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Antithrombotic therapy for venous thromboembolic disease.

(CHEST 2001; 119:176S‐193S) S tasis of blood, abnormalities of the vessel wall, and changes in the soluble and formed elements of the blood are the major contributors to thrombosis. All of these alterations can contribute to venous thrombosis, depending on the specific risk factors that are present in a given patient. Antithrombotic regimens modify one or more of these abnormalities. These regimens include drugs that inhibit blood coagulation, such as the various heparins and heparinoids; warfarin; direct thrombin inhibitors; drugs that inhibit platelet function, such as aspirin and dextran; and techniques that counteract venous stasis, such as compression stockings and pneumatic compression devices. In this broad sense, thrombolytic agents are also antithrombotic (Table 1). This section will describe the effectiveness of antithrombotic agents in the treatment of venous thromboembolism (VTE), a disease that encompasses both deep venous thrombosis (DVT) and pulmonary embolism (PE). Several of these agents are also useful for the primary prevention of VTE, and this application of antithrombotic therapy is reviewed in the preceding chapter. All antithrombotic therapy with either anticoagulants or platelet-active drugs is prophylactic, since these agents interrupt progression of the thrombotic process; but unlike thrombolytic agents, they do not as a rule actively resolve it. Unfractionated heparin, low-molecular-weight (LMW) heparin, thrombolytic agents, and warfarin are used to treat venous thromboembolic disease. 1. Treatment of VTE 1.1. Effective Regimens Treatment regimens for DVT and PE are similar because the two conditions are manifestations of the same disease process. When patients with VTE are carefully studied, the majority of those with proximal DVT also have PE (symptomatic or asymptomatic) and vice versa. Furthermore, clinical trials in patients with DVT alone have validated treatment regimens that are similar to regimens used in patients with both DVT and PE and in patients known to have only PE. None of these studies established the superiority of a treatment regimen for patients with PE in stable condition that was substantially different than regimens for patients with DVT. Patients with VTE who receive adequate anticoagulation generally do not die of recurrent disease. However, it should be noted that patients who are treated for PE are almost four times more likely (1.5% vs 0.4%) to die of recurrent VTE in the next year than are patients who are treated for DVT. 1 The major exception to the statement that the two conditions are treated similarly is that patients with symptomatic proximal DVT may benefit from fitted compression stockings for at least 3 months to reduce the incidence of the postthrombotic syndrome. 2 Heparin: Heparin, an acidic glycosaminoglycan, is a time-honored and relatively effective antithrombotic agent, but it requires careful monitoring and dose adjustment when used to treat active disease. Clinical preparations vary over a molecular weight range of 5,000 to 30,000 d, with a mean molecular weight of approximately 15,000 d. The drug acts by catalyzing the effect of a plasma inhibitor, antithrombin III, so that the inhibitor more efficiently combines with and inactivates a number of serine proteinases, notably thrombin (factor IIa), factor Xa, and factor IXa. Heparin also acts to inhibit activation of factors V and VIII by thrombin. 3,4 Neither hepatic nor renal disease seem to interfere notably with the clearance of the drug at therapeutic concentrations. 5 Heparin is currently obtained from the gut mucosa of animals and is available as a sodium or calcium salt.