A 70-year-old man underwent coronary artery bypass grafting and double valve replacement (Carpentier-Edwards Magna: 33-mm prosthesis for rheumatic severe mitral regurgitation and 23 mm for moderate aortic stenosis).
After cardiopulmonary bypass (CPB), his pulmonary artery wedge pressure (PAWP) was elevated to 31 mm Hg and central venous pressure to 18 mm Hg compared to pre-CPB values of 24 and 12 mm Hg, respectively. Transesophageal echocardiography (TEE) in the midesophageal 4-chamber and long-axis view revealed a left atrial (LA) linear structure of homogeneous intensity and random motion, dividing the LA into a small anterior (adjacent to the aortic valve, along the anterior mitral annulus) and a large posterior (along the posterior mitral annulus) compartments (Video Clips 1 and 2, see Supplemental Digital Content 1, http://links.lww.com/AA/A912, Supplemental Digital Content 2, http://links.lww.com/AA/A913; Fig. 1, A and B). In addition, a freely oscillating mass was noticed inside the left ventricle (LV) (Video Clip 1, see Supplemental Digital Content 1, http://links.lww.com/AA/A912; Fig. 1A).
Color flow Doppler examination of the LA showed antegrade diastolic blood flow from the anterior LA compartment through the mitral prosthesis with proximal flow acceleration (Video Clip 2, see Supplemental Digital Content 2, http://links.lww.com/AA/A913; Fig. 1, C and D). Continuous-wave Doppler revealed a mean diastolic transmitral pressure gradient of 16 mm Hg (Fig. 2B). In a modified midesophageal 4-chamber view, a continuous left-to-right shunt from the anterior LA compartment across the interatrial septum (IAS) was also seen, with a peak gradient of 23 mm Hg (Video Clip 3, see Supplemental Digital Content 3, http://links.lww.com/AA/A914; Fig. 2C).
The posterior LA compartment communicated with the LV through a mitral paraprosthetic defect adjacent to posterior mitral annulus (Video Clip 2, see Supplemental Digital Content 2, http://links.lww.com/AA/A913; Fig. 2A), with blood flow during systole and diastole.
The free-floating LV structure was identified as part of the anterolateral papillary muscle (Video Clip 3, see Supplemental Digital Content 3, http://links.lww.com/AA/A914) in a transgastric midpapillary short-axis view. Pulsed-wave Doppler examination of the pulmonary veins, prosthetic aortic valve, tricuspid valve, and 2-dimensional examination of LV function were normal.
The patient was placed on CPB again and surgical inspection revealed an LA dissection flap, a large posterior LA cavity communicating to the LV through a small paravalvular defect, an anterior LA cavity communicating with the mitral prosthesis, and the right atrium (RA) via an IAS defect. The dissection flap was excised, and the IAS defect was closed. After the repair, TEE examination revealed a unified LA cavity and a normal diastolic transmitral pressure gradient (Fig. 2D). The PAWP and central venous pressure decreased to 10 and 6 mm Hg, respectively.
LA dissection is a rare complication that occurs predominantly after mitral valve (MV) repair/replacement and occasionally after blunt cardiac trauma, acute myocardial infarction, prosthetic endocarditis, and aortic valve surgery.1–3 The dissection usually originates from the posterior mitral annulus to involve the posterior LA wall; it rarely originates from the anterior mitral annulus to involve the IAS.4 The dissection creates a large expanding cavity between the LA endocardium and the myocardium. In the acute setting, rapid expansion of this dissection cavity may encroach onto the adjacent structures and lead to a decrease in the size of the true LA cavity and obstruction of the LV inlet, pulmonary veins, or even rupture into the true LA cavity, RA, or pericardial cavity.1–4
In our case, the large LA posterior dissection cavity compressed the anterior, true LA cavity and encroached on the mitral prosthesis to cause obstruction of the LV inlet. It communicated with the LV via a small mitral paraprosthetic defect, through which it received blood during LV systole and returned it back to LV during diastole. In addition, an IAS defect allowed the communication between the anterior, true LA cavity and the RA.
On TEE examination, an LA dissection cavity appears as a hypoechoic space, extending from the mitral or tricuspid annulus plane and extending along the IAS or lateral LA wall.5 The LA dissection flap has a homogeneous acoustic intensity and moves randomly. This differentiates it from an LA linear artifact, which shows gradually fading acoustic intensity, moves with the cardiac motion, and traverses the LA anatomic boundaries. M-mode may help to detect the subtle motion of a dissection flap. The origin of the LA dissection may or may not be apparent; however, when imaged, it shows a high velocity, regurgitant jet, which is directed from the LV to the LA dissection cavity. The direction of this jet helps to diagnose the direction of the propagation of dissection. Examination with color flow Doppler is helpful to detect whether adjacent structures are compressed by showing turbulent flow or any fistulous communication.
In our case, the expanding LA posterior compartment caused the dissection flap to obstruct the LV inlet, thus resulting in functional stenosis of the mitral prosthesis. That might have been the reason for the increased PAWP, which decreased to normal levels after repair of the LA dissection, because neither LV contractility nor diastolic dysfunction appeared abnormal. The transmitted pressure from the LA posterior dissection cavity facilitated the shunt between the LA anterior compartment and the RA. The involvement of the IAS in LA dissection, when arising from the anterior mitral annulus, has been described4; however, in this case, the LA dissection originated from the posterior mitral annulus.
The hypoechoic LA dissection cavity may become hyperechoic after heparin reversal, suggestive of blood stagnation and hematoma formation.2 The lack of this feature, despite heparin reversal in our case, was most likely due to the bidirectional blood flow between the LV and the posterior LA dissection cavity.
In the case of LA dissection, it is necessary to examine all 4 pulmonary veins to exclude possible obstruction by the flap or communication with the dissection cavity. A normal pulmonary venous flow pattern excludes obstruction. The pulmonary vein flow pattern will show systolic blunting in case of systolic LA hypertension and diastolic blunting or sudden interruption of diastolic flow5 in case of obstruction of LV inflow.
In our case, the MV repair was performed through a left atriotomy and the chordae attached to the anterior mitral leaflet were sutured to the corresponding commissures. The posterior mitral leaflet segments devoid of chordae were excised and the MV was replaced using interrupted sutures. During weaning off CPB, concurrent to the increasing LV pressure, one posterior suture cut through the annulus and created a mitral paraprosthetic defect, through which blood from the LV entered the LA wall to create the LA dissection cavity (Fig. 3). The observed IAS shunt was most likely iatrogenic from the use of a metallic suction tip.
This case underscores the importance of correlating hemodynamics with TEE findings to diagnose complications during the intraoperative period.
Clinician’s Key Teaching Points
By Nikolaos J. Skubas, MD, FASE, Donald Oxorn, MD, and Martin J. London MD
* Left atrial dissection is a rare complication of mitral valve surgery. It is usually the result of excessive annular traction or aggressive decalcification of the posterior annulus causing left atrial endocardial injury. Expansion of the left atrial false cavity, contained between the endocardium and myocardium, may encroach on the pulmonary veins or the mitral valve, limiting the size of the left atrium or even rupture into the pericardium resulting in tamponade.
* In the midesophageal views, the left atrial dissection flap appears as a linear structure that exhibits random motion. It should be differentiated from linear artifact, which traverses anatomic boundaries, is synchronous with cardiac motion, and generates weaker echo reflections. The dissection flap may obstruct the orifice of the pulmonary veins or the mitral valve. If blood stagnates in the false chamber, thrombus may develop.
* In this case, after placement of a prosthetic mitral valve and separation from cardiopulmonary bypass, elevated pulmonary capillary wedge (31 mm Hg) and central venous pressures (18 mm Hg) prompted examination of the left atrium with transesophageal echocardiography, confirming the presence of a left atrial dissection flap. Imaging revealed a small anterior left atrial chamber receiving blood from the pulmonary veins, allowing flow through the mitral prosthesis. An expanding posterior left atrial false chamber, communicating with the left ventricle via a paraprosthetic mitral valve leak, caused functional stenosis of the prosthetic mitral valve (continuous-wave Doppler-derived mean pressure gradient of 16 mm Hg).
* Although a rare event, left atrial dissection should be suspected when after mitral valve surgery, left-sided or biventricular filling pressures unexpectedly increase. An expanding false left atrial chamber dissection flap or Doppler signs of obstruction, such as systolic blunting or abrupt cessation of diastolic velocity in the pulmonary veins or an increased mean gradient across the mitral valve, may indicate the need for surgical repair.
Name: Virendra Kumar Arya, MD.
Contribution: This author helped write the manuscript and was the anesthetist for the case.
Attestation: Virendra Kumar Arya approved the final manuscript.
Name: Bhupesh Kumar, MD, DM.
Contribution: This author helped assisted in conducting anesthesia and preparation of the manuscript.
Attestation: Bhupesh Kumar approved the final manuscript.
Name: Anand Kumar Mishra, MS, MCh.
Contribution: This author was the operating surgeon.
Attestation: Anand Kumar Mishra approved the final manuscript.
Name: Shyam K.S. Thingnam, MS, MCh.
Contribution: This author helped the operating surgeon.
Attestation: Shyam K.S. Thingnam approved the final manuscript.
This manuscript was handled by: Martin J. London, MD.