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

Patients with atherosclerotic carotid artery stenosis commonly have arterial disease elsewhere, especially coronary artery disease. The aim of the medical treatment is to reduce the incidence of stroke, myocardial infarction and vascular death. Both primary and secondary prevention of these vascular events requires control of vascular risk factors, particularly lowering elevated blood pressure, lowering of elevated blood cholesterol and stopping smoking. Aspirin and ticlopidine are effective in reducing vascular events in patients with atherosclerosis, with a relative reduction of about 25% for the composite outcome event "stroke, myocardial infarction or vascular death". Whether low dose (less than 100 mg/d), medium (300 mg/d) or high dose (1,000 mg/d or more) of aspirin confer the same degree of protection against vascular events is unclear. The gastrointestinal side effects are greater for the high dose than for the medium dose, but the difference between the medium dose and the low dose is very small. Ticlopidine conveys a modest risk of reversible severe neutropenia and is often used as a second-line drug, but this is a controversial issue. Heparin is often used as a short-term preventive treatment in patients with transient ischaemic attacks or minor stroke, especially in those with "crescendo" transient ischaemic attacks, progressing stroke, severe carotid stenosis or intraluminal thrombus.
 ...
PMID:[Medical treatment of atherosclerotic carotid stenoses]. 815 33

Durable, covalently bonded, heparin-coated cardiopulmonary bypass (CPB) circuits with oxygenators have been developed. Proposed advantages of heparin-coated CPB circuits include improved biocompatibility and thromboresistance. The purpose of this study was to evaluate our experience with heparin-coated CPB circuits in 20 patients. Heparin was given to maintain an activated clotting time equal to or greater than 200 seconds, while flow rates were kept equal to or greater than 2 L/min. Indications for use of this circuit included recent stroke, posttraumatic injuries, recent gastrointestinal bleeding, protamine allergies, combined cardiac and noncardiac procedures, and ventricular assist. Mean heparin dosage was 0.50 +/- 0.18 mg/kg and protamine dosage was 57.14 +/- 39.36 mg. Postoperative blood loss and transfusion requirements were minimal. Postoperative complement levels of C3a and C5a were normal, suggesting excellent biocompatibility. There were no deaths or perioperative complications. Heparin-coated CPB circuits using a pump oxygenator can be used safely with low-dose heparin administration in select patients requiring CPB.
 ...
PMID:Safe use of heparin-coated bypass circuits incorporating a pump-oxygenator. 816 24

The need for improvements in materials and equipment for extracorporeal circulation has been obvious for years. Among the surfaces with biologically active compounds, those with heparin binding have been found sufficiently thromboresistant and particularly suitable for different types of artificial perfusion. Partial left heart bypass (LHBP) was performed in 10 anesthetized, acutely instrumented, and open-chested mongrel dogs (weight 23 to 50 kg) with a servo-controlled roller pump. The pump flow was maintained at 50 mL/kg/min for 6 hours. Heparin surface-coated equipment was used without additional heparin. For LHBP with a standard circuit, the total amount of heparin during the study period was (mean +/- SD) 487 +/- 124 IU/kg. The right atrial, pulmonary artery, and left ventricular end-diastolic pressures, cardiac output, left ventricular output, right and left ventricular stroke work, pulmonary gas exchange, and acid-base balance changed similarly with both systems. Blood loss (204 +/- 78 v 1,240 +/- 586 mL, P < 0.0005), volume substitution requirements (647 +/- 48 v 1,860 +/- 764 mL, P < 0.0025), and oxygen extraction ratio (mean 25.4 to 32.0 v 25.4 to 56.4%, P < 0.025) were significantly lower, and mean aortic pressure (mean 65 to 69 v 62 to 38 mmHg, P < 0.025) and hemoglobin concentration (mean 9.1 to 8.1 v 9.4 to 3.9 g/dL, P < 0.05) were significantly higher during 6 hours of LHBP without systemic heparinization. Low but stable oxygen delivery was provided with heparin-coated LHBP, whereas it showed a descending trend (mean 14.0 to 10.8 v 13.4 to 5.5 mL/kg/min, P < 0.1) with the standard circuit.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Assisted circulation without systemic heparinization. 820 9

Heparin-induced Extracorporeal LDL < total cholesterol, triglycerides, fibrinogen > Precipitation (H.E.L.P.) was applied in cases of acute thromboembolic stroke within 48 to 96 hours after onset. 42 patients had been randomized for the trial. In Group A 12 patients underwent a single H.E.L.P. application, while remaining 10 patients formed a control group. In group B 10 patients had 10 H.E.L.P. applications, the other 10 patients firmed as controls. Results of group A: 4 days after H.E.L.P. an improvement in the Mathew Scale and in the Mini Mental State Examination could be obtained (p < 0.05 each). 10 days after H.E.L.P. all the tests showed significant changes (p < 0.05 in the Mathew Scale and in the Mini Mental State Examination and p < 0.01 in the Activities-of-Daily-Living Score). Relatet to the controls there appeared a statistically significant difference 4 days after H.E.L.P. in the Mini Mental State Examination and in the Activities-of-Daily-Living Score (p < 0.05 each). At day 10 all the tests showed a difference to the controls (p < 0.05 in the Mathew Scale and p < 0.01 in the other tests). Results of group B 10: One day after 1st H.E.L.P. a statistically significant difference could be observed in all the tests (p < 0.05 in the Mathew Scale and the Mini Mental State Examination and p < 0.01 in the Activities-of-Daily-Living Score). At that time even a difference to the controls became visible (p < 0.05 in the Mathew scale, p < 0.01 in the other tests).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:First experience in application of heparin-induced extracorporeal LDL precipitation (H.E.L.P.) in acute thromboembolic stroke. 831 80

Risk factors, pathogenesis, clinical manifestations, diagnosis, and surgical and pharmacological treatment of ischemic stroke are reviewed. Risk factors play an important part in the pathogenesis of ischemic stroke. Knowledge of the complex metabolic and cellular changes that occur during ischemic stroke is rapidly growing. Choosing the correct treatment is dependent upon obtaining a thorough and accurate clinical assessment of the patient. Diagnostic tests help in determining the size, location, etiology, and characteristics of the lesion. Currently no single agent or mode of therapy appears to be most efficacious. Many drugs are still in the human clinical testing stage; promising agents include thrombolytics, low-molecular-weight heparin, and heparinoids. Hemodilution, pentoxifylline, epoprostenol, nimodipine, naloxone, and GM1 therapy have had mixed results in clinical trials, partly because some of these agents were not tested in enough patients to provide an accurate assessment of their efficacy. Atenolol and propranolol are ineffective. Ticlopidine and aspirin decrease the incidence of subsequent stroke but have not been tested in acute ischemic stroke. Heparin may be effective in preventing further cardioembolic stroke or in treating stroke in progress. Nondrug therapies include carotid endarterectomy and surgical decompression for cerebellar stroke. No single agent can be recommended for treatment of ischemic stroke at this time. Promising regimens include ancrod, low-molecular-weight heparin and heparinoids, or thrombolytics.
 ...
PMID:Pathophysiology and treatment of acute ischemic stroke. 831 20

A formal statistical overview of all truly randomised trials was undertaken to determine whether antithrombotic therapy is effective and safe in the early treatment of patients with acute stroke. There were 15 completed randomised controlled trials of the value of early antithrombotic treatment in patients with acute stroke. The regimes tested in acute presumed or confirmed ischaemic stroke were: heparin, 10 trials with 1047 patients: oral anticoagulants, one trial with 51 patients: antiplatelet therapy, three trials with 103 patients. Heparin was tested in one trial with 46 patients with acute haemorrhagic stroke. Outcome measures were deep venous thrombosis (confirmed by I125 scanning or venography), pulmonary embolism, death from all causes, haemorrhagic transformation of cerebral infarction, level of disability in survivors. In patients with acute ischaemic stroke, allocation to heparin was associated with a highly significant 81% (SD 8, 2p < 0.00001) reduction in deep venous thrombosis detected by I125 fibrinogen scanning or venogram. Only three trials systematically identified pulmonary emboli, which occurred in 6/106 (5.7%) allocated control vs 3/132 (2.3%) allocated heparin, a non-significant 58% reduction (SD 45.7, 2p > 0.1). There were relatively few deaths in the trials in patients with presumed ischaemic stroke: 94/485 (19.4%) among patients allocated to the control group vs 79/497 (15.9%) among patients who were allocated heparin. The observed 18% (SD 16) reduction in the odds of death was not statistically significant. The least biased estimated of the effect of treatment on haemorrhagic transformation of the cerebral infarct (HTI) comes from trials where all patients were scanned at the end of treatment, irrespective of clinical deterioration; using this analysis, haemorrhagic transformation occurred in 7/102 (6.9%) control vs 8/106 (7.5%) treated, a non-significant 12% increase (SD 56, 2p > 0.1). These data cannot exclude the possibility that heparin substantially increases the risks of HTI. No data on disability in survivors could be obtained. Early heparin treatment might be associated with substantial reductions in deep venous thrombosis (and probably also pulmonary embolism) and possibly a one fifth reduction in mortality (equivalent to the avoidance of 20-40 early deaths per thousand patients treated.) However, the data were wholly inadequate on safety, particularly on the risk of haemorrhagic transformation of the infarct and on the hazards of heparin therapy in patients with known intracerebral haemorrhage. The trials of oral anticoagulants (15 deaths among 57 patients) and antiplatelet therapy (two deaths among 103 patients) were too small to be informative. Much larger randomized trials-comparing aspirin, heparin and the combination of both drugs against control-in patients with acute ischaemic stroke are justified (and several are now planned or underway).
 ...
PMID:Antithrombotic therapy in acute ischaemic stroke: an overview of the completed randomised trials. 812 24

To evaluate the effects of the short-term, high-dose sodium heparin therapy on biochemical markers of bone metabolism, we studied 20 patients (11 males and 9 females) with pulmonary embolism, treated with sodium heparin (daily dose range: 40,000-45,000 I.U. by continuous i.v. infusion). Heparin therapy lasted 5-7 days, after which patients received warfarin over 12 months. Eleven patients (6 males and 5 females) with ischaemic stroke, treated with i.v. glycerol and pentoxifilline, were used as controls. Before and after therapy serum and urinary markers of bone metabolism were evaluated; in 12 heparin-treated pts., the parameters were also evaluated 4 months after discontinuation of warfarin therapy. After heparin therapy a significant reduction vs. basal value was observed in levels of serum osteocalcin (ng/ml;mean + SEM): 3.32 & 0.19 vs. 2.05 + 0.21; p < 0.001. In the 12 patients evaluated 4 months after discontinuation of warfarin therapy, serum osteocalcin levels returned to basal value: 3.41 + 0.12 ng/ml (p:n.s.). No significant changes of the examined parameters were observed in controls. In conclusion, our data seem to indicate an effect of i.v. short-term heparin therapy on bone metabolism. This effect seems to be characterized by an inhibition of osteoblast function as suggested by the reduction of serum osteocalcin levels.
 ...
PMID:Effects of short-term, high dose, heparin therapy on biochemical markers of bone metabolism. 860 85

The authors describe a patient with stroke, treated with heparin for unstable angina, whose clinical features mimicked those of thrombotic thrombocytopenic purpura (TTP). His condition eventually proved to be caused by heparin-induced thrombocytopenia (HIT), complicated by thrombosis (HITT). The absence of microangiopathic hemolytic anemia should question the diagnosis in a presumed TTP patient. Early diagnosis of HITT is possible since recently two highly sensitive and specific tests have become available. Heparin treatment has to be stopped immediately if HITT is diagnosed. First-choice antithrombotic treatment in HITT patients is danaparoid.
 ...
PMID:Heparin-induced thrombocytopenia with multiple cerebral infarctions simulating thrombotic thrombocytopenic purpura. A case report. 861 15

Physiological changes occurring during pregnancy and puerperium may increase the risk of stroke. However, the incidence rate of ischemic stroke is of 3.8 to 5 in 100,000 pregnancies, i.e. quite similar to that of ischemic strokes occurring in non pregnant women of child bearing age. Whereas eclampsia, choriocarcinoma and amniotic emboli occur only during pregnancy or puerperium, peripartum cardiomyopathy and benign cerebral angiopathy are less specific. All other causes of cerebral ischemia may also occur during pregnancy and puerperium. The management of an ischemic stroke should not differ between pregnant and non pregnant women of child bearing age. Strokes associated with pregnancy require a complete diagnostic work-up including angiography if necessary. Low doses of aspirin (60-80 mg/d) can be used after 3 months of pregnancy. Heparin is the anticoagulant of choice during pregnancy, but warfarin may be used between 13 and 36 weeks of gestation; heparin and warfarin can be used during breast feeding. There is no neurological reason to recommend a systematic use of cesarean section. Subsequent prescription of oral contraceptive therapy is not recommended except in patients with a definite cause of ischemic stroke which is not influenced by hormones.
 ...
PMID:Arterial ischemic strokes associated with pregnancy and puerperium. 910 39

Heparin is commonly, but by no means universally, used after acute myocardial infarction. When used the dose, route of administration, and duration of therapy varies considerably. The role of heparin is reviewed with particular reference to its use in conjunction with other commonly used therapies, such as aspirin and thrombolytic agents. Intravenous heparin after thrombolytic therapy remains untested in patients treated with aspirin. When used, benefit is seen in a narrow aPTT range, and there have been unexpected increases in mortality in patients with the greatest heparin effect. The addition of delayed subcutaneous heparin to aspirin and thrombolytic therapy does not provide a mortality benefit. In patients not treated with thrombolysis, there is no clear evidence that heparin confers significant mortality benefit if patients are treated with aspirin. Heparin therapy may reduce the incidence of intraventricular thrombus after anterior wall infarction, but there is no clear evidence that it reduces the clinically important sequelae of cerebral embolism and stroke. Given concerns about increased hemorrhagic rates with heparin and unknown benefit, it is reasonable to conclude that its role in the management of patients with acute myocardial infarction remains unclear.
 ...
PMID:Heparin after acute myocardial infarction. 914 Jun 86


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>