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.