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

Lupus anticoagulants (LAs) are immunoglobulins which prolong 1 or more of the in vitro phospholipid-dependent tests of coagulation (e.g., activated partial thromboplastin time [APTT], dilute Russell viper venom time [dRVVT], kaolin clotting time [KCT], and textarin time [TT]). Paradoxically, patients with LAs rarely experience hemorrhagic problems. Approximately 1/3 of individuals with LAs experience thromboembolic complications such as stroke, deep vein thrombosis, and pulmonary emboli. LAs are members of the antiphospholipid antibody (APA) family. The APA family includes: LAs, anticardiolipin antibodies (ACAs), and reagin (the antibody responsible for the positive serologic test for syphilis). In approximately 60% of the patients, a LA and an ACA will both be present. The diagnosis of LAs requires an organized approach. Careful preparation of platelet poor plasma (PPP) is essential to assure maximum detection of LA. In order to rule out LAs, it is necessary to perform at least 2 screening tests (e.g., APTT, dRVVT). Additional steps in the diagnosis of LAs include mixing studies to identify the presence of an inhibitor and confirmatory procedures to demonstrate phospholipid-dependence of the inhibitor. It is also important to rule out any other potential coagulopathies which may account for the prolonged screening studies.
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PMID:Lupus anticoagulants: diagnostic dilemma and clinical challenge. 1016 22

The International Normalized Ratio (INR) system was introduced a decade ago as a way of standardizing the results of prothrombin time testing for patients taking oral anticoagulants. A strong emphasis has been placed upon using thromboplastin reagents that are very sensitive to the effects of oral anticoagulants upon the prothrombin time [i.e. reagents with low International Sensitivity Index (ISI)]. In order to assess how well the INR system functions as currently used in clinical laboratories, we compared the INRs determined using thromboplastins of differing ISIs in samples collected during a large clinical trial of oral anticoagulation for atrial fibrillation (Stroke Prevention in Atrial Fibrillation III trial). Frozen plasma was subjected to prothrombin time testing using thromboplastins with ISIs ranging from 0.97 to 2.49. INRs were calculated using machine-specific ISIs and Westgard's rules were followed to maintain quality control. An unanticipated coagulometer failure allowed a determination of the effect of machine recalibration upon the INR of control plasmas. The correlation between each pair of INRs obtained from 1181 plasmas was high (> 0.9), but the differences between reagents were statistically different from zero (P<0.001 for pairwise comparisons). Plasmas had INRs within the therapeutic range (2.0-3.0) with one reagent but not with another in an average of 20% of instances. Among the 20% discordant pairings, 43% (8.5% of the total tested) showed a difference in INR of more than 0.2 INR units above or below the target range. Low ISI thromboplastins did not perform better in this pairwise comparison than other reagents or the locally determined INR. Recalibration of a coagulometer resulted in a significant change in the INRs obtained from control plasmas (P<0.0001), which confirms and extends the observations of other authors concerning the sensitivity of the INR to coagulometer-related variables. There was a clinically significant difference in the INRs obtained with different thromboplastins, and low ISI reagents did not perform better than others. Since the risk of thrombosis rises sharply below the lower limit of the currently recommended target ranges, consideration should be given to narrowing the recommended range, or advising clinicians to aim for its mid-point. These findings illustrate the difficulties in imposing standardization upon coagulation testing after a test is in widespread use.
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PMID:Clinically significant differences in the International Normalized Ratio measured with reagents of different sensitivities. SPAF Investigators. Stroke Prevention in Atrial Fibrillation. 1045 11

During an 8-year period, 32 consecutive patients with chronic renal failure on maintenance hemodialysis were diagnosed to have cerebral hemorrhage. The outcome was determined using the activity of daily life (ADL) at 6 months after hemorrhage. The overall mortality was 64%. Of the 12 surviving patients, no one made a good recovery (back to normality), 5 recovered to ADL grade II, 4 to grade III, 1 to grade IV, and 2 to grade V. Up to 91% of the patients had a history of hypertension. On admission, Glasgow coma scale (GCS) was 15 in 8 cases, 8-14 in 10, and below 8 in 14. The poor prognostic factors showing statistical significance included a poor admission GCS, age above 65 years, and blood sugar level of more than 200 mg/dl. Other factors which apparently were not related to the outcome included sex, history of stroke, acute myocardial infarction, hypertension, and diabetes mellitus, the locations of hemorrhage, the duration of hemodialysis, treatment modality (surgery vs non-surgery), and the laboratory data (blood urea nitrogen, creatinine, platelet count, hemoglobin, prothromin time, and partial thromboplastin time). This study confirmed a poor prognosis for hemodialysis patients with cerebral hemorrhage. More attention should be paid to the control of blood sugar in this group to improve the outcome of cerebral hemorrhage in hemodialysis patients, especially in elderly patients with poor admission GCS.
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PMID:Prognosis of spontaneous intracerebral hemorrhage in hemodialysis patients. 1051 65

Physicians face a therapeutic dilemma in patients with acute hemorrhagic stroke requiring long-term, high-intensity anticoagulants because this treatment increases the risk of intracranial hemorrhage (ICH) 8- to 11-fold. We retrospectively studied 15 patients with ICH which occurred under anticoagulation with phenprocoumon, with an international norrmalized ratio (INR) of 2.5-6.5 on admission. Hemispheric, thalamic, cerebellar, intraventricular, or subarachnoid hemorrhage without aneurysm occurred. Absolute indications for anticoagulation were double, mitral, or aortic valve replacement, combined mitral valve failure with atrial fibrillation and atrial enlargement, internal carotid artery-jugular vein graft, frequently recurring deep vein thrombosis with risk of pulmonary embolism, and severe nontreatable ischemic heart disease. As soon as the diagnosis of ICH was established, INR normalization was attempted in all patients by administration of prothrombin complex, fresh frozen plasma, or vitamin K. After giving phenprocoumon antagonists (and neurosurgical therapy in four patients) heparin administration was started. Nine patients received full-dose intravenous and six low-dose subcutaneous heparin. The following observations were made: (a) All patients with effective, full-dose heparin treatment with a 1.5- to 2-fold elevation in partial thromboplastin time after normalization of the INR were discharged without complication. (b) Three of four of the patients with only incomplete correction of the INR (> 1.35) experienced relevant rebleeding within 3 days (all patients with an INR higher than 1.5), two of whom were on full-dose heparin. (c) Three of seven of the patients with normalized INR and without significant PTT elevation developed severe cerebral embolism. Although our data are based on a retrospective analysis, they support treatment with intravenous heparin (partial thromboplastin time 1.5-2 times baseline value) after normalization of the INR in patients with an ICH and an urgent need for anticoagulation.
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PMID:Managing the therapeutic dilemma: patients with spontaneous intracerebral hemorrhage and urgent need for anticoagulation. 1078 17

Particulate matter air pollution (PM) has been associated with morbidity and mortality from ischemic heart disease and stroke in humans. It has been hypothesized that alveolar inflammation, resulting from exposure to PM, may induce a state of blood hypercoagulability, triggering cardiovascular events in susceptible individuals. Previous studies in our laboratory have demonstrated acute lung injury with alveolar inflammation in rats following exposure to residual oil fly ash (ROFA), an emission source particulate. In addition, increased mortality has been documented following exposure to ROFA in rats with preexistent cardiopulmonary disease. ROFA's toxicity derives from its soluble metal content, which appears also to drive the toxicity of ambient PM. The present study was conducted to test the hypothesis that exposure of rats to a toxic PM, like ROFA, would adversely alter hemostatic parameters and cardiovascular risk factors thought to be involved in human epidemiologic findings. Sixty-day-old male Sprague-Dawley rats were exposed by intratracheal instillation (IT) to varying doses (0.3, 1. 7, or 8.3 mg/kg) of ROFA, 8.3 mg/kg Mt. Saint Helen's volcanic ash (MSH, control particle), or 0.3 ml saline (SAL, control). At 24 h post-IT, activated partial thromboplastin time (APTT), prothrombin time (PT), plasma fibrinogen (PF), plasma viscosity (PV), and complete blood count (CBC) were performed on venous blood samples. No differences from control were detected in APTT and PT in ROFA-exposed rats; however, ROFA exposure did result in elevated PF, at 8.3 mg/kg only. In addition, PV values were elevated in both ROFA and MSH-exposed rats relative to SAL-control rats, but not significantly. Although no changes were detected in APTT and PT, alteration of important hematologic parameters (notably fibrinogen) through PM induction of an inflammatory response may serve as biomarkers of cardiovascular risk in susceptible individuals.
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PMID:Oil fly ash-induced elevation of plasma fibrinogen levels in rats. 1086 47

A 15-year-old woman with a history of transient dysarthria two years before, suddenly developed weakness of right upper extremity, right facial palsy, and dysarthria. She was admitted to our hospital on the third day. She had no hypertension, heart murmur and oedema. On neurological examination, she had mild right hemiparesis including face muscles and mild dysarthria. The right knee jerk was brisk with no Babinski's sign. Ataxia and sensory disturbance were not present. T2-weighted MRI showed a hyperintensity at the posterior limb of the left internal capsule. Cerebral angiography was unremarkable. Ultracardiography and 24-hour electrocardiography were normal. Laboratory data revealed no inflammatory findings, liver dysfunction, hyperglycemia and hyperlipidemia. Antinuclear and anticardiolipin antibodies were negative. Prothrombin time was normal, but activated partial thromboplastin time was slightly prolonged (35.4 sec, normal 25.2-34.4). Protein C, protein S and antithrombin III were normal. Heparin cofactor II (HC II) activity was decreased (44%) with normal HC II antigen (79%) and so she was diagnosed as heparin cofactor II deficiency type II (heparin cofactor II abnormality). Her father manifesting thromboangitis obliterans also had low HC II activity with normal HC II antigen. However, on her genetic analysis, we didn't detect any mutations in the coding region of HC II gene. Until now she has no recurrence of cerebrovascular attacks. On the basis of these results, we suspect that HC II deficiency was a possible risk factor of cerebral infarction in this case because she was so young and had no general risk factors except for HC II. No stroke associated with HC II deficiency type II has been reported up to date. This case is worth considering etiologies of juvenile cerebral infarction.
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PMID:[Juvenile cerebral infarction associated with heparin cofactor II abnormality. A case report]. 1096 62

In the United States, there are approximately 217,000 patients with deep-vein thrombosis hospitalized each year. The cause for these thrombotic events include surgery, trauma, malignancy, hereditary thrombotic disorders, stroke, spinal cord injury, and idiopathic. Frequently, a number of these patients are cared for in rehabilitation units or centers to improve their functional status. This rehabilitation process is often interrupted with the development of deep vein thrombosis and or pulmonary embolism. These patients are placed on bedrest and, often, are transferred to an acute care hospital to receive continuous infusion unfractionated heparin with a targeted activated partial thromboplastin time of 1.5-2.5 times the baseline value and warfarin to achieve an international normalized ratio of 2-3. Recently, the low-molecular-weight heparins have been shown to be as or more effective than unfractionated heparin, have less major bleeding complications, and do not require laboratory monitoring of coagulation tests to adjust medications. The purpose of this article is to review the efficacy and safety of low-molecular-weight heparins and provide physiatrists with a rationale approach for managing patients with deep vein thrombosis and or pulmonary embolism on their respective units.
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PMID:Low-molecular-weight heparins versus unfractionated heparin in the treatment of deep vein thrombosis and pulmonary embolism. 1099 98

The life-span of stroke-prone spontaneously hypertensive rats (SHRSP) has been reported to become shorter by ingestion of some vegetable oils, including rapeseed oil, when given as the sole dietary fat. The present study was undertaken to examine if the ingestion of rapeseed (canola) oil affects blood coagulating time and erythrocyte membranes. Namely, SHRSP were orally given canola oil or soybean oil as the only dietary fat (10% of diet) for 4 weeks. After the 4-week feeding, activated partial thromboplastin time (APTT) in the canola oil group (19.9+/-0.5 s, N=8) was significantly shorter than that in the soybean oil group (21.6+/-0.6 s, N=8, P<0. 05), though there were no between-group differences in plasma Ca(2+), platelet density and platelet aggregation. Erythrocytes from the canola oil group were less tolerant to low osmotic pressure than those from soybean oil group; the EC(50) values for NaCl concentration to cause hemolysis were 0.42+/-0.004 and 0.40+/-0.005% in the canola oil and the soybean oil groups, respectively (N=10, P<0.01). The canola oil-induced shortening of blood coagulation time and increased fragility in erythrocyte membranes may have relevance to the promotion of strokes in SHRSP.
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PMID:Blood coagulation and osmolar tolerance of erythrocytes in stroke-prone spontaneously hypertensive rats given rapeseed oil or soybean oil as the only dietary fat. 1099 82

This paper aimed to investigate the effect of lumbrokinase on the anticoagulation and fibrinolysis in treating cerebral infarction. Lumbrokinase was used in patients with cerebral infarction. Patients were randomly divided into treatment group (n = 31) and control group (n = 20). Single blind method was used in this investigation. The Chinese stroke score was used to evaluate the results of treatment before and after administration of lumbrokinase. Kaolin partial thromboplastin time (KPTT), prothrombin time (PT), fibrinogen content, vWF content were analyzed, and tissue plasminogen activator (t-PA) activity, plasminogen activator inhibitor (PAI) activity, D-dimer level were assayed. In both groups, the stroke score decreased after administration, but in the treatment group, it was more obvious. In the treatment group, KPTT was prolonged, t-PA activity and D-dimer level increased, while the content of fibrinogen decreased significantly. There were no significant changes of PT and PAI activity in both groups. It is concluded that lumbrokinase is beneficial to the treatment of cerebral infarction. The effect of lumbrokinase is related to the inhibition of intrinsic coagulation pathway and the activation of fibrinolysis via an increase of t-PA activity.
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PMID:Changes in coagulation and tissue plasminogen activator after the treatment of cerebral infarction with lumbrokinase. 1132 42

The authors hypothesized that divergent influences of the APOE epsilon4 allele on ischemic and hemorrhagic stroke survival might result from differences in coagulation profiles. In 49 hemorrhagic stroke patients, epsilon4 carriers had higher partial thromboplastin time ratios (p < 0.01) than non-epsilon4 carriers. Among 529 ischemic stroke patients, increasing epsilon4 allele dose was associated with improved survival (p = 0.03) after adjusting for baseline NIH stroke scale (p = 0.00001) and partial thromboplastin time ratio (p = 0.01). Relative anticoagulation does not fully explain the survival advantage in epsilon4-carrying ischemic stroke patients.
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PMID:Apolipoprotein E genotype, coagulation, and survival following acute stroke. 1157 42


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