We developed a new murine model to study MY and the potential role of viral infection in cardiomyopathy of pregnancy. Pregnant (P) and nonpregnant (NP) mice were inoculated intravenously with Theiler's virus, a murine enterovirus, or with BHK 21 cell lysate (controls). P animals were inoculated at 6-7 days(early) gestation and sacrificed (sacr) either 6 or 12 days later. Hearts were evaluated by viral culture, histologic grading and in-situ hybridization. Histologic grading and culture results of cardiac tissue were as follows: Table Although MY occurred at comparable rates in P (22/34, 65%) and NP (9/16, 56%) virus-infected mice, severe MY (m2 or m3) occurred more frequently in P mice (13/34, 38% vs 2/16, 13%). Hearts from P mice were more likely culture positive than hearts from NP mice (15/34, 44% vs 3/16, 19%) and hearts from mice with MY were more likely culture positive than hearts without MY. In-situ hybridization detected viral RNA within myocytes of 3 P infected mice, each of which had MY histologically. With longer duration from inoculation, culture positivity decreased but histologic damage persisted. This model demonstrates both enhanced susceptibility to cardiac viral infection and increased severity of MY in pregnancy.

Table 1