Bui Quan M, Ang Lawrence, Phreaner Nicholas
Division of Cardiovascular Medicine, Department of Medicine, University of California, San Diego, San Diego, 9452 Medical Center Drive #7411 La Jolla, CA 92037-7411, USA.
Eur Heart J Case Rep. 2021 Apr 21;5(4):ytab127. doi: 10.1093/ehjcr/ytab127. eCollection 2021 Apr.
A subset of patients with takotsubo cardiomyopathy will develop significant dynamic left ventricular outflow tract (LVOT) obstruction leading to cardiogenic shock. However, traditional therapies for cardiogenic shock that focus on increased inotropy and afterload reduction can be detrimental in this situation.
We describe a 71-year-old woman who presented to the emergency department with typical, substernal chest pain found to be hypotensive with ST-elevations in the lateral leads. Coronary angiography showed no significant coronary artery disease, but a left ventriculogram demonstrated takotsubo cardiomyopathy. Right heart catheterization revealed cardiogenic shock and elevated filling pressures. Haemodynamics and symptoms worsened with the initiation of dopamine and placement of intra-aortic balloon pump but improved with the initiation of phenylephrine. Follow-up echocardiogram demonstrated dynamic LVOT obstruction with concomitant severe mitral regurgitation (MR). The patient recovered in the intensive care unit for 5 days after successful weaning of phenylephrine and initiation of low-dose beta-blocker. Repeat echocardiogram 3 weeks later showed complete resolution of apical akinesis, LVOT obstruction, and MR.
Elucidating whether dynamic LVOT obstruction is contributing to cardiogenic shock physiology is paramount since the management radically differs depending on the presence or absence of obstruction. Corrective therapy focuses on reducing the LVOT gradient and includes fluid administration to improve preload, beta-blocker therapy to increase diastolic filling time, and vasopressors to raise afterload.
一部分应激性心肌病患者会出现显著的动态左心室流出道(LVOT)梗阻,进而导致心源性休克。然而,针对心源性休克的传统治疗方法侧重于增加心肌收缩力和降低后负荷,在这种情况下可能有害。
我们描述了一名71岁女性,她因典型的胸骨后胸痛就诊于急诊科,发现血压降低且侧壁导联ST段抬高。冠状动脉造影显示无明显冠状动脉疾病,但左心室造影显示为应激性心肌病。右心导管检查显示心源性休克和充盈压升高。使用多巴胺并置入主动脉内球囊反搏后,血流动力学和症状恶化,但使用去氧肾上腺素后有所改善。随访超声心动图显示动态LVOT梗阻并伴有严重二尖瓣反流(MR)。在成功停用去氧肾上腺素并开始使用小剂量β受体阻滞剂后,患者在重症监护病房恢复了5天。3周后复查超声心动图显示心尖运动消失、LVOT梗阻和MR完全消失。
明确动态LVOT梗阻是否导致心源性休克的病理生理过程至关重要,因为根据梗阻的有无,治疗方法有很大差异。纠正治疗的重点是降低LVOT压力阶差,包括补液以改善前负荷、使用β受体阻滞剂以增加舒张期充盈时间,以及使用血管升压药以提高后负荷。