Case Presentation
A 69-year-old man with no history of cardiac disease was transported to
a previous hospital with a fever of 39°C and fainting. An
electrocardiogram (ECG) showed ST-segment elevation and elevated
myocardial desensitization enzymes. Echocardiography revealed severe
diffuse hypokinesis and pericardial effusion. Additionally, remarkable
stenosis was not observed during coronary artery angiography. He was
admitted to the previous hospital with suspected myocarditis. Three days
after admission, the level of consciousness decreased, hepatobiliary
enzymes increased, renal function worsened, and blood pressure
decreased, thereafter he was transferred to our hospital.
On physical examination at our emergency department, his Glasgow coma
scale was eyes: 4, verbal: 4, motor: 6; blood pressure (BP): 112/90
mmHg; heart rate (HR): 132 beats per minute (bpm), regular with no
catecholamine support; respirations: 27 breaths per minute, oxygen
saturation: 96% with a 4 L oral mask, and temperature was 37.2°C. The
laboratory data at the time of arrival are shown in Table 1. Overall,
white blood cells, C-reactive protein (CRP), and myocardial enzymes were
prominently elevated. Troponin I levels were above 2000 ng/L. A 12-lead
ECG showed ST-segment elevation in all guides (Figure 1). After
admission to the intensive care unit, considering the possibility of a
bacterial infection, relevant treatment was initiated. On day two, his
HR increased to 180 bpm and his systolic BP dropped to 60 mmHg
Echocardiography revealed significant decrease in ejection fraction to
approximately 10%. The patient then fell into pulseless electrical
activity; cardiopulmonary resuscitation occurred immediately, and the
patient was resuscitated after administration of 1 mg of adrenaline.
Since circulatory dynamics remained unstable, veno-arterial ECMO (V-A
ECMO) and intra-aortic balloon pumping (IABP) were introduced.
Intravenous high-dose methylprednisolone therapy (1000 mg for 3 days)
and immunoglobulin therapy (0.5 kg/kg for 2 days) were also initiated.
On day four ECG showed asystole; however, systolic BP was maintained at
80 mmHg under V-A ECMO with a flow of approximately 3 L/min and IABP
with an internal trigger mode. Circulatory dynamics were maintained,
therefore, intensive care was continued. After 38 h of asystole,
electrical activity revived on ECG with a HR of 50-60 bpm (Figure 2). He
responded to a call, suggesting cerebral function was maintained to some
level. Cardiac function gradually improved, and the patient was weaned
off V-A ECMO on day 14. The cause of fulminant myocarditis in this case
was unclear, as we did not perform magnetic resonance imaging or
myocardial biopsy at our hospital. Laboratory data that screened for
causative viruses also showed no significant findings. On day 15,
echocardiography showed an improved ejection fraction of approximately
60%. The patient was weaned from the IABP and extubated on day 18.
After extubation, consciousness continued without any obvious higher
functional impairment. On day 25, the patient was transferred to another
hospital.