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  1. YOSHIKAZU YAZAKI,
  2. WATARU TAKAHASHI,
  3. KEISHI KUBO
  1. yyazaki2{at}madmac.com

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A 52 year old man was admitted with dyspnoea and hypotension. An ECG taken on admission showed complete atrioventricular block with a heart rate of 40 beats per minute and ST segment elevation in broad leads, and a temporary pacemaker was inserted. Echocardiography revealed extremely severe left ventricular hypertrophy and systolic dysfunction with a fine granular echodensity of the ventricular wall. Right heart catheterisation showed that the pulmonary capillary wedge pressure was 22 mm Hg, and the cardiac index was 1.4 l/min/m2. Cardiogenic shock caused by acute fulminant myocarditis was suspected. Despite intravenous administration of inotropes, high doses of corticosteroids, intra-aortic balloon pumping, and percutaneous cardiopulmonary support, the patient died of refractory heart failure six days after admission.

Histological diagnosis of giant cell myocarditis was confirmed by necropsy. Microscopic examination revealed a dense diffuse inflammatory infiltrate, composed of lymphocytes, macrophage, eosinophils, and multinucleated giant cells (top right). Immunohistochemical analysis was performed to identify the phenotype of inflammatory infiltrate and expression of cell adhesion molecules. CD-56 positive natural killer cells and CD-8 positive T lymphocytes were the predominant cells. Perforin was expressed in a large amount of the infiltrate (bottom right). Enhanced expression of intercellular adhesion molecule-I and vascular cell adhesion molecule-I was also observed. These observations suggest that cell mediated cytotoxity related to these adhesion molecules and perforin included in killer lymphocytes may be considered as a possible mechanism for severe myocardial cell damage in human giant cell myocarditis.

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