Author’s Accepted Manuscript A new regional wall motion abnormality after aortic dissection repair: What is the next step? Stephen H. Gregory, Jonathan K. Zoller, Anand Lakshminarasimhachar www.elsevier.com/locate/buildenv
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S1053-0770(17)30474-3 http://dx.doi.org/10.1053/j.jvca.2017.04.050 YJCAN4132
To appear in: Journal of Cardiothoracic and Vascular Anesthesia Cite this article as: Stephen H. Gregory, Jonathan K. Zoller and Anand Lakshminarasimhachar, A new regional wall motion abnormality after aortic dissection repair: What is the next step?, Journal of Cardiothoracic and Vascular Anesthesia, http://dx.doi.org/10.1053/j.jvca.2017.04.050 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
A new regional wall motion abnormality after aortic dissection repair: What is the next step?
1. Author: Stephen H. Gregory, MD1 · · ·
Title: Fellow, Cardiothoracic Anesthesiology Email:
[email protected] Conflicts of Interest: None
2. Author: Jonathan K. Zoller, MD1 · · ·
Title: Fellow, Cardiothoracic Anesthesiology Email:
[email protected] Conflicts of Interest: None
3. Author: Anand Lakshminarasimhachar, MD · · ·
Title: Associate Professor, Anesthesiology Email:
[email protected] Conflicts of Interest: None
1. Department of Anesthesiology, Washington University in St. Louis. Campus Box 8054. 660 S. Euclid Ave. St. Louis, MO 63110
Corresponding Author: Name: Stephen H. Gregory, MD Department: Department of Anesthesiology Institution: Washington University in St. Louis Mailing address: Campus Box 8054. 660 S. Euclid Ave. St. Louis, MO 63110 Phone: 1-618-578-8280 Email:
[email protected] Funding: No funding was used in the construction of this manuscript. Introduction:
The management of the patient presenting with an ascending aortic dissection represents a significant clinical challenge, with multiple acute and subacute complications that may present during perioperative management. Myocardial ischemia is a known complication of aortic dissection, with the
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right coronary artery being most commonly involved.1 While myocardial ischemia is typically present prior to surgical intervention, patients may also present with new onset regional wall motion abnormalities (RWMA) following the discontinuation of cardiopulmonary bypass (CPB). These patients present both a diagnostic and therapeutic challenge, as there are multiple potential mechanisms of ischemia and options for management. We present a case of a patient with a new RWMA following repair of an ascending aortic dissection and discuss the challenges in clinical management.
Case report: A 78 year-old woman with a history of Stanford Type B aortic dissection with prior thoracic endovascular aortic repair presented with acute onset of chest and back pain. Computed tomography (CT) imaging demonstrated a new Stanford Type A aortic dissection, likely due to retrograde stent-graft migration. The patient was transferred to the operating room for emergent surgical repair. Transesophageal echocardiography (TEE) prior to cardiopulmonary bypass showed normal left ventricular systolic function and an ascending aortic hematoma consistent with aortic dissection. (Figure 1) Although there was proximal extension of the dissection flap to near the origin of the right coronary artery, there was no preoperative evidence of coronary dissection. The patient underwent total arch replacement with reconstruction of the sinotubular junction under moderate hypothermic circulatory arrest with antegrade cerebral perfusion. The aortic root was not replaced and the coronary arteries did not require re-implantation. After weaning from cardiopulmonary bypass (CPB), heart function was initially noted to be normal. Following the administration of 1/3 of the protamine, the patient developed gradual decompensation with severe hypokinesis of the anterior and anterolateral wall noted on TEE. (Video 1)
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Clinical Challenge: What was the mechanism of this patient’s new regional wall motion abnormality? What is the next step in management? The possible etiologies for the patient’s decompensation were felt to be either (a) occlusion of the left coronary artery by a suture placed during reconstruction of the sinotubular junction, (b) preexisting coronary artery disease with acute arterial occlusion, (c) undiagnosed retrograde dissection into the coronary artery, or (d) coronary arterial air embolism resulting in decompensation. Due to the delayed presentation of the RWMA following the discontinuation of CPB, it was felt that preexisting coronary artery disease was the most likely etiology, although a delayed presentation of mechanical coronary obstruction remained high on the differential diagnosis. Unfortunately, the patient had no prior left heart catheterization available to help corroborate this suspicion or direct therapy. Undiagnosed retrograde dissection was felt to be unlikely given that the aortic root was carefully examined during surgical repair, and the exclusive involvement of the left coronary artery distribution and a lack of observable air on TEE examination suggested against air embolism. The management of this new RWMA was discussed with the surgical team. Potential options for intervention included performing coronary artery bypass grafting guided by TEE imaging or transfer to the cardiac catheterization laboratory for possible percutaneous coronary intervention. If attempts at revascularization were unsuccessful, it was felt that the patient would likely require postoperative mechanical circulatory support.
Clinical course: Due to the patient’s progressive and rapid clinical deterioration with escalating inotropic requirements, the patient was emergently returned to cardiopulmonary bypass. Reexamination of the aortic root revealed no evidence of mechanical coronary occlusion, but significant difficulty was encountered when inserting a 1.5 mm coronary artery probe, suggesting that severe coronary artery disease was the most likely etiology of decompensation. Therefore, two saphenous vein grafts were
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placed to the left anterior descending and obtuse marginal arteries, corresponding to the distribution of the new RWMA as diagnosed by TEE. The patient was then weaned from cardiopulmonary bypass on an epinephrine infusion with significant improvement in myocardial function. Assessment of the saphenous vein grafts with ultrasound demonstrated excellent flow, and the patient was transferred to the intensive care unit for postoperative management. (Video 2)
Discussion: Coronary ischemia is a known complication of ascending aortic dissection, occurring in approximately 15% of patients presenting for operative repair.1 While ischemia evident preoperatively is typically the result of proximal extension of the aortic dissection into the coronary arteries, a new RWMA following the discontinuation of cardiopulmonary bypass has a number of possible etiologies.1-4 The approach to the patient with a new RWMA following aortic dissection repair should be guided by (a) the specific operative repair performed, (b) echocardiographic assessment of the distribution of the RWMA, (c) the time to onset of ischemia following weaning from CPB, and (d) an assessment of patient-specific risk factors for coronary artery disease. Patients who have a surgical repair that involves replacement of the aortic root and re-implantation of the coronary arteries are at increased risk of mechanical obstruction due to kinking or obstruction of the coronary artery button.4 Similarly, patients who demonstrate evidence of myocardial ischemia prior to cardiopulmonary bypass are likely to have mechanical obstruction from proximal extension of the aortic dissection into the right or left coronary artery ostia. A new RWMA immediately following weaning from CPB is also more likely to be due to mechanical occlusion, as full anticoagulation required for cardiopulmonary bypass is likely to protect against acute coronary thrombosis. In this case, the proximal aortic anastomosis was performed above the level of the aortic root, suggesting mechanical occlusion was less likely. Additionally, the patient’s advanced age, delayed time to presentation (corresponding with administration of protamine), and the presence of a distinct RWMA in
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the distribution of the left anterior descending artery increased the likelihood that coronary artery disease was responsible for the new RWMA. Percutaneous coronary intervention (PCI) and rescue coronary artery bypass grafting (CABG) have both been described as potential management strategies for patients with acute coronary occlusion following aortic dissection repair.2, 4 While PCI allows for a more directed approach to therapy, it typically requires transport of an unstable patient to the cardiac catheterization laboratory. Furthermore, PCI with stent placement necessitates the use of antiplatelet agents to maintain stent patency, which may worsen postoperative bleeding. In contrast, rescue CABG may be performed immediately when a new RWMA is identified following CPB.4 Shahriari and colleagues reported three patients who required rescue CABG shortly after aortic root replacement, including two patients who received saphenous vein graft placement during their initial operation.4 This suggests that, while preoperative left heart catheterization may be beneficial to define coronary anatomy, TEE guidance may also be used exclusively to direct emergent CABG in the case of severe hemodynamic instability. In this case, the presence of a clear, well-defined RWMA was essential to direct surgical therapy. Patients with ongoing hemodynamic instability unresponsive to inotropic or vasopressor support may require mechanical circulatory support following repair of an aortic dissection. Given this patient’s hemodynamic decompensation, unsuccessful revascularization likely would have necessitated extracorporeal support. Venoarterial ECMO (VA-ECMO) following repair of an ascending aortic dissection is associated with a dramatic increase in perioperative mortality.5 However, VA-ECMO remains the primary means for hemodynamic support in patients with refractory cardiogenic shock following aortic dissection repair, as intraaortic balloon counterpulsation is contraindicated in this setting. Fortunately, this patient showed a dramatic improvement in myocardial function following revascularization and mechanical circulatory support was unnecessary.
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Conclusions: The presence of a new RWMA after repair of an ascending aortic dissection is a clinical challenge that requires consideration of patient comorbidities and the operative repair to determine the most likely etiology. Thoughtful TEE examination may allow for rapid diagnosis and intervention to improve clinical outcomes in this challenging patient population.
References
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Hori D, Noguchi K, Yamaguchi A, et al.: Successful percutaneous coronary intervention in a case of acute aortic dissection complicated with malperfusion of the left main coronary artery after replacement of the ascending aorta. Gen Thorac Cardiovasc Surg. 60:381-385, 2012.
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Marchetti M, Scacciatella P, Di Rosa E, et al.: Coronary Thrombosis and Type A Aortic Dissection. J Card Surg. 30:583-585, 2015.
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Shahriari A, Eng M, Tranquilli M, et al.: Rescue coronary artery bypass grafting (CABG) after aortic composite graft replacement. J Card Surg. 24:392-396, 2009.
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Figure/Video Legends Figure 1: Midesophageal aortic valve long-axis view demonstrating the presence of an ascending aortic hematoma consistent with Stanford Type A aortic dissection. LA = left atrium; AV = aortic valve; RV = right ventricle.
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