A Dual Pathogen for Arterial and Venous Thrombosis
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- arterial thrombosis
- body mass index
- vascular diseases
- venous thromboembolism
Article, see p 7
Traditional book learning and clinical training of common risk factors for venous thromboembolism (VTE) did not include cigarette smoking. I recall as a medical student, after giving the history of a patient presenting with deep venous thrombosis, being told that smoking was not a risk factor for venous disease, only arterial disease. This perplexed me. If smoking was known to “thicken the blood,” as evidenced by the increased fibrinogen, and venous thromboses typically represent a larger clot burden compared with arterial thromboses, why wouldn't cigarette smoking be a dual pathogen for venous and arterial disease?
Prior evaluations have compared the risk of smoking and other traditional arterial risk factors (ie, diabetes mellitus, hypertension, and elevated cholesterol) for arterial vascular disease with the risk of these factors for VTE.1 Our understanding of the pathophysiology of arterial vascular diseases is based on atherosclerosis, which becomes atherothrombosis when plaque rupture occurs, platelets are recruited, and the coagulation cascade is activated. Clinically apparent venous thrombosis is usually the result of venous stasis (immobility or obstruction), stimulation of the coagulation cascade from circulating or exogenous inciters leading to a hypercoagulable state, or mechanical injury to the vessel wall. One may expect that there are unique risk factors for arterial and venous thrombosis and some shared risk factors for which stasis conditions, hypercoagulable states, and vessel injury are the inciters (Figure).
Some evidence supports a shared pathogenesis of arterial and venous thrombosis. The Tromsø study of 21 624 subjects recruited from Norway showed that a family history of myocardial infarction is associated with a 52% increased risk of myocardial infarction and a 26% increased risk of VTE after …