Smoking and Deep Vein Thrombosis Risk

Mechanism and Clinical Context

Smoking-induced polycythemia contributes to thrombotic risk through increased blood viscosity caused by carbon monoxide exposure, which triggers compensatory erythropoiesis, with carbon monoxide binding hemoglobin with 200-250 times greater affinity than oxygen, creating a hypoxic state that increases red blood cell production in the general population 1

A history of prior VTE is associated with an odds ratio of 6.08, thrombophilia with an odds ratio of 5.88, active malignancy with an odds ratio of 2.65, immobility with an odds ratio of 3.17, and critical illness with an odds ratio of 1.65, compared to smoking, which has a relatively weaker effect, according to the American College of Cardiology 2
The American Heart Association notes that history of prior VTE, thrombophilia, active malignancy, immobility, and critical illness are associated with odds ratios of 6.08, 5.88, 2.65, 3.17, and 1.65, respectively, compared to smoking, in patients with deep vein thrombosis 3

Daily smoking before pregnancy increases post-thrombotic syndrome risk with an odds ratio of 2.9 in women with pregnancy-associated DVT, according to the American Heart Association 4

Smoking cessation reduces thrombotic risk, with risk reduction beginning within 1 year and returning to baseline after 5 years, similar to the pattern seen with stroke risk reduction, in the general population 1
The American College of Cardiology recommends that smoking cessation should be strongly recommended as part of VTE risk reduction strategies, particularly in patients with multiple risk factors, with a strength of evidence based on observational studies and expert consensus 5