Association of Traditional Cardiovascular Risk Factors with Venous Thromboembolism: An Individual Participant Data Meta-analysis of Prospective Studies
BACKGROUND—There is much controversy surrounding the association of traditional cardiovascular disease (CVD) risk factors with venous thromboembolism (VTE). METHODS—We performed an individual level random-effect meta-analysis including 9 prospective studies with measured baseline CVD risk factors an...
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| Published in | Circulation (New York, N.Y.) Vol. 135; no. 1; pp. 7 - 16 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
by the American College of Cardiology Foundation and the American Heart Association, Inc
03.01.2017
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0009-7322 1524-4539 |
| DOI | 10.1161/CIRCULATIONAHA.116.024507 |
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| Abstract | BACKGROUND—There is much controversy surrounding the association of traditional cardiovascular disease (CVD) risk factors with venous thromboembolism (VTE).
METHODS—We performed an individual level random-effect meta-analysis including 9 prospective studies with measured baseline CVD risk factors and validated VTE events. Definitions were harmonized across studies. Traditional CVD risk factors were modeled categorically, as well as continuously using restricted cubic splines. Estimates were obtained for overall VTE, provoked (i.e., VTE occurring in the presence of one or more established VTE risk factors) and unprovoked VTE, pulmonary embolism (PE) and deep-vein thrombosis (DVT).
RESULTS—The studies included 244,865 participants with 4,910 VTE events occurring during a mean follow-up 4.7−19.7 years per study. Age, sex, and body-mass index adjusted hazard ratios for overall VTE were 0.98 (95%CI, 0.89−1.07) for hypertension, 0.97 (0.88−1.08) for hyperlipidemia, 1.01 (0.89−1.15) for diabetes and 1.19 (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 (HR=0.79 [95% CI, 0.68−0.92] at systolic blood pressure 160 vs. 110 mmHg), 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 with 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 (0.90−1.29), respectively.
CONCLUSIONS—Except the association of cigarette smoking with provoked VTE, which is potentially mediated through comorbid conditions such as cancer, the modifiable traditional CVD risk factors are not associated with increased VTE risk. Higher systolic blood pressure showed inverse association with VTE. |
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| AbstractList | Much controversy surrounds the association of traditional cardiovascular disease risk factors with venous thromboembolism (VTE).
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.
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.
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—There is much controversy surrounding the association of traditional cardiovascular disease (CVD) risk factors with venous thromboembolism (VTE). METHODS—We performed an individual level random-effect meta-analysis including 9 prospective studies with measured baseline CVD risk factors and validated VTE events. Definitions were harmonized across studies. Traditional CVD risk factors were modeled categorically, as well as continuously using restricted cubic splines. Estimates were obtained for overall VTE, provoked (i.e., VTE occurring in the presence of one or more established VTE risk factors) and unprovoked VTE, pulmonary embolism (PE) and deep-vein thrombosis (DVT). RESULTS—The studies included 244,865 participants with 4,910 VTE events occurring during a mean follow-up 4.7−19.7 years per study. Age, sex, and body-mass index adjusted hazard ratios for overall VTE were 0.98 (95%CI, 0.89−1.07) for hypertension, 0.97 (0.88−1.08) for hyperlipidemia, 1.01 (0.89−1.15) for diabetes and 1.19 (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 (HR=0.79 [95% CI, 0.68−0.92] at systolic blood pressure 160 vs. 110 mmHg), 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 with 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 (0.90−1.29), respectively. CONCLUSIONS—Except the association of cigarette smoking with provoked VTE, which is potentially mediated through comorbid conditions such as cancer, the modifiable traditional CVD risk factors are not associated with increased VTE risk. Higher systolic blood pressure showed inverse association with VTE. BACKGROUNDMuch controversy surrounds the association of traditional cardiovascular disease risk factors with venous thromboembolism (VTE).METHODSWe 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.RESULTSThe 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.CONCLUSIONSExcept 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. |
| Author | Hammerstrøm, Jens Manson, JoAnn E. Brækkan, Sigrid K. Holst, Anders G. Folsom, Aaron R. Bos, Willem Jan Zakai, Neil A. Allison, Matthew A. Mahmoodi, Bakhtawar K. Matsushita, Kunihiro Lakoski, Susan G. Næss, Inger Anne Overvad, Kim Prescott, Eva Puurunen, Marja Sang, Yingying Rossouw, Jacques E. Lutsey, Pamela L. Cannegieter, Suzanne C. Cushman, Mary ten Berg, Jur Gona, Philimon N. Martin, Lisa W. Severinsen, Marianne T. Meijer, Karina Gansevoort, Ron T. Hansen, John-Bjarne Heckbert, Susan |
| AuthorAffiliation | 1Department of Cardiology and Internal Medicine, Saint Antonius Hospital, Nieuwegein, the Netherlands; 2Department of Haematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; 3Departments of Medicine and Pathology, University of Vermont, Burlington, VT; 4Departments of Hematology, Trondheim University Hospital, Trondheim, Norway; 5Department of Family and Preventive Medicine, University of California San Diego, La Jolla, CA; 6K.G.Jebsen – Thrombosis Research and Expertise Center (TREC) Department of Clinical Medicine, University of Tromsø, Tromsø, Norway; 7Department of Clinical Epidemiology, Leiden University Medical Center, University of Leiden, Leiden, the Netherlands; 8Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; 9Department of Exercise and Health Sciences, University of Massachusetts, Boston, MA; 10Department of Epidemiology and Cardiovascular Health Research |
| AuthorAffiliation_xml | – name: 1Department of Cardiology and Internal Medicine, Saint Antonius Hospital, Nieuwegein, the Netherlands; 2Department of Haematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; 3Departments of Medicine and Pathology, University of Vermont, Burlington, VT; 4Departments of Hematology, Trondheim University Hospital, Trondheim, Norway; 5Department of Family and Preventive Medicine, University of California San Diego, La Jolla, CA; 6K.G.Jebsen – Thrombosis Research and Expertise Center (TREC) Department of Clinical Medicine, University of Tromsø, Tromsø, Norway; 7Department of Clinical Epidemiology, Leiden University Medical Center, University of Leiden, Leiden, the Netherlands; 8Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; 9Department of Exercise and Health Sciences, University of Massachusetts, Boston, MA; 10Department of Epidemiology and Cardiovascular Health Research Unit, University of Washington, Seattle, WA; 11Laboratory for Molecular Cardiology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark; 12Department of Clinical Cancer Prevention and Cardiology, the University of Texas MD Anderson Cancer Center, Houston, TX; 13Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN; 14Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA; 15Division of Cardiology, George Washington University School of Medicine and Health Sciences, Washington DC; 16Johns Hopkins Bloomberg School of Public Health, Baltimore, MD; 17Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus, and Department of Cardiology, Aalborg University Hospital, Aalborg, Denmark; 18Department of Cardiology, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark; 19Framingham Heart Study of Boston University School of Medicine and NHLBI, Framingham, MA; 20National Heart, Lung, and Blood Institute, Bethesda, MD; 21Department of Hematology, Aalborg University Hospital, Aalborg, Denmark – name: 4 Departments of Hematology, Trondheim University Hospital, Trondheim, Norway – name: 17 Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus, and Department of Cardiology, Aalborg University Hospital, Aalborg, Denmark – name: 10 Department of Epidemiology and Cardiovascular Health Research Unit, University of Washington, Seattle, Washington, USA – name: 11 Laboratory for Molecular Cardiology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark – name: 6 K.G.Jebsen – Thrombosis Research and Expertise Center (TREC) Department of Clinical Medicine, University of Tromsø, Tromsø, Norway – name: 7 Department of Clinical Epidemiology, Leiden University Medical Center, University of Leiden, Leiden, the Netherlands – name: 15 Division of Cardiology, George Washington University School of Medicine and Health Sciences, Washington DC, USA – name: 16 Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA – name: 1 Department of Cardiology and Internal Medicine, Sint Antonius Hospital, Nieuwegein, the Netherlands – name: 13 Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, Minnesota, USA – name: 9 Department of Exercise and Health Sciences, University of Massachusetts, Boston, Massachusetts, USA – name: 20 National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA – name: 8 Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands – name: 12 Department of Clinical Cancer Prevention and Cardiology, the University of Texas MD Anderson Cancer Center, Houston, Texas, USA – name: 21 Department of Hematology, Aalborg University Hospital, Aalborg, Denmark – name: 2 Department of Haematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands – name: 19 Framingham Heart Study of Boston University School of Medicine and NHLBI, Framingham, Massachusetts, USA – name: 18 Department of Cardiology, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark – name: 14 Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA – name: 5 Department of Family and Preventive Medicine, University of California San Diego, La Jolla, California, USA – name: 3 Departments of Medicine and Pathology, University of Vermont, Burlington, Vermont, USA |
| Author_xml | – sequence: 1 givenname: Bakhtawar surname: Mahmoodi middlename: K. fullname: Mahmoodi, Bakhtawar K. organization: 1Department of Cardiology and Internal Medicine, Saint Antonius Hospital, Nieuwegein, the Netherlands; 2Department of Haematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; 3Departments of Medicine and Pathology, University of Vermont, Burlington, VT; 4Departments of Hematology, Trondheim University Hospital, Trondheim, Norway; 5Department of Family and Preventive Medicine, University of California San Diego, La Jolla, CA; 6K.G.Jebsen – Thrombosis Research and Expertise Center (TREC) Department of Clinical Medicine, University of Tromsø, Tromsø, Norway; 7Department of Clinical Epidemiology, Leiden University Medical Center, University of Leiden, Leiden, the Netherlands; 8Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; 9Department of Exercise and Health Sciences, University of Massachusetts, Boston, MA; 10Department of Epidemiology and Cardiovascular Health Research Unit, University of Washington, Seattle, WA; 11Laboratory for Molecular Cardiology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark; 12Department of Clinical Cancer Prevention and Cardiology, the University of Texas MD Anderson Cancer Center, Houston, TX; 13Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN; 14Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA; 15Division of Cardiology, George Washington University School of Medicine and Health Sciences, Washington DC; 16Johns Hopkins Bloomberg School of Public Health, Baltimore, MD; 17Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus, and Department of Cardiology, Aalborg University Hospital, Aalborg, Denmark; 18Department of Cardiology, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark; 19Framingham Heart Study of Boston University School of Medicine and NHLBI, Framingham, MA; 20National Heart, Lung, and Blood Institute, Bethesda, MD; 21Department of Hematology, Aalborg University Hospital, Aalborg, Denmark – sequence: 2 givenname: Mary surname: Cushman fullname: Cushman, Mary – sequence: 3 givenname: Inger surname: Næss middlename: Anne fullname: Næss, Inger Anne – sequence: 4 givenname: Matthew surname: Allison middlename: A. fullname: Allison, Matthew A. – sequence: 5 givenname: Willem surname: Bos middlename: Jan fullname: Bos, Willem Jan – sequence: 6 givenname: Sigrid surname: Brækkan middlename: K. fullname: Brækkan, Sigrid K. – sequence: 7 givenname: Suzanne surname: Cannegieter middlename: C. fullname: Cannegieter, Suzanne C. – sequence: 8 givenname: Ron surname: Gansevoort middlename: T. fullname: Gansevoort, Ron T. – sequence: 9 givenname: Philimon surname: Gona middlename: N. fullname: Gona, Philimon N. – sequence: 10 givenname: Jens surname: Hammerstrøm fullname: Hammerstrøm, Jens – sequence: 11 givenname: John-Bjarne surname: Hansen fullname: Hansen, John-Bjarne – sequence: 12 givenname: Susan surname: Heckbert fullname: Heckbert, Susan – sequence: 13 givenname: Anders surname: Holst middlename: G. fullname: Holst, Anders G. – sequence: 14 givenname: Susan surname: Lakoski middlename: G. fullname: Lakoski, Susan G. – sequence: 15 givenname: Pamela surname: Lutsey middlename: L. fullname: Lutsey, Pamela L. – sequence: 16 givenname: JoAnn surname: Manson middlename: E. fullname: Manson, JoAnn E. – sequence: 17 givenname: Lisa surname: Martin middlename: W. fullname: Martin, Lisa W. – sequence: 18 givenname: Kunihiro surname: Matsushita fullname: Matsushita, Kunihiro – sequence: 19 givenname: Karina surname: Meijer fullname: Meijer, Karina – sequence: 20 givenname: Kim surname: Overvad fullname: Overvad, Kim – sequence: 21 givenname: Eva surname: Prescott fullname: Prescott, Eva – sequence: 22 givenname: Marja surname: Puurunen fullname: Puurunen, Marja – sequence: 23 givenname: Jacques surname: Rossouw middlename: E. fullname: Rossouw, Jacques E. – sequence: 24 givenname: Yingying surname: Sang fullname: Sang, Yingying – sequence: 25 givenname: Marianne surname: Severinsen middlename: T. fullname: Severinsen, Marianne T. – sequence: 26 givenname: Jur surname: ten Berg fullname: ten Berg, Jur – sequence: 27 givenname: Aaron surname: Folsom middlename: R. fullname: Folsom, Aaron R. – sequence: 28 givenname: Neil surname: Zakai middlename: A. fullname: Zakai, Neil A. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27831499$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2016 by the American College of Cardiology Foundation and the American Heart Association, Inc. 2016 American Heart Association, Inc. |
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| Keywords | cardiovascular disease hyperlipidemia risk factors venous thromboembolism smoking diabetes mellitus hypertension |
| Language | English |
| License | 2016 American Heart Association, Inc. |
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| PublicationTitle | Circulation (New York, N.Y.) |
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| Snippet | BACKGROUND—There is much controversy surrounding the association of traditional cardiovascular disease (CVD) risk factors with venous thromboembolism (VTE).... Much controversy surrounds the association of traditional cardiovascular disease risk factors with venous thromboembolism (VTE). We performed an individual... BACKGROUNDMuch controversy surrounds the association of traditional cardiovascular disease risk factors with venous thromboembolism (VTE).METHODSWe performed... |
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| SubjectTerms | Age Factors Blood Pressure Body Mass Index Diabetes Complications Humans Hyperlipidemias - complications Hypertension - complications Lipids - blood Proportional Hazards Models Prospective Studies Pulmonary Embolism - etiology Risk Factors Sex Factors Smoking Venous Thromboembolism - etiology Venous Thrombosis - etiology |
| Title | Association of Traditional Cardiovascular Risk Factors with Venous Thromboembolism: An Individual Participant Data Meta-analysis of Prospective Studies |
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