Pregnancy requires significantly increased cardiac output (~30%) achieved through peripheral vasodilation and increased stroke volume, due to increased end-diastolic volume. Most women resolve these physiological changes within 6 months of delivery; however, some women progress to heart failure late in pregnancy or in the immediate post-partum period. Peri-partum cardiomyopathy (PPCM) is a rare condition of largely unknown etiology which, at its most-severe and life-threatening, requires cardiac transplantation. Pre-eclampsia occurs at much higher rates in the PPCM population (~40%) compared with the generally pregnant population (~2-5%). We have previously shown that transgenic mice expressing the human-specific isoform of the TBXA2R gene (TPβ) spontaneously develop pre-eclampsia accompanied by all the associated hallmarks expected from the human disease. We now show TPβ transgenic (TPβ-Tg) mice are a model of PPCM. Using trans-thoracic echocardiographic imaging, TPβ-Tg mice had no basal phenotype; however, unlike C57/Bl6J (WT) mice that resolved the pregnancy-induced cardiac remodeling, TPβ-Tg mice had exaggerated cardiac dilatation at term (E18.5; P<0.01) which increased in severity over the subsequent 6 months (P<0.005). In addition, TP-Tg mice exhibited reduced ejection fraction (22±13% vs 67% in WT), significant LV wall thinning (1.12±0.16 mm vs 1.6±0.17 mm WT), and loss of LV mass (66.55±9 mg vs 95±11mg WT). Analysis of myocardium of human PPCM patients undergoing heart transplant (n=12) compared to healthy myocardium from non-diseased donors (n=42) by RT-PCR and IHC showed highly expressed TPβ in PPCM patients. In human PPCM samples, there was a significant (p<0.01) dysregulation of genes associated with circadian rhythm as determined by RNAseq analysis. Quantitative PCR analysis of hearts from non-pregnant (WT=8; TPβ-Tg=4) and pregnant (WT=10; TPβ-Tg=13) mice found similar dysregulation of multiple genes associated with circadian rhythm compared to WT mice (p<0.01). This indicates that PPCM may be associated with failure to terminate CLOCK signaling as a result of TPβ activation. Our results support dysregulation of TBXA2R splicing as part of the pathogenesis of PPCM and identify new therapeutic targets for this condition.

Characterization of a Novel Clinically Relevant Mouse Model of Postpartum Cardiomyopathy

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