TY - JOUR
T1 - Myocardial damage assessed by indium-111-antimyosin
T2 - Correlation with persistent enteroviral ribonucleic acid in dilated cardiomyopathy
AU - Bengel, Frank M.
AU - Feistel, Herbert
AU - Moshage, Werner
AU - Bachmann, Kurt
AU - Wolf, Friedrich
PY - 1997
Y1 - 1997
N2 - The persistence of enteroviral ribonucleic acid (RNA) in the myocardium has been implicated as a pathogenetic factor in idiopathic dilated cardiomyopathy. Enteroviral persistence may lead to myocardial cell membrane damage, resulting in increased uptake of antimyosin antibodies. To further evaluate this hypothesis, a direct comparison of myocardial antimyosin uptake with the presence of enteroviral RNA was performed in ten patients (one female, nine male; 53 ± 8 years) with chronic dilated cardiomyopathy. Planar antimyosin images were obtained 48 h after the injection of indium-111-labelled antimyosin Fab. Using a region of interest technique, the heart to lung uptake ratio (HLR) was calculated as a semiquantitative parameter of myocardial tracer uptake. Cardiac catheterization was performed to assess left ventricular function and to obtain myocardial biopsy samples. In the biopsy samples, gene amplification by polymerase chain reaction (PCR) was used to specifically detect enteroviral RNA. In the ten patients, the left ventricular ejection fraction was 39% ± 11% and the enddiastolic volume 131 ± 46 ml/m2. The HLR was 1.72 ± 0.21 and showed no correlation with functional parameters. In two patients with a positive PCR consistent with persisting enteroviral RNA, the HLR was not higher than that in eight patients with a negative PCR (1.46 ± 0.18 vs 1.78 ± 0.18, respectively). These results suggest that increased uptake of 111In-antimyosin in chronic idiopathic dilated cardiomyopathy cannot be explained by pure persistence of enteroviral RNA. Other pathogenetic factors such as myocardial autoantibodies or microvascular spasm may be responsible for myocyte membrane damage detected by antimyosin.
AB - The persistence of enteroviral ribonucleic acid (RNA) in the myocardium has been implicated as a pathogenetic factor in idiopathic dilated cardiomyopathy. Enteroviral persistence may lead to myocardial cell membrane damage, resulting in increased uptake of antimyosin antibodies. To further evaluate this hypothesis, a direct comparison of myocardial antimyosin uptake with the presence of enteroviral RNA was performed in ten patients (one female, nine male; 53 ± 8 years) with chronic dilated cardiomyopathy. Planar antimyosin images were obtained 48 h after the injection of indium-111-labelled antimyosin Fab. Using a region of interest technique, the heart to lung uptake ratio (HLR) was calculated as a semiquantitative parameter of myocardial tracer uptake. Cardiac catheterization was performed to assess left ventricular function and to obtain myocardial biopsy samples. In the biopsy samples, gene amplification by polymerase chain reaction (PCR) was used to specifically detect enteroviral RNA. In the ten patients, the left ventricular ejection fraction was 39% ± 11% and the enddiastolic volume 131 ± 46 ml/m2. The HLR was 1.72 ± 0.21 and showed no correlation with functional parameters. In two patients with a positive PCR consistent with persisting enteroviral RNA, the HLR was not higher than that in eight patients with a negative PCR (1.46 ± 0.18 vs 1.78 ± 0.18, respectively). These results suggest that increased uptake of 111In-antimyosin in chronic idiopathic dilated cardiomyopathy cannot be explained by pure persistence of enteroviral RNA. Other pathogenetic factors such as myocardial autoantibodies or microvascular spasm may be responsible for myocyte membrane damage detected by antimyosin.
KW - Dilated cardiomyopathy
KW - Indium-111 antimyosin
KW - Pathogenesis
KW - Polymerase chain reaction
KW - Viral persistence
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U2 - 10.1007/BF01254244
DO - 10.1007/BF01254244
M3 - Article
C2 - 9283105
AN - SCOPUS:0030815205
SN - 0340-6997
VL - 24
SP - 1128
EP - 1131
JO - European Journal of Nuclear Medicine
JF - European Journal of Nuclear Medicine
IS - 9
ER -