右冠状动脉痉挛导致急性下壁心梗和电风暴一例

2018-01-25 佚名 中华心血管病杂志

患者男性,47岁

【一般资料】

患者男性,47岁

【主诉】

因"发作性胸痛8h,加重1.5h",于2015年12月9日入院。

【体格检查】

血压80/50mmHg(1mmHg=0.133kPa);双肺呼吸音清,未闻及干湿性啰音;心率44次/min,心音低钝,无杂音;腹软,无压痛,肝脾未触及。

【辅助检查】

入院时心电图:窦性心律,P波与QRS波无关,心室率44次/min,Ⅰ、aVL导联ST段压低0.1mV,Ⅱ、Ⅲ、aVF导联ST段抬高0.3mV(图1)。肌钙蛋白I50%。意识恢复后1h复查心电图,示窦性心律,Ⅱ、Ⅲ、aVF导联ST段回落至等电位线。急诊经桡动脉途径行冠状动脉造影,结果显示:左主干正常;左前降支中段可见肌桥,收缩期压缩70%;左回旋支未见狭窄;右冠状动脉未见狭窄,未见血栓影(图5)。患者未行PCI,返回病房。检查心肌坏死标志物,肌钙蛋白I>25μg/L,肌酸激酶(CK)为5407U/L,肌酸激酶同工酶(CK-MB)为283U/L,天门冬氨酸氨基转移酶(AST)为388U/L,乳酸脱氢酶(LDH)为677U/L。给予阿司匹林、氯吡格雷、地尔硫和他汀等药物治疗后,患者未再发作胸痛等症状。出院前心电图示窦性心律,Ⅱ导联呈qR型,Ⅲ、aVF导联呈Qr型,T波低平(图6)。患者拒绝植入植入型心律转复除颤器(implantablecardioverterdefibrillator,ICD),住院10d后病情好转出院。













【讨论】

电风暴是指24h内自发室性心动过速或心室颤动≥2次,血液动力学不稳定,需要电除颤或电击紧急治疗的临床症候群。其发生于10%~20%的急性心肌梗死患者,多见于左前降支或右冠状动脉近端闭塞后,病死率高(60%~97%)。发病机制包括交感神经过度激活、β受体的反应性增高、希浦系统传导异常和心室颤动阈值降低。急性心肌梗死多发生于有冠状动脉粥样硬化病变基础的患者,但是随着冠状动脉造影技术的广泛开展,发现10%~15%的急性心肌梗死患者冠状动脉未见狭窄病变。研究认为其可能与冠状动脉痉挛有关。冠状动脉痉挛的发病机制目前尚未完全明确,与遗传因素、吸烟、饮酒、劳累、心理应激、运动、自主神经张力过高、冠状动脉内斑块破裂、冠状动脉支架置入和硝酸甘油突然撤药等有关。Lanza等认为,冠状动脉痉挛与血栓形成互为因果关系,持续冠状动脉痉挛可引起缺氧、血管内皮细胞损伤、血小板激活和黏附,从而诱发血栓形成,发生急性心肌梗死。本例患者的冠状动脉造影示右冠状动脉未见狭窄病变,无血栓形成,血流TIMI3级;心电图为三度房室传导阻滞,下壁导联ST-T动态演变;服用地尔硫卓治疗后未再发作胸痛。因此,考虑右冠状动脉痉挛是引起急性下壁心肌梗死及电风暴的主要原因。然而,本例患者虽然未见右冠状动脉狭窄病变、斑块和血栓,仍不能除外血栓自溶和无法识别的轻度粥样硬化斑块破裂的可能。值得注意的是,本例患者的心电图出现Lambda波,这是一个心室除极与复极均有异常的心电图波,是独立的识别猝死高危的心电图标志。Lambda波在2004年由Gussak等命名,表现为下壁导联出现ST段下斜型抬高,近似于非缺血性"动作电位样"或不典型的"墓碑样"的QRS-ST复合波,其上升支的终末部及降支均有切迹,因其形态类似于希腊字母λ(Lambda)而得名。左胸前导联表现为ST段水平压低的镜像性改变,常合并恶性室性心律失常、短阵心室颤动及心脏骤停。Potet等的研究发现,SCN5A基因上的G752R位点突变时,可以引起Ⅱ、Ⅲ、aVF导联ST段抬高和明显的J波,因此考虑Lambda波的产生主要与G752R位点突变有关。人体心肌细胞动作电位2相平台期由缓慢持续的内向钙电流、内向钠电流及短暂锐减的瞬间外向钾电流共同组成。SCN5A基因突变引起钠通道改变和复极加速,导致2相平台期复极不均衡,构成了2相折返的基础,进而导致室性心动过速和心室颤动的发生。Lambda波的出现提示患者为心脏性猝死的高危人群,建议植入ICD预防心脏性猝死。目前对Lambda波的研究及报道罕见,其临床特点及干预措施有待进一步研究。综上所述,对于急性心肌梗死患者应密切注意心电图变化,尽早判断和识别可能发生室性心动过速、心室颤动和电风暴的高危人群,针对危险因素积极采取早期干预措施,避免不良事件的发生。

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    2018-01-27 apoenzyme
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    2018-01-26 AAAAA-郑富文

    谢谢分享!

    0

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    2018-01-25 惠映实验室

    学习.谢谢分享.

    0

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