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Q J Med 2001; 94: 179-185
© 2001 Association of Physicians

Review

Current trends in the management of thromboembolic events

F. De Lorenzo, A. Noorani1 and V.V. Kakkar

From the Thrombosis Research Institute, London, and 1 Ashford Hospital, Middlesex, UK


   Introduction
 
Thrombus formation on a disrupted atherosclerotic plaque is the main pathogenetic mechanism for the acute coronary syndromes of myocardial infarction and unstable angina. Myocardial infarction results from an acute total occlusion of the artery, while unstable angina is secondary in most cases to mural thrombus formation. Thrombus formation has also been implicated in chronic atherosclerotic disease progression, and in restenosis following coronary angioplasty. Therapeutic measures to treat thrombus rely on the ability of drugs either to prevent thrombus extension, to dissolve its fibrin component, or to prevent further platelet aggregation.

Following arterial vessel wall injury, platelets adhere to the subendothelial collagen. Glycoprotein Ib on the platelet membrane is the primary receptor for this single layer of platelets, and it binds von Willebrand factor as its extracellular ligand. Platelet aggregation involves activation of several different pathways leading to exposure of the glycoprotein IIb/IIIa receptor on the platelet. These receptors bind either . . . [Full Text of this Article]


   Thrombosis in ischaemic heart disease
 

   Medical therapy for the treatment of intracoronary thrombus
 
Unfractionated heparin
Low-molecular-weight heparins
Other antithrombin agents
Conclusion

   Venous thrombosis
 
Prophylaxis and treatment for venous thromboembolism
Treatment with LMWH outside hospital
Treatment of pulmonary embolism
Dosage and administration
Conclusion

   Notes
 

   References
 

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