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Risk marker associations with venous thrombotic events: a cross-sectional analysis.
- Author(s): Golomb, Beatrice A;
- Chan, Virginia T;
- Denenberg, Julie O;
- Koperski, Sabrina;
- Criqui, Michael H
- et al.
Published Web Locationhttps://doi.org/10.1136/bmjopen-2013-003208
ObjectiveTo examine the interrelations among, and risk marker associations for, superficial and deep venous events-superficial venous thrombosis (SVT), deep venous thrombosis (DVT) and pulmonary embolism (PE).
SettingSan Diego, California, USA.
Participants2404 men and women aged 40-79 years from four ethnic groups: non-Hispanic White, Hispanic, African-American and Asian. The study sample was drawn from current and former staff and employees of the University of California, San Diego and their spouses/significant others.
Outcome measuresSuperficial and deep venous events, specifically SVT, DVT, PE and combined deep venous events (DVE) comprising DVT and PE.
ResultsSignificant correlates on multivariable analysis were, for SVT: female sex, ethnicity (African-American=protective), lower educational attainment, immobility and family history of varicose veins. For DVT and DVE, significant correlates included: heavy smoking, immobility and family history of DVEs (borderline for DVE). For PE, significant predictors included immobility and, in contrast to DVT, blood pressure (BP, systolic or diastolic). In women, oestrogen use duration for hormone replacement therapy, in all and among oestrogen users, predicted PE and DVE, respectively.
ConclusionsThese findings fortify evidence for known risk correlates/predictors for venous disease, such as family history, hormone use and immobility. New risk associations are shown. Striking among these is an association of PE, but not DVT, to elevated BP: we conjecture PE may serve as cause rather than consequence. Future studies should evaluate the temporal direction of this association. Oxidative stress and cell energy compromise are proposed to explain and predict many risk factors, operating through cell-death mediated triggering of coagulation activation.
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