Venous thromboembolism (VTE) comprises deep vein thrombosis (DVT) and pulmonary embolism (PE). It is the third most frequent cardiovascular disease with an overall annual incidence rate between 75 and 270 cases per 100,000 inhabitants.1 The risk of VTE approximately doubles with each subsequent decade after the age of 40; therefore, a larger number of patients are expected to be diagnosed with VTE in aging societies in the coming future.1 PE is the most serious clinical presentation of VTE with 1- and 3-month mortality rates between 9% and 11% and up to 17%, respectively.2,3,4 Following the acute PE episode, resolution of emboli is frequently incomplete despite optimal anticoagulant therapy,5 which may lead to the development of chronic thromboembolic pulmonary hypertension (CTEPH).6 Although a number of patients die of comorbidities that predispose them to the thromboembolic event, approximately one-third of patients die from PE within the first hours of presentation, often before the diagnosis can be confirmed and therapy initiated or because the diagnosis was overlooked.7 Despite advances in diagnostic imaging tests and therapeutic interventions, PE remains underdiagnosed, and prophylaxis continues to be dramatically underused. Globally, improvements in length of stay and changes in the initial treatment are being accompanied by a reduction in short-term all-cause and PE-specific mortality.8,9
Over the past decade, a number of valuable insights into the natural history of venous thrombosis and PE have enhanced our diagnostic and therapeutic approaches.10 One such insight is the awareness that patients hospitalized for medical problems face a thromboembolic risk similar to that of their surgical counterparts. Another is an understanding of the substantial thromboembolic recurrence risk among patients with idiopathic or unprovoked venous thrombosis.11 Yet another insight is the awareness that the presence of right ventricular (RV) dysfunction and increased levels of troponins and/or natriuretic peptides in the setting of PE may be associated with an increased risk of adverse consequences, including subsequent cardiovascular collapse and death.12 Anticoagulation with heparin, low-molecular-weight heparin (LMWH), or fondaparinux as a “bridge” to oral anticoagulation is still considered the standard treatment for PE. The spectrum of anticoagulant drugs has been expanded recently with the new generation of oral direct thrombin inhibitors and factor Xa inhibitors.
RISK FACTORS AND PATHOGENESIS OF VENOUS THROMBOEMBOLISM
In 1856, Virchow proposed his triad of factors leading to intravascular coagulation, including stasis, vessel wall injury, and hypercoagulability. Risk factors for VTE are based on these processes (Table 75–1). VTE is considered to be provoked in the presence of a temporary or reversible, usually acquired, risk factor (eg, surgery, trauma, immobilization, pregnancy) within the last 3 months before the diagnosis and unprovoked in the absence thereof.13 The presence of a persistent, sometimes inherited, risk factor may affect the decision of the duration of anticoagulation therapy after a first episode of VTE. The overwhelming majority of ...