case_images: PMC5813737_01
case_images: The 12-lead electrocardiogram of the patient upon admission to the intensive care unit. Sinus rhythm, low-voltage R-wave, and intraventricular conduction disturbance in all leads were seen
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case_images: PMC5813737_01_40981_2016_67_Fig1_HTML.jpg
case_images: Fig1
case_images: His chest radiograph and chest computed tomography showed pulmonary congestion and bilateral pleural effusion without cardiomegaly, and the electrocardiogram showed low voltage of R-wave and intraventricular conduction disturbance in all leads (Fig. 1).
case_images: Microscopic examination from the endomyocardial biopsy of the right ventricle. Characteristic infiltrations of multinucleated giant cells in the myocardium (open circle) were seen
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case_images: PMC5813737_01_40981_2016_67_Fig2_HTML.jpg
case_images: Fig2
case_images: He was eventually diagnosed with giant cell myocarditis (Fig. 2).  In addition, sudden elevation of PaCO2 from 31 to 62.5 mmHg was also observed despite the preservation of both the steady PCPS output and the mechanical ventilation setting (Fig. 4 and Table 2).
case_images: Electrocardiogram strips on the next morning. Complete atrioventricular block was seen
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case_images: PMC5813737_01_40981_2016_67_Fig3_HTML.jpg
case_images: Fig3
case_images: On the next morning, he developed complete atrioventricular block (Fig. 3), subsequent decreased blood pressure from 100/50 to 70/40 mmHg, and increased pulmonary arterial pressure from 35/15 to 60/20 mmHg.
case_images: The change in the hemodynamic status around the onset of the atrioventricular block. HR heart rate, ABP arterial blood pressure, PAP pulmonary artery pressure, P
  E
  tCO
  2 end-tidal carbon dioxide tension, PaCO
  2 arterial carbon dioxide tension, SvO
  2 mixed venous oxygenation saturation, PCPS percutaneous cardiopulmonary support, CO cardiac output. (1) The onset of the complete atrioventricular block. (2) The start of the ventricular pacing. After the onset of the complete atrioventricular block, the decrease of BP and the increase of PAP and PaCO2 continued until the point when the blood flow and the gas flow of the PCPS were augmented. The hemodynamics of the patient improved along with the recovery of the ventricular contraction by the ventricular pacing
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case_images: PMC5813737_01_40981_2016_67_Fig4_HTML.jpg
case_images: Fig4
case_images: In addition, sudden elevation of PaCO2 from 31 to 62.5 mmHg was also observed despite the preservation of both the steady PCPS output and the mechanical ventilation setting (Fig. 4 and Table 2).
case_images: Transesophageal echocardiography (TEE) after the onset of atrioventricular block. a Mid-esophageal 4-chamber (ME 4ch) view showed thrombus formations and congestion in the left ventricle. b Mid-esophageal aortic valve short-axis (ME AV SAX) view showed thrombus formations in the Valsalva sinus and aortic valve closure. c Mid-esophageal long-axis (ME AV LAX) view showed thrombus formations in the left ventricular tract and the Valsalva sinus
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case_images: PMC5813737_01_40981_2016_67_Fig5_HTML.jpg
case_images: Fig5
case_images: Hence, we performed transesophageal echocardiography (TEE), which indicated widespread thrombus formations and marked congestion in his left ventricular outlet tract and Valsalva sinus and closure of the aortic valve; however, there is no thrombus in his right ventricle (Fig. 5).
case_images: The mechanism of thrombus formation in this case. PCPS percutaneous cardiopulmonary support, AV-block atrioventricular block, BP systemic blood pressure, PAP pulmonary artery pressure, PaCO
  2 arterial carbon dioxide tension. Giant cell myocarditis induced the left ventricular distension and subsequent thrombus formation tendency. The retrograde perfusion by the PCPS and the complete atrioventricular block further enhanced thrombus formation tendency. As a result, widespread thrombi were formed in the left ventricular tract and the Valsalva sinus
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case_images: PMC5813737_01_40981_2016_67_Fig6_HTML.jpg
case_images: Fig6
case_images: In this case, the complete atrioventricular block induced a critical decrease of the left ventricular ejection, which resulted in the further left ventricle distension, which might trigger the thrombosis (Fig. 6). 