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