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Cardiovascular Anesthesiology: Echo Rounds

Accessory Left Ventricular Chamber

Intraoperative Echocardiographic Assessment

Usoltsev, Nikolay A., MD*; Alfirevic, Andrej, MD; Trombetta, Carlos, MD

Author Information
doi: 10.1213/ANE.0b013e3182a4e453


A 38-year-old woman presented with a year-long history of progressive dyspnea as well as hypertension, epilepsy, and rheumatoid arthritis. Preoperative transthoracic echocardiography and computed tomography scan revealed a mildly thickened, nonstenotic, but regurgitant aortic valve (AV) and left ventricular (LV) septation creating an accessory chamber. Coronary catheterization was normal. Written consent for the presentation of this report was obtained.

Intraoperative transesophageal echocardiography revealed an LV accessory chamber formed by the apical septal, anterior, and lateral walls extending to mid and basal anterior, anteroseptal, and anterolateral segments of the LV (Figs. 1 and 2 and Video 1, Loops 1, 2, and 3, see Supplemental Digital Content 1, The walls surrounding the LV accessory chamber appeared hypokinetic, thin, and hyperechoic (suggestive of fibrotic tissue). The LV ejection fraction was estimated to be 45% to 50%. The tract of tissue connecting the accessory chamber with the AV left coronary cusp provided for in-and-out blood flow (Fig. 2 and Video 1, Loops 2, 4, and 5,, with no direct communication between the accessory and main LV chambers. Color flow Doppler interrogation in diastole revealed moderate aortic insufficiency (Video 1, still image 1, and regurgitant flow filling the accessory chamber responsible for its rhythmic fluctuation in size. Color flow Doppler interrogation in systole revealed 2 laminar flows in the LV outflow tract and LV accessory chamber (Fig. 2A). Continuous wave Doppler aligned across the LV outflow tract and AV revealed a peak gradient of 15 mm Hg (Video 1, still image 2,

Figure 1
Figure 1:
Midesophageal 4-chamber view (left) demonstrating a left ventricular accessory chamber adjacent to the apex of the left ventricle (LV). The same chamber is seen in a midesophageal 2-chamber view (right) adjacent to the anterior wall of the LV. RV = right ventricle. LA = left atrium.
Figure 2
Figure 2:
Midesophageal long-axis view demonstrating the long axis of the left ventricle (LV) accessory chamber connecting to the aorta via a tract proximal to the left coronary cusp. In systole (A), ejection flow is seen from the LV and accessory chamber. In diastole (B), regurgitation flow fills the LV accessory chamber. RV = right ventricle. LA = left atrium.

Surgical exploration confirmed dehiscence of the left coronary cusp from the annulus with the large accessory chamber separated from the LV with a thick remnant of fibrotic endocardium. The AV appeared retracted with mildly thickened leaflets. In addition to AV replacement, the procedure included a partial transaortic resection of the basal and mid portions of the endocardial aspect of the accessory chamber producing a unified cavity with a residual ridge arising from the LV apex (Video 2, Loops 1, 2, 3, and 4, see Supplemental Digital Content 2, The patient required minimal inotropic support for separation from bypass followed by postoperative medical therapy optimization for treatment of decreased heart function.


The LV accessory chamber appears as an echolucent space within the LV wall surrounded by the thin, hypokinetic or akinetic, and hyperechoic walls directly communicating with the aorta. However, a similar echocardiographic appearance may be seen with the LV dissection, dual-chambered LV, aneurysm, pseudoaneurysm, noncompaction, and neocavities within mural thrombus1–6 (Table 1). A transverse tear across the LV septum may lead to ventricular septal defect, while a tear across the free wall leads to tamponade or pseudoaneurysm formation. In contrary, with a linear tear extending along the wall, blood spreads myocardial spiral fibers, resulting in a neocavity formation such as LV wall dissection.1 The LV wall dissection is seen as a complication of cardiac surgery or nonsurgical conditions such as myocardial infarction, catheterization, or trauma.2,7 When related to myocardial infarction, it is confined to the area supplied by the respective coronary artery and has been associated with decreased ejection fraction, decline in functional status, and increased mortality.1 In addition, presentation of the LV dissection can be variable because of its dynamic nature and different acoustic properties of the organized thrombus and moving blood. Visualization of an intramyocardial echolucent cyst-like space is typical, with the possibility of an echodense mass appearance due to thrombus formation or neocavity obliteration.1 The surrounding intact endocardial and epicardial walls appear thin and hyperechoic due to fibrotic tissue and may be associated with regional wall motion abnormalities1 without a direct communication with the main LV cavity. The etiology of an LV accessory chamber in our patient remained unclear because of a lack of coronary artery disease or trauma. In a dual-chambered LV, the chamber is surrounded by full thickness walls which contract in synchrony with the main LV chamber and has a wide-neck communication with the LV. The LV wall aneurysm is formed by all 3 layers that appear thin, hyperechoic, dyskinetic and has a wide-neck communication with the LV that persists in diastole. The stagnated blood in the aneurysm increases the chance of thrombus formation. In contrast, the LV pseudoaneurysm results from a wall perforation contained by the parietal pericardium. Typically, the outpouch has a narrow-necked communication with the LV and may be filled with thrombus. The surrounding LV walls may be normal or have regional wall motion abnormalities. The LV noncompaction is characterized by thickened and hypokinetic LV wall segments that consist of compacted epicardial and noncompacted endocardial layers with hypertrabeculations seen in end diastole as a result of an arrested endomyocardial morphogenesis.3 Mural thrombus is a laminar or pedunculated mass along the akinetic LV segment. Depending on the maturity of the thrombus, it may present with echolucent areas.

Table 1
Table 1:
Accessory Left Ventricular Chamber Differential Findings

In conclusion, attention to the following echocardiographic characteristics may help establish the diagnosis of an LV accessory chamber: integrity of the endocardium and epicardium, intramyocardial echolucency, identification of an entry site, blood flow within the cavity, and abnormal myocardial wall motion.

Clinician’s Key Teaching Points

By Kent H. Rehfeldt, MD and Nikolaos J. Skubas, MD

  • A left ventricular (LV) accessory chamber is a rare abnormality in which an echolucent space is imaged adjacent to the LV. The size and site of communication and the consistency of the walls are used to differentiate the various pathologies of an LV accessory chamber.
  • A dual chamber LV is a form of a congenital accessory chamber with full thickness walls and synchronous contraction with the LV. In LV hypertrabeculation, the congenital noncompaction of the endomyocardium layer may also present as accessory chambers in diastole. The differential diagnoses must include acquired diseases such as: (a) LV dissection, which is a noncommunicating cavity contained within the myocardium and is usually the result of a myocardial infarction or iatrogenic injury, (b) aneurysms, either true or false, with wide or narrow communicating neck, and thinned out or absent walls, respectively, with abnormal or absent contraction, and (c) cavities resulting resorption in the center of an LV mural thrombus.
  • In this case, a dehiscence of the left coronary cusp of the aortic valve led to a dissection of the LV septal, anterior, and lateral walls and an accessory chamber with thin, hypokinetic walls that mimicked LV dissection, despite the absence of coronary disease or history of iatrogenic injury. The accessory LV chamber communicated with the aortic root directly, filling in diastole and emptying in systole.
  • The echocardiographic characteristics of an accessory LV chamber are used to define the proper treatment, which in cases of false aneurysms or associated lesions, as in this case, are always surgical.


Name: Nikolay A. Usoltsev MD.

Contribution: This author helped collect data, prepared manuscript, and worked with media files.

Attestation: Nikolay A. Usoltsev approved the final manuscript.

Name: Andrej Alfirevic MD.

Contribution: This author helped collect data, prepared manuscript, and worked with media files.

Attestation: Andrej Alfirevic approved the final manuscript.

Name: Carlos Trombetta, MD.

Contribution: This author helped collect data, prepared manuscript, and worked with media files.

Attestation: Carlos Trombetta approved the final manuscript.

This manuscript was handled by: Martin J. London, MD.


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