3D TEE, a boon for the diagnosis of Left Atrial Appendage thrombus!

Selvi Mahalingam, Krishnakumar

Senior Consultant, Cardiac Anaesthesia Department, Kauvery Hospital, Tirunelveli

PDCC, Cardiac Anaesthesia Department, Kauvery Hospital, Tirunelveli

*Correspondence: krishdr86@gmail.com

Background

Atrial fibrillation (AF) is a potentially problematic cardiac arrhythmia affecting approximately 1% of adults. Stroke occurs in 5% of non-anticoagulated patients. The gold standard for preventing atrial fibrillation-related strokes is oral anticoagulation. However, contraindications and reluctance to comply with long-term use due to increased risk of bleeding make it a problematic therapy. In fact, as much as 50% of patients with atrial fibrillation who qualify for anticoagulation do not receive it.

The left atrial appendage (LAA) is suggested to be the source of more than 90% of emboli in chronic atrial fibrillation.

LAA anatomy

The LAA is an anterolateral structure and the smallest part of the left atrium. It originates anterior to the left pulmonary vein ostium. The LAA body usually extends anteriorly toward the right ventricle. The LAA morphology is heterogeneous, but can be divided into the ostium, neck, and lobes. The OS is the junction between the atrium and the LAA. It is anterior to the left pulmonary veins and separated by the left atrial ridge, which is a 5 mm in-folding of the left atrial wall. Inferior to the OS is the mitral valve, which is separated by a muscle band. Some reports have stated that the shape of the OS is more elliptical than round. This suggests that to seal the LAA orifice adequately without oversizing, circular devices may be less appropriate: a round rigid implant over an oval shaped orifice may leave crevices on either side of the implant, leading to incomplete sealing.

Anatomical structures surrounding LAA

The left anterior descending (LAD) coronary artery is in close proximity to the LAA and is a vulnerable structure during device implantation. In human specimen dissections, the LAD was located within 1 cm of the OS of the LAA when epicardial adipose tissue was removed in nearly half of the examined cases. The circumflex artery, close to the LAD and the LAA OS, is also at risk of trauma during device implantation, particularly with surgical occlusion or devices larger than the LAA OS.

The left phrenic nerve runs across the top of the LAA. It is the most important branch of the left cervical plexus and originates from the fourth cervical nerve. Vulnerability of the left phrenic nerve may be greater in epicardial left atrial appendage procedures. The great cardiac vein originates at the apex of the heart and runs along the interventricular groove. Risk of injury to this structure is low. However, reports exist describing LAA to great cardiac vein fistula complicating LAA closure, pulmonary artery injury and left circumflex coronary artery occlusion. Selecting the appropriate device and avoiding aggressive oversizing may reduce risk of injuring surrounding LAA structures.

Excision of the left atrial appendage (LAA) is becoming an increasingly popular adjunct to either a mitral valve repair/replacement or as part of a thoracoscopically performed Maze procedure in patients with atrial fibrillation (AF). A comprehensive echocardiographic examination of the LAA before ligation to exclude the presence of thrombi and after excision and ligation to ensure the absence of a residual stump of LAA is considered an integral part of the procedure.

Case Presentation

A 65-year-old woman presented for an elective mitral valve replacement (MVR) for severe mitral stenosis (MS) (mitral valve area of 0.8 cm2). A Coronary Angiogram preoperatively did not reveal any coronary artery disease. Transesophageal echocardiography (TEE) performed before surgery confirmed these diagnoses and also showed normal biventricular systolic function with a dilated left atrium (LA).

There was also a history of well-controlled hypertension and paroxysmal AF. Because of her paroxysmal AF, she had been on oral coumadin for the last 6 years. Her preoperative medications included digoxin, lisinopril, furosemide, and coumadin. Her oral coumadin had been withheld 3 days before surgery, she was admitted to the hospital and simultaneously started on an intravenous heparin infusion, which was titrated to achieve a therapeutic partial thromboplastin time of 55 s. In the holding area, she was found to be in sinus rhythm, and she was being administered an intravenous heparin infusion at a rate of 600 U/h.

After the placement of 2 large-bore intravenous cannulae and a radial arterial catheter with adequate premedication, the heparin infusion was discontinued immediately before transport to the operating room for surgery. The induction of general anesthesia was smooth and uneventful endotracheal intubation was done.

TEE

The TEE examination confirmed preoperative echocardiographic findings of severe MS. There was also moderate spontaneous echo contrast in a severely dilated LA. The LAA was then interrogated with 2-dimensional (2D) and pulse-wave Doppler imaging. With the TEE probe in the mid esophageal position and scan plane at 0°, keeping the LAA in the middle of the image, visualization was started with 5° incremental rotations of the scan plane from 0o to 180o.

A suspicious echo density was visualized in the LAA (1-0.75 cm); it had a homogenous consistency and a smooth outline and was attached to the wall of the LAA. The pulse-wave Doppler-measured LAA ejection velocity was approximately equal to 20 cm/s. The RT3D imaging in the en- face view of the mitral valve clearly showed that the visualized echo density was a thrombus in the LAA.

3d-1

Discussion

The present case highlights the importance and impact of perioperative RT3D transesophageal echocardiography during cardiac surgery involving LAA ligation. This case also is a reminder that it is important to have a high index of suspicion for an LAA thrombus in high-risk patients (MS and dilated LA) even if these patients are on anticoagulation. The present patient presented for elective MVR for severe MS. Her preoperative TEE (4 weeks before surgery) had not revealed a thrombus in the LAA. During her brief preoperative hospitalization, she was on intravenous heparin, and her partial thromboplastin time was kept within the therapeutic range.

Despite being on anticoagulant medications, she still formed thrombus in the LAA. Because of a normal TEE examination a few weeks before surgery and adequate anticoagulation in the interim, the authors were not absolutely sure of the nature of the echo density despite having multiple risk factors for thrombus formation in the LAA. This is because the formation of LAA thrombi in patients with adequate anticoagulation is quite uncommon but not rare

The authors’ ability to identify the echo density in the LAA on 2D examination and then conclusively diagnose it with RT3D in the pre- cardiopulmonary bypass period helped in the correct management of the case (no cardiac manipulation and extraction of thrombus before LAA ligation).

Because of the shape and location of the LAA, it is a major source of cardiogenic thrombus formation. It is embryologically distinct from the main LA body. It has parallel-running pectinate muscles in the cavity, which are 1 mm in diameter in almost 97% of cases, and the LAA is often congenitally multilobed.

The comprehensive 2D echocardiographic examination of the LAA is limited by the oblique orientation of the LAA to the long axis of the heart and requires interrogation in multiple views at different rotations of the scan plane. Conventional 2D imaging with TEE is considered the “gold standard” diagnostic tool for diagnosing LAA thrombi, with a sensitivity and specificity of 100% and 90%, respectively. Recently, however, the utility of RT3D. over and above the conventional 2D imaging for LAA examination has been shown in multiple reports.

In the previous case reports, the RT3D imaging was used to correctly identify a bilobed LAA or a prominent pectinate muscle, which appeared as a thrombus in patients otherwise at risk for LAA thrombus formation. A dilated LA, MS, and the presence of spontaneous echo contrast are all considered risk factors for LAA thrombus formation.

However, pericardial fluid accumulation in the transverse sinus and coumadin ridge (the tissue between the LAA and the left upper pulmonary vein) can cause acoustic shadowing in the LAA that can be confused with LAA thrombus. The superiority of intraoperative RT3D transesophageal echocardiography over 2D imaging already has been shown in multiple studies. The “live zoom” mode of the matrix 3D TEE probe was used, which provided high-quality live en- face images of the LAA.

In the present patient, the LAA visualization in conventional 2D TEE did show the presence of a possible thrombus in the LAA.

By obtaining 3D volumetric imaging and using the crop-adjust function, the authors were able to visualize the detailed LAA structure and conclusively identify the clot in the LAA and establish its mobility and hence the risk of embolization. This unexpected finding alerted the surgical team to be cautious and careful to avoid cardiac manipulation before aortic cross-clamp application and extract the thrombus before external ligation of the LAA.

Lastly, RT-3D imaging was used after the procedure to ensure a “flush ligation” of the LAA and the absence of a residual stump of the LAA and avoid further risk of stroke.

The availability of RT3D TEE in the operating room is providing new perspectives into intracardiac and valvular anatomy. Cardiac structures such as the LAA and mitral valve, which are difficult to comprehensively interrogate with conventional 2D TEE imaging, are particularly visualized in greater detail with this modality. The value of RT3D TEE has been appreciated as a valuable modality during cardiac surgery.

It has the potential to revolutionize the understanding of cardiac structure and function and improve outcome. The use of RT3D TEE during LAA ligation has shown particular promise to impact the surgical decision making.

References

  1. Jacka MJ, et al. The use of and preferences for the transesophageal echocardiogram and pulmonary artery catheter among cardiovascular anesthesiologists, Anesth Analg. 2002;94:1065-71.
  2. Mahmood F, et al. Transesophageal echocardiography and noncardiac surgery. Semin Cardiothorac Vasc Anesth. 2008;12:265-89.
  3. American Society of Anesthesiologists and Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography Practice guidelines for perioperative transesophageal echocardiography. Anesthesiol. 2010;112:1084-96.
  4. Bergman R, et al. Major surgery, hemodynamic instability, and left atrial appendage clot: What to do? J Cardiothorac Vasc Anesth. 2013;27(3):625-6.
  5. Cummisford K, et al. Real-time three-dimensional transesophageal echocardiography and a congenital bilobar left atrial appendage. J Cardiothorac Vasc Anesth. 2010;24(3):P475-477.

Journals

Find Doctor
Book Appointment