PMC9127081_01
Twelve-lead electrocardiograms revealing atrial fibrillation (A), atrial flutter with mild ST-segment elevation in leads V2-V5 (arrows) (B), atrial tachycardia with a rapid ventricular rate of 238 beats/min was recorded when he was experiencing attacks of atrial tachycardia (C), and sinus rhythm at 6-month follow-up (D).
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F1
He had sinus rhythm with paroxysmal AF (Figure 1A) and normal blood pressure (111/68 mmHg). Thereafter, he was experiencing paroxysmal atrial tachycardia with mild ST-segment elevation in leads V2-V5 (Figure 1B). On day 17, the patient was frequently experiencing attacks of atrial tachycardia with a very rapid ventricular rate of 200-240 beats/min (Figure 1C) and reduced blood pressure to 80-90/50-60 mmHg. At 6-month follow-up, he was still in sinus rhythm (Figure 1D) and free of adverse events.
The brain computed tomography scans at admission revealed (A) massive cerebral infarction in the right-sided frontotemporal insula (red circle) and (B) the basal ganglia area with right middle cerebral artery thrombus (white arrow). (C) The chest X-ray in the cardiology department demonstrating the abnormal left heart border. Transthoracic echocardiography (TTE), apical four-chamber view (D), and the view with color doppler (E) revealing an echo-free cavity (red star) adjacent to and compressing the LV and the probable communication of the cavity with the LA; TTE with contrast showing the contrast filling in the LA and the cavity simultaneously without filling defect in the cavity (F); TEE, the mid-esophageal 2-chamber and LAA view demonstrating a giant cavity (red star) measuring 9.3 cm x 5.7 cm (G) and its connection to LA via a 2.6 cm-wide orifice (white arrow) (H) and the to-and-fro blood flows between LA and the cavity (red star) through the orifice (white arrow) (I). Axial computed tomography scan (J) and 3D reconstruction (K) demonstrate a 9.3 cm x 6.4 cm x 3.8 cm giant LAAA. AO: aorta; RA: right atrium; LA: left atrium; RV: right ventricle; LV: left ventricle.
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F2
Computed tomography (CT) revealed massive cerebral infarction in the right-sided frontotemporal insula (Figure 2A) and the basal ganglia area with the right middle cerebral artery thrombus (Figure 2B). The chest x-ray revealed a greatly enlarged left border of the heart (Figure 2C). Transthoracic echocardiography (TTE) (Vivid E9; GE Healthcare, Norway) revealed a giant echo-free cystic structure adjacent to the posterolateral wall of the left ventricle (LV) and compressed the anterolateral LV wall during the entire cardiac cycle (Figure 2D). The apical 4-chamber views with color Doppler demonstrated that this cavity was probably related to and communicated with the left atrium (LA) via a broad neck (Figure 2E). Contrast-enhanced echocardiography was performed then, which showed that the contrast agent filled the LA and the cystic structure was simultaneously with no filling defect (Figure 2F). Further transesophageal echocardiography (TEE) confirmed that the enlarged cavity measuring 9.3 cm x 5.7 cm was arising from the LA and communicating with the LA through a 2.6 cm-wide orifice, with a big chicken-wing morphology and with intense spontaneous echo contrast but no obvious thrombi (Figures 2G,H). To-and-fro blood flows through the orifice were detected by color Doppler image (Figure 2I). Computed tomography (CT) confirmed the echocardiographic findings and showed a giant LAAA measuring 9.3 cm x 6.4 cm x 3.8 cm that was compressing the LV wall (Figures 2J,K).
Intraoperative views (A) and the surgical specimen of the LAAA with no thrombus inside the cavity of the aneurysm (B). Hematoxylin and eosin staining of the resected left atrial appendage tissues showing the wall of the aneurysm composed of the myocardium and fibrotic tissue [(C,D), 2007x].
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F3
A huge LAAA measuring about 9.5 cm in long axis was visualized with intact pericardium during the operation (Figures 3A,B). There was no thrombus inside the cavity of the aneurysm (Figure 3B). Histopathology examination revealed focal chronic inflammation with myocardial atrophy and degeneration and increased interstitial fibrosis, which are typical histological features of LAAA (Figures 3C,D).