Systematic histopathological analysis revealed that cardiac rupture accounts for only 50% of deaths in C57BL/6J mice following nonreperfused myocardial infarction, indicating that gross autopsy criteria often overestimate rupture rates.
Hemothorax is a low-specificity criterion for cardiac rupture in mouse MI models, and rupture is associated with an imbalance between inflammatory and reparative responses.
We show that cardiac rupture accounts for 50% of deaths in C57BL/6J mice undergoing nonreperfused myocardial infarction protocols. Overestimation of rupture events in published studies likely reflects the low specificity of hemothorax as a criterion for documentation of rupture. In contrast, identification of a gross rupture site has high specificity and low sensitivity. We also show that mice dying of rupture have increased macrophage influx and attenuated myofibroblast infiltration in the infarct. These findings are consistent with a role for perturbations in the balance between inflammatory and reparative responses in the pathogenesis of postinfarction cardiac rupture. We also report that the male predilection for rupture in infarcted mice is not associated with increased inflammatory activation of myeloid cells.
Hanna et al. (Fri,) conducted a other in Myocardial infarction (n=49). Nonreperfused myocardial infarction vs. Unexposed/reference group (not applicable, descriptive study of post-MI deaths) was evaluated on Proportion of post-MI deaths attributed to cardiac rupture by systematic histopathological analysis. Systematic histopathological analysis revealed that cardiac rupture accounts for only 50% of deaths in C57BL/6J mice following nonreperfused myocardial infarction, indicating that gross autopsy criteria often overestimate rupture rates.