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

Oral anticoagulant therapy is effective antithrombotic treatment for several indications. The results of prothrombin time monitoring should be reported as the International Normalized Ratio (INR). An INR of 2 to 3 is the recommended therapeutic range for all indications except for the prevention of systemic embolism in patients with mechanical heart valves and for the long-term treatment of patients with myocardial infarction, for whom an INR range of 2.5 to 3.5 is recommended. Oral anticoagulant therapy with warfarin sodium is the preferred approach for preventing stroke in most patients with atrial fibrillation. The available data suggest that warfarin is more effective than aspirin. Aspirin, 325 mg/d, is indicated for patients in whom warfarin is contraindicated or in patients less than 75 years of age who are at low risk for stroke because risk factors are absent. In patients 75 years of age or more, close monitoring of warfarin treatment is prudent to avoid major bleeding due to poor anticoagulant control. In selected patients, patient-self-monitoring and adjustment of warfarin treatment using a portable prothrombin time monitor may be effective and safe.
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PMID:Oral anticoagulant therapy. 937 2

Postmenopausal hormone replacement therapy is associated with a reduction in the incidence of coronary heart disease. However, inconclusive results have been reported with respect to the risk of stroke, and recent studies consistently showed an increased risk of venous thromboembolism in postmenopausal women using oral estrogen. There are surprisingly few interventional studies to assess the true effects of estrogen-progestin regimens on blood coagulation and fibrinolysis, and the impact of the route of estrogen administration on hemostasis has not been well documented. Therefore, we investigated the effects of oral and transdermal estradiol/progesterone replacement therapy on hemostatic variables. Forty-five healthy postmenopausal women, aged 45 to 64 years, were assigned randomly to one of the three following groups: cyclic oral or transdermal estradiol, both combined with progesterone, or no hormonal treatment. Hemostatic variables were assayed at baseline and after a 6-month period. Pairwise differences in the mean change between the three groups were compared using nonparametric tests. Oral but not transdermal estradiol regimen significantly increased the mean value of prothrombin activation peptide (F1 + 2) and decreased mean antithrombin activity compared with no treatment. Differences in fragment F1 + 2 levels between active treatments were significant. The oral estrogen group was associated with a significant decrease in both mean tissue-type plasminogen (t-PA) concentration and plasminogen activator inhibitor (PAI-1) activity and a significant rise in global fibrinolytic capacity (GFC) compared with the two other groups. A transdermal estrogen regimen had no significant effect on PAI-1, t-PA, and GFC levels. There were no significant changes in mean values of fibrinogen, factor VII, von Willebrand factor, protein C, fibrin D-dimer, and plasminogen between and within the three groups. We conclude that oral estrogen/progesterone replacement therapy may result in coagulation activation and increased fibrinolytic potential, whereas opposed transdermal estrogen appears without any substantial effects on hemostasis. Whereas these results may account for an increased risk of venous thromboembolism in users of oral postmenopausal estrogen, they emphasize the potential importance of the route of estrogen administration in prescribing hormone replacement therapy to postmenopausal women, especially to those at high risk of thrombotic disease.
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PMID:Effects of oral and transdermal estrogen/progesterone regimens on blood coagulation and fibrinolysis in postmenopausal women. A randomized controlled trial. 940 95

We analysed the results of coagulation studies in an unselected series of young adults with acute cerebral ischaemia. Our aims were (a) to determine the prevalence of coagulation disorders among these patients, (b) to investigate the relation between the presence of coagulation abnormalities and large vessel disease or potential sources of cardiac embolism and (c) to evaluate the occurrence of thrombotic events in patients with or without coagulation disorders. One hundred and twenty consecutively admitted patients (53 men, 67 women, median age 38 years, range 15-45) who presented with acute cerebral infarction (n = 89) or a transient ischaemic attack (n = 31) were evaluated. Diagnostic studies consisted of electrocardiography, echocardiography, duplex scanning, and/or angiography. Coagulation studies included activity tests of protein S, protein C, antithrombin, plasminogen, measurement of immunoglobulin G (IgG) anticardiolipin antibodies (ACLA), and a dilute prothrombin assay. Initially, 30 patients had increased ACLA titres and 28 had an abnormal dilute prothrombin assay, suggesting lupus anticoagulant. Decreased protein S, protein C and antithrombin activity were detected in 20, 3 and 3 patients, respectively, excluding patients in whom the abnormalities could be explained by the use of medication, by pregnancy or puerperium. We detected a decreased activity of plasminogen in 5 patients. The disorders could be confirmed by a second assessment in only 2 patients with a protein S deficiency, in none of the patients with a protein C or antithrombin deficiency and in 1 patient with plasminogen deficiency. However, the abnormalities persisted in 19 of 21 patients with increased anticardiolipin IgG titres and in 9 of 20 patients with lupus anticoagulant. A confirmed coagulation disorder was not associated with stroke type or vascular risk factors, but it was more common among patients with large vessel disease (odds ratio: 3.8, 95% confidence interval (CI): 1.1-12.8). Sixteen patients had a recurrent thromboembolic event, but the risk of recurrence was not increased among patients with a confirmed coagulation disorder. Our results suggest that idiopathic coagulation disorders are found in about a quarter of young stroke patients. They are difficult to predict and probably interact with other risk factors.
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PMID:Coagulation disorders in young adults with acute cerebral ischaemia. 945 24

In order to clarify the coagulation profile accompanying ischemic stroke, which may have implications on therapeutic strategies, we performed a prospective study to evaluate the hemostatic parameters in the first 24 h after the onset of cortical atherothrombotic infarct and lacunar infarction. Twenty-seven patients with cortical atherothrombotic infarction and 27 patients with lacunar infarction, diagnosed on clinical and CT-scan criteria, had blood samples taken within the first 24 h after onset of the stroke, and before anticoagulant treatment had been started. Levels of fibrinogen, von Willebrand factor, D-dimers, prothrombin factors 1 + 2, anti-thrombin III, and C-protein and S-proteins, were measured. Laboratory tests detected the following abnormalities: a protein C deficiency was observed in 1 case of cortical infarction and in 1 case of lacunar infarction; a decrease in S-protein was observed in 1 case of cortical infarction, and the presence of lupus anticoagulant in 4 cases (2 in cortical and 2 in lacunar infarction). Various degrees of coagulation activation were observed. Statistically significant activation of the coagulation was observed in the patients with cortical infarction, compared to normal patients adjusted for age: the levels of DDI were significantly raised (2298 +/- 2221 ng ml-1 vs. 750 +/- 400 ng ml-1) (p < 0.03) as were F1 + 2 levels (3.9 +/- 2.8 nmol l-1 vs. 1.5 +/- 0.9 nmol l-1). (p < 0.01). In the lacunar infarction group, there was a significant rise in F1 + 2 compared with normal patients adjusted for age (2.2 +/- 1.7 nmol l-1 vs. 1.5 +/- 0.9 nmol l-1) (p < 0.01), while the DDI level was in the normal range, when age was taken into account. In the cortical infarction group, we observed a significantly raised fibrinogen level (4.8 +/- 1.7 g l-1 vs. 3.7 +/- 1.0 g l-1) (p < 0.05) and von Willebrand factor level (271 +/- 104% vs. 178 +/- 103%) (p < 0.01) compared to the lacunar infarction group. In addition, we observed a significantly low level of S-protein in the cortical infarction group (105 +/- 29%) compared to the lacunar infarction group (127 +/- 28%) (p < 0.01). Confirmation of the role of enhanced thrombin activity in the pathogenesis of acute stroke may be an important determinant in its therapeutic management.
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PMID:Coagulation abnormalities in lacunar and cortical ischemic stroke are quite different. 947 Oct 97

Although stroke is a great public health challenge in Korea, there have have been few epidemiologic studies of the risk factors stroke. A case-control study was performed to evaluate the risk factors for hemorrhagic stroke in Wonju, Korea. Ninety-five subarachnoid hemorrhage (SAH) and 102 intracerebral hemorrhage (ICH) patients aged 21-86 years, and 267 controls were recruited among the inpatients of Wonju Christian Hospital during 1994-1995. Information was gathered through interview and examinations. After adjustment for age and sex, family and past history of hypertension, drinking habits, age of menarche, height, weight, body mass index, waist and hip circumference, earlobe crease, prothrombin time, white blood cell count, hemoglobin, and total cholesterol were all found to be significantly associated with both SAH and ICH. The risk factor significantly associated only with ICH was smoking habits. In multiple logistics analyses, the independent risk factors for SAH and ICH were the same. Those included family and past history of hypertension, age of menarche, earlobe crease, prothrombin time, white blood cell count, hemoglobin and total cholesterol. In general, the risk factors for SAH and ICH were similar with each other, except smoking habits. Risk factors found in this study congruent with previous studies were family and past history of hypertension, drinking habits, body mass index, prothrombin time, white blood cell count, and hemoglobin. Those incongruent or rather newly found were age of menarche, a big physique, earlobe crease, and total cholesterol.
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PMID:Risk factors for hemorrhagic stroke in Wonju, Korea. 966 27

The prevalence of the prothrombin gene variant (allele 20.210 A), factor V Leiden mutation, and homozygosity for transition 677C-->T in the methylenetetrahydrofolate reductase (MTHFR) gene was determined among patients with sickle cell disease (SCD). The group included 73 patients with median age of 32.3 years with a diagnosis of sickle cell anemia in 53 patients, hemoglobinopathy SC in 16 patients, and four with S/beta(0) thalassemia. Vascular complications such as ischemic stroke or deep vein thrombosis were diagnosed in nine patients. Heterozygosity for the prothrombin gene variant or factor V Leiden mutation was identified in four patients. However, only one patient, who developed ischemic stroke, was identified as a carrier of factor V Leiden mutation. None of the patients presented homozygosity for the thermolabile variant of the MTHFR. These data suggest a low clinical impact of inherited hypercoagulability risk factors in developing thrombosis, occlusive stroke, or mortality data among patients with SCD in Brazil.
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PMID:Prothrombin mutant, factor V Leiden, and thermolabile variant of methylenetetrahydrofolate reductase among patients with sickle cell disease in Brazil. 972 76

Antiphospholipid antibodies associated with the antiphospholipid syndrome (APS) have been shown to bind plasma proteins, particularly beta 2-glycoprotein I (beta2-GPI). In this study the incidence of antibodies to solid-phase prothrombin was examined in patients with antiphospholipid syndrome and a variety of other inflammatory disorders. Significantly elevated levels of IgG anti-prothrombin (anti-PT) antibodies were detected in 63% of patients with APS (n = 27, median 22 arbitrary units: AU), 33% with SLE (n = 92, median 14 AU). 45% with rheumatoid factor (n = 22, median 16 AU), 21% with carotid artery stenosis (n = 21, median 15 AU), 32% with stroke (n = 38, median 13 AU). 67% of patients with a false positive serology for syphilis (n = 21, median 24 AU), 37% with HIV (n = 30, median 14 AU), 29% with syphilis (n = 14, median 19 AU) and 3% with infectious mononucleosis (n= 30, median 9 AU). In addition, a group of lupus anticoagulant (LA) positive patients (n = 48) was examined for antibodies to prothrombin, beta2-GPI and cardiolipin. 10 (21%) patients had raised levels of IgG anti-PT antibodies, 30 (62%) had significantly elevated levels of anti-beta2-GPI antibodies and 15 (31%) had elevated levels of anticardiolipin antibodies (ACA). Of the LA-positive patients, 15 (43%) were identified with definite APS, eight (23%) with probable APS, two (6%) with possible APS and 10 (28%) patients had no clinical evidence of APS. In conclusion, antibodies to prothrombin were found in a variety of inflammatory disorders and were therefore not specific for the APS. However, identification of the plasma proteins recognized by antibodies from patients with APS may provide insight into the pathogenic mechanisms involved in the heterogenous clinical manifestations of the APS.
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PMID:Antibodies to prothrombin in antiphospholipid syndrome and inflammatory disorders. 973 36

The cardiovascular, coagulation and haematological effects of prothrombin activator from Tiger Snake (Notechis scutatus) venom were investigated in anaesthetized mechanically ventilated dogs. Infusion caused dose-related systemic hypotension, marked decreases in cardiac output and stroke volume, marked increases in pulmonary artery pressure, pulmonary artery occlusion pressure and pulmonary vascular resistance. Effects occurred within several minutes but abated over 30 to 40 minutes. Evidence of procoagulation included prolongation of prothrombin and partial thromboplastin times and depletion of serum fibrinogen. Thrombocytopenia and leucopenia occurred. All effects were prevented by prior administration of heparin but none by inhaled nitric oxide. Oesophageal echocardiography during infusion identified thrombi within the heart, right ventricular dilatation and dyskinesia. Electrocardiography suggested myocardial ischaemia. Pulmonary thromboemboli were identified histologically post mortem. Cardiovascular effects of the activator were not due to a variety of endogenous substances as indicated by use of antagonists to platelet activating factor and thromboxane A2 indomethacin, dexamethasone, serotonin, ketanserin, histamine, promethazine and ondansetron. Tiger Snake prothrombin activator causes bilateral ventricular failure by thrombotic obstruction of the pulmonary vasculature and possibly by coronary ischaemia.
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PMID:The cardiovascular, coagulation and haematological effects of tiger snake (Notechis scutatus) prothrombin activator and investigation of release of vasoactive substances. 980 10

Today, more than 40% of all patients who develop a thrombosis are found to have inherited thrombophilia. The most common cause of this is APC resistance, which can usually be traced back to factor V-Leiden. In the commonly heterozygous patients the risk of thrombosis is increased about 7-fold (life-long risk of thrombosis 10 to 15%). In most cases, however, additional thrombogenic stimuli are required (oral contraception, pregnancy, surgery, immobilization). In combination with oral contraceptives, the risk is increased roughly 30-fold. In contrast, APC resistance does not present an increased risk for thrombosis in the arterial system (myocardial infarction, stroke). Four further inherited or acquired disorders of the hemostatic system are known: prothrombin dimorphism, antithrombin, protein C and protein S deficiencies. Prothrombin dimorphism, the second most common form of inherited thrombophilia, has been known only for the past two years and elevates the risk of thrombosis only to a moderate degree. Today, a search for thrombophilic factors should be carried out not only in young patients with spontaneous development of thrombosis, but also in elderly patients, even when an additional risk for the occurrence of thrombosis such as traumatization or immobilization is present. Therapeutic consequences are discussed.
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PMID:[Thrombophilia caused by congenital disorders of blood coagulation]. 984 71

A genetic variation in the prothrombin gene is located in the 3-untranslated region at position 20210 where a G-->A transition occurs. The prevalence of the mutation is 1% to 2% in white populations, and the mutation is associated with an increased risk of venous thrombosis and myocardial infarction. We report the prevalence of the A allele in blacks at birth; in black control subjects with no history of heart attack, stroke, or blood clots; in black patients with venous thrombosis; and in black patients with myocardial infarction. Among 318 infants, the prevalence of the A allele was 0.2% (1 heterozygote), with an exact, one-sided upper 95% confidence limit of 0.7%. Among 185 control subjects the variant was absent, yielding an exact, one-sided upper 95% confidence limit of 0.8% for the A allele. The heterozygous genotype was found in 2 of 91 subjects with deep vein thrombosis and in none of 123 subjects with myocardial infarction. The very low prevalence of the A allele indicates that the prothrombin variant is not a major cause of venous thrombosis or myocardial infarction in blacks.
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PMID:Prevalence of the prothrombin 20210 G-to-A variant in blacks: infants, patients with venous thrombosis, patients with myocardial infarction, and control subjects. 985 30


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