Pregnancy mitigates cardiac pathology in a mouse model of left ventricular pressure overload.


In Western countries heart disease is the leading cause of maternal death during pregnancy. The effect of pregnancy on the heart is difficult to study in patients with preexisting heart disease. Since experimental studies are scarce, we investigated the effect of pressure overload, produced by transverse aortic constriction (TAC) in mice, on the ability to conceive, pregnancy outcome, and maternal cardiac structure and function. Four weeks of TAC produced left ventricular (LV) hypertrophy and dysfunction with marked interstitial fibrosis, decreased capillary density, and induced pathological cardiac gene expression. Pregnancy increased relative LV and right ventricular weight without affecting the deterioration of LV function following TAC. Surprisingly, the TAC-induced increase in relative heart and lung weight was mitigated by pregnancy, which was accompanied by a trend towards normalization of capillary density and natriuretic peptide type A expression. Additionally, the combination of pregnancy and TAC increased the cardiac phosphorylation of c-Jun, and STAT1, but reduced phosphoinositide 3-kinase phosphorylation. Finally, TAC did not significantly affect conception rate, pregnancy duration, uterus size, litter size, and pup weight. In conclusion, we found that, rather than exacerbating the changes associated with cardiac pressure overload, pregnancy actually attenuated pathological LV remodeling and mitigated pulmonary congestion, and pathological gene expression produced by TAC, suggesting a positive effect of pregnancy on the pressure-overloaded heart.

DOI: 10.1152/ajpheart.00056.2016

Cite this paper

@article{Xu2016PregnancyMC, title={Pregnancy mitigates cardiac pathology in a mouse model of left ventricular pressure overload.}, author={Hong Xu and Elza D van Deel and Mark R. D. Johnson and Petra Opi{\'c} and Bronwen R. Herbert and Els Moltzer and Suren R Sooranna and Heleen MM van Beusekom and Wang-fu Zang and Dirk Jan Duncker and Jolien W Roos-Hesselink}, journal={American journal of physiology. Heart and circulatory physiology}, year={2016}, volume={311 3}, pages={H807-14} }