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Heart:全身性炎症反应作为一种新的QT间期延长的危险因素?

2017-05-11 xing.T MedSci原创

这些数据首次表明,通过IL-6水平升高反映的全身性炎症可能是一个新的QT间期延长的危险因素,在其他经典危险因素的存在情况下有助于Tdp的发生发展。如果得到证实,这可能开辟抗心律失常治疗的新途径。

越来越多的证据表明全身炎症作为获得性长QT综合征(LQTS)的一种新的潜在原因,通过细胞因子介导的心肌细胞离子通道改变。尖端扭转型室性心动过速(Tdp)是一种危及生命的发生在LQTS患者中的多形性室性心动过速,通常与多QT间期延长因素同时存在。由于经典的危险因素不能完全解释一些患者的Tdp事件,研究人员假设全身性炎症可能是一种目前被忽视的危险因素,在一般人群中可以促进Tdp的发生发展。

四十例连续就诊的经历了Tdp的患者(Tdp队列)被招募入研究,研究人员测量了其循环的C-反应蛋白(CRP)和促炎性细胞因子(白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、白细胞介素-1(IL-1))并与类风湿关节炎的患者(RA)、合并症或健康对照者进行了比较。额外有46例不同的炎症性疾病的患者(急性感染,n=31;免疫介导性疾病,n=12;其他,n=3)以及升高的CRP患者(炎症组)被前瞻性的招募入研究,校正的QT间期(QTc)和细胞因子水平在疾病活动期和随后的治疗CRP下降>75%的时期进行测量。

在Tdp队列研究中,80%的患者的CRP水平升高(中位数:3 毫克/分升),40例病例中有18例患者有明确的炎症性疾病(急性感染,n=12;免疫介导性疾病,n=5;其他,n=1)。在这些患者中,IL-6,而不是TNF-α和IL-1,比对照者和RA患者要高15-20 倍。在炎症队列中,其中QTc间期延长是常见的现象(平均值为:456.6±30.9ms),C反应蛋白降低与IL-6水平降低和QTc间期显著缩短(-22.3ms)相关。

这些数据首次表明,通过IL-6水平升高反映的全身性炎症可能是一个新的QT间期延长的危险因素,在其他经典危险因素的存在情况下有助于Tdp的发生发展。如果得到证实,这可能开辟抗心律失常治疗的新途径。

原始出处:

Pietro Enea Lazzerini,et al. Systemic inflammation as a novel QT-prolonging risk factor in patients with torsades de pointes. Heart. 2017. http://dx.doi.org/10.1136/heartjnl-2016-311079

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    2017-06-11 I come

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    0

  4. 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    2017-05-26 I come

    学习了谢谢分享

    0

  5. 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    2017-05-13 ylzr123

    感谢小编为我们精心准备了如此精辟的精神大餐,小编辛苦了,点个赞吧!

    0

  6. 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  7. 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createdBy=80d715270048, createdName=slcumt, createdTime=Sat May 13 04:02:00 CST 2017, time=2017-05-13, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=197115, encodeId=0a7519e1151f, content=学习了,谢谢, beContent=null, objectType=article, channel=null, level=null, likeNumber=91, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=, createdBy=28761705280, createdName=cuiyejia, createdTime=Fri May 12 12:57:13 CST 2017, time=2017-05-12, status=1, ipAttribution=)]
    2017-05-13 zhaojie88
  8. 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  9. 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createdBy=80d715270048, createdName=slcumt, createdTime=Sat May 13 04:02:00 CST 2017, time=2017-05-13, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=197115, encodeId=0a7519e1151f, content=学习了,谢谢, beContent=null, objectType=article, channel=null, level=null, likeNumber=91, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=, createdBy=28761705280, createdName=cuiyejia, createdTime=Fri May 12 12:57:13 CST 2017, time=2017-05-12, status=1, ipAttribution=)]
    2017-05-13 slcumt
  10. 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createdBy=80d715270048, createdName=slcumt, createdTime=Sat May 13 04:02:00 CST 2017, time=2017-05-13, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=197115, encodeId=0a7519e1151f, content=学习了,谢谢, beContent=null, objectType=article, channel=null, level=null, likeNumber=91, replyNumber=0, topicName=null, topicId=null, topicList=[], attachment=null, authenticateStatus=null, createdAvatar=, createdBy=28761705280, createdName=cuiyejia, createdTime=Fri May 12 12:57:13 CST 2017, time=2017-05-12, status=1, ipAttribution=)]
    2017-05-12 cuiyejia

    学习了,谢谢

    0

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血浆TNF-α的持续升高是全身低水平炎症反应的标志物。软脂酸(PA)是人体中最丰富的饱和脂肪酸类型。PA与血浆中的白蛋白结合,不能自由通过内皮屏障。白蛋白结合的PA必须通过细胞内胞吞作用穿过单层内皮细胞,但这一过程不是细胞间扩散。近期,一项发表在杂志Sci Rep上的研究发现TNF-α可能刺激心脏微血管内皮细胞的PA胞吞作用,这一过程进一步削弱了心肌细胞中胰岛素刺激的葡萄糖摄取,并促进了胰岛素抵抗

PNAS:为什么孤独的人更易患病?终于有答案了!

尽管既往研究已经证明,孤独会对健康产生负面影响,但人们并不知道这种关联的机制。现在,芝加哥大学心理学教授John T. Cacioppo和他的同事们进行的一项研究表明,孤独可以改变免疫系统细胞,进而增加民众的疾病易感性。这篇研究发表在Proceedings of the National Academy of Sciences。

PNAS:细胞色素P450环氧化活性调控炎症反应

单核细胞以及巨噬细胞在慢性炎症过程中起了关键的作用,而分泌一些脂类的调控分子是其发挥作用的主要手段之一。细胞色素P450(CYP)具有环氧化催化活性,能够对花生四烯酸等底物进行特异性修饰。 过去15年来,随着研究的逐步深入,我们了解到脂肪酸代谢产物参与调控了多种炎症的信号通路。但是CYP对炎症发生的调节作用目前仍不清楚。为了研究这一问题,来自英国伦敦学院大学的David Bishop-Bail

JCI:特殊基因突变或可致机体出现过度的炎症反应

近日,来自卡迪夫大学的研究人员通过研究发现了一种特殊的遗传突变,或能帮助解释为何某些免疫系统会对病毒反应过度,相关研究刊登于国际杂志Journal of Clinical Investigation 此前研究中,研究人员发现,名为Ifitm3的基因能够影响某些人群对流感病毒的易感性,而这种

Cell Death Dis:TLR4调节听觉损伤炎症反应机制

声损伤(Acoustic trauma)是成年人群中患后天性失聪的主要原因,它主要由耳蜗结构受到的压力过大而引发的。作为防护性的机制,耳蜗的免疫系统参与了由于声损伤引发的生理反应。动物实验表明一些免疫调节因子参与了耳蜗组织的免疫反应,其中包括促炎性因子TNFa、IL-6以及IL-1b,它们能够促进炎症反应;另外,一些流动性的单核细胞能够进入耳蜗分化为巨噬细胞发挥功能。耳蜗巨噬细胞参与了耳蜗的炎症反

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