E. Arbustini et al., ENTEROVIRAL RNA AND VIRUS-LIKE PARTICLES IN THE SKELETAL-MUSCLE OF PATIENTS WITH IDIOPATHIC DILATED CARDIOMYOPATHY, The American journal of cardiology, 80(9), 1997, pp. 1188-1193
The role of chronic viral infection in the etiopathogenesis of idiopat
hic dilated cardiomyopathy [IDC) has generated considerable research,
Enteroviruses were the favorite candidates as etiologic agents of IDC.
However, enteroviruses were rarely demonstrated in affected hearts. W
e investigated whether enteroviral infection persists in the heart and
in extracardiac sites, particularly in skeletal muscle, in patients w
ith IDC, Blood and myocardial and skeletal muscle samples were collect
ed at cardiac transplantation from 31 IDC patients, 24 non-IDC heart d
isease patients, and 3 heart donors. Samples underwent ultrastructural
studies and ribonucleic acid (RNA) extraction. RNA was reverse-transc
ribed, and 2 nested fragments (bps 179 and 126) were amplified in the
highly conserved 5' noncoding region of enteroviral genomic RNA. Enter
oviral RNA was found in the skeletal muscle of 12 cases, whereas only
4 hearts (2 of which with positive skeletal muscle) were positive. Of
the 24 controls, 2 were positive (1 muscle and heart, 1 muscle only).
Automated sequencing confirmed the enteroviral nature of the amplified
products. Ultrastructural study showed enterovirus-like particles in
4 of the enterovirus-positive muscles, and myopathic changes in ail en
terovirus-positive cases. Skeletal muscle hosts chronic enteroviral in
fection in more than one third of patients with sporadic IDC. Two hypo
theses may explain this link, Myocardial damage may derive directly fr
om recurrent subclinical heart infections caused by enteroviruses harb
ored in skeletal muscle, Alternatively, enterovirus-related myopathy m
ay trigger an autoimmune response to antigens shared by muscle and myo
cardium, Further studies are needed to assess the importance of these,
non-mutually exclusive mechanisms in IDC pathogenesis. (C) 1997 by Ex
cerpta Medica, Inc.