Bakhtawar K Mahmoodi1, Mary Cushman2, Inger Anne Næss2, Matthew A Allison2, Willem J Bos2, Sigrid K Brækkan2, Suzanne C Cannegieter2, Ron T Gansevoort2, Philimon N Gona2, Jens Hammerstrøm2, John-Bjarne Hansen2, Susan Heckbert2, Anders G Holst2, Susan G Lakoski2, Pamela L Lutsey2, JoAnn E Manson2, Lisa W Martin2, Kunihiro Matsushita2, Karina Meijer2, Kim Overvad2, Eva Prescott2, Marja Puurunen2, Jacques E Rossouw2, Yingying Sang2, Marianne T Severinsen2, Jur Ten Berg2, Aaron R Folsom2, Neil A Zakai2. 1. From Department of Cardiology and Internal Medicine, Sint Antonius Hospital, Nieuwegein, The Netherlands (B.K.M., W.J.B., J.t.B.); Department of Haematology, University Medical Center Groningen, University of Groningen, The Netherlands (B.K.M., K. Meijer); Departments of Medicine and Pathology, University of Vermont, Burlington (M.C., N.A.Z.); Department of Hematology, Trondheim University Hospital, Norway (I.A.N., J.H.); Department of Family and Preventive Medicine, University of California San Diego, La Jolla (M.A.A.); K. G. Jebsen-Thrombosis Research and Expertise Center, Department of Clinical Medicine, University of Tromsø, Norway (S.K.B., J.- B.H.); Department of Clinical Epidemiology, Leiden University Medical Center, University of Leiden, The Netherlands (S.C.C.); Department of Internal Medicine, University Medical Center Groningen, University of Groningen, The Netherlands (R.T.G.); Department of Exercise and Health Sciences, University of Massachusetts, Boston (P.N.G.); Department of Epidemiology and Cardiovascular Health Research Unit, University of Washington, Seattle (S.H.); Laboratory for Molecular Cardiology, Copenhagen University Hospital, Rigshospitalet, Denmark (A.G.H.); Department of Clinical Cancer Prevention and Cardiology, University of Texas MD Anderson Cancer Center, Houston (S.G.L.); Division of Epidemiology and Community Health, University of Minnesota, Minneapolis (P.L.L., A.R.F.); Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (J.E.M.); Division of Cardiology, George Washington University School of Medicine and Health Sciences, Washington, DC (L.W.M.); Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (K. Matsushita, Y.S.); Department of Public Health, Section for Epidemiology, Aarhus University, and Department of Cardiology, Aalborg University Hospital, Denmark (K.O.); Department of Cardiology, Bispebjerg Hospital, University of Copenhagen, Denmark (E.P.); Framingham Heart Study, Boston University School of Medicine, MA (M.P.); National Heart, Lung, and Blood Institute, Bethesda, MD (J.E.R.); and Department of Hematology, Aalborg University Hospital, Denmark (M.T.S.). b.k.mahmoodi@umcg.nl. 2. From Department of Cardiology and Internal Medicine, Sint Antonius Hospital, Nieuwegein, The Netherlands (B.K.M., W.J.B., J.t.B.); Department of Haematology, University Medical Center Groningen, University of Groningen, The Netherlands (B.K.M., K. Meijer); Departments of Medicine and Pathology, University of Vermont, Burlington (M.C., N.A.Z.); Department of Hematology, Trondheim University Hospital, Norway (I.A.N., J.H.); Department of Family and Preventive Medicine, University of California San Diego, La Jolla (M.A.A.); K. G. Jebsen-Thrombosis Research and Expertise Center, Department of Clinical Medicine, University of Tromsø, Norway (S.K.B., J.- B.H.); Department of Clinical Epidemiology, Leiden University Medical Center, University of Leiden, The Netherlands (S.C.C.); Department of Internal Medicine, University Medical Center Groningen, University of Groningen, The Netherlands (R.T.G.); Department of Exercise and Health Sciences, University of Massachusetts, Boston (P.N.G.); Department of Epidemiology and Cardiovascular Health Research Unit, University of Washington, Seattle (S.H.); Laboratory for Molecular Cardiology, Copenhagen University Hospital, Rigshospitalet, Denmark (A.G.H.); Department of Clinical Cancer Prevention and Cardiology, University of Texas MD Anderson Cancer Center, Houston (S.G.L.); Division of Epidemiology and Community Health, University of Minnesota, Minneapolis (P.L.L., A.R.F.); Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (J.E.M.); Division of Cardiology, George Washington University School of Medicine and Health Sciences, Washington, DC (L.W.M.); Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (K. Matsushita, Y.S.); Department of Public Health, Section for Epidemiology, Aarhus University, and Department of Cardiology, Aalborg University Hospital, Denmark (K.O.); Department of Cardiology, Bispebjerg Hospital, University of Copenhagen, Denmark (E.P.); Framingham Heart Study, Boston University School of Medicine, MA (M.P.); National Heart, Lung, and Blood Institute, Bethesda, MD (J.E.R.); and Department of Hematology, Aalborg University Hospital, Denmark (M.T.S.).
Abstract
BACKGROUND: Much controversy surrounds the association of traditional cardiovascular disease risk factors with venous thromboembolism (VTE). METHODS: We performed an individual level random-effect meta-analysis including 9 prospective studies with measured baseline cardiovascular disease risk factors and validated VTE events. Definitions were harmonized across studies. Traditional cardiovascular disease risk factors were modeled categorically and continuously using restricted cubic splines. Estimates were obtained for overall VTE, provoked VTE (ie, VTE occurring in the presence of 1 or more established VTE risk factors), and unprovoked VTE, pulmonary embolism, and deep-vein thrombosis. RESULTS: The studies included 244 865 participants with 4910 VTE events occurring during a mean follow-up of 4.7 to 19.7 years per study. Age, sex, and body mass index-adjusted hazard ratios for overall VTE were 0.98 (95% confidence interval [CI]: 0.89-1.07) for hypertension, 0.97 (95% CI: 0.88-1.08) for hyperlipidemia, 1.01 (95% CI: 0.89-1.15) for diabetes mellitus, and 1.19 (95% CI: 1.08-1.32) for current smoking. After full adjustment, these estimates were numerically similar. When modeled continuously, an inverse association was observed for systolic blood pressure (hazard ratio=0.79 [95% CI: 0.68-0.92] at systolic blood pressure 160 vs 110 mm Hg) but not for diastolic blood pressure or lipid measures with VTE. An important finding from VTE subtype analyses was that cigarette smoking was associated with provoked but not unprovoked VTE. Fully adjusted hazard ratios for the associations of current smoking with provoked and unprovoked VTE were 1.36 (95% CI: 1.22-1.52) and 1.08 (95% CI: 0.90-1.29), respectively. CONCLUSIONS: Except for the association between cigarette smoking and provoked VTE, which is potentially mediated through comorbid conditions such as cancer, the modifiable traditional cardiovascular disease risk factors are not associated with increased VTE risk. Higher systolic blood pressure showed an inverse association with VTE.
BACKGROUND: Much controversy surrounds the association of traditional cardiovascular disease risk factors with venous thromboembolism (VTE). METHODS: We performed an individual level random-effect meta-analysis including 9 prospective studies with measured baseline cardiovascular disease risk factors and validated VTE events. Definitions were harmonized across studies. Traditional cardiovascular disease risk factors were modeled categorically and continuously using restricted cubic splines. Estimates were obtained for overall VTE, provoked VTE (ie, VTE occurring in the presence of 1 or more established VTE risk factors), and unprovoked VTE, pulmonary embolism, and deep-vein thrombosis. RESULTS: The studies included 244 865 participants with 4910 VTE events occurring during a mean follow-up of 4.7 to 19.7 years per study. Age, sex, and body mass index-adjusted hazard ratios for overall VTE were 0.98 (95% confidence interval [CI]: 0.89-1.07) for hypertension, 0.97 (95% CI: 0.88-1.08) for hyperlipidemia, 1.01 (95% CI: 0.89-1.15) for diabetes mellitus, and 1.19 (95% CI: 1.08-1.32) for current smoking. After full adjustment, these estimates were numerically similar. When modeled continuously, an inverse association was observed for systolic blood pressure (hazard ratio=0.79 [95% CI: 0.68-0.92] at systolic blood pressure 160 vs 110 mm Hg) but not for diastolic blood pressure or lipid measures with VTE. An important finding from VTE subtype analyses was that cigarette smoking was associated with provoked but not unprovoked VTE. Fully adjusted hazard ratios for the associations of current smoking with provoked and unprovoked VTE were 1.36 (95% CI: 1.22-1.52) and 1.08 (95% CI: 0.90-1.29), respectively. CONCLUSIONS: Except for the association between cigarette smoking and provoked VTE, which is potentially mediated through comorbid conditions such ascancer, the modifiable traditional cardiovascular disease risk factors are not associated with increased VTE risk. Higher systolic blood pressure showed an inverse association with VTE.
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