Ann Thorac Surg 2007;84:2101-2103. doi:10.1016/j.athoracsur.2007.06.075
© 2007 The Society of Thoracic Surgeons
Case Reports
Another Pitfall in Minimally Invasive Mitral Valve Repair
Maiken B. Jensen, MDa,*,
Peter B. Hansen, MDa,
Jacob E. Moller, MDb,
Jens T. Lund, MDc
a Department of Cardiothoracic Anesthesiology, The Heart Centre, Rigshospitalet, Copenhagen, University Hospital, Copenhagen, Denmark
b Department of Cardiology, The Heart Centre, Rigshospitalet, Copenhagen, University Hospital, Copenhagen, Denmark
c Department of Cardiothoracic Surgery, The Heart Centre, Rigshospitalet, Copenhagen, University Hospital, Copenhagen, Denmark
Accepted for publication June 27, 2007.
* Address correspondence to Dr Jensen, The Heart Centre, 4142, Blegdamsvej 9, Copenhagen, 2100, Denmark (Email: maikenjensen{at}dad/net.dk).
 |
Abstract
|
|---|
We report a case of severe systolic anterior motion (SAM) and dynamic left ventricular outflow obstruction after repair of a flail posterior leaflet of the mitral valve. The reason for SAM was found to be due to traction on the pericardial stay sutures placed to expose the surgical field. The SAM and the outflow obstruction were completely resolved by cutting these sutures. Our case demonstrates the contribution of geometric factors in the development of SAM and left ventricular outflow obstruction and emphasizes the need to evaluate the heart in its natural position within the mediastinum.
|
Introduction
|
|---|
Mitral valve repair has many advantages compared with valve replacement and has proven to be feasible in the majority of patients with mitral regurgitation. A well-recognized risk of repair is dynamic left ventricular outflow tract obstruction (LVOTO) due to systolic anterior motion (SAM) of the anterior mitral leaflet [1]. In various series, SAM is identified by intraoperative transesophageal echocardiography in 8% to 9% [2, 3] of patients, with resultant LVOTO in 1% to 3% [1, 2].
The mechanism of SAM and LVOTO is multifactorial. Risk factors include the presence of excess mitral leaflet tissue, repair of the posterior leaflet, a more anteriorly placed coaptation point, a bulging septum, a nondilated hyperdynamic left ventricle, and a narrow mitral-aortic angle [1, 2].
We report an unusual cause of severe SAM, which was diagnosed by intraoperative transesophageal echocardiography after repair of a flail posterior mitral leaflet.
A 63-year-old man with increasing shortness of breath on exertion presented for mitral valve repair. Preoperative echocardiography demonstrated severe mitral regurgitation with estimated effective regurgitant orifice of 0.50 cm2, which was caused by chordal rupture to the middle scallop of the posterior leaflet (P2). Left and right ventricular function and dimensions were normal; the outflow tract was estimated to be 21 mm. No significant epicardial coronary artery disease was found on coronary angiography.
Anesthetic induction was uneventful. Post-induction transesophageal echocardiography confirmed prolapse of P2 with chordal rupture and a severe mitral regurgitation. A partial upper sternotomy was performed through an 8-cm skin incision. The upper half part of the pericardium was opened in the midline, and stay sutures were placed on both sides for maximal exposure of the surgical field. After cannulation, cardiopulmonary bypass was instituted using vacuum-assisted drainage. The aorta was clamped and blood cardioplegia given. Both venae cavae were snared and the mitral valve was exposed through the atrial septum. The prolapsing segment of P2 was identified, and a classic quadrangular resection was made. Both leaflets appeared otherwise normal in terms of structure and size. Prior to the insertion of a flexible Duran Ring (No. 33 [Medtronic Inc, Kerkrade, Holland]), a localized annuloplasty was made to reapproximate the two sides of the posterior leaflet. By filling the left ventricle with saline, we tested the competence of the valve.
Weaning from cardiopulmonary bypass proved difficult; the hemodynamic status of the patient was characterized by instability and hypotension. The arterial tracing appeared dampened with a protracted upstroke and the dicrotic notch close to the peak of the tracing ("M-configuration"). Transesophageal echocardiography disclosed a classical case of SAM and LVOTO. Two-dimensional transesophageal echocardiography (mid-esophageal long-axis view) showed LVOTO was caused by anterior motion and intrusion of the anterior mitral leaflet into the left ventricular outflow tract (Fig 1). Color Doppler showed turbulence in the outflow tract. In the transgastric long-axis view, continuous wave Doppler measurement could demonstrate a dynamic LVOTO with a characteristic dagger-shaped flow curve and an outflow peak gradient of 68 mm Hg (Fig 1). There was a discrete, posteriorly-directed regurgitation jet into the left atrium. The ventricle did not appear under loaded. Cardiopulmonary bypass was terminated and the cannulas were removed. Additional volume load and vasopressor therapy stabilized the hemodynamics to some extent, but the situation remained unsatisfactory.
View larger version (59K):
[in this window]
[in a new window]
|
Fig 1. Perioperative echocardiography. Top panel demonstrates the systolic anterior motion (SAM) (left) on two-dimensional echocardiography and left ventricular outflow tract obstruction (LVOTO) on continuous wave Doppler. Bottom panel demonstrates the SAM disappeared and no LVOTO could be detected with Doppler after removal of pericardial stay sutures. (AML = anterior mitral leaflet; AO = aorta; LVOT = left ventricular outflow tract.)
|
|
Tensions on the stay sutures in the pericardium were removed, which allowed the heart to sink back into its natural position. This maneuver resulted in an immediate improvement in the hemodynamics. The hypotension resolved and the arterial tracing appeared normal. The mitral valve was competent on transesophageal echocardiography, the SAM and LVOTO had disappeared, and the continuous wave Doppler gradient and pattern normalized (Fig 1). By re-establishing the traction on the stay sutures, the SAM and LVOTO reappeared with a prompt hemodynamic compromise. This response of creating and relieving SAM by applying and releasing tension on the sutures could be reproduced.
The immediate postoperative course was uneventful; discharge echocardiography did not reveal any SAM or LVOTO, but a mild pericardial effusion was noted. However, the patient was readmitted 2 weeks postoperatively due to severe shortness of breath. Echocardiography showed a large pericardial effusion and recurrence of the SAM and LVOTO (Fig 2). An uncomplicated pericardiocentesis was performed (1,200 mL serosanguineous pericardial fluid was removed from non-loculated pericardial space), and the SAM as well as the LVOTO disappeared. Aggressive preload reduction was performed using the Valsalva maneuver, and administration of nitroglycerin was given without the SAM reappearing.
View larger version (103K):
[in this window]
[in a new window]
|
Fig 2. Postoperative echocardiography. Top panel demonstrates the systolic anterior motion (SAM) (left) on two-dimensional echocardiography and left ventricular outflow tract obstruction (LVOTO) on continuous wave Doppler during significant pericardial effusion. Bottom panel demonstrates the SAM disappeared and no LVOTO could be detected with Doppler after pericardiocentesis. Please note the difference in scaling of Doppler images. (AML = anterior mitral leaflet; AO = aorta; LVOT = left ventricular outflow tract.)
|
|
|
Comment
|
|---|
A partial upper sternotomy provides excellent exposure of the mitral valve. However, in using this technique there may be a risk of creating an unfavorable mitral-aortic angle by traction of the pericardial sutures placed close to the aorta. The lower part of the heart will stay in situ due to the intact inferior part of the sternum, whereas the aorta will be displaced anteriorly. The sutures may already pre-repair, having caused a significant change in the geometry of the heart, creating the conditions for the SAM. Numerous causes of SAM have been proposed. We believe that the pericardial stay sutures have never been described as the sole reason for the SAM. The hemodynamic problems caused by the SAM may resolve with conservative therapy, such as volume loading, β-blockade, vasopressor, and cessation of inotropic support [2, 3]. The main purposes of these maneuvers are to keep the left ventricle optimally expanded and create a geometry that permits unobstructed flow in the left ventricular outflow tract. In refractory cases, re-repair is mandatory to reduce the amount of leaflet tissue and move the coaptation line further backward [1]. The stay sutures in our case may have narrowed the mitral-aortic angle so the conditions for obstruction were set. The fact that the SAM reappeared during the pericardial effusion episode is most likely a result of geometric changes of the left ventricular outflow tract and poor left ventricular filling.
Thus, our case underscores the importance of geometric factors in the development of the SAM and emphasizes the need to evaluate the geometry with the heart in its natural position. This may be particularly important in a minimally invasive technique through a partial sternotomy in which there is a risk of "kinking" the heart. In addition, this proves the importance of having transesophageal echocardiographic support, not only for evaluating the result of the repair, but also for visualizing complications.
|
References
|
|---|
- Lee KS, Stewart WJ, Lever HM, Underwood PL, Cosgrove DM. Mechanism of outflow tract obstruction causing failed mitral valve repairAnterior displacement of leaflet coaptation. Circulation 1993;88:II24-II29.[Medline]
- Brown ML, Abel, MD, Click RL, et al. Systolic anterior motion after mitral valve repair: is surgical intervention necessary? J Thorac Cardiovasc Surg 2007;133:136-143.[Abstract/Free Full Text]
- Charles LM. SAM-systolic anterior motion of the anterior mitral valve leaflet post-surgical mitral valve repair Heart Lung 2003;32:402-406.[Medline]
Top
Abstract
Introduction
