JA Clinical Reports (Nov 2016)

A case of a giant cell myocarditis that developed massive left ventricular thrombus during percutaneous cardiopulmonary support

  • Yusuke Takei,
  • Yutaka Ejima,
  • Hiroaki Toyama,
  • Kana Takei,
  • Takahisa Ota,
  • Masanori Yamauchi

DOI
https://doi.org/10.1186/s40981-016-0067-0
Journal volume & issue
Vol. 2, no. 1
pp. 1 – 8

Abstract

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Abstract Background Giant cell myocarditis, characterized by infiltration of multinucleated giant cells in the myocardium, is a rare type of myocarditis. It often progresses rapidly into fulminant heart failure and indicates a poor prognosis. When a patient with giant cell myocarditis develops into severe myocarditis presenting with a cardiogenic shock, we should use a percutaneous cardiopulmonary support (PCPS), which could occur complications. We experienced a patient with giant cell myocarditis, who developed left ventricular thrombus formations during the circulation support therapy with PCPS for cardiogenic shock. Case presentation A 60-year-old man who developed a cardiogenic shock was transferred to our hospital. After the admission, inotropic agents were increased and an intra-aortic balloon pumping was started. But these therapies did not improve his hemodynamic status. He was placed PCPS. Then, he underwent endomyocardial biopsy and was diagnosed with giant cell myocarditis. On the next morning, he developed complete atrioventricular block, and subsequently, thrombus formations occurred in his left ventricular outlet tract and Valsalva sinus despite an anticoagulant therapy. Thereafter, we intensified the anticoagulant therapy to prevent further thrombus formation, but he developed an intracranial hemorrhage. He did not recover from heart failure and died 16 days after the admission. Conclusions We present a patient with giant cell myocarditis who developed widespread thrombosis in the left ventricle during the circulatory support with PCPS, despite anticoagulant therapy. In this case, decreased left myocardial contractility caused by giant cell myocarditis and increased left ventricular afterload by the retrograde perfusion from the PCPS induced the thrombotic tendency and congestion in the left ventricle. In addition, he developed complete atrioventricular block, which reduced the left ventricular ejection and enhanced the thrombus formation. Because patients with giant cell myocarditis have a low probability of spontaneous recovery, heart transplantation or ventricular assist device implantation may be required for circulatory support. We should establish mechanical circulatory support rapidly to improve the prognosis of patients with giant cell myocarditis. Moreover, a ventricular assist device, which can prevent both ventricular congestion and retrograde blood flow, might be suitable to prevent complications as this case.

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