Walter Ageno1, Matteo N D Di Minno2, Cihan Ay2, Moon Ju Jang2, John-Bjarne Hansen2, Lyn M Steffen2, Amparo Vayà2, Marcello Rattazzi2, Ingrid Pabinger2, Doyeun Oh2, Giovanni Di Minno2, Sigrid K Braekkan2, Mary Cushman2, Elena Bonet2, Paolo Pauletto2, Alessandro Squizzato2, Francesco Dentali2. 1. From the Department of Clinical and Experimental Medicine, University of Insubria, Varese, Italy (W.A., A.S., F.D.); Unit of Cell and Molecular Biology in Cardiovascular Diseases, Centro Cardiologico Monzino, IRCCS, Milan, Italy (M.N.D.D.M.); Department of Experimental and Clinical Medicine, Federico II University, Napoli, Italy (M.N.D.D.M., G.D.M.); Clinical Division of Haematology and Haemostaseology, Department of Medicine I, Medical University of Vienna, Vienna, Austria (C.A., I.P.); Department of Internal Medicine, School of Medicine, CHA University, Seongnam, Korea (M.J.J., D.O.); Department of Clinical Medicine, University of Tromso, Tromso, Norway (J.-B.H., S.K.B.); Division of Epidemiology and Community Health, University of Minnesota School of Public Health, Minneapolis (L.M.S.); Department of Medicine, University of Vermont College of Medicine, Burlington (M.C.); Hemostasis Unit, Service of Clinical Pathology, La Fe University Hospital, Valencia, Spain (A.V., E.B.); and Department of Internal Medicine, Ca' Foncello Hospital, Treviso, Italy (M.R., P.P.). agewal@yahoo.com. 2. From the Department of Clinical and Experimental Medicine, University of Insubria, Varese, Italy (W.A., A.S., F.D.); Unit of Cell and Molecular Biology in Cardiovascular Diseases, Centro Cardiologico Monzino, IRCCS, Milan, Italy (M.N.D.D.M.); Department of Experimental and Clinical Medicine, Federico II University, Napoli, Italy (M.N.D.D.M., G.D.M.); Clinical Division of Haematology and Haemostaseology, Department of Medicine I, Medical University of Vienna, Vienna, Austria (C.A., I.P.); Department of Internal Medicine, School of Medicine, CHA University, Seongnam, Korea (M.J.J., D.O.); Department of Clinical Medicine, University of Tromso, Tromso, Norway (J.-B.H., S.K.B.); Division of Epidemiology and Community Health, University of Minnesota School of Public Health, Minneapolis (L.M.S.); Department of Medicine, University of Vermont College of Medicine, Burlington (M.C.); Hemostasis Unit, Service of Clinical Pathology, La Fe University Hospital, Valencia, Spain (A.V., E.B.); and Department of Internal Medicine, Ca' Foncello Hospital, Treviso, Italy (M.R., P.P.).
Abstract
OBJECTIVE: The metabolic syndrome (MetS) may contribute to the pathogenesis of venous thromboembolism (VTE), but this association requires additional investigation. APPROACH AND RESULTS: We performed a patient-level meta-analysis of case-control and cohort studies that evaluated the role of MetS and risk of unprovoked VTE. For case-control studies, odds ratios and 95% confidence intervals were calculated using logistic regression analysis to estimate the influence of individual variables on the risk of VTE; χ(2) tests for trend were used to investigate the effect of increasing number of components of MetS on the risk of VTE and to explore the influence of abdominal obesity on this relationship. For cohort studies, hazard ratios and 95% confidence interval were calculated using multivariable Cox regression analysis. Six case-control studies were included (908 cases with unprovoked VTE and 1794 controls): in multivariate analysis, MetS was independently associated with VTE (odds ratio, 1.91; 95% confidence interval, 1.57-2.33), and both MetS and abdominal obesity were better predictors of unprovoked VTE than obesity defined by the body mass index. Two prospective cohort studies were included (26,531 subjects and 289 unprovoked VTE events): age, obesity, and abdominal obesity, but not MetS were associated with VTE. CONCLUSIONS: Case-control but not prospective cohort studies support an association between MetS and VTE. Abdominal adiposity is a strong risk factor for VTE.
OBJECTIVE: The metabolic syndrome (MetS) may contribute to the pathogenesis of venous thromboembolism (VTE), but this association requires additional investigation. APPROACH AND RESULTS: We performed a patient-level meta-analysis of case-control and cohort studies that evaluated the role of MetS and risk of unprovoked VTE. For case-control studies, odds ratios and 95% confidence intervals were calculated using logistic regression analysis to estimate the influence of individual variables on the risk of VTE; χ(2) tests for trend were used to investigate the effect of increasing number of components of MetS on the risk of VTE and to explore the influence of abdominal obesity on this relationship. For cohort studies, hazard ratios and 95% confidence interval were calculated using multivariable Cox regression analysis. Six case-control studies were included (908 cases with unprovoked VTE and 1794 controls): in multivariate analysis, MetS was independently associated with VTE (odds ratio, 1.91; 95% confidence interval, 1.57-2.33), and both MetS and abdominal obesity were better predictors of unprovoked VTE than obesity defined by the body mass index. Two prospective cohort studies were included (26,531 subjects and 289 unprovoked VTE events): age, obesity, and abdominal obesity, but not MetS were associated with VTE. CONCLUSIONS: Case-control but not prospective cohort studies support an association between MetS and VTE. Abdominal adiposity is a strong risk factor for VTE.
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