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

728 patients aged 50-75 years who had had Q-wave myocardial infarction 6-18 months previously were enrolled in a randomised, multicentre trial of low-dose heparin in prevention of reinfarction. The control group (365 patients) received their study centres' usual therapy; the heparin group (363 patients) also received subcutaneous calcium heparin (12,500 IU daily). Mean (SD) follow-up was 708 (265) days in the heparin group and 687 (251) in the control group. The reinfarction rate was 63% lower in the heparin than in the control group (4/303, 1.32% v 13/365, 3.56%). The difference in cumulative reinfarction rate between the groups was significant by both drug-efficacy (chi 2 = 3.99, p less than 0.05) and intention-to-treat analysis (chi 2 = 3.84, p = 0.05). Heparin treatment reduced the cumulative general mortality rates by 48% on drug-efficacy analysis (chi 2 = 3.88, p less than 0.05) and by 34% on intention-to-treat analysis (chi 2 = 2.05, not significant). Cardiovascular mortality was also reduced (33%) but not significantly. However, fatal events attributable to thromboembolism (fatal reinfarction, stroke, pulmonary embolism) were significantly less frequent in the heparin than in the control group (1 v 7, p less than 0.05). 60 patients (16.5%) discontinued heparin treatment, but only 23 patients (6.3%) stopped because of side-effects. Low-dose heparin appears to be effective, safe, well tolerated, and free from haemorrhagic risk for the prevention of myocardial reinfarction.
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PMID:Effectiveness of low-dose heparin in prevention of myocardial reinfarction. 288 39

We studied platelet function in whole blood, a situation that better reflects the in vivo state, from 85 patients with acute ischemic stroke and from 19 healthy controls. Patients receiving no antithrombotic drugs demonstrated increased platelet dense body secretion without an associated increase in platelet aggregation, thus raising the possibility that dense body secretion may be of separate importance in cerebral infarction. Our results also suggest that dense body secretion may occur independently of aggregation. Heparin and heparin plus warfarin were ineffective in reducing the high level of dense body secretion seen in acute cerebral infarction, whereas treatment with aspirin plus dipyridamole inhibited both dense body secretion and platelet aggregation. It seems worthwhile to investigate the usefulness of antiplatelet drugs in the treatment of acute ischemic stroke wherein clinical outcome is correlated with the extent of suppression of platelet dense body secretion.
Stroke 1989 Jan
PMID:Whole blood platelet function in acute ischemic stroke. Importance of dense body secretion and effects of antithrombotic agents. 291 33

Functional alterations in arterial acidic glycosaminoglycans (AGAG) may be related to the pathogenesis of some forms of cerebrovascular disease. We measured the AGAG, lipid and water content of human cerebral artery of 275 normal males at various ages. These measures were separately carried out in the main trunk and distal branches. The AGAG components were analyzed by an enzymatic assay method employing specific enzymes which digest AGAG to assess topographic change and aging variations. The total AGAG content was higher in the main cerebral artery than in the distal branches. The main AGAG component of the normal main cerebral artery was heparan sulfates (HS), constituting half the total AGAG, followed by moderate amounts of dermatan sulfate (DS), chondroitin-6-sulfate (C-6S) and chondroitin-4-sulfate (C-4S). Hyaluronic acid (HA) was a minor component and it was more prominent in young arteries. Heparin could be occasionally detected. With advancing age, the relative amounts of HS, HA, chondroitin and C-4S both in the main trunk and distal branches decreased but those of DS and C-6S increased. The total lipid, cholesterol ester and triglyceride content was greater in the main trunk than in the distal branches; the total lipid content increased with age. A possible function of the cerebral arterial AGAG is discussed with respect to change in lipid and water content according to topographic sites and aging.
Stroke
PMID:Distribution of acidic glycosaminoglycans, lipids and water in normal human cerebral arteries at various ages. 402 82

Heparin-associated thrombocytopenia is a relatively common complication of heparin therapy occurring in approximately 5% of the patients who receive this drug. The incidence is higher with bovine heparin then with porcine heparin. Onset of heparin-associated thrombocytopenia usually occurs 6 to 12 days after initiation of treatment and by itself has a low morbidity. Heparin-associated thrombocytopenia plus arterial thrombosis can cause major complications including stroke, heart attack, and death. The incidence of heparin-associated thrombocytopenia plus arterial thrombosis is lower than that for heparin-associated thrombocytopenia alone. The diagnosis of heparin-associated thrombocytopenia remains one of exclusion, but testing for the presence of a heparin-dependent platelet-aggregating factor may prove to be useful. Analysis of the time of onset suggests a strategy for prevention. Oral anticoagulants could be started concomitantly with the heparin so that it could be discontinued in several days. This approach may prevent most episodes of heparin-associated thrombocytopenia.
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PMID:Heparin-associated thrombocytopenia. 636 79

Thrombus formation depends on adherence of blood-formed elements to the intimal surface through platelet-vessel surface interaction, platelet release phenomena and aggregation, formation of fibrin, and the enmeshing of blood cells. Arterial thrombi involve platelet aggregation, whereas venous thrombi found in low flow or during stasis have greater proportions of erythrocytes and fibrin. It is not known if or how abnormalities of flow resistance, platelet thrombus formation, or endothelial and dynamic parameters affect the microcirculation, largely due to the difficulty of obtaining comprehensive data from these systems. Increases of fibrinogen observed in many disorders may result in minor changes in blood viscosity without known physiologic consequence, but in most disorders in which thrombosis is observed, the pathophysiologic mechanisms are multifactorial and abnormal blood viscosity is presumed to be a significant but not limiting component. Therapeutic approaches in thrombotic disorders should recognize which elements of the thrombotic triad predominate. In arterial disorders focus should be on platelet activity, and the objectives of venous thrombosis treatment include prevention of morbidity and death from pulmonary embolism, reduction of morbidity resulting from the acute thrombotic episode, and prevention of the postphlebitic syndrome. Pathology, mechanism, and treatment for specific thrombogenic disorders are described. Treatments suggested for hyperviscosity involve giving antibiotics during crises. Also discussed are thalassemia, paroxysomal nocturnal hemoglobinuria, polycythemia, cryoglobulinemia, paraproteinemia, diabetes mellitus, and disseminated intravascular coagulation. Studies have established a relationship between thromboembolic disease and oral contraceptives (OCs). The risk is only increased while the patient is taking OCs but is compounded in women undergoing surgery or who have a disorder which predisposes to venous disease. The risk for myocardial infarction or stroke is significantly increased when OCs are taken over age 35 and when there is hypertension, smoking, type-II hyperlipoproteinemia, and diabetes mellitus. The risk appears to be a function of estrogen dosage, causing a 25% mean increase in calf venous volume and 30% decrease in vein velocity of venous blood compared to controls. Low flow rates may contribute to venous thromboembolism. OCs may alter precisely regulated systems of coagulation and fibrinolysis and recent studies confirm abnormalities in the hemostatic system attributed to OCs. 16% of women taking OCs have a 60% or greater reduction in antithrombin III activity. The multiple effects of OCs often result in low-grade activation of the hemostatic system, potentially lowering the threshold to precipitate thrombus formation and possibly explaining the increased incidence of thromboembolic disease. Heparin appears to reverse many of these problems.
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PMID:Blood viscosity and thrombosis: clinical considerations. 676 12

Adequate management of a patient with progressing stroke should include the following. (1) Understanding of the pathophysiologic mechanisms causing cerebral infarction. (2) prompt diagnosis. When the possibility of progressing stroke is considered by the physician, it automatically becomes the priority diagnosis. (3) Prompt clinical and laboratory evaluation should be initiated. (4) Prompt institution of anticoagulant treatment unless contraindicated is appropriate. Heparin followed by coumadin is used most commonly. (5) If there is not prompt cessation of progression over the next 1--3 hr (following adequate anticoagulation), the patient should have a repeat CAT scan, and in many instances, a carotid angiogram to investigate the possibility of misdiagnosis or that an ulcerated atherosclerotic plaque is present releasing emboli not affected by anticoagulation. (6) If any progression occurs, the question of antiedema treatment should be raised.
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PMID:Treatment of progressing stroke. 737 45

This is a critical review of the role of heparin in the acute phase of ischemic cerebral vascular accident (CVA). Completed clinical trials lead to the following conclusions: 1. The efficacy of heparin in the acute phase of CVA is unknown, given the many biases and methodological imprecisions contained in the studies performed so far, among them a reliance on temporal rather than etiological classification of infarctions and the small number of patients treated. 2. Heparin-related complications have been explored only anecdotally and retrospectively, even though the risk of hemorrhage would depend on the magnitude of the prolongation of PTTa. The severity of neurological deficit, infarction size and patient age, on the other hand, would be contributing factors. 3. Delay in start of heparin therapy based on the severity of clinical symptoms is not supported by the evidence. There are prospective studies, on the other hand, that indicate a lack of correlation between early instauration of heparin therapy and the appearance of complications in severe stroke. 4. PTTa must be controlled carefully in the heparinized patient and administration of the drug in continuous perfusion or by subcutaneous injection is recommended.
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PMID:[Critical analysis of early heparin therapy in cerebral ischemic infarction]. 757 34

New technology has made it possible to identify cardiogenic cerebral emboli more easily and reliably. In recent years echocardiography, and in particular transesophageal echocardiography, has become the gold standard for the identification of cardiogenic sources of emboli, whereas transcranial Doppler is an important technique for the detection of cerebral emboli. Treatment strategies are better established and more accurate, if more complex, since the completion of large randomized trials. For primary prevention of stroke in elderly patients with nonvalvular atrial fibrillation, warfarin is generally indicated, yet in patients aged 60-75 years with no risk factors, aspirin may be sufficient. Warfarin is hazardous in older high-risk patients even at the 'low intensity' of the anticoagulation regimen; even lower doses are therefore being tested. Heparin and aspirin are indicated for short-term treatment of acute myocardial infarction, whereas for long-term treatment aspirin is still the drug of choice. However, if mobile left ventricular thrombi are present, warfarin is superior and new studies have shown its effectiveness for all myocardial infarction survivors. Combined treatment of warfarin and aspirin appears to be most effective in patients with mechanical prosthetic valves.
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PMID:Cardiogenic cerebral emboli: diagnosis and treatment. 774 16

The question of whether or not to reverse heparin following carotid endarterectomy is a topic of debate. The potential reduction of the risk of thrombosis at the endarterectomy site with non-reversal has to be measured against a potential increase in the risk of wound haematoma. This study prospectively followed activated clotting time (ACT) of 42 consecutive patients undergoing carotid endarterectomy. A standard heparin dose of 100 units/kg was used, and heparin reversal was employed only if the wound appeared excessively haemorrhagic at the procedure's completion. Heparin was reversed in 11 patients. Following heparin administration, ACT increased to a mean 2.72 +/- 0.09 times baseline (range 1.84-4.07), and fell with time, until at 3 h after heparin administration mean ACT in the non-reversed patients was 1.48 +/- 0.03 times baseline (range 1.1-2.03). There was one postoperative neurological event (2%), a contralateral hemisphere stroke. No patient developed a frank wound haematoma requiring evacuation, although three patients (7% of the total study group, 9% of patients not receiving heparin reversal) developed neck swelling and symptoms of airway compromise, and were intubated. Measurements of ACT suggest that a heparin dose of 100 units/kg achieves an adequate anticoagulant level in the operative and early postoperative phase, when thrombosis is most likely to occur, and is not associated with an increased risk of wound haematoma. If heparin is to be selectively reversed in patients felt to be at high risk of postoperative haematoma, the decision should be based on an objective measurement such as ACT, and not the surgeon's impression of wound haemostasis.
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PMID:Peri-operative anticoagulant effects of heparinization for carotid endarterectomy. 794 64

In the natural history of patients with peripheral obliterative arterial disease (POAD) the prognosis of the complaint "intermittent claudication" is relatively good and the amputation rate is presently only about 3%. However, POAD patients carry a high risk of cardiovascular events and their cumultative mortality rate within 10 years is as high as 40-50%. Atherothrombotic events in the coronary and, less frequently, cerebral arteries are by far the first cause of death and disability in these patients. The rationale for antithrombotic drugs in the treatment of POAD lies in the pivotal role of platelet activation and thrombin formation in the evolution of the atherothrombotic lesions, but also in the effect of some of these drugs on the regulation of microcirculatory responses. In acute thrombotic arterial occlusion, Heparin is the "first application" drug, especially in support of interventional revascularisation procedures. Regional thrombolysis often coupled with angioplasty (PTA), or systemic thrombolysis, are effective in revascularisation of especially infrainguinal-supra popliteal occlusions. However, controlled clinical trials are needed. In chronic POAD, intermittent claudication can be improved with a rational walking exercise programme, but, besides pentoxyphilline, especially ticlopidine significantly adds to the benefits of exercise. Regarding districtual progression of atherothrombosis and especially cardiovascular events, both aspirin and ticlopidine have been shown effective in single studies or meta-analyses. In a recent observational study of pooled data the cumulative endpoint including myocardial infarction, stroke and vascular death was reduced by 25 +/- 10% in the generality of patients treated with antiplatelet drugs. Finally, in critical limbs ischemia (CLI), some prostanoid compounds as Iloprost and Prostaglandin E1 favourably influence rest pain and ulcer healing, but less evidence is available on their effects on hard events as amputation and death. In conclusion, following the general indication to "be conservative" in the treatment of these patients, it seems clear that antithrombotic drugs have become by far a key medication in all different phases of POAD.
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PMID:Antithrombotic drugs in peripheral obliterative arterial diseases. 795 59


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