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Venous thromboembolism: Epidemiology and magnitude of the problem

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Pulmonary embolism is the third most common cardiovascular disease after myocardial infarction and stroke. The death rate from pulmonary embolism exceeds the death rate from myocardial infarction, because myocardial infarction is much easier to detect and to treat. Among survivors of pulmonary embolism, chronic thromboembolic pulmonary hypertension occurs in 2–4 of every 100 patients. Post-thrombotic syndrome of the legs, characterized by chronic venous insufficiency, occurs in up to half of patients who suffer deep vein thrombosis or pulmonary embolism. We have effective pharmacological regimens using fixed low dose unfractionated or low molecular weight heparin to prevent venous thromboembolism among hospitalized patients. There remains the problem of low rates of utilization of pharmacological prophylaxis. The biggest change in our understanding of the epidemiology of venous thromboembolism is that we now believe that deep vein thrombosis and pulmonary embolism share similar risk factors and pathophysiology with atherothrombosis and coronary artery disease.

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Relationship between VTE and atherothrombosis

VTE and atherothrombosis share common risk factors (Table 1) and the common pathophysiology of inflammation, hypercoagulability, and endothelial injury [34]. A meta-analysis of cardiovascular risk factors and VTE in more than 63,000 patients in cohort or case–control studies found that compared with control subjects, the odds ratio for the risk of VTE was 2.33 for obesity, 1.51 for hypertension, 1.42 for diabetes mellitus, 1.18 for cigarette smoking [35], and 1.16 for hypercholesterolemia [36].

Risk factors for VTE

VTE is a multifactorial disorder that arises as a result of genetic and environmental factors that interact. Inherited thrombophilias are frequently suspected in patients with VTE at a young age, multiple family members with VTE, idiopathic or recurrent VTE, or recurrent spontaneous abortions. Major inherited thrombophilias include factor V Leiden, prothrombin gene mutation 20210, and deficiencies of protein C, protein S, or antithrombin. Prevalence of inherited thrombophilias varies by

Conflict of interest

Dr. Goldhaber discloses the following possible conflicts: Research support from Daiichi Sankyo, Eisai, and EKOS, Johnson & Johnson, and Sanofi Aventis.

Dr. Goldhaber serves as a Consultant for: Baxter, Boehringer Ingelheim, Bristol Myers Squibb, Daiichi Sankyo, Eisai, Medscape, Merck Portola, and Sanofi Aventis.

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