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

The relationship between haemostatic factors and recurrent cardiovascular events was investigated in patients enrolled with acute coronary syndrome (acute non-Q myocardial infarction or unstable angina pectoris). One hundred and fifteen patients, aged 64 +/- 10 years, were included in the study. Haemostatic parameters [prothrombin time, activities of factor VII, factor VIII, factor X, antithrombin (AT) and protein C (PC), and concentrations of free protein S, fibrinogen, D-dimer, prothrombin fragment 1+2, and thrombin-antithrombin complex] were measured four times: within 48 h of hospitalization, at discharge (days 5-8), at 3 months and after 1 year. Screening for factor V Leiden mutation was also performed. Patients were followed for cardiovascular endpoints (new or refractory unstable angina pectoris, non-fatal myocardial infarction, stroke, or death) for an average of 555 days. Of all patients, 35 had an endpoint during the follow-up ("endpoint" group) and 80 patients did not ("no endpoint" group). Analysing the whole follow-up period, PC (P < 0.01) and AT (P < 0.01) were lower in the "endpoint" than in the "no endpoint" group. With 50% percentiles at enrollment, the odds ratio for getting an endpoint in the low (cut-off value < 100%) versus high PC group was 2.72 (95% confidence interval, 1.18-6.29; P < 0.05). Lower levels of AT (P < 0.05) and PC (P < 0.05) during the whole follow-up were associated with a shorter event-free time. In conclusion, lower PC and AT values, even within the normal range, seem to be associated with elevated risk for recurrent cardiovascular events and shorter event-free time in acute coronary syndrome patients.
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PMID:Low normal level of protein C or of antithrombin increases risk for recurrent cardiovascular events. 1587 May 47

There is current interest in the associations of circulating inflammatory markers (C-reactive protein, fibrinogen, white cell count, albumin, erythrocyte sedimentation rate, the factor VIII:von Willebrand factor complex, the tissue plasminogen activator:plasminogen activator inhibitor type 1 complex, fibrin D-dimer) not only with prognosis in acute coronary syndromes and acute stroke, but also in prediction of cardiovascular events in the general population. Recent meta-analyses of long-term prospective studies have established their associations with coronary heart disease (CHD) events, which may be cause, consequence or coincidence. These markers are also associated in epidemiologic studies of general populations with many cardiovascular risk factors (which may confound their associations with CHD risk), and also with asymptomatic arterial disease (of which they be consequences: 'reverse causality'). The causality of their associations with cardiovascular events is questioned by their lack of specificity for risk of cardiovascular events; and by the lack of association of their functional genotypes with CHD in 'Mendelian randomized trials'. Hence, proof of causality awaits testing in randomized-controlled trials of long-term selective reduction by future agents. Markers are of little additional predictive value to current cardiovascular risk scores, and it is premature to advocate their use in screening for cardiovascular risk prior to careful evaluation of costs, risks, and benefits.
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PMID:Circulating inflammatory markers and risks of cardiovascular and non-cardiovascular disease. 1610 27

A 4-year-old boy was admitted with left hemiplegia. Thrombophilia marker examination resulted with factor V Leiden mutation heterozygosity, a deficiency of antithrombin III and a high level of factor VIII. Cranial computed tomography scan revealed an ischemic infarct in the region of right anterior cerebral artery. In the literature, combinations of multiple thrombophilia risk factors that trigger cerebral ischemic stroke in children have been emphasized. To our knowledge, this is the first child with these combinations of thrombophilia risk factors and ischemic stroke to be reported in the literature.
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PMID:Factor V Leiden mutation, deficiency of antithrombin III and elevation of factor VIII in a child with ischemic stroke: a case report. 1664 63

Several hematologic disorders and hemostatic defects increase risk of ischemic stroke. A common feature of these disorders is the creation of a prothrombotic state, now commonly referred to as "hypercoagulable state." Hematologic diseases such as essential thrombocythemia, polycythemia vera, and thrombotic thrombocytopenic purpura clearly cause stroke. Effective treatment is now available for these disorders. Association of hemostatic defects with stroke risk is still at the investigational stage. Although a number of factors such as soluble thrombomodulin, fibrinogen, factor VIII, von Willebrand factor, and plasminogen activator inhibitor-1 are associated with stroke risk, their predictive values remain unknown. Furthermore, causal relationship has not been established.
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PMID:Hypercoagulable states and strokes. 1682 99

The pathomechanism of acute complications of atheromatosis, i.e. arterial thrombosis, still remains unclear. Conventional cardiovascular risk factors can explain only about 50% of cases of arterial thrombosis. The activation of intrinsic and extrinsic pathways of the coagulation system on damaged atherosclerotic plaque is one of the most important mechanisms. The role of clotting factors in the development of arterial thrombosis is also considered. From among a few clotting factors (V, VIII, XIII), factor VIII arouses interest due to the well-known observation that the morbidity for cardiovascular reasons is less among hemophiliacs than in the general population. A high factor VIII level predicts the occurrence of episodes of venous thromboses, but its role in the pathogenesis of arterial thromboses is still unclear. In clinical studies, a high factor VIII level predicts episodes of stroke, myocardial infarct, and acute lower-limb ischemia over a short period of observation. A high factor VIII level may the cause of about 5% of all episodes of arterial thrombosis. The reasons for elevated factor VIII levels in some persons remain unclear. Although heritability can play an important role, the influence of other factors (e.g. activation of the sympathetic nervous system) has been reported. The pathomechanism is the subject of investigation as well. An explanation for the occurrence of severe complications of arterial thrombosis in patients without significant risk factors may result in the development of methods of detection and prevention.
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PMID:[Factor VIII and the risk of arterial thrombosis]. 1719 1

Superior sagittal sinus thrombosis (SSST) is associated with a variety of hypercoaguable states. Although coagulation disturbances are reported in hyperthyroidism, a direct link between hyperthyroidism and cerebral venous thrombosis is not established. We report a 39-year-old man who developed increased intracranial pressure, seizures, and rapid atrial fibrillation. Neuroimaging showed SSST, and laboratory studies were consistent with hyperthyroidism. No other causes of a hypercoaguable state were identified. Prompt treatment of his hyperthyroidism led to recanalization of the superior sagittal sinus and a full neurological recovery. Given the known effects of hyperthyroidism on factor VIII activity, we hypothesize that hyperthyroidism is an independent risk factor for SSST. A high index of suspicion for SSST is warranted in patients with hyperthyroidism and neurological symptoms. Furthermore, thyroid dysfunction should be excluded in patients with unexplained SSST.
J Stroke Cerebrovasc Dis
PMID:Superior sagittal sinus thrombosis secondary to hyperthyroidism. 1789 4

Risk factors of children with arterial ischemic stroke were retrospectively evaluated. The children were grouped according to values on developing diagnostic tools: 13 in the old era (1987-1994) and 18 in the new era (1995-2004). The old era battery included 5 tests: protein C, protein S, antithrombin, lupus anticoagulants, and anticardiolipin antibodies. The new era battery added 5 more tests: homocystine level, factor VIII level, mutations for factor V Leiden and prothrombin G20210A, and lipoprotein (a) level. At least 1 risk factor was found in 5 of 13 children (38.5%) in the old era and in 8 of 18 (44.4%) in the new era. The extended battery for prothrombotic disorders revealed 7 risk factors in 4 children (22.2%) in the new era, whereas the limited battery identified a single risk factor in 1 child (7.7%) in the old era. For the correct etiologic identification, prothrombotic risk factors should be extensively evaluated in patients with arterial ischemic stroke.
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PMID:Arterial ischemic stroke in childhood: risk factors and outcome in old versus new era. 1794 Feb 47

Atrial fibrillation (AF) is a common cardiac arrhythmia with a 5-20% annual risk of stroke. Warfarin reduces this risk by at least 60%. Despite adequate anticoagulation within the target International Normalized Ratio (INR) range of 2.0-3.0, some patients still experience thrombotic and bleeding events. It is now possible to assess the intensity of anticoagulation with automated thrombin generation (TG) tests, such as the calibrated automated thrombogram (CAT). These tests were compared and an inverse relationship was found between the INR and CAT in 143 elderly AF patients. There was equally good correlation between the concentration of factors II, VII, IX and X and the INR and TG parameters. The peak thrombin was most strongly associated with the concentration of prothrombin fragment 1 + 2 in plasma. There was wide variability in TG parameters in patients with identical INR values, sometimes up to a fourfold difference. This TG variability in individuals with the same INR is not due to inflammation, at least when the latter is measured as the concentration of factor VIII coagulant activity, von Willebrand factor antigen, high sensitivity C-reactive protein and fibrinogen. It was concluded that, although the TG and INR were closely correlated there was wide variability in peak thrombin and endogenous thrombin potential in patients within the INR therapeutic range, the cause of which remains unclear.
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PMID:Wide variation in thrombin generation in patients with atrial fibrillation and therapeutic International Normalized Ratio is not due to inflammation. 1857 10

The aim of the authors is to examine the relationship between the cytokine levels that are thought to be involved in stroke etiopathogenesis (tumor necrosis factor [TNF]-alpha, interleukin [IL]-2, IL-6, IL-8, IL-11), soluble protein C receptor (sEPCR), and factor VIII (FVIII) levels. The study included 27 patients with stroke and 30 healthy controls, aged 0 to 18. In the comparison of the sEPCR, cytokine, and FVIII levels between patient and control groups, median levels of TNF-alpha, IL-2, IL-6, and IL-8 are found to be high in the patient group when compared with controls, whereas there is no difference in sEPCR, IL-11, and FVIII levels. In the patient group, a positive correlation is seen between TNF-alpha levels and IL-2 and IL-6 levels, between IL-2 and IL-6 levels, and between IL-6 and IL-8 levels, whereas a negative relationship is seen between sEPCR and FVIII. In the control group apart from the patient group, a negative relationship is seen between TNF-alpha and FVIII, whereas there is a positive relationship between IL-11 and sEPCR levels. Median sEPCR levels in patients who have normal or low FVIII levels are significantly high when compared with those with high FVIII levels. In conclusion, in the pediatric population, an increase in TNF-alpha, IL-2, IL-6, and IL-8 levels is seen. Also, an inverse relationship of sEPCR and FVIII levels is shown for the first time. This study provides a basis for ongoing studies that aim to clarify stroke etiopathogenesis. Studies with larger series of patients are warranted to confirm this hypothesis.
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PMID:The relation between cytokines, soluble endothelial protein C receptor, and factor VIII levels in Turkish pediatric stroke patients. 1859 Nov 80

In a 12-member, 3-generation kindred with conjoint inheritance of G1691A factor V Leiden (FVL) and G20210A prothrombin gene (PTG) mutations, identified through a proband with amaurosis fugax and his father with nonarteritic ischemic optic neuropathy (NAION), the authors' hypothesis was that ocular thrombosis was a diagnostic window to familial thrombophilia-thrombosis. The authors used polymerase chain reaction (PCR) measures for thrombophilia (FVL, PTG, C677T-A1298C methylenetetrahydrofolate reductase [MTHFR], platelet glycoprotein PLA1A2) and hypofibrinolysis (plasminogen activator inhibitor-1 4G4G). The 39-year-old white male proband, with amaurosis fugax and transient ischemic attacks (TIA), was found to be a compound heterozygote for FVL and PTG mutations. His symptoms resolved only after coumadin. His 44-year-old brother (deep venous thrombosis [DVT]) and 46-year-old sister (DVT, pulmonary embolus [PE]) were compound FVL-PTG gene heterozygotes. Of 4 asymptomatic children born to these 3 siblings, 2 were FVL heterozygotes and 2 PTG heterozygotes. The proband's 69-year-old father, with NAION and ischemic stroke, had PTG heterozygosity, familial high factor VIII, and compound MTHFR C677T-A1298C mutation with homocysteinemia. The proband's 61-year-old aunt had PTG heterozygosity, recurrent DVT, and mesenteric artery thrombosis. The proband's 67-year-old mother, free of thrombotic events, was a FVL heterozygote, had high factor VIII, and PAI-1 4G4G homozygosity. In this extended kindred, ocular thrombotic events (amaurosis fugax, NAION) were associated with variegated thrombotic events, including TIA, ischemic stroke, DVT, PE, and mesenteric artery thrombosis, and opened a diagnostic window to family screening and treatment for complex thrombophilias, which had previously been undiagnosed.
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PMID:Ocular vascular thrombotic events: a diagnostic window to familial thrombophilia (compound factor V Leiden and prothrombin gene heterozygosity) and thrombosis. 1879 59


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