Myocardial Inflammatory Cell Infiltrates in Cases of Dilated Cardiomyopathy as a Determinant of Outcome Following Partial Left Ventriculectomy.

  • Kanzaki Yumiko
    The Third Division, Department of Internal Medicine, Osaka Medical College
  • Terasaki Fumio
    The Third Division, Department of Internal Medicine, Osaka Medical College
  • Okabe Makoto
    The Third Division, Department of Internal Medicine, Osaka Medical College
  • Hayashi Tetsuya
    The Third Division, Department of Internal Medicine, Osaka Medical College
  • Toko Haruhiro
    The Third Division, Department of Internal Medicine, Osaka Medical College
  • Shimomura Hiroaki
    The Third Division, Department of Internal Medicine, Osaka Medical College
  • Fujioka Shigekazu
    The Third Division, Department of Internal Medicine, Osaka Medical College
  • Kitaura Yasushi
    The Third Division, Department of Internal Medicine, Osaka Medical College
  • Kawamura Keishiro
    The Third Division, Department of Internal Medicine, Osaka Medical College
  • Horii Yasuhiro
    Division of Cardiovascular Surgery, Hayama Heart Center, Hayama
  • Isomura Tadashi
    Division of Cardiovascular Surgery, Hayama Heart Center, Hayama
  • Suma Hisayoshi
    Division of Cardiovascular Surgery, Hayama Heart Center, Hayama

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Partial left ventriculectomy (PLV) can be used to treat refractory congestive heart failure caused by dilated cardiomyopathy (DCM). In order to understand the relationship between the underlying myocardial injury and early clinical outcomes after PLV, histopathologic, immunohistochemical and virologic studies of the resected myocardium were performed. The posterolateral left ventricular walls from 27 patients with idiopathic DCM were examined. Cardiomyocyte diameter, degree of myocardial fibrosis, degree of cardiomyocyte degeneration, and degree of inflammatory cell infiltration were compared with mortality rates. Polymerase chain reaction was performed to detect enterovirus genome in the myocardium. Some patients had inflammatory cell infiltrates with focal accumulations of lymphocytes and macrophages, including both cytotoxic/suppressor T-cells and helper/inducer T-cells. The number of inflammatory cells (activated lymphocytes plus macrophages/mm2) was significantly greater in patients who died of cardiac insufficiency after surgery (27.8±5.7; n=7) than in the survivors (11.1±2.5; n=15). There was no significant difference in the degree of myocardial fibrosis, cardiomyocyte diameter or degree of cardiomyocyte degeneration between the 2 groups. Enterovirus genome was detected in the myocardium of 9 (38%) of 24 patients examined and 5 of these enterovirus-positive hearts had severe inflammatory cell infiltrates (37.9±2.5/mm2). Early survival in patients undergoing PLV for DCM is significantly affected by the degree of myocardial inflammation, so patients with more severe or ongoing inflammation may have poor clinical outcomes. Chronic myocarditis may play an important role in the etiology and pathophysiology of idiopathic DCM. (Jpn Circ J 2001; 65: 797 - 802)

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