CASE REPORT |
https://doi.org/10.5005/jp-journals-10034-1133 |
Mitral Valve Repair Surgery—When the Right Ventricle is Not Just an Innocent Bystander: A Case Report
1,2,5Department of Cardiovascular and Thoracic Anaesthesiology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Trivandrum, Thiruvananthapuram, Kerala, India
3Department of Anaesthesia, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India
4Department of Cardiovascular and Thoracic Surgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Thiruvananthapuram, Kerala, India
Corresponding Author: Unnikrishnan P Koniparambil, Department of Cardiovascular and Thoracic Anaesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Thiruvananthapuram, Kerala, India, Phone: +91 9446177521, e-mail: unnikp@sctimst.ac.in
Received: 15 September 2023; Accepted: 05 November 2023; Published on: 20 February 2024
ABSTRACT
Aim: To assess rare causes of systolic anterior motion (SAM) of the mitral valve (MV) after MV repair.
Background: A preoperative assessment of the MV apparatus is done to predict postoperative SAM in all patients undergoing MV surgery. These parameters include the lengths of MV leaflets and the ratio between them, the aortomitral angle, the distance between the coaptation point and septum, and septal thickness. When predicted, surgical repair is planned with the goal of avoiding the occurrence of SAM.
Case description: A 45-year-old man with MV prolapse and severe mitral regurgitation (MR) underwent MV repair after intraoperative transesophageal echocardiography (TEE) assisted confirmation of feasibility. The postoperative risk of SAM was ruled out. Although there was no SAM in the immediate postrepair TEE, he developed hemodynamic instability, which, on reevaluation, was found to be due to new onset SAM. Transgastric imaging revealed inferior wall hypokinesia and right ventricle (RV) dysfunction, which infrequently causes SAM. Medical management was sufficient to address this manifestation.
Conclusion: Systolic anterior motion (SAM) may be caused by right ventricular dysfunction even in the absence of other TEE-described predictors.
Clinical significance: It is important to identify medically reversible causes of SAM so as to avoid a redo of surgical intervention with a return to cardiopulmonary bypass, especially in the absence of preoperative predictors.
How to cite this article: Thomas D, Hanumansetty K, Aspari A, et al. Mitral Valve Repair Surgery—When the Right Ventricle is Not Just an Innocent Bystander: A Case Report. J Perioper Echocardiogr 2021;9(2):37–40.
Source of support: Nil
Conflict of interest: None
Patient consent statement: The author(s) have obtained written informed consent from the patient for publication of the case report details and related images.
Keywords: Case report, Intraoperative echo, Mitral valve repair, Mitral valve surgery, Right ventricle dysfunction, Systolic anterior motion, Transesophageal echocardiography
INTRODUCTION
Systolic anterior motion (SAM) of the mitral valve (MV) is defined as the anterior translational motion of the mitral leaflets into the left ventricular outflow tract (LVOT) during systole, resulting in a variable LVOT obstruction and distortion of mitral leaflets leading to mitral regurgitation (MR).1 With an incidence ranging from 6 to 10% after MV reconstruction surgeries, SAM continues to be a relevant clinical challenge that needs to be identified and addressed in the perioperative period.2,3
We will here discuss an unusual cause of SAM that developed after MV repair surgery in a patient with severe MR and no anatomical risk factors.
This manuscript adheres to the applicable Enhancing the Quality and Transparency of Health Research Network guidelines.
CASE DESCRIPTION
A 45-year-old man with a history of exertional dyspnea and palpitations for 3 months underwent MV repair surgery for severe MR.
After induction of anesthesia following standard institute protocol, transesophageal echocardiography (TEE) was done to evaluate MV pathology. TEE showed the presence of severe MR with an anteriorly directed eccentric jet with jet area >10 cm2 and vena contracta >7 mm. There was neither mitral stenosis nor other valve pathology, and biventricular function was found satisfactory. Further examination was directed at determining the feasibility of MV repair. The P2 segment of the posterior mitral leaflet (PML) had a definitive flail motion (Fig 1) (type 2 Carpentier functional class) associated with chordal rupture. The valve pathology was restricted to the P2 segment; therefore, its height was measured to evaluate the redundancy of tissue and found to be 22 mm (Fig 1). The P1 segment measured 14 mm, and the P3 segment measured 10 mm (Fig. 1). The height of the anterior mitral leaflet (AML) was determined to be 28 mm without including the coaptation segment and 33 mm when including it. The MV annulus had a 41 mm anteroposterior diameter (Fig. 1) and a 44 mm intercommissural diameter. There was no vegetation or calcification on the MV apparatus. Since MR was found to be solely due to the flail P2 segment with excessive tissue, a decision was made to perform quadrangular resection of the affected segment, neochord placement (to address chordal rupture), and flexible ring annuloplasty following the American correction.4 Intertrigonal distance was assessed for annuloplasty and derived as 32 mm with the aid of aortic root diameter (Fig. 2A) and 30.5 mm by three-dimensional (3D) imaging (Fig. 2B). Hence, a decision to place a 31 mm flexible ring was made.
Fig. 1: Preoperative transesophageal echocardiography assessment of MV showing flail motion of P2 segment of posterior mitral leaflet
Further assessment of the risk of SAM was done. Although the individual leaflet heights and AML:PML ratio of 1.27 (<1.3) were suggestive of a possible risk, a Coaptation point to the septum (C-sept) distance of 32 mm indicated a low risk of SAM (Fig. 2), also supported by the fact that the long pathological P2 segment was to be resected during repair.
Figs 2A and B: (A) Assessment of intertrigonal distance to determine annuloplasty ring size: Direct measurement of intertrigonal distance by 3D imaging, 30.5 mm; (B) C-sept distance measured as 32 mm indicating low risk of postoperative SAM of the MV
After the planned surgical repair was done via standard left atriotomy with ongoing CO2 insufflation, cardiac chambers were deaired, and the patient was weaned off bypass with dobutamine 5 μg/kg/minute to sinus rhythm and stable hemodynamics. Postrepair TEE assessment was aimed at determining the adequacy of repair. MV leaflet motion had been resolved to type 1 Carpentier functional class, that is, normal leaflet motion, leaflets coapted at the annular plane, and a trivial MR was noted at the junction of P1-A1 (Fig. 3A). The durability of repair was assured by a coaptation length of 9.4 mm (Fig. 3B). Annuloplasty was found to be satisfactory, with the partial flexible ring seated normally with no rocking movement and the MR jet not hitting the ring. There was no evidence of SAM, as suggested by laminar flow in the LVOT (Fig. 3A and Video 1).
Deeming an adequate MV repair, heparin reversal was done, and the aorta decannulated. However, from this point, the patient developed progressive hypotension and atrial fibrillation. Dobutamine infusion was hiked to 7.5 μg/kg/minute, and noradrenaline infusion started at 0.05 μg/kg/minute. TEE assessment was done to diagnose a possible new pathology, which showed an increase in MR and development of LVOT flow turbulence suggestive of SAM (Video 2). Dobutamine was immediately discontinued, and intravascular volume expansion was initiated with crystalloids. Further TEE in the transgastric view revealed inferior wall hypokinesia and a drastically reduced tricuspid annular plane systolic excursion (TAPSE) suggestive of right ventricle (RV) systolic dysfunction (Fig. 3, Videos 3 and 4). The lateral wall of the left ventricle (LV) had normal contractility, ruling out left circumflex artery injury, which is a known complication during MV annuloplasty. Right coronary artery air embolism was suspected, and a directed TEE revealed air shadows in the LV. Coronary air embolism requires a similar line of management, namely an increase in mean arterial pressure with vasopressors to mechanically clear the emboli. Atrial fibrillation was addressed with an intravenous bolus dose of amiodarone, and sinus rhythm was recovered subsequently. As right coronary arterial air emboli were cleared, RV and LV contractility improved, and SAM decreased to a minimal grade (Video 5).
Figs 3A and B: (A) Postrepair transesophageal echocardiography assessment of MV: coaptation length of 9.4 mm; (B) Drastically reduced TAPSE suggestive of RV systolic dysfunction
Once echocardiography demonstrated the absence of SAM and sustainable MV repair, the chest was closed, and the patient was shifted to the postsurgical intensive care unit (ICU) for postoperative monitoring and management. He was electively ventilated for 12 hours and had a further uneventful course till discharge.
DISCUSSION
The most common iatrogenic complication after MV repair is SAM.5 The preliminary theory expounding this phenomenon was largely based on the presence of large MV leaflets and a narrow LVOT causing the Venturi effect and a dynamic LVOT obstruction.6 First described in hypertrophic obstructive cardiomyopathy, this began to be described in non-hypertrophic hearts after MV repair procedures and drag theory was founded. It was proven with sustainable evidence as the foremost cause of SAM.7 Further understanding and echocardiographic demonstrations have added the role of left ventricular kinetics in propagating abnormal mitral leaflet motion and dynamic LVOT obstruction.8 All this has reduced the need for redoing surgery to ≤1%.9
RV dysfunction causing SAM is, however, a rare occurrence. Hoshino et al. described an incidence of SAM in a patient with chronic thromboembolic pulmonary hypertension and RV dysfunction after undergoing pulmonary thromboendarterectomy.10 They recognized the role of RV in systolic interventricular dependence, which, in the face of RV dysfunction, causes the septum to straighten out and narrow an otherwise normal LVOT.
Without a pathologic RV, air embolism into the right coronary artery is the most common cause of RV dysfunction postopen heart surgery, as evidenced by this report. The dysfunctional RV caused the interventricular septum to bulge into the LV, reducing the C-sept distance, especially in an already underfilled LV, leading to a narrow LVOT. Flow across this narrowed orifice generated both venturi and drag forces, causing the anterior MV leaflet to be sucked into the LVOT. This led to a significant increase in MR and generated a turbulent flow across LVOT. Atrial fibrillation further worsened LV filling and mean arterial pressure, leading to inadequate coronary perfusion. This failed to remove air from the right coronary artery and worsened LV contractility by reducing perfusion into the left coronary artery.
Early recognition of this phenomenon and the vicious cycle that resulted helped direct conservative management toward two targets to achieve the common goal of eliminating SAM. Target one was to reduce the propagation of SAM by reducing LV hypercontractility, which was done by withholding Dobutamine infusion and increasing LV volume by fluid resuscitation. Target two was to remove the initiator of this sequence of events, that is, air embolism in the right coronary artery, which was achieved by raising the mean arterial pressure and coronary perfusion pressure by administering noradrenaline. The absence of sinus rhythm had further worsened LV filling, and therefore, amiodarone was administered to treat atrial fibrillation. With the above steps, RV function improved, sinus rhythm was achieved, SAM resolved, MR was reduced to an insignificant level, LVOT flow returned to a laminar pattern, and blood pressure normalized.
Once lasting hemodynamic stability was achieved, chest closure was done, and the patient was shifted to the ICU for postoperative care. He had an uneventful postoperative course. Predischarge transthoracic echocardiography showed a normally functioning MV prosthesis, absence of SAM, and good biventricular function.
Clinical Significance
Although RV function assessment has not been emphasized strongly in assessing risk for SAM, this report shows that SAM may develop in the postoperative period due to RV dysfunction due to right coronary artery air embolism, which can be extrapolated to any other cause of postoperative RV dysfunction such as inadequate myocardial protection and cardioplegia delivery.
Early recognition was of paramount significance in this case, as the cycle of events was self-propagating, and an acute and severe hemodynamic collapse was imminent. Real-time TEE imaging helped identify the pathology and avoid redoing surgery.
SUPPLEMENTARY MATERIAL
The supplementary videos 1 to 5 are available online on the website of www.jpecardio.com
Video 1: Mid-esophageal (ME) LV long axis view showing laminar flow across the LVOT, implying the absence of SAM of the MV
Video 2: Focused view of the LVOT from ME five-chamber view (ME-5C) showing significant MR and turbulent flow across LVOT
Video 3: Transgastric mid-papillary short axis view showing inferior wall hypokinesia
Video 4: Mid-esophageal 5C (ME-5C) depicting dysfunctional left and RVs
Video 5: After intravascular volume expansion and withdrawal of inotropic drugs—ME-5C showing significant reduction in MR and return of laminar flow across LVOT suggesting resolution of SAM of MV.
ORCID
Diana Thomas https://orcid.org/0000-0001-5737-3818
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