Acute aortic insufficiency (AI) is an established class I indication for surgical aortic valve replacement.¹ In contrast to chronic AI where the left ventricle (LV) has time to compensate and adapt to the demands of the additional regurgitant volume, acute severe AI results in a precipitous rise in left ventricular end-diastolic pressure (LVEDP) that in turn results in pulmonary edema and hemodynamic instability. The sudden drop in aortic diastolic blood pressure accompanied by the previously mentioned rise in LVEDP can markedly reduce coronary perfusion pressure (diastolic blood pressure LVEDP) and mimic LV dysfunction due to an acute coronary syndrome.

We present a case of a patient with homograft failure resulting in acute severe AI that is illustrative of these physiological principles. Due to high surgical risk from his hemodynamic compromise, depressed ejection fraction, and prior homograft operation, the patient underwent a successful emergent transcatheter aortic valve implantation with subsequent rapid improvement of hemodynamics and normalization of LV function.

A 65-year-old male with history of hypertension, gout, seizure disorder, and bicuspid aortic stenosis who underwent a cadaveric homograft in 1995 presented to his local emergency department with acute-onset dyspnea. From a cardiopulmonary standpoint, he had been asymptomatic since his remote homograft surgery. He had been appropriately monitored with serial echocardiograms, which previously showed only mild AI. Social and family histories were noncontributory.

His physical exam was notable for tachycardia, significant hypoxia requiring 5 liters oxygen by nasal cannula, and a short diastolic murmur heard at the left lower sternal border with expiration. With the exception of rales at the lung bases, the remainder of his physical exam was unremarkable. His initial ECG showed sinus tachycardia with a heart rate of 119 beats per minute and ST depressions in the lateral leads (V₅ through V₆). He was transferred to our institution for further evaluation and management. Results of his basic metabolic panel and complete blood count were normal. His initial cardiac biomarkers were elevated (fourth generation troponin T 0.267 ng/mL). His echocardiogram demonstrated a dilated LV with reduced ejection fraction (28%) with an apical wall motion abnormality (Movie IA in the Data Supplement). Although the AI was relatively unremarkable on color Doppler (a consequence of rapid equalization of pressures), holodiastolic flow reversal was noted in the descending thoracic aorta confirming severe aortic regurgitation (Figure 1). While in the cardiac intensive care unit, a Swan-Ganz catheter was placed, and the patient was initiated on sodium nitroprusside with the goal of decreasing systemic arterial impedance which can result in a decreased LVEDP and increased systemic diastolic blood pressure.² Coronary angiography showed no significant epicardial coronary artery disease (Movie II in the Data Supplement).

Figure 1. Select images illustrating echo findings in acute aortic regurgitation.A, Apical 3 chamber view with color flow underestimating severe aortic insufficiency. B, M-mode through the mitral valve in the parasternal long-axis view showing premature closure of the mitral valve. C, Continuous wave Doppler across aortic valve with a pressure half-time of 74 ms suggestive of severe aortic insufficiency. D, Pulse wave Doppler in the descending aorta showing holodiastolic flow reversal.

Due to the depressed ejection fraction, overt heart failure, and his history of prior sternotomy in the setting of a prior homograft with marked calcification of the aorta, he was deemed high risk for emergent surgical intervention. The patient successfully underwent transfemoral approach transcatheter aortic valve implantation with a 29 mm Edwards Sapien S3 Valve. Hemodynamic pressure measurements immediately postdeployment of valve revealed a marked decline in LVEDP, rise in aortic diastolic pressures, and recovery of aortic dicrotic notch (Figure 2). Similar improvements were evident both clinically and echocardiographically with an immediate reduction in oxygen requirement, improvement in heart rate and mild recovery of left ventricular function (Movie IB in the Data Supplement). Echocardiography performed 2 weeks after the procedure showed a significant recovery in LV function and trivial AI (Movie IC in the Data Supplement).

Figure 2. Select hemodynamic tracings obtain in the catheterization laboratory.A, Pre-transcatheter aortic valve implantation (TAVI) hemodynamics: simultaneous hemodynamic tracings of the left ventricle (LV) and aorta on 200 mm Hg scale showing near equalization of LV end-diastolic pressure (LVEDP) and aortic diastolic pressure which lead to decreased coronary perfusion. B, Pre-TAVI: simultaneous hemodynamic tracings of the LV (40 mm Hg scale) and aorta (200 mm Hg scale) show loss of the aortic dicrotic notch which represents closure of the aortic valve. C, Post-TAVI: simultaneous hemodynamic tracings of the LV and aorta on 200 mm Hg scale showing significant reduction in LVEDP after transcatheter aortic valve implantation. D, Post-TAVI: simultaneous hemodynamic tracings of the LV (40 mm Hg scale) and aorta (200 mm Hg scale) show recovery of the aortic dicrotic notch.

The impact of a sudden loss of coronary perfusion pressure on LV function is highlighted by this case. The apical wall motion abnormality noted resembles that often seen with a stress-induced cardiomyopathy, but is likely a manifestation of this phenomenon. Previous studies have shown that severe AI can lead to a reduction in coronary blood flow potentiating myocardial ischemia due to increased LVEDP with a concomitant fall in aortic diastolic pressure.³ The immediate normalization of LVEDP and rise in aortic diastolic pressure with correction of the regurgitation illustrates the dramatic effect of acute AI on the unprepared LV. The subsequent echocardiogram showing significant improvement of systolic function further supports this observation.

This clinical vignette highlights several salient features of acute AI. Recognition of the cause of acute heart failure is pivotal to implementing an appropriate therapeutic intervention.

Support for publication was provided by the Ralph C. Wilson Jr. Fellow Leadership Education endowment.

None.

The Data Supplement is available at https://www.ahajournals.org/doi/suppl/10.1161/CIRCHEARTFAILURE.119.005896.

急性主动脉瓣关闭不全（AI）是手术主动脉瓣置换的公认I类适应症。¹与慢性AI相比，左室（LV）有时间补偿和适应额外的反流量的需求，急性严重AI会导致左心室舒张末期压力（LVEDP）急剧上升在肺水肿和血液动力学不稳定。主动脉舒张压的突然下降，伴随着先前提到的LVEDP的升高，可以显着降低冠状动脉的灌注压（舒张压LVEDP）并模仿急性冠状动脉综合征所致的LV功能障碍。

我们介绍了一个患者，其同种移植失败导致急性严重AI的发生，这说明了这些生理原理。由于血液动力学受损，射血分数降低和先前进行的同种异体移植手术，手术风险较高，因此患者成功地成功完成了经导管主动脉瓣植入手术，随后迅速改善了血液动力学，并使左室功能正常化。

一名65岁的男性，有高血压，痛风，癫痫发作和二尖瓣主动脉狭窄的病史，于1995年接受了尸体同种异体移植术，并因急性发作的呼吸困难向当地急诊科就诊。从心肺的角度来看，自远程异体移植手术以来，他一直没有症状。连续超声心动图对他进行了适当的监测，以前仅显示了轻度的AI。社会和家庭的历史是无贡献的。

他的身体检查主要表现为心动过速，明显的缺氧，需要通过鼻插管注入5升氧气，并且在胸骨左下边界处听到一小段舒张期杂音，并伴有呼气。除了肺基部的罗音外，他的其余体检情况均不明显。他的最初心电图显示窦性心动过速，心律为每分钟119拍，侧导联ST压低（V ₅至V ₆）。他被转移到我们的机构进行进一步评估和管理。他的基本代谢指标和全血细胞计数结果正常。他最初的心脏生物标志物升高（第四代肌钙蛋白T 0.267 ng / mL）。他的超声心动图显示左室扩张，左室射血分数降低（28％），并伴有根尖壁运动异常（数据补充中的电影IA）。尽管AI在彩色多普勒检查中相对不显着（压力快速均衡的结果），但在降主动脉中注意到了舒张性逆流，证实了严重的主动脉瓣关闭不全（图1）。在心脏重症监护室中，放置了Swan-Ganz导管，²冠状动脉造影未显示明显的心外膜冠状动脉疾病（数据补充资料中的Movie II）。

图1. 选择的图像说明在急性主动脉瓣关闭不全中的回声发现。A，心尖3房视图，其中血流低估了严重的主动脉瓣关闭不全。B，通过胸骨旁长轴视图中的二尖瓣的M模式显示二尖瓣的过早关闭。C，横跨主动脉瓣的连续波多普勒，压力半衰期为74 ms，提示严重的主动脉瓣关闭不全。D，在降主动脉中的脉搏波多普勒，显示出总体舒张期逆流。

由于射血分数降低，明显的心力衰竭，以及在先行同种异体移植且主动脉钙化明显的情况下进行过先前的胸骨切开术的历史，他被认为是急诊手术干预的高风险。该患者成功地用29 mm Edwards Sapien S3瓣膜经股动脉入路经主动脉瓣膜植入术。瓣膜放行后立即进行血流动力学压力测量，发现LVEDP明显下降，主动脉舒张压升高以及主动脉二尖瓣切迹的恢复（图2）。在临床和超声心动图检查中，类似的改善是明显的，可立即减少氧气需求，提高心律和左心室功能轻度恢复（数据补充资料中的Movie IB）。

图2. 选择在导管实验室获得的血液动力学示踪图。A，经导管前主动脉瓣植入术（TAVI）的血流动力学：左心室（LV）和主动脉在200 mm Hg刻度上同时进行血流动力学示踪，显示LV舒张末期压力（LVEDP）和主动脉舒张压几乎相等，从而导致降低冠状动脉灌注。B，TAVI之前：LV（40毫米汞柱刻度）和主动脉（200毫米汞柱刻度）的同时血流动力学示踪显示主动脉二尖瓣切迹消失，这表示主动脉瓣关闭。C，TAVI后：LV和主动脉同时在200 mm Hg量表上进行血流动力学示踪，显示经导管主动脉瓣植入后LVEDP显着降低。d，TAVI后：LV（40 mm Hg刻度）和主动脉（200 mm Hg刻度）的同时血流动力学示踪显示主动脉二尖瓣切迹已恢复。

这种情况强调了冠脉灌注压力突然丧失对左室功能的影响。注意到的心尖壁运动异常类似于在压力诱发的心肌病中经常见到的现象，但很可能是这种现象的一种表现。先前的研究表明，严重的AI会导致LVEDP升高，并伴随主动脉舒张压下降，从而导致冠状动脉血流量减少，从而增强心肌缺血。³ LVEDP的即时正常化和主动脉舒张压的升高以及反流的纠正说明了急性AI对未准备好的LV的巨大作用。随后的超声心动图显示了收缩功能的显着改善，进一步支持了这一观察结果。

此临床插图强调了急性AI的几个显着特征。认识急性心力衰竭的原因对于实施适当的治疗干预至关重要。

拉尔夫·C·威尔逊（Ralph C. Wilson Jr.）资深领导力教育基金会提供了出版支持。

没有。

数据补充资料可在https://www.ahajournals.org/doi/suppl/10.1161/CIRCHEARTFAILURE.119.005896上获得。