Mahmoodi Bakhtawar K, Cushman Mary, Anne Næss Inger, Allison Matthew A, Bos Willem J, Brækkan Sigrid K, Cannegieter Suzanne C, Gansevoort Ron T, Gona Philimon N, Hammerstrøm Jens, Hansen John-Bjarne, Heckbert Susan, Holst Anders G, Lakoski Susan G, Lutsey Pamela L, Manson JoAnn E, Martin Lisa W, Matsushita Kunihiro, Meijer Karina, Overvad Kim, Prescott Eva, Puurunen Marja, Rossouw Jacques E, Sang Yingying, Severinsen Marianne T, Ten Berg Jur, Folsom Aaron R, Zakai Neil A
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.).
Circulation. 2017 Jan 3;135(1):7-16. doi: 10.1161/CIRCULATIONAHA.116.024507. Epub 2016 Nov 9.
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.
传统心血管疾病风险因素与静脉血栓栓塞症(VTE)之间的关联存在诸多争议。
我们进行了一项个体水平的随机效应荟萃分析,纳入了9项前瞻性研究,这些研究测量了基线心血管疾病风险因素并验证了VTE事件。各研究的定义进行了统一。传统心血管疾病风险因素采用分类和连续方式建模,使用受限立方样条。获得了总体VTE、诱因性VTE(即在存在1种或多种既定VTE风险因素的情况下发生的VTE)、非诱因性VTE、肺栓塞和深静脉血栓形成的估计值。
这些研究纳入了244865名参与者,每项研究在平均4.7至19.7年的随访期间发生了4910例VTE事件。高血压、高脂血症、糖尿病和当前吸烟在年龄、性别和体重指数调整后的总体VTE风险比分别为0.98(95%置信区间[CI]:0.89 - 1.07)、0.97(95% CI:0.88 - 1.08)、1.01(95% CI:0.89 - 1.15)和1.19(95% CI:1.08 - 1.32)。完全调整后,这些估计值在数值上相似。连续建模时,观察到收缩压与VTE呈负相关(收缩压160 mmHg与110 mmHg时的风险比 = 0.79 [95% CI:0.68 - 0.92]),但舒张压或血脂指标与VTE无此关联。VTE亚型分析的一个重要发现是,吸烟与诱因性VTE相关,但与非诱因性VTE无关。当前吸烟与诱因性和非诱因性VTE关联的完全调整风险比分别为1.36(95% CI:1.22 - 1.52)和1.08(95% CI:0.90 - 1.29)。
除了吸烟与诱因性VTE之间的关联(可能通过癌症等合并症介导)外,可改变的传统心血管疾病风险因素与VTE风险增加无关。较高的收缩压与VTE呈负相关。