A Double-Blind Trial of Low Doses of Subcutaneous Heparin in the Prevention of Deep-Vein Thrombosis After Myocardial Infarction*1

Warlow, Charles; Terry, G; Kenmure, A. C. F.; Beattie, A. G.; Ogston, D.; Douglas, A.G.

doi:10.1016/s0140-6736(73)92597-x

Cited by 142 publications

(36 citation statements)

References 8 publications

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“…In patients with myocardial infarction, low-dose heparin has reduced the incidence of deep-vein thrombosis from about 25 to 4% [3][4][5][6]. In patients with acute stroke, the incidence of deep-vein thrombosis was reduced by lowdose heparin from about 70 to 20% [7][8][9][10], However, hemorrhage, local hematomas, al lergy and thrombocytopenia are the main side effects of heparin and may limit its therapeu tic use.…”

Section: Introductionmentioning

confidence: 99%

Subcutaneous Low-Molecular-Weight Heparin versus Standard Heparin and the Prevention of Thromboembolism in Medical Inpatients

Harenberg¹,

Roebruck

Heene³

1996

Pathophysiol Haemos Thromb

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In a multicenter, double-blind clinical trial in 1,968 inpatients 1 daily subcutaneous administration of LMW heparin plus 2 placebo injections or 3 × 5,000 IU unfractionated (UF) heparin was given for 10 (8-11) days. The primary end point was the incidence of proximal deep-vein thrombosis or pulmonary embolism. Patients were assessed during the study period for development of proximal deep-vein thrombosis by compression sonography at days 1 and 10 and for pulmonary embolism by scintigraphy in symptomatic patients. Aim of the study was to demonstrate the equivalence of both treatment regimens. A total of 1,968 patients were randomized to receive UF or LMW heparin. Of these, 378 patients were excluded during the study period, so that 780 patients on UF and 810 on LMW heparin were included in the efficacy analysis. Four primary end points were observed with UF and 6 with LMW heparin, demonstrating the equivalence of treatments (p = 0.012). Additionally, pulmonary embolism was suspected as the cause of death in 6 patients who died during the study (3 per treatment group). A higher frequency of death (n = 32) was observed in the LMW-heparin group (p = 0.02) particularly documented in a part of the centers. Safety analysis showed a higher frequency of local pruritus, local erythema and subcutaneous hematoma, a higher increase in plasma levels of triglycerides, total cholesterol, alanine aminotransferase and aspartate aminotransferase, and a decrease of antithrombin III in patients receiving UF heparin. A decrease in platelet count (values ranging between 40,000 and 80,000/μl) was observed in 4 patients with UF and in none with LMW heparin. No severe thrombocytopenia was observed. Subcutaneous LMW heparin is as effective as UF heparin for prophylaxis of thromboembolism in bedridden, hospitalized medical patients.

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Section: Introductionmentioning

confidence: 99%

Subcutaneous Low-Molecular-Weight Heparin versus Standard Heparin and the Prevention of Thromboembolism in Medical Inpatients

Harenberg¹,

Roebruck

Heene³

1996

Pathophysiol Haemos Thromb

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“…It is known that patients with arterial thromboses are at increased risk of venous thrombosis. [18][19][20][21] The etiology of the brainstem infarction, in the absence of past medical history of arterial thrombotic events, atherosclerosis or arrhythmias, was thought to be a venous thromboembolism that traversed the patent foramen ovale.…”

Section: Discussionmentioning

confidence: 99%

Successful anticoagulation with hirudin in a patient with mesenteric venous thrombosis and multiple coagulation abnormalities

Gordon

Beckman

2000

Vasc Med

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A case of multiple thrombotic diatheses discovered in the setting of mesenteric venous infarction is discussed. The patient had deficiencies of protein C, protein S, antithrombin III; was heterozygous for factor V Leiden; and had polycythemia vera. Adequate anticoagulation could not be established with heparin administration and hirudin was used. The diagnosis of mesenteric venous infarction, thrombotic tendency of multiple coagulation diatheses, and use of hirudin are discussed.

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“…1), and always in the paralysed leg; in fact, this stroke complication had first been described in 1810 by Ferriar [3], which reminded me of one of my favourite quotations, from Murphy, the first novel by Samuel Beckett: ‘The sun shone, having no alternative, on the nothing new’ [4]. Along the way I did my first randomised trial, of heparin to prevent DVT in acute myocardial infarction [5], and learnt a lot about platelets and the effect of aspirin on them, which had only been discovered a few years earlier. All this was the result of a lucky chance, without any real planning at all – or any bad luck or battles in those early days.…”

Section: Stumbling Into Stroke Researchmentioning

confidence: 99%

Chances and Battles in Stroke Research

Warlow

2007

Cerebrovasc Dis

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Here I have reviewed how good luck, bad luck and barriers determined my research directions in stroke over the last 30 or so years. Good luck should be exploited, and very often barriers can be not just overcome but put to good use as well. It is crucial for the young researcher to find mentors as good as I have had, and to move around to gain a broad experience, and for the experienced researchers to bring on the younger generation as I have tried to do.

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A Double-Blind Trial of Low Doses of Subcutaneous Heparin in the Prevention of Deep-Vein Thrombosis After Myocardial Infarction*1

Cited by 142 publications

References 8 publications

Subcutaneous Low-Molecular-Weight Heparin versus Standard Heparin and the Prevention of Thromboembolism in Medical Inpatients

Subcutaneous Low-Molecular-Weight Heparin versus Standard Heparin and the Prevention of Thromboembolism in Medical Inpatients

Successful anticoagulation with hirudin in a patient with mesenteric venous thrombosis and multiple coagulation abnormalities

Chances and Battles in Stroke Research

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