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Antithrombotic Therapy in Peripheral Arterial Occlusive Disease

Mark R. Jackson, MD, Chair; G. Patrick Clagett, MD
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Correspondence to: Mark R. Jackson, MD, Department of Surgery, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75235-9157.



Chest. 2001;119(1_suppl):283S-299S. doi:10.1378/chest.119.1_suppl.283S
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Atherosclerosis is the cause of the vast majority of cases of chronic peripheral arterial occlusive disease. The arteries most frequently involved, in order of occurrence, are the femoropopliteal-tibial, aortoiliac, carotid and vertebral, splanchnic and renal, and brachiocephalic. Fibromuscular dysplasia, inflammatory arteritides, and congenital arterial malformations are much rarer causes of arterial insufficiency. The causes of acute arterial occlusion are embolism, thrombosis, and trauma. The goals of therapy in chronic arterial occlusive disease are to relieve ischemic symptoms (intermittent claudication and rest pain), to alleviate disability, and to prevent progression that might lead to gangrene and limb loss. The objectives of therapy in acute arterial occlusion are to restore blood flow and to preserve life and limb. Antithrombotic therapy is a rational consideration in patients with peripheral arterial occlusive disease. In chronic disease, antithrombotic therapy is designed to prevent progression and thrombotic occlusion or to prevent thrombotic complications after vascular reconstructions and other interventions. In acute arterial occlusion from embolism or thrombosis, effective anticoagulant therapy will prevent propagation of thrombi into proximal and distal arterial branches with attendant compromise of collateral flow; may prevent reocclusion after surgical or interventional procedures to reestablish flow; or, in the case of embolism, may prevent recurrence. The antithrombotic agents available are anticoagulants, antiplatelet agents, thrombolytic drugs, and dextran (Table 1 ).

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