High-Sensitivity C-Reactive Protein and Lipoprotein-Associated Phospholipase A2 Stability Before and After Stroke and Myocardial Infarction
High-Sensitivity C-Reactive Protein and Lipoprotein-Associated Phospholipase A2 Stability Before and After Stroke and Myocardial Infarction
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DOI：
10.1161/strokeaha.109.552802
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发表时间：
2009-10-01
期刊：
影响因子：
8.3
通讯作者：
Sacco, Ralph L.
中科院分区：
文献类型：
--
作者：
Elkind, Mitchell S. V.;Leon, Vladimir;Sacco, Ralph L.
背景和目的：超敏C反应蛋白（hsCRP）和脂蛋白相关磷脂酶A（2）（Lp-PLA（2））被假设为全身炎症和心肌梗死（MI）和卒中风险的生物标志物。然而，关于这些标记物随时间的稳定性，特别是关于急性血管事件对这些标记物水平的影响，知之甚少。方法：从北方曼哈顿研究（NOMAS）中的52名无中风参与者中以4年的间隔收集血清样品，并使用标准技术测定hsCRP和Lp-PLA（2）质量和活性水平。根据需要进行水平的对数转换，以稳定方差。使用未调整和调整人口统计学和其他风险因素的随机效应模型评估标志物水平随时间的稳定性。此外，37名最初无卒中的卒中（n = 17）或MI（n = 20）参与者的样本可用于血管事件前后的测量（中位数5天，范围2 - 40天）。结果：HsCRP和Lp-PLA（2）活性水平随时间推移保持稳定，而Lp-PLA（2）质量水平平均每年下降5%（P = 0.0015）。使用可接受的阈值来定义Lp-PLA（2）质量的风险类别，随时间推移无显著变化。HsCRP在卒中后（从卒中前的中位数2.2 mg/L增加到卒中后的中位数6.5 mg/L; P = 0.0067）和MI后（从MI前的中位数2.5 mg/L增加到MI后的中位数13.5 mg/L; P < 0.0001）增加。Lp-PLA（2）质量和活性水平在卒中和MI后均显著降低（对于Lp-PLA（2）质量，中风后从中值210.0 ng/mL到169.4 ng/mL，P = 0.0348，MI后从中值233.0 ng/mL到153.9 ng/mL，P < 0.0001）。而hsCRP和Lp-PLA（2）活性随时间推移而稳定。急性卒中和MI后，hsCRP升高，而Lp-PLA（2）质量和活动水平降低。这些变化意味着在卒中和MI后不久进行的测量不能反映卒中前的水平，并且对于长期危险分层可能不太可靠。（中风。2009;40：3233-3237）。
Background and Purpose-High-sensitivity C-reactive protein (hsCRP) and lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) are hypothesized to be biomarkers of systemic inflammation and risk of myocardial infarction (MI) and stroke. Little is known, however, about the stability of these markers over time, and in particular, about the effects of acute vascular events on these marker levels.Methods-Serum samples were collected at 4 annual intervals in 52 stroke-free participants from the Northern Manhattan Study (NOMAS) and assayed for hsCRP and Lp-PLA(2) mass and activity levels using standard techniques. Log transformation of levels was performed as needed to stabilize the variance. Stability of marker levels over time was assessed using random effects models unadjusted and adjusted for demographics and other risk factors. In addition, samples from 37 initially stroke-free participants with stroke (n = 17) or MI (n = 20) were available for measurement before and after the vascular event (median 5 days, range 2 to 40 days). Levels before and after events were compared using nonparametric tests.Results-HsCRP and Lp-PLA(2) activity levels were stable over time, whereas Lp-PLA(2) mass levels decreased on average 5% per year (P = 0.0015). Using accepted thresholds to define risk categories of Lp-PLA(2) mass, there was no significant change over time. HsCRP increased after stroke (from median 2.2 mg/L prestroke to 6.5 mg/L poststroke; P = 0.0067) and MI (from median 2.5 mg/L pre-MI to 13.5 mg/L post-MI; P < 0.0001). Lp-PLA(2) mass and activity levels both decreased significantly after stroke and MI (for Lp-PLA(2) mass, from median 210.0 ng/mL to 169.4 ng/mL poststroke, P = 0.0348, and from median 233.0 ng/mL to 153.9 post-MI, P < 0.0001).Conclusion-Lp-PLA(2) mass levels decrease modestly, whereas hsCRP and Lp-PLA(2) activity appear stable over time. Acutely after stroke and MI, hsCRP increases whereas Lp-PLA(2) mass and activity levels decrease. These changes imply that measurements made soon after stroke and MI are not reflective of prestroke levels and may be less reliable for long-term risk stratification. (Stroke. 2009;40:3233-3237.)