An animal model of congestive (dilated) cardiomyopathy: dilatation and hypertrophy of the heart in the chronic stage in DBA/2 mice with myocarditis caused by encephalomyocarditis virus.
Author(s) -
Akira Matsumori,
C Kawai
Publication year - 1982
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.66.2.355
Subject(s) - medicine , ventricle , interventricular septum , myocarditis , cardiology , heart failure , dilated cardiomyopathy , viral myocarditis , cardiomyopathy , muscle hypertrophy , fibrosis
To investigate whether lesions that develop in the chronic stage of viral myocarditis are similar to those seen in congestive (dilated) cardiomyopathy, we studied myocarditis in inbred strains of DBA/2 mice infected with encephalomyocarditis (EMC) virus. Myocardial necrosis with calcification appeared on day 4. Thereafter, myocardial necrosis became more extensive and mononuclear cell infiltration was evident and was most marked on day 14. On day 90, cellular infiltration had decreased and myocardial fibrosis was prominent. At this stage, the heart weight was significantly greater in the infected mice than in the controls (0.190 +/- 0.028 g vs 0.122 +/- 0.013 g, mean +/- SD) (p less than 0.001) and the cavity dimensions of the left ventricle were larger (1.67 +/- 0.29 mm vs 1.11 +/- 0.20 mm) (p less than 0.001). The diameters of myocardial fibers of the right ventricle, the interventricular septum and the left ventricle were significantly larger than those of the controls (right ventricle, 16.6 +/- 1.8 vs 13.4 +/- 1.5 micrometer; interventricular septum, 17.8 +/- 1.5 vs 13.8 +/- 1.5 micrometer; left ventricle, 19.4 +/- 1.7 vs 14.8 +/- 1.1 micrometer) (p less than 0.001). This study demonstrates that in viral myocarditis in the chronic stage, lesions develop that resemble those seen in congestive cardiomyopathy.
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