes and phases of stroke. 750 62

The aim of the present study was to determine whether the level of plasma atrial natriuretic peptide (ANP), an indicator of atrial stretching, correlates with the formation of a thrombus in the left atrium during cardioembolic stroke with atrial fibrillation. Plasma concentrations of immunoreactive ANP and thrombin-antithrombin III complex (TAT) were measured in five age-matched groups including: 16 patients with acute cardioembolic stroke and atrial fibrillation (group 1), 26 patients with chronic cardioembolic stroke and atrial fibrillation (group 2), 27 patients with atrial fibrillation without previous stroke (group 3), 21 patients with acute lacunar stroke (group 4), and 27 healthy controls. The plasma ANP levels were higher in group 1, regardless of the stage, than those estimated at chronic stage in group 4 and in healthy controls. There were no stage-related differences between groups 1, 2 and 3. Plasma levels of ANP in group 2, a high risk group of cardioembolic stroke, were higher than in group 3, a low risk group. There was no correlation between plasma levels of ANP and mean blood pressure, pulse rate or plasma levels of TAT in any group. These results indicate that the determination of plasma ANP concentration is useful to distinguish a high risk patient from a low risk patient and also a cardioembolic stroke patient from a lacunar stroke patient. They also underscore the difficulties in recognizing left atrial thrombus formation by determining the plasma ANP concentration in cardioembolic stroke.
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PMID:Plasma concentrations of atrial natriuretic peptide in cardioembolic stroke with atrial fibrillation. 756 67

Antiplatelet therapy has become a useful means of preventing acute thromboembolic artery occlusions in cardiovascular diseases. The rationale for this is an enhanced activity of circulating platelets and release of platelet-derived vasoactive mediators, probably due to endothelial dysfunction. This review discusses the current status of 4 major classes of antiplatelet compounds: (i) aspirin and related drugs active via cyclo-oxygenase product formation; (ii) thienopyridines (ticlopidine and clopidogrel); (iii) direct thrombin inhibitors (e.g. hirudin); and (iv) GPIIb/IIIa receptor antagonists [e.g. abciximab (c7E3 Fab)]. It is concluded that aspirin is the drug of choice for long term oral treatment, specifically for secondary prevention of myocardial infarction, and is also a suitable basic but not maximally efficient drug in percutaneous transluminal coronary angioplasty (PTCA) and platelet activation during clot lysis. Ticlopidine has a similar indication and may be superior to aspirin in prevention of ischaemic stroke and peripheral arterial occlusion. Direct thrombin inhibitors and glycoprotein GPIIb/IIIa receptor antagonists need further investigation in clinical trials. To date, these compounds have a higher bleeding risk and currently they are available only for short term parenteral application. They are superior to aspirin in acute platelet-dependent ischaemic syndromes, such as unstable angina, and in connection with therapeutic PTCA because of their high potency in preventing platelet-dependent reocclusion. Future developments include more selective thromboxane inhibitors, i.e. combined-mode agents; nonpeptide clot-specific thrombin inhibitors with longer lasting action and nonpeptide fibrinogen receptor antagonists.
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PMID:Antiplatelet drugs. A comparative review. 758 91

The relevance of coagulation abnormalities in ischemic stroke remains uncertain. The purpose of this study was to identify abnormal patterns of coagulation in established ischemic stroke. We measured coagulation parameters in 86 patients with acute ischemic stroke: 10 lacunar, 55 atherothrombotic and 21 cardioembolic. Statistical comparisons were made between different stroke groups and between all stroke patients and 60 healthy controls. A decrease in functional antithrombin III and plasminogen and an increase in thrombin-antithrombin III complexes, total protein S, tissue plasminogen activator, plasminogen activator inhibitor and D-dimer were observed in the stroke group (p < 0.05). A positive correlation was found between tissue plasminogen activator and thrombin-antithrombin III levels in cardioembolic stroke (p < 0.05). Protein C levels showed significant differences between the three groups, and in the cardioembolic group they were lower than in controls (p < 0.05). Antiphospholipid antibodies were positive in two cases. We conclude that activation of coagulation and fibrinolytic pathways was observed during the acute phase of ischemic stroke. Protein C activity is different in the three types of strokes analyzed, and higher levels seem to be associated with lacunar lesions. Antiphospholipid antibodies do not seem to play an important role in the pathogenesis of stroke in a nonselected population.
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PMID:Hemostatic disturbances in acute ischemic stroke: a study of 86 patients. 765 7

We investigated in rats fed a purified diet for 2 and 4 months whether wine drinking was associated with the rebound effect on thrombin-induced platelet aggregation observed after alcohol withdrawal. With 6% ethanol drinking or its equivalent in red or white wine, platelet aggregation was reduced similarly by 70% when the animals drank the alcoholic beverages up to the venipuncture. Depriving the rats of alcoholic beverages for 18 hours was associated with an increase in the platelet response of 124% in those receiving 6% ethanol, of 46% with white wine but a decrease of 59% in those with red wine. The protective effect of red wine on platelets could be reproduced by tannins (procyanidins) extracted from grape seeds or red wine and added to 6% ethanol, but not by glycerol or wine without alcohol. That was related to inhibition of the alcohol-induced lipid peroxidation as shown by the lowering of conjugated dienes, lipid peroxides, and the increase in vitamin E in plasma. Owing to tannins, the platelets of rats drinking red wine did not exhibit the rebound effect observed hours after alcohol drinking, eventually associated with sudden death and stroke in humans.
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PMID:Platelet rebound effect of alcohol withdrawal and wine drinking in rats. Relation to tannins and lipid peroxidation. 774 10

Intracerebral hemorrhagic transformation is one of the most important complications of thrombolytic therapy for acute ischemic stroke. The relationship between changes in markers for the coagulation and fibrinolytic systems and occurrence of hemorrhagic transformation was determined after local intra-arterial thrombolytic therapy using urokinase (UK) (24 patients) or recombinant tissue plasminogen activator (t-PA) (10 patients) within 6 hours of onset. All 34 patients had no hypodensity areas on initial computed tomography scans. Plasma concentrations of fibrinogen-fibrin degradation products (FDP), fibrinogen, alpha 2-plasmin inhibitor (alpha 2-PI), plasmin-alpha 2 plasmin inhibitor complex (PIC), thrombin-antithrombin III complex (TAT), and D-dimer were measured. Hemorrhagic transformation occurred in seven patients (21%) with complete or partial recanalization; four in the UK group and three in the t-PA group. Doses of the thrombolytic agents did not correlate with the incidence of hemorrhagic transformation. The FDP levels in the hemorrhagic transformation group treated with UK significantly increased immediately and 1 hour after the therapy. The alpha 2-PI activities decreased and PIC levels increased in both the hemorrhagic transformation and the nonhemorrhagic groups after the therapy. The TAT levels in both groups tended to be higher than the normal range, but there was no significant difference from the pretreatment levels. The D-dimer levels in the hemorrhagic transformation group were higher than those in the nonhemorrhagic group at 24 hours after the therapy. Furthermore, the D-dimer levels were significantly higher in patients with complete recanalization compared with those with none or partial recanalization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in coagulation and fibrinolytic system after local intra-arterial thrombolysis for acute ischemic stroke. 777 Jan 6

To determine the prevalence of the factor V Leiden gene mutation in relation to the phenotypes of cerebral infarction and cerebral hemorrhage, we studied 386 randomly selected cases of acute stroke and 247 control subjects. Factor V genotype was determined by amplification of a 267-bp sequence of exon/intron 10 of the factor V gene. Levels of prothrombin fragment F(1 + 2), a marker of thrombin generation, were determined in both acute and convalescent stroke and related to factor V genotype. Prothrombin fragment F(1 + 2) was assessed by using an enzyme-linked immunosorbent assay. Sixteen stroke cases (4.1%) were identified as having the mutation compared with 14 (5.6%) control subjects. Prothrombin fragment F(1 + 2) levels were estimated in 191 cases and found to be elevated both acutely and after 3 months, but they were not related to factor V genotype. Prothrombin fragment F(1 + 2) is elevated in acute stroke and requires further evaluation in relation to cerebrovascular disease. These results suggest that the factor V Leiden gene mutation is not a risk factor for arterial thrombosis causing stroke.
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PMID:Factor V Leiden gene mutation and thrombin generation in relation to the development of acute stroke. 777 34

General recognition of the thrombotic component in ischaemic heart disease (IHD) is comparatively recent. Despite the obvious role of platelets, it has in many ways--and certainly epidemiologically--been work on the coagulation system that has been more rewarding in characterising those at high risk of IHD on account of haemostatic abnormalities. Raised plasma fibrinogen levels are clearly and independently associated with the onset of both clinically manifest IHD and stroke and probably with lower extremity arterial disease as well. High fibrinogen levels also increase recurrence rates and the progression of these conditions. High factor VII activity levels are associated with increased mortality from IHD but not with non-fatal episodes. Low fibrinolytic activity and raised factor VIII levels are also associated with increased IHD incidence. High fibrinogen levels predispose to thrombosis by effects on viscosity, platelet aggregability, fibrin deposition and the atherogenic process. There is increasing evidence that raised factor VII activity levels lead to increased thrombin production. Associations of several personal characteristics--notably smoking in the case of fibrinogen and dietary fat intake in the case of factor VII activity--influence the coagulation system in ways that are likely to predispose to thrombosis. Besides well known agents such as aspirin and anticoagulants, increasing attention ought now to be given to the antithrombotic potential of fibrinogen-lowering agents.
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PMID:Haemostatic function and arterial disease. 780 29


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