title: Myocardial inflammatory cell infiltrates in cases of dilated cardiomyopathy as a determinant of outcome following partial left ventriculectomy.
abstract: 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.
authors.affiliation: Department of Internal Medicine, Osaka Medical College, Takatsuki, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Kanzaki
authors.forename: F
authors.initials: F
authors.lastname: Terasaki
authors.forename: M
authors.initials: M
authors.lastname: Okabe
authors.forename: T
authors.initials: T
authors.lastname: Hayashi
authors.forename: H
authors.initials: H
authors.lastname: Toko
authors.forename: H
authors.initials: H
authors.lastname: Shimomura
authors.forename: S
authors.initials: S
authors.lastname: Fujioka
authors.forename: Y
authors.initials: Y
authors.lastname: Kitaura
authors.forename: K
authors.initials: K
authors.lastname: Kawamura
authors.forename: Y
authors.initials: Y
authors.lastname: Horii
authors.forename: T
authors.initials: T
authors.lastname: Isomura
authors.forename: H
authors.initials: H
authors.lastname: Suma
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D006348:Cardiac Surgical Procedures / Q000401:mortality; D002311:Cardiomyopathy, Dilated / Q000401:mortality / Q000473:pathology / Q000601:surgery*; D002633:Chemotaxis; D004279:DNA, Viral / Q000032:analysis; D004770:Enterovirus / Q000235:genetics; D005260:Female; D006352:Heart Ventricles / Q000473:pathology / Q000601:surgery*; D006801:Humans; D007150:Immunohistochemistry; D007962:Leukocytes / Q000502:physiology; D008264:Macrophages / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009205:Myocarditis / Q000401:mortality / Q000473:pathology* / Q000821:virology; D011379:Prognosis; D016896:Treatment Outcome
chemical_list: D004279:DNA, Viral