PMC8818743_01
(A) ECG for the woman patient when admitted to hospital: Sinus rhythm Right bundle branch block; (B) ECG of the man patient when admitted to hospital; V1-V3 lead ST-elevation and third-degree atrioventricular block; (C) ECG of the man patient when implanted with temporary pacing; (D) ECG of the man patient at discharge: Sinus rhythm, Right bundle branch block.
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F1
An emergency electrocardiogram revealed a third-degree atrioventricular block (AVB) (Figure 1B). Physical examination revealed a body temperature of 36.2 C, blood pressure of 101/60 mmHg, pulse of 77 bpm (pacemaker heart rate, Figure 1C), respiratory rate of 18 bpm, and blood oxygen saturation of 99% while the patient was breathing ambient air. After 9 days, the LVEF recovered to 59% with a normal sinus rhythm (Figure 1D) when he was discharged with oral beta-blockers (47.5 mg/day), perindopril (4 mg/day), and prednisone 20 mg/day.
Coronary angiography results for Case 1 (A-C): (A) Left coronary artery: Cranial 30 ; (B) Left coronary artery: Caudal 30 ; (C) Right coronary artery: Left anterior oblique 45 ; Coronary angiography results for Case 2 (D-F): (D) Left anterior oblique 30 + Cranial 30 ; (E) Left coronary artery: Caudal 30 ; (F) Right coronary artery: Left anterior oblique 45 .
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F2
Urgent coronary angiography excluded coronary artery disease (Figures 2A-C); therefore, transthoracic echocardiography (TTE) with strain analysis revealed diffuse left ventricular hypokinesia and increased thickness of the mid-ventricular septal wall (septal wall 13 mm; inferior wall 11 mm), and markedly reduced LV ejection fraction (LVEF 30%) (Figures 3B,D).
The echocardiographic and cardiac magnetic resonance images recorded at admission and the findings of pathological specimens compatible with fulminant myocarditis. (A) LV ejection fraction was mildly reduced (EF value, 28%); (B) LV ejection fraction was mildly reduced (EF value = 30%); (C) Representative images of global longitudinal strains (GLS) presented as "bullseye" displays in case 1 (GLS = -12.1%); (D) Representative images of global longitudinal strains (GLS) presented as "bullseye" displays in case 2 (GLS = -9.8%); (E) Increased myocardial signal in the outer layer of the apical ventricular septum (edema) (arrow); (F) Late gadolinium enhancement imaging suggests myocardial enhancement in the outer layer of the apical ventricular septum (myocardial necrosis) (arrow); (G) Long-axis late gadolinium enhancement imaging suggests myocardial necrosis in the middle ventricular septum (red arrow), thinning, and enhancement of the lateral wall (yellow arrow); (H) Short axial late gadolinium enhancement imaging demonstrates myocardial necrosis in the middle ventricular septum (red arrow) with thinning of the lateral wall and formation of fibrosis (yellow arrow); (I) in T1 mapping, ventricular septal myocardial edema was observed, and the value of myocardial T1 was significantly increased, T1=1380 ms (normal value T1 = 1,180 +- 20 ms); (J) Myocardial edema in the lower interventricular septum was observed in T1 mapping, and the value of myocardial T1 was significantly increased, T1 = 1,364 ms (normal value T1 = 1,180 +- 20 ms); (K) Biopsy from myocardium showing myocardial fibers were slightly edematous and interstitial edema was accompanied by infiltration of inflammatory cells; (L) Biopsy from myocardium showing myocardial atrophy, hypertrophy of some cardiomyocytes, myocardial interstitial edema, local fibrosis, scattered focal necrosis of cardiomyocytes accompanied by infiltration of inflammatory cells.
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F3
Immediate transthoracic echocardiography with strain analysis documented diffuse left ventricular hypokinesia and increased thickness in the mid-ventricular septal wall (13 mm), and LVEF severely reduced to 26% (Figures 3A,C). Five days later, his temporary pacemaker was withdrawn with regular sinus rhythm, and at this time, the CMR test revealed a corresponding extensive myocardial edema and necrosis with predominant subepicardial/mid-ventricular septal distribution highly suggestive of a myocarditis pattern (Figures 3E,F). Ventricular septal myoedema was observed on T1 mapping, and the value of myocardial T1 was significantly increased (1,380 ms in the male patient, Figures 3I,J).
PMC8818743_02
(A) ECG for the woman patient when admitted to hospital: Sinus rhythm Right bundle branch block; (B) ECG of the man patient when admitted to hospital; V1-V3 lead ST-elevation and third-degree atrioventricular block; (C) ECG of the man patient when implanted with temporary pacing; (D) ECG of the man patient at discharge: Sinus rhythm, Right bundle branch block.
fcvm-08-769616-g0001.jpg
PMC8818743_02_fcvm-08-769616-g0001.jpg
F1
An emergency electrocardiogram revealed a third-degree atrioventricular block (AVB) (Figure 1B). Physical examination revealed a body temperature of 36.2 C, blood pressure of 101/60 mmHg, pulse of 77 bpm (pacemaker heart rate, Figure 1C), respiratory rate of 18 bpm, and blood oxygen saturation of 99% while the patient was breathing ambient air. After 9 days, the LVEF recovered to 59% with a normal sinus rhythm (Figure 1D) when he was discharged with oral beta-blockers (47.5 mg/day), perindopril (4 mg/day), and prednisone 20 mg/day.
The echocardiographic and cardiac magnetic resonance images recorded at admission and the findings of pathological specimens compatible with fulminant myocarditis. (A) LV ejection fraction was mildly reduced (EF value, 28%); (B) LV ejection fraction was mildly reduced (EF value = 30%); (C) Representative images of global longitudinal strains (GLS) presented as "bullseye" displays in case 1 (GLS = -12.1%); (D) Representative images of global longitudinal strains (GLS) presented as "bullseye" displays in case 2 (GLS = -9.8%); (E) Increased myocardial signal in the outer layer of the apical ventricular septum (edema) (arrow); (F) Late gadolinium enhancement imaging suggests myocardial enhancement in the outer layer of the apical ventricular septum (myocardial necrosis) (arrow); (G) Long-axis late gadolinium enhancement imaging suggests myocardial necrosis in the middle ventricular septum (red arrow), thinning, and enhancement of the lateral wall (yellow arrow); (H) Short axial late gadolinium enhancement imaging demonstrates myocardial necrosis in the middle ventricular septum (red arrow) with thinning of the lateral wall and formation of fibrosis (yellow arrow); (I) in T1 mapping, ventricular septal myocardial edema was observed, and the value of myocardial T1 was significantly increased, T1=1380 ms (normal value T1 = 1,180 +- 20 ms); (J) Myocardial edema in the lower interventricular septum was observed in T1 mapping, and the value of myocardial T1 was significantly increased, T1 = 1,364 ms (normal value T1 = 1,180 +- 20 ms); (K) Biopsy from myocardium showing myocardial fibers were slightly edematous and interstitial edema was accompanied by infiltration of inflammatory cells; (L) Biopsy from myocardium showing myocardial atrophy, hypertrophy of some cardiomyocytes, myocardial interstitial edema, local fibrosis, scattered focal necrosis of cardiomyocytes accompanied by infiltration of inflammatory cells.
fcvm-08-769616-g0003.jpg
PMC8818743_02_fcvm-08-769616-g0003.jpg
F3
Immediate transthoracic echocardiography with strain analysis documented diffuse left ventricular hypokinesia and increased thickness in the mid-ventricular septal wall (13 mm), and LVEF severely reduced to 26% (Figures 3A,C). Five days later, his temporary pacemaker was withdrawn with regular sinus rhythm, and at this time, the CMR test revealed a corresponding extensive myocardial edema and necrosis with predominant subepicardial/mid-ventricular septal distribution highly suggestive of a myocarditis pattern (Figures 3E,F). Ventricular septal myoedema was observed on T1 mapping, and the value of myocardial T1 was significantly increased (1,380 ms in the male patient, Figures 3I,J).