Seminars in thrombosis and hemostasis
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Semin. Thromb. Hemost. · Jan 1999
ReviewLow molecular weight heparins in the prevention of venous thromboembolism in nonsurgical patients.
Hospitalized nonsurgical patients are at risk of developing venous thromboembolic disease (VTED) but, in contrast to surgical patients, only a limited number of prevention trials have been performed. Guidelines for optimal prophylaxis, particularly with respect to low molecular weight heparins (LMWHs), are not definitive. The Fifth American College of Chest Physicians' (ACCP) Consensus on Antithrombotic Therapy makes limited recommendations on the use of LMWH in patients. ⋯ Enoxaparin was at least as effective as UFH in reducing the risk of thromboembolic events by 19%. In high-risk pre-defined subgroups with heart failure, enoxaparin was significantly more effective. It is not possible to recommend a specific LMWH for prophylaxis in medical patients, but the recent position adopted by the United States Food and Drug Administration and the World Health Organization that LMWHs are noninterchangeable drugs suggests that thromboprophylaxis guidelines should be strengthened to reflect the level of evidence for each individual LMWH.
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The identified main causes of inherited thrombophilia are deficiencies of antithrombin, protein C and protein S, activated protein C (APC) resistance and the factor V Leiden mutation, mutant factor II, and inherited hyperhomocysteinemia. In women from symptomatic families these defects may be associated with an increased risk of venous thrombosis in pregnancy and recurrent fetal loss. Inherited thrombophilia is common and appears to be a multigene disorder. ⋯ Fetal loss may be increased in women with inherited thrombophilia. The risk appears greatest in women with antithrombin deficiency and women with more than one thrombophilia defect. A number of reports have claimed that prophylactic treatment with heparin during pregnancy has resulted in successful pregnancy in women with recurrent fetal death and inherited thrombophilia.
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Semin. Thromb. Hemost. · Jan 1999
ReviewOptimizing anticoagulant therapy in the management of pulmonary embolism.
Pulmonary embolism (PE) continues to command a high price in terms of mortality and recurrence, despite full-dose initial anticoagulation and long-term warfarin therapy. Embolectomy, thrombolysis, and vena cava filters may be life saving in patients with massive PE and cardiogenic shock, but their use in other groups remains controversial. Recent progress has been made in identifying key markers of a poor prognosis; these markers may assist in tailoring treatment to patient risk. ⋯ Although enoxaparin for PE treatment is currently licensed for therapy exclusively in the hospital setting, brief hospitalization or home treatment for nonmassive PE may be possible in the future. Expert management of long-term warfarin therapy is also crucial to optimize clinical outcomes. Recognition of potential causes of excessive anticoagulation and the use of self-monitoring by patients may improve the efficacy and safety of long-term warfarin administration.
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The sticky platelet syndrome (SPS) is an autosomal dominant platelet disorder associated with arterial and venous thromboembolic events. It is characterized by hyperaggregability of platelets in platelet-rich plasma with adenosine diphosphate (ADP) and epinephrine (type I), epinephrine alone (type II), or ADP alone (type III). Clinically, patients may present with angina pectoris, acute myocardial infarction (MI), transient cerebral ischemic attacks, stroke, retinal thrombosis, peripheral arterial thrombosis, and venous thrombosis, frequently recurrent under oral anticoagulant therapy. ⋯ Normal levels of platelet factor 4 (PF4) and beta-thromboglobulin in plasma suggest that the platelets are not activated at all times; they appear to become hyperactive upon ADP or adrenaline release. In vivo clumping could temporarily or permanently occlude a vessel, leading to the described clinical manifestations. The syndrome appears to be prominent especially in patients with unexplained arterial vascular occlusions.
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Semin. Thromb. Hemost. · Jan 1998
Review Clinical Trial Controlled Clinical TrialHyperhomocysteinemia and venous thrombosis.
In recent years hyperhomocysteinemia has been established as a new risk factor for neural tube defects, arterial cardiovascular disease, and venous thrombosis. Concerning vascular problems, it first became clear that hyperhomocysteinemia might be (though not proven) a risk factor for arterial disease as observed in case-control studies, as well as in prospective analysis. More recently, the subject of hyperhomocysteinemia and venous thrombosis has received much attention. ⋯ Briefly, the possible mechanisms of how hyperhomocysteinemia can lead to venous thrombosis are discussed. The article ends with therapeutic options to treat hyperhomocysteinemia (hyperhomocysteinemia can easily be treated with vitamins) and the description of a study that is presently being undertaken in an international multicenter design. This placebo-controlled study might resolve the question of whether lowering of homocysteine levels is of any clinical relevance in preventing recurrent venous thrombosis.