Y. Kanzaki et al., Myocardial inflammatory cell infiltrates in cases of dilated cardiomyopathy as a determinant of outcome following partial left ventriculectomy, JPN CIRC J, 65(9), 2001, pp. 797-802
Citations number
37
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Partial left ventriculectomy (PLV) can be used to treat refractory congesti
ve heart failure caused by dilated cardiomyopathy (DCM). In order to unders
tand the relationship between the underlying myocardial injury and early cl
inical outcomes after PLV, histopathologic, immunohistochemical and virolog
ic studies of the resected myocardium were performed. The posterolateral le
ft ventricular walls from 27 patients with idiopathic DCM were examined. Ca
rdiomyocyte diameter, degree of myocardial fibrosis, degree of cardiomyocyt
e degeneration, and degree of inflammatory cell infiltration were compared
with mortality rates. Polymerase chain reaction was performed to detect ent
erovirus genome in the myocardium. Some patients had inflammatory cell infi
ltrates 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/mm(2)) was sign
ificantly greater in patients who died of cardiac insufficiency after surge
ry (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, cardiomyocy
te diameter or degree of cardiomyocyte degeneration between the 2 groups. E
nterovirus 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/mm(2)). Early survival in patients undergoin
g PLV for DCM is significantly affected by the degree of myocardial inflamm
ation, so patients with more severe or ongoing inflammation may have poor c
linical outcomes. Chronic myocarditis may play an important role in the eti
ology and pathophysiology of idiopathic DCM.