Kubota Yasuhiko, Alonso Alvaro, Folsom Aaron R
Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, USA; Public Health, Department of Social Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
Thromb Res. 2017 Jul;155:116-120. doi: 10.1016/j.thromres.2017.05.016. Epub 2017 May 17.
Although it has been suggested that increased concentrations of activated platelet biomarkers are associated with increased risk of incident cardiovascular disease (CVD) in the general population, evidence for this association is still controversial. Thus, we tested the hypothesis that activated platelets, measured by higher concentrations of β-thromboglobulin, are associated with increased risk of incident CVD (coronary heart disease, heart failure ischemic stroke, and atrial fibrillation).
We prospectively followed a cohort random sample of the Atherosclerosis Risk in Communities (ARIC) cohort, aged 45-64years, and free of CVD at baseline who had previous measurements of plasma β-thromboglobulin. We identified incident CVD from 1987 through 2013, and used a weighted Cox proportional hazard models to estimate hazard ratios (HRs) and their 95% confidence intervals (CIs).
During the 14,387person-years of follow-up for the 746 participants, we identified 140 coronary heart diseases, 123 heart failures, 54 ischemic strokes, and 126 atrial fibrillations. The age-, sex-, and race-adjusted model showed no association between plasma β-thromboglobulin and CVD, regardless of subtypes. After further adjustment for other CVD risk factors, including antiplatelet agent use, β-thromboglobulin remained unassociated with CVD risk.
In the prospective population-based ARIC cohort, β-thromboglobulin was not associated with CVD risk. Our results do not support the hypothesis that a blood marker of higher platelet activity reflects increased future risk of CVD in the general population.
尽管有人提出,在普通人群中,活化血小板生物标志物浓度升高与心血管疾病(CVD)发病风险增加有关,但这种关联的证据仍存在争议。因此,我们检验了以下假设:通过较高浓度的β-血小板球蛋白测量的活化血小板与CVD(冠心病、心力衰竭、缺血性卒中和房颤)发病风险增加有关。
我们对社区动脉粥样硬化风险(ARIC)队列中年龄在45 - 64岁、基线时无CVD且之前测量过血浆β-血小板球蛋白的队列随机样本进行了前瞻性随访。我们确定了1987年至2013年期间发生的CVD病例,并使用加权Cox比例风险模型来估计风险比(HRs)及其95%置信区间(CIs)。
在对746名参与者进行的14387人年的随访中,我们确定了140例冠心病、123例心力衰竭患者、54例缺血性卒中患者和126例房颤患者。年龄、性别和种族调整后的模型显示,无论CVD亚型如何,血浆β-血小板球蛋白与CVD之间均无关联。在进一步调整其他CVD风险因素(包括使用抗血小板药物)后,β-血小板球蛋白与CVD风险仍无关联。
在基于人群的前瞻性ARIC队列中,β-血小板球蛋白与CVD风险无关。我们的结果不支持以下假设:较高血小板活性的血液标志物反映了普通人群未来CVD风险增加。