PMC8586196_01
Serial changes of electrocardiography (ECG). (A) Extensive ST elevation with bizarrely wide QRS complexes immediately after extracorporeal membrane oxygenation (ECMO) application. (B) Ventricular and atrial electrical standstill during ECMO management. (C) Decreased but remained extensive ST elevation with narrowing and low voltage of QRS complexes on ECG on the third hospital day. (D) Normalization of ST segment elevation and QRS width; an increased but remained low voltage QRS complex on pre-discharge ECG.
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F1
The ECG showed an extensive ST segment elevation with bizarrely wide QRS complexes in the entire precordial and limb leads except for lead aVR (Figure 1A). It eventually progressed into a total ventricular and atrial electrical standstill lasting for more than 2 h (Figure 1B) and returned to the previous ECG pattern thereafter. In addition, the ECG showed a more decreased ST segment elevation with the narrowing of QRS complexes (Figure 1C). Predischarge ECG revealed the normalization of previously noted ST segment elevation and QRS width, and an increased but low voltage QRS complex that remained (Figure 1D).
Serial changes of echocardiography. (A,B) Global akinesia with severe left ventricular (LV) dysfunction and marked edematous left ventricular wall thickening on portable echocardiography performed just after extracorporeal membrane oxygenation application. (C,D) Normalized LV function and wall thickness on pre-discharge echocardiography.
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F2
Portable echocardiography revealed global akinesia with severe left and right ventricular dysfunction (ejection fraction <10% by visual estimation) and marked edematous left ventricular (LV) wall thickening (13 mm) (Figures 2A,B) (Supplementary Videos 1, 2). LV function (ejection fraction: 58%) and wall thickness were normalized on the predischarge echocardiography (Figures 2C,D) (Supplementary Videos 3, 4), and the patient was discharged and followed up at an outpatient clinic without clinical events.
Histopathologic examination of endomyocardial biopsy revealed marked and diffused infiltration of lymphocytes (thick arrow) within the myocardium (thin arrow) (x40, Hematoxylin-eosin stain).
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F3
ECMO weaning was done on the sixth day. EMB demonstrated compatible findings of acute lymphocytic myocarditis (Figure 3).
Cardiac magnetic resonance imaging (MRI) findings. (A) T2-weighted short TI inversion recovery MRI at 3T in a short-axis view shows multifocal high signal intensities at the mid anterior and lateral wall (arrow) indicating myocardial edema. (B) Late gadolinium enhancement imaging in a four-chamber view displays multifocal mid wall enhancement (arrow) indicating inflammatory myocardial necrosis. (C) T1 mapping and T2 mapping in a short-axis view show elevated T1 and T2 relaxation times at the mid ventricular level, indicating an acute myocardial injury (regional T1 relaxation time-1,418 ms at the anterolateral wall and 1,461 ms at the septal wall, regional T2 relaxation time-45 ms at the anterolateral wall and 47 ms at the septal wall; institution-specific cutoff values for acute myocarditis- T1 global: >=1,230 ms and T2 global: >=36 ms).
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F4
On the tenth day, cardiac magnetic resonance imaging was performed, which showed multifocal lesions with high signal intensity in T2 weighted images (Figure 4A) and a positive late gadolinium enhancement (Figure 4B) which implies myocardial edema and necrosis, respectively. In addition, both T1 and T2 relaxation times at the LV wall were also increased (Figure 4C).