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Circulation. 1982;65:1230-1235

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Circulation, Vol 65, 1230-1235, Copyright © 1982 by American Heart Association


ARTICLES

An experimental model for congestive heart failure after encephalomyocarditis virus myocarditis in mice

A Matsumori and C Kawai

Severe myocarditis was induced in inbred BALB/c mice inoculated with the M variant of encephalomyocarditis (EMC) virus. The mortality rate was maximal on the fourth day, then decreased gradually, but increased again between the eleventh and fourteenth days. Gross myocardial lesions were seen on the surface of the ventricles in 62 of 125 mice (49.6%) after the fifth day. These myocardial lesions were observed more frequently in the dead mice (46 of 49, 93.9%). Cavity dimensions and wall thickness were measured in two groups of mice with myocarditis. On days 5-7, the cavity dimensions of the right (RV) and left (LV) ventricles in inoculated mice (0.92 +/- 0.51 mm and 1.21 +/- 0.18 mm, respectively) were significantly larger than those in controls (RV 0.54 +/- 0.17, LV 1.01 +/- 0.15; p less than 0.05). The wall thickness of the RV (0.46 +/- 0.09, controls 0.64 +/- 0.11; p less than 0.001) and the LV (0.97 +/- 0.13, controls 1.12 +/- 0.19; p less than 0.05) was significantly decreased. On days 8-14, dilatation of the LV was more pronounced (1.48 +/- 0.37, p less than 0.005) than during days 5-7, and the interventricular septum was also thinner. Pleural effusion, ascites and congestion of the lungs and liver were noted, and death seemed due to congestive heart failure. This study is the first documentation of congestive heart failure after viral infection is an experimental animal.


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