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Cardiovascular Anesthesiology: Echo Rounds

Left Ventricular Outflow Tract Obstruction After a Mitral Valve Repair

Musuku, Sridhar Reddy MD, FRCA*; Akujuo, Adanna MD; Pani, Saroj MD, FASE*; Bennett, Edward V. Jr. MD

Author Information
doi: 10.1213/ANE.0000000000000955

This submission is an IRB-approved and patient-consented report. A 58-year-old man with symptomatic bileaflet myxomatous mitral valve (MV) disease and atrial fibrillation was scheduled for MV repair. Intraoperative transesophageal echocardiogram (TEE) confirmed a posterior mitral regurgitation (MR) jet secondary to anterior MV leaflet prolapse with flail of A2 segment (Fig. 1A). Mitral and tricuspid annuli were dilated, and the patient had moderate tricuspid regurgitation. The left ventricular outflow tract (LVOT) diameter was measured at 2.4 cm (Fig. 1A). Aortic valve (AV) leaflet motion and biventricular function were normal (Fig. 2A). MV, tricuspid valve repair, and a Maze procedure were planned.

Figure 1
Figure 1:
Intraoperative transesophageal echocardiography images showing the left ventricular outflow tract (LVOT) before and after the application of a medial trigone suture during mitral valve repair. Inset A is a still image in the midesophageal (ME) long-axis view using color flow Doppler showing a posteriorly directed mitral regurgitation (MR) jet secondary to A2 leaflet flail. The baseline LVOT measured 2.4 cm; inset B is an attempted ME long-axis view after the trigonal suture showing the narrowed LVOT (0.9 cm). Please note the displaced interventricular septum (IVS). LA = left atrium; LV = left ventricle; RV = right ventricle.
Figure 2
Figure 2:
Intraoperative 2D transesophageal echocardiography images of the aortic valve (AV) before and after application of the trigone suture. Inset A is midesophageal (ME) AV short-axis view using a color flow Doppler view showing normal AV leaflets opening in midsystole. Inset B shows the AV in midsystole after application of the trigone suture. Compared with inset A, the AV leaflet opening (in midsystole) is restricted. The noncoronary and left coronary cups are opening, and the right coronary cusp is severely restricted (Video 3, Supplemental Digital Content 3, LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle; PA = pulmonary artery.

The surgical technique was composed of an MV repair with a resection of prolapsed A2 segment and attachment of a Gore-Tex NeoChordae (W. L. Gore & Associates, Inc., Flagstaff, AZ) to the lateral side of the A2. The posterior mitral annulus was reinforced from one trigone to another. Mitral annuloplasty was performed with a 36 CG Future annuloplasty partial band (Medtronic, Minneapolis, MN). A tricuspid annuloplasty was performed with an Edwards MC3 tricuspid annuloplasty ring (Edwards Lifesciences Corp., Irvine, CA). After weaning from cardiopulmonary bypass (CPB), 2+ residual MR was observed at the repaired A2 area.

To address the residual MR, CPB was reinitiated to attach another neochord along the medial side of the A2 region. In addition, a double-running suture was required to address the weakened medial trigone (likely because of sutures used during the mitral annuloplasty). Upon weaning from CPB, there was no residual MR. However, TEE in the midesophageal (ME) long-axis view with color flow Doppler (CFD) showed flow acceleration starting at the LVOT progressing across the AV (Video 1, Supplemental Digital Content 1, Deep transgastric 5-chamber 2D and CFD views showed LVOT narrowing and flow turbulence (part 1 of Video 2, Supplemental Digital Content 2, The interventricular septum (IVS) was overriding the aortic annulus. Pulse wave Doppler sampled at the LVOT revealed a peak velocity of 195.81 cm/s (part 2 of Video 2, Supplemental Digital Content 2, Continuous wave Doppler (CWD) across the LVOT and AV showed a peak gradient of 32 mm Hg (part 3 of Video 2, Supplemental Digital Content 2, Motion of all AV leaflets was restricted, particularly that of the right coronary cusp, as confirmed by the ME AV short-axis with 2D and live 3D TEE (Video 3, Supplemental Digital Content 3, This resulted in a “bow tie” TEE appearance of the AV in midsystole.

A third and final CPB was performed to address the narrowed LVOT. An aortotomy coupled with a digital examination across the LVOT revealed that one of the trigone sutures was compromising the LVOT. Releasing this suture restored the LVOT to its normal diameter. There was no flow acceleration across the LVOT and AV. The AV leaflets regained their normal motion. After suture release, the LVOT pulse wave Doppler revealed a reduced velocity of 80.81 cm/s. The CWD across the LVOT and AV revealed a peak gradient of 5 mm Hg (part 3 of Video 2, Supplemental Digital Content 2, The total CPB time was 3 hours and 20 minutes. The patient was tracheally extubated on the first postoperative day. A telephone call 3 months after surgery and the electronic records indicated the patient’s good functional status.


LVOT obstruction (LVOTO) may be classified as dynamic or fixed after an MV repair. Dynamic LVOTO in the form of systolic anterior motion occurs in 8.4% of patients after MV repair,1 a condition not present in this patient. A fixed LVOTO may result from various valvular and subvalvular2 causes in addition to rare causes such as protruding MV rings3 and abnormal papillary muscles.4 In this complex MV repair, we encountered a narrowed LVOT, AV dysfunction, and an overriding IVS, a very rare clinical presentation.

The LVOT is part of the AV complex, and unlike the right ventricular outflow tract, the LVOT is in direct communication with the MV within the fibrous framework of the heart. This anatomic arrangement results in a complex interaction between the ventricular inflow and the outflow tract at different stages of the cardiac cycle. The LVOT5 is surrounded by several key structures of fibrous network, including the IVS, the aortomitral curtain (AMC) bound by medial and lateral trigones (Fig. 3). The AMC is in continuity with the anterior MV leaflet that, via the annulus of the MV, is in turn attached to the left coronary and noncoronary cusps (Fig. 3). The AMC maintains the anatomical and functional integrity of both the AV and the MV.6 Neither trigone is imaged by TEE. The trigones act as a hinge mechanism for the movement of the AMC and anterior MV leaflet.

Figure 3
Figure 3:
A, The structures surrounding the left ventricular outflow tract (LVOT). In this image, the LVOT is viewed from aorta into the left ventricle where the papillary muscles are seen. The LVOT is surrounded by membranous interventricular septum (IVS) medially and muscular IVS laterally. The aortomitral curtain (AMC) is posterior, and the right coronary cusp is located anteriorly opposite to the AMC. The medial and lateral trigones are on each side of the AMC. Schematic image B is an attempt to show the mechanism of the LVOT narrowing. The red arrow represents the trigone suture (just below the aortic valve [AV]) and direction of the pulling force. This force is responsible for pulling the aortic root posteriorly. Secondary to this suture, the noncoronary cusp (N) and the left coronary cusp (L) are affected. The right coronary cusp that is located more anteriorly followed the distorted fibrous architecture. This pulling force along with the altered flow pattern may have caused severe restriction and characteristic AV appearance on the transesophageal echocardiograph. AMVL = anterior mitral valve leaflet; LT = lateral trigone; MT = medial trigone; N = noncoronary cusp; PV = pulmonary valve; R = right coronary cusp; TV = tricuspid valve.

Because of these interconnections among various structures of the fibrous network, MV repair involving the trigones can impact the structure and function of not only the LVOT but also the surrounding structures. In this case, a medial trigone suture not only caused a narrowed LVOT but the suture also affected the IVS and the aortic root, causing abnormal AV movement.

In a myxomatous MV disease, the fibrous network is weaker because of deficient connective tissue components and reinforcement sutures to the thinned out medial trigone, which in our case compromised the LVOT and its surrounding structures. Abnormal AV movement and the flow pattern across the LVOT and AV can also be explained by an altered fibrous framework after MV repair. In our patient, although all 3 AV leaflets were restricted, the right coronary cusp was severely immobile. It is worth noting that the severely restricted right coronary cusp is anatomically anterior and farthest away from the medial trigone and the AMC (Fig. 3). Perhaps, the pulling force generated by the culprit suture resulted in posterior displacement of the aortic root complex, thus causing severe LVOTO. The bow tie appearance of the AV in midsystole was a characteristic TEE finding in this patient. The normalized LVOT and the restoration of the structure and function of the AV leaflets after the release of the suture signify the importance of the interlinking fibrous framework and support our contention that the medial trigonal suture was the culprit suture that caused the LVOTO after MV repair.

CFD findings in the ME long-axis view indicated that the flow was accelerating beyond the LVOT into the aortic root. This finding may be explained by the fact that the velocity of fluid must increase immediately distal to the constriction. After the release of the trigonal suture, CWD across the LVOT and AV showed a decreased peak gradient from 32 to 5 mm Hg. The TEE and surgical findings suggest an iatrogenic LVOT narrowing after an MV repair, which was resolved after an aortotomy and release of the trigonal suture.

In conclusion, this case suggests that a deep trigone intervention during MV repair especially with an underlying myxomatous condition may alter the LVOT and its surrounding structures. Although our diagnosis was retrospective, TEE was instrumental in understanding the mechanism of LVOT narrowing and the importance of an intact interlinking fibrous framework of the heart.

Clinician’s Key Teaching Points

By J. Skubas, MD, and Roman M. Sniecinski, MD

  • The borders of the left ventricular outflow tract (LVOT) are the interventricular septum and the fibrous aortomitral curtain, which is adjacent to the left and noncoronary aortic valve cusps. This complex LVOT geometry is dynamically changing during the cardiac cycle.
  • LVOT obstruction after mitral valve repair or replacement is typically dynamic as seen with systolic anterior motion of the anterior mitral valve leaflet. This often improves after volume loading, elevation of afterload, and reduction in excessive LV contractility. However, fixed obstruction can result from protruding struts of a prosthetic mitral valve and may need to be addressed surgically.
  • In this case of mitral valve repair, a surgical stitch along the aortomitral curtain that was meant to stabilize a floppy annulus distorted LVOT anatomy, resulting in fixed LVOT obstruction and altered movement of the right coronary cusp of the aortic valve. Transesophageal echocardiography imaging revealed turbulent flow (by color flow Doppler) and high velocities (by spectral Doppler) within the LVOT. This prompted a return to bypass and removal of the stitch, thus correcting the problem.
  • Myxomatous disease involves the breakdown of connective tissue. Although this generally refers to the leaflets, the neighboring fibrous network may also be involved, necessitating additional surgical maneuvers to stabilize the annulus. After a complex mitral valve repair, a high-velocity LVOT systolic jet should prompt detailed interrogation of the subaortic valve region, particularly in the absence of mitral regurgitation jet suggestive of systolic anterior motion.


Name: Sridhar Reddy Musuku, MD, FRCA.

Contribution: This author was responsible for the perioperative patient care and prepared the manuscript after taking a written informed consent. This author also prepared the figures and run freeze run videos and prepared the videos with the help of Dr. Kareem Kassel, MD.

Attestation: Sridhar Reddy Musuku approved the final manuscript. He attests to the integrity of the original data and he is the archival author.

Name: Adanna C. Akujuo, MD.

Contribution: This author helped edit the surgical procedure part of the manuscript.

Attestation: Adanna C. Akujuo attests to the final manuscript.

Name: Saroj Pani, MD, FASE.

Contribution: This author helped edit the manuscript.

Attestation: Saroj Pani attests to the final manuscript.

Name: Edward V. Bennett, Jr., MD.

Contribution: This author was the primary surgeon who was responsible for the perioperative patient care. This author also helped in understanding the mechanism of the problem encountered.

Attestation: Edward V. Bennett, Jr., attests to the final manuscript.

This manuscript was handled by: Martin London, MD.


We thank Dr. Kevin Roberts (Chair, Department of anesthesiology) and the department staff and residents for the support. Our sincere regards to the CT surgeons (Edward V. Bennett, Harry J. DePan, and Lewis W. Britton) for giving their valuable input into the manuscript. Dr. Kareem Kassel is appreciated for the help with the video clips.


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