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Table of Contents
Year : 2020  |  Volume : 10  |  Issue : 3  |  Page : 148-151

Aggressive treatment of afterload mismatch to address left ventricular dysfunction after mitral valve repair: A case report

1 Department of Anesthesiology, The Ohio State University Wexner Medical Center, Columbus, OH, USA
2 Department of Cardiac Surgery, The Ohio State University Wexner Medical Center, Columbus, OH, USA

Date of Submission05-Dec-2019
Date of Acceptance25-Feb-2020
Date of Web Publication22-Sep-2020

Correspondence Address:
Dr. Charles Vinsant
Department of Anesthesiology, The Ohio State University Wexner Medical Center, 411 Doan Hall, 410 West 10th Avenue, Columbus, OH 43210
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/IJCIIS.IJCIIS_101_19

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Mitral regurgitation (MR), one of the most common valvulopathies, occurs in at least 10% of the individuals older than 75 years. The long-standing volume overload occurring in severe MR inevitably leads to left ventricular (LV) enlargement and dysfunction; untreated, severe MR can progress to heart failure and death. Hypotension following separation from cardiopulmonary bypass after mitral valve intervention should alert an anesthesiologist to consider a myriad of differential diagnoses. This includes, but is not limited to, afterload mismatch, which can contribute to severe LV dysfunction, even in patients with seemingly normal preoperative ejection fraction. We present a case of acute on chronic biventricular failure after mitral valve repair due to afterload mismatch and discuss its management intraoperatively. Admittedly, identifying the causes of hypotension to guide treatment after mitral valve surgery in patients with severe MR is challenging. High index of suspicion and transesophageal echocardiogram guidance are important for prompt diagnosis, increasing the likelihood of successful outcomes with appropriate clinical management.

Keywords: Cardiac anesthesia, cardiac inotropism, heart failure, mitral valve annuloplasty

How to cite this article:
Vinsant C, Holecko J, Whitson BA, Turner K. Aggressive treatment of afterload mismatch to address left ventricular dysfunction after mitral valve repair: A case report. Int J Crit Illn Inj Sci 2020;10:148-51

How to cite this URL:
Vinsant C, Holecko J, Whitson BA, Turner K. Aggressive treatment of afterload mismatch to address left ventricular dysfunction after mitral valve repair: A case report. Int J Crit Illn Inj Sci [serial online] 2020 [cited 2022 Nov 30];10:148-51. Available from: https://www.ijciis.org/text.asp?2020/10/3/148/295773

   Introduction Top

Mitral regurgitation (MR) is one of the most common valvulopathies, occurring in at least 10% of the individuals older than 75 years.[1] The long-standing volume overload occurring in severe MR inevitably leads to left ventricular (LV) enlargement and dysfunction; untreated, severe MR can progress to heart failure and death.[2] Optimal timing of mitral valve repair or replacement is dependent on multiple factors, including symptomatology, evidence of LV dysfunction, chronicity of the MR, and likelihood of a successful and durable repair versus replacement.[2],[3] In patients undergoing corrective mitral valve surgery for MR, hypotension following separation from cardiopulmonary bypass (CPB) should alert an anesthesiologist to consider a myriad of differential diagnoses including, but not limited to, iatrogenic mitral valve stenosis, hemorrhage, ischemia, and right heart failure [Table 1].[4],[5],[6],[7] In addition, hypotension in this setting warrants consideration of an afterload mismatch. Afterload is generally considered to be the force or load against which the LV must eject during systole. In the setting of long-standing MR, the left atrium offers an additional, low-resistance system into which the LV can eject.[4] Following corrective surgical elimination of this low-resistance pathway, the LV must now eject against an “unmasked” afterload. This afterload mismatch can contribute to LV dysfunction following separation from CPB, even in patients with seemingly normal preoperative ejection fraction (EF). We present a case of acute-onset chronic biventricular failure after mitral valve repair due to LV afterload mismatch and its management intraoperatively.
Table 1: Etiology of left ventricular failure following mitral valve repair/replacement

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   Case Report Top

A 64-year-old male with a medical history notable for atrial fibrillation and severe MR presented for mitral valve repair. Preoperative transthoracic echocardiography and transesophageal echocardiogram (TEE) demonstrated severe MR with a flail P2 segment, resulting in an anteriorly directed regurgitant jet, a severely dilated left atrium measuring 8.9 cm, LV inferior wall hypokinesis contributing to mildly reduced LV systolic function with an EF of 40%–45%, as well as mild right ventricular (RV) dysfunction with free wall hypokinesis [Figure 1] and [Video 1]. On the day of surgery, the patient's baseline blood pressure was noted to be 106/76 mmHg, with mean arterial pressure of 85 mmHg and heart rate of 94 beats/min. Following an uneventful induction of general anesthesia, right internal jugular introducer and pulmonary artery catheter were placed showing systolic/diastolic/mean pulmonary artery pressures of 50/35/44 mmHg, respectively, and a central venous pressure of 18 mmHg. Intraoperative preintervention TEE confirmed the mitral valve pathology, as well as mild biventricular dysfunction. Additional hemodynamic data included a cardiac index of 1.5.
Figure 1: Preprocedural transesophageal echocardiograms midesophageal four-chamber view showing left ventricular ejection fraction 40%–45% and mild right ventricular dilation with mild-free wall hypokinesis

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Following initiation of CPB utilizing anterograde and retrograde cardioplegia, the patient underwent a mitral valve repair with posterior leaflet quadrangular resection and placement of a Carpentier-Edwards 34-mm mitral valve annuloplasty ring (Edwards Lifesciences Corp., Irvine, CA, USA). In preparation for the weaning of CPB, biventricular cardiac function and vasomotor tone were supported with epinephrine (0.08 mcg/kg/min), milrinone (0.2 mcg/kg/min), and inhaled epoprostenol at a paced heart rate of 90 beats/min. Pharmacologic agents were chosen based on preprocedural biventricular dysfunction and anticipation of post-CPB vasoplegia. Attempting to separate from CPB was initially unsuccessful due to refractory hypotension, severe global LV dysfunction, and mild RV dysfunction, which slowly worsened despite the above-described pharmacologic support [Table 2] for hemodynamic measurements]. Despite returning on CPB and escalating pharmacologic support by increasing epinephrine (0.15 mcg/kg/min) and adding norepinephrine to the afore-mentioned agents, the patient's hemodynamic parameters deteriorated further [Table 2], resulting in a second unsuccessful wean from CPB. TEE revealed a moderately dilated RV and severely reduced LV systolic function (LV ejection fraction [LVEF] of ~20%) with spontaneous echo contrast (SEC) formation in the left atrium [Figure 2] and [Video 2]. Interrogation of the newly repaired valve demonstrated peak and mean gradients of 2 and 1 mm Hg, respectively, with no residual MR, decreasing the likelihood of iatrogenic mitral stenosis. The patient was placed back on CPB, at which time an intra-aortic balloon pump (IABP) was placed by the surgical team to improve coronary perfusion and reduce afterload. With the presumption that the afterload mismatch was contributing to LV failure in the setting of SEC, pharmacological support was modified with the goal to increase inotropy while reducing afterload. Along with milrinone, dobutamine was initiated (10 mcg/kg/min), epinephrine was decreased (0.1 mcg/kg/min), and vasopressor therapy was modified to vasopressin (0.04 mcg/kg/min) with discontinuation of norepinephrine. A third attempt to separate from CPB proved successful with greatly improved biventricular function on TEE and resolution of previously observed SEC [Table 2], [Figure 3] and [Video 3]. On the postoperative day (POD) 3, the patient was weaned off inotropic support, and the IABP was removed. Throughout the hospitalization, he remained hemodynamically stable and was eventually discharged on POD 14 after an uneventful postoperative course in which he was initiated on guideline-directed medical therapy for heart failure. Postoperative TEE assessment of the mitral valve approximately 2 months after the operation was notable for a mean gradient across the mitral valve of 3 mmHg and an LVEF of 35%–40%. Follow-up discussion with the patient was notable for reported good functional status with ultimate return to work in his woodshop at 8 weeks postoperatively.
Table 2: Hemodynamic data during weaning of cardiopulmonary bypass

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Figure 2: Transesophageal echocardiograms midesophageal four-chamber view showing acute-onset chronic left ventricular dysfunction, severe right ventricular dilation, severe right atrial enlargement, and biatrial spontaneous echo contrast status postmitral valve repair and ring annuloplasty

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Figure 3: Transesophageal echocardiograms midesophageal four-chamber view showing improved acute-onset chronic left ventricular dysfunction, improved right ventricular ejection fraction, and resolution of spontaneous echo contrast following initiation of inodilator therapy

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   Discussion Top

Cardiac adaptations to chronic MR are complex, demonstrating early eccentric hypertrophy in response to the volume-overloaded state. However, in contrast to other volume-overload-related valvulopathies (such as aortic regurgitation), the wall stress during systole remains normal due to low impedance flow into the left atrium through the mitral valve during ventricular systole, leading to chronic asymptomatic phase of MR.[1],[8] However, progressive LV enlargement due to volume overload inevitably stretches cardiac myocytes beyond normal contractile length, resulting in systolic dysfunction. As the LV fails, the higher intraventricular pressures translate to the left atrium and subsequently the pulmonary vasculature, resulting in dyspnea, atrial fibrillation secondary to left atrial enlargement, and pulmonary hypertension which can be detrimental to the RV.

Surgical correction of a regurgitant mitral valve can have profound impacts on the loading conditions of the LV. With chronic MR, the impedance to LV ejection is low due to anterograde flow through the LV outflow tract, as well as retrograde flow into the left atrium, oftentimes resulting in seemingly normal preoperative LVEF on echocardiogram. Eliminating this low-resistance leak into the left atrium results in the LV ejecting primarily into the afterload of the aorta and arterial system. This unmasking of the “true” afterload can result in acute LV failure. Predictors of LV dysfunction following mitral valve surgery include increased LV size, worsening heart failure symptoms, pulmonary hypertension, atrial fibrillation, and low preoperative EF.[9],[10] However, Quintana et al. found that approximately one in five patients undergoing mitral valve surgery for severe MR with assumed “preserved” LV function (EF >60%) developed early LV dysfunction, which recovered in only 30% of patients, 5 years after repair.[11]

Afterload mismatch following surgical repair of a regurgitant mitral valve should be considered whenever refractory hypotension, LV dysfunction, and low cardiac output syndrome are evident immediately following repair.[11] Although well described in the literature as pertains to MitraClip repair, intraoperative diagnosis of afterload mismatch following mitral valve surgery is difficult because a myriad of other conditions can mimic similar presentations, in particular de novo mitral stenosis.[4],[5],[12] TEE is invaluable in the prompt recognition of the afterload mismatch following mitral valve surgery. Afterload mismatch should be considered if there is echocardiographic evidence of new or worsening LV systolic dysfunction, acute LV dilation, and formation of SEC in the left atrium or LV, particularly in the setting of normal transmitral pressure gradients.[4],[5],[6],[12]

Medical treatment of the afterload mismatch should be focused on increasing forward flow through optimization of RV and LV function while reducing LV afterload.[5] While hypotension often is the presenting symptom, the use of pure vasopressors should be avoided because the resulting increased afterload could further worsen LV contractility.[5] Inodilators, such as milrinone and dobutamine, can be ideal first-line agents as they offer inotropic support with mild vasodilating properties, which effectively decreases afterload. However, their use as solo agents in the setting of general anesthesia with reduced afterload has the potential to further worsen hypotension and compromise coronary perfusion pressure, which in turn could worsen ventricular function. In hypotensive patients, inotropic therapy with epinephrine alone, or in combination with an inodilator, can promote cardiac output without compromising coronary circulation.[4],[5],[6] Temporary mechanical circulatory support using an IABP can help accomplish two important goals through counterpulsation of a balloon placed in the descending aorta: (1) afterload reduction created by deflation of the balloon during ventricular systole and (2) maintenance of coronary perfusion pressure through inflation of the balloon following the closure of the aortic valve. Veno-arterial extracorporeal membrane oxygenation can also provide lifesaving therapy in the setting of acute LV dysfunction that is refractory to medical and mechanical support.[5],[13] In our patient, the combination of vasopressors, inodilators, and mechanical support in the form of an IABP improved forward flow and allowed successful separation from CPB with stabilization of acute on chronic biventricular failure.

Declaration of patient consent

The authors certify that they have obtained appropriate patient consent documentation, and the patient has given permission for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed. Applicable reporting guideline for case reports (CARE) was followed by the authors.


We would like to thank the Department of Cardiac Anesthesia at Ohio State University for their support and guidance at editing this article.

Financial support and sponsorship

This study was financially supported by the Department of Anesthesiology, Ohio State Wexner Medical Center.

Conflicts of interest

There are no conflicts of interest.

Ethical conduct of research

The authors of this manuscript declare that this scientific work complies with reporting quality, formatting, and reproducibility guidelines set forth by the EQUATOR Network. The authors also attest that this clinical investigation was determined to not require Institutional Review Board/Ethics Committee Review, and the corresponding protocol/approval number is not applicable.

   References Top

Nishimura RA, Vahanian A, Eleid MF, Mack MJ. Mitral valve disease–current management and future challenges. Lancet 2016;387:1324-34.  Back to cited text no. 1
Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP 3rd, Fleisher LA, et al. 2017 AHA/ACC focused update of the 2014 AHA/ACC guideline for the management of patients with valvular heart disease: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol 2017;70:252-89.  Back to cited text no. 2
Zhou T, Li J, Lai H, Zhu K, Sun Y, Ding W, et al. Benefits of early surgery on clinical outcomes after degenerative mitral valve repair. Ann Thorac Surg 2018;106:1063-70.  Back to cited text no. 3
Dalia AA, Essandoh M. Acute hypotension after mitraclip implantation due to acute left ventricular failure. Semin Cardiothorac Vasc Anesth 2018;22:332-4.  Back to cited text no. 4
Essandoh MK. Afterload mismatch after mitraclip implantation: The potential impact of pharmacologic support. J Cardiothorac Vasc Anesth 2017;31:702-6.  Back to cited text no. 5
Melisurgo G, Ajello S, Pappalardo F, Guidotti A, Agricola E, Kawaguchi M, et al. Afterload mismatch after MitraClip insertion for functional mitral regurgitation. Am J Cardiol 2014;113:1844-50.  Back to cited text no. 6
Nguyen L, Roth DM, Shanewise JS, Kaplan JA. Discontinuing Cardiopulmonary Bypass. Kaplan's Essentials of Cardiac Anesthesia. 2nd ed. Philadelphia, PA: Elsevier; 2018. p. 715-40.  Back to cited text no. 7
Ross J Jr., Afterload mismatch in aortic and mitral valve disease: Implications for surgical therapy. J Am Coll Cardiol 1985;5:811-26.  Back to cited text no. 8
Varghese R, Itagaki S, Anyanwu AC, Milla F, Adams DH. Predicting early left ventricular dysfunction after mitral valve reconstruction: The effect of atrial fibrillation and pulmonary hypertension. J Thorac Cardiovasc Surg 2014;148:422-7.  Back to cited text no. 9
Suri RM, Schaff HV, Dearani JA, Sundt TM 3rd, Daly RC, Mullany CJ, et al. Determinants of early decline in ejection fraction after surgical correction of mitral regurgitation. J Thorac Cardiovasc Surg 2008;136:442-7.  Back to cited text no. 10
Quintana E, Suri RM, Thalji NM, Daly RC, Dearani JA, Burkhart HM, et al. Left ventricular dysfunction after mitral valve repair—the fallacy of “normal” preoperative myocardial function. J Thorac Cardiovasc Surg 2014;148:2752-60.  Back to cited text no. 11
Tang GH, Cohen M, Dutta T, Undemir C. Afterload mismatch after transcatheter mitral valve repair with MitraClip for degenerative mitral regurgitation in acute cardiogenic shock. Catheter Cardiovasc Interv 2018;92:E168-71.  Back to cited text no. 12
Rihal CS, Naidu SS, Givertz MM, Szeto WY, Burke JA, Kapur NK, et al. 2015 SCAI/ACC/HFSA/STS clinical expert consensus statement on the use of percutaneous mechanical circulatory support devices in cardiovascular care: Endorsed by the American Heart Association, the Cardiological Society of India, and Sociedad Latino Americana de Cardiologia Intervencion; Affirmation of Value by the Canadian Association of Interventional Cardiology-Association Canadienne de Cardiologie d'intervention. J Am Coll Cardiol 2015;65:e7-26.  Back to cited text no. 13


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2]


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