The most common sources of pulmonary embolism (PE) are proximal leg deep venous thromboses (DVTs) or pelvic veinthromboses; therefore, any risk factor for DVT also increases the risk of PE. Approximately 15% of patients with a DVT will develop a PE. In these chapters on venous thromboembolism (VTE), the word risk factors refers to those epidemiologic and genetic variables that expose someone to a higher risk of developing venous thrombosis. The word triggers refer to those factors in the patients immediate history or environment that may have lead to the occurrence of the venous thrombosis. The risk factors for VTE are a constellation of predisposing conditions which stem from the three principles of Virchow's triad: stasis of the blood flow, damage to the vascular endothelial cells, and hypercoagulability. Approximately 5 to 8% of the U.S. population has one of several genetic risk factors, also known as inheritedthrombophilias in which a genetic defect can be identified that increases the risk for thrombosis.[1][2] The risk factors for VTE can be classified as temporary, modifiable and non-modifiable. It is suggested that venous thrombosis also shares risk factors with arterial thrombosis, such as obesity, hypertension, smoking, and diabetes mellitus.[3]
Shown below is a list of predisposing factors for VTE.[4][5] The risk factors are classified as moderate or weak depending on how strongly they predispose for a VTE.
In addition, surgery, trauma, cancer and immobilization are associated with provoked PE.
Risk Factors from the Physician's Health Study[edit | edit source]
The following factors have been associated with elevated risk of VTE among subjects in the Physicians Health Study. The relative risk for the occurrence of VTE among patients who have these factors compared to those who don't is provided below.
↑Vayá A, Martínez-Triguero ML, España F, Todolí JA, Bonet E, Corella D (2011). "The metabolic syndrome and its individual components: its association with venous thromboembolism in a Mediterranean population". Metab Syndr Relat Disord. 9 (3): 197–201. doi:10.1089/met.2010.0117. PMID21352080.CS1 maint: Multiple names: authors list (link)
↑Goldhaber SZ, Grodstein F, Stampfer MJ, Manson JE, Colditz GA, Speizer FE; et al. (1997). "A prospective study of risk factors for pulmonary embolism in women". JAMA. 277 (8): 642–5. PMID9039882.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Ginsburg KS, Liang MH, Newcomer L, Goldhaber SZ, Schur PH, Hennekens CH; et al. (1992). "Anticardiolipin antibodies and the risk for ischemic stroke and venous thrombosis". Ann Intern Med. 117 (12): 997–1002. PMID1443986.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Ridker PM, Hennekens CH, Lindpaintner K, Stampfer MJ, Eisenberg PR, Miletich JP (1995). "Mutation in the gene coding for coagulation factor V and the risk of myocardial infarction, stroke, and venous thrombosis in apparently healthy men". N Engl J Med. 332 (14): 912–7. doi:10.1056/NEJM199504063321403. PMID7877648.CS1 maint: Multiple names: authors list (link)