Department of Clinical Medicine, UiT The Arctic University of Norway, Tromsø, Norway
Department of Neurology, University Hospital of North Norway, Tromsø, Norway.
J Am Heart Assoc. 2018 May 17;7(11):e008951. doi: 10.1161/JAHA.118.008951.
The joint effect of atherosclerosis and CRP (C-reactive protein) on risk of ischemic stroke (IS) and myocardial infarction (MI) has been sparsely studied. The aim of this study was to explore whether CRP mediates the risk of events in subjects with prevalent carotid plaque, examine synergism, and test whether CRP and carotid plaque add to risk prediction beyond traditional risk factors.
CRP and carotid total plaque area (TPA) were measured in 10 109 participants in the Tromsø Study from 1994 to 2008. Incident IS (n=671) and MI (n=1079) were registered until December 31, 2013. We calculated hazard ratios (HRs) of MI and IS according to categories of CRP (<1, 1-3, and >3 mg/L) and plaque status (no plaque and TPA below and above median) in Cox proportional hazard models with time-varying covariates. Multivariable-adjusted CRP >3 versus <1 mg/L was associated with risk of IS (HR, 1.84; 95% confidence interval, 1.49-2.26) and MI (HR, 1.46; 95% confidence interval, 1.23-1.73). TPA above median versus no plaque was associated with risk for IS (HR, 1.65; 95% confidence interval, 1.36-2.01) and MI (HR, 1.64; 95% confidence interval, 1.41-1.92). In participants with plaque, adjustment for CRP minimally attenuated the risk estimates. The highest incidence rates for MI and IS were seen in the group with both CRP >3 mg/L and TPA is above the median. TPA and CRP combined added to risk prediction beyond traditional risk factors.
The simultaneous presence of subclinical atherosclerosis and elevated CRP was associated with increased risk of IS and MI. The combined assessment of subclinical atherosclerosis and inflammatory biomarkers may improve cardiovascular disease risk stratification.
动脉粥样硬化和 C 反应蛋白（CRP）对缺血性中风（IS）和心肌梗死（MI）风险的联合影响研究较少。本研究旨在探讨 CRP 是否介导有颈动脉斑块的受试者发生事件的风险，检验协同作用，并检验 CRP 和颈动脉斑块是否比传统危险因素更能增加风险预测。
1994 年至 2008 年，在特罗姆瑟研究中对 10109 名参与者测量 CRP 和颈动脉总斑块面积（TPA）。截至 2013 年 12 月 31 日，登记了 IS（n=671）和 MI（n=1079）的发病情况。我们在 Cox 比例风险模型中，根据 CRP（<1、1-3 和>3mg/L）和斑块状态（无斑块和 TPA 低于和高于中位数）的类别计算 MI 和 IS 的危险比（HR），采用时变协变量。多变量调整后 CRP>3 与<1mg/L 与 IS（HR，1.84；95%置信区间，1.49-2.26）和 MI（HR，1.46；95%置信区间，1.23-1.73）风险相关。TPA 高于中位数与无斑块与 IS（HR，1.65；95%置信区间，1.36-2.01）和 MI（HR，1.64；95%置信区间，1.41-1.92）风险相关。在有斑块的参与者中，调整 CRP 可使风险估计值最小化。CRP>3mg/L 且 TPA 高于中位数的组中，MI 和 IS 的发病率最高。TPA 和 CRP 的联合评估可改善心血管疾病风险分层。
亚临床动脉粥样硬化和 CRP 升高的同时存在与 IS 和 MI 风险增加相关。亚临床动脉粥样硬化和炎症生物标志物的联合评估可能改善心血管疾病风险分层。
