Acute deep vein thrombosis (DVT) occurs in approximately 300,000 persons per year in the United States alone (1). Because pulmonary embolism (PE) can be fatal, its prevention using anticoagulant therapy has been the mainstay of DVT therapy for nearly 50 years (2). However, anticoagulant drugs do not actively eliminate venous thrombus, so in many cases, their use is not sufficient to prevent serious DVT complications. Early thrombus progression occurs in a minority of anticoagulated DVT patients and can threaten life, limb, or organ function; prolong hospitalization; and exacerbate DVT symptoms such as limb pain, swelling, and ambulatory difficulties. Despite use of anticoagulant therapy, 25% to 50% of proximal DVT patients will develop significant quality of life (QOL) impairment from the postthrombotic syndrome (PTS), a debilitating late DVT complication characterized by chronic leg fatigue or heaviness, swelling, pain, paresthesias, venous claudication, stasis dermatitis, and/or skin ulceration (3,4). PTS can also affect the upper extremity, particularly when the subclavian vein from the dominant arm is involved with
the initial DVT episode. The development of PTS is directly related to the continued presence of thrombus within the deep venous system during the initial weeks and months after DVT via at least two pathways: (a) residual thrombus physically blocks blood flow (“obstruction”) and (b) thrombosis stimulates inflammation, which directly damages the venous valves, causing valvular incompetence (“reflux”). When reflux and/or obstruction is present, ambulatory venous hypertension develops and ultimately leads to the edema, tissue hypoxia and injury, progressive calf pump dysfunction, subcutaneous fibrosis, and skin ulceration of PTS (5). It is therefore logical that rapid thrombus elimination and restoration of unobstructed deep venous flow using catheter-directed thrombolysis (CDT) should rapidly improve initial DVT symptoms and prevent late valvular reflux, venous obstruction, and PTS.