肌钙蛋白I(cTnI)如此之高,竟是因为脑血管意外?

2021-12-20 检验之声 网络

中医来讲,脑血管和心血管疾病,存在空间、时间和直接的相互作用。心脏疾病可诱发缺血性脑卒中,缺血性脑事件可导致心脏功能紊乱,脑心相互作用,剪不断、理不乱。

 

胶州市人民医院--王晓燕,赵而玉

 

2021年10月,中国医师协会检验分会心血管专家委员会组织撰写的《心肌肌钙蛋白实验室检测与临床应用中国专家共识》正式刊出。共识介绍,心肌肌钙蛋白(cTn)的临床应用从根本上改变了急性冠脉综合征(ACS)诊断、预后判断、治疗和危险分层的格局,其对急性心肌梗死(AMI)的诊断被相关国际指南列为I级a类推荐。但在实际工作中,cTn的检测受到多种内外源性干扰因素的影响,而且部分非冠状动脉缺血事件也会引起肌钙蛋白的显著升高,因而由此引发的临床困惑时有发生。

案例简介

肌钙蛋白I(cTnI)检测

肌钙蛋白I(cTnI)异常升高,结果:70.64ng/ml,检测参数如下:

分析处理及思维导图

虽然患者副诊断有动脉粥样硬化性心脏病和主动脉夹层,但与临床沟通中,并未出现ACS相关临床症状,cTnI如此之高,实验室首先要进行假阳性的排除和其他检测系统的比对。参考试剂说明书:

思维导图

标本处理

更换检测系统(拜明化学发光检测平台),cTnI结果也是明显升高。

确定了cTnI结果的真阳性,与临床沟通,通过会诊排除了急性心梗的可能。

患者cTnI如此之高,却没有明显的急性冠脉综合征表现,难道主要是因为脑血管意外吗?

资料查阅

研究表明,急性脑梗死后心肌标志物升高的机制,可能为:① 神经源性增高:大脑中动脉区域的梗死有更高的儿茶酚胺水平,提示这个区域的梗死更易发生交感活化及儿茶酚胺水平升高,继之导致心脏损伤[1]。② 心源性增高,患者的年龄越老,心脏基础疾病的概率就会越高,而且有时心脏症状不典型,有时不易辨认究竟是脑梗死本身还是心脏基础疾病引起的心肌标志物升高。

脑血管意外中的急性非创伤性脑出血(ICH)患者,cTnI增高与患者是否合并蛛网膜下腔出血、累及岛叶相关区以及脑出血量显著正相关,年龄、岛叶相关区出血是cTnI增高的独立影响因素[2]。机制为大脑中岛叶是心血管调节中枢位置,岛叶卒中可能更容易起心肌损伤和心电活动异常。由于临床单纯岛叶出血并不多见,但与其位置毗邻的区域如额叶、颞叶、顶叶出血水肿也压迫岛叶,对岛叶功能产生潜在影响。蛛网膜下腔出血导致的心肌损伤报道较多,可能与交感神经过度激活有关。

另有研究显示,小儿病毒性脑炎患儿的cTnI水平明显升高,而且急性期水平要高于缓解期。同时发现,cTnI水平与病情严重程度呈正相关[3]。这与小儿病毒性脑炎患儿机体供氧不足时,导致过氧化物及酸性代谢产物等堆积,损伤心肌细胞膜,提升了细胞的通透性,造成cTnI进入血液,促使cTnI检测升高。

中医来讲,脑血管和心血管疾病,存在空间、时间和直接的相互作用。心脏疾病可诱发缺血性脑卒中,缺血性脑事件可导致心脏功能紊乱,脑心相互作用,剪不断、理不乱。

参考文献:

[1]李乐燕,王建国等.老年急性脑梗死患者心电图和心肌标志物变化与预后的关系[J].心血管康复医学杂志,2014,6(23):262-265.

[2]胡正涛,张勇等.急性非创伤性脑出血患者肌钙蛋白I升高的影响因素及临床意义[J].临床急诊杂志,2021,7(22):453-457.

[3]宋冰.心肌酶和肌钙蛋白I在小儿病毒性脑炎的诊断意义[J].现代实用医学,2017,9(6):786-787.

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    2022-04-21 shanyongle
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    2021-12-20 1561fd8b97m

    脑心是相通的

    0

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主动脉僵化或提示神经炎症和神经变性

Stroke:既往脑血管疾病患者的COVID-19死亡率增加

该研究的主要结局是COVID-19阳性后任何原因的死亡率。研究人员使用针对合并症调整的Cox比例回归分析,并对性别和年龄(<60、60-79和80岁以上)进行分层分析。