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Impact of placental ischemia on cardiac structure and function during pregnancy and Post‐Partum
Author(s) -
Bakrania Bhavisha,
Granger Joey P.
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.851.4
Subject(s) - medicine , preeclampsia , endothelial dysfunction , pregnancy , cardiac function curve , cardiology , gestational hypertension , uterine artery , placenta , ischemia , placentation , diastole , gestation , blood pressure , obstetrics , fetus , heart failure , genetics , biology
Preeclampsia (PE) is a disorder prevalent in 5–7% of pregnancies. It is characterized by maternal hypertension and endothelial dysfunction. PE is thought to develop in response to impaired spiral artery remodelling of the placenta, which leads to placental ischemia and ultimately the release of anti‐angiogenic and pro‐inflammatory factors into the maternal circulation. More recently, it has been shown that cardiac function is impaired in women with PE, including hypertrophy and, systolic and diastolic dysfunction, with symptoms persisting one year post‐partum. In addition to the significant health risks imposed during pregnancy, multiple studies report increased risk of cardiovascular disease for mother and baby later in life. The placental factors, sFlt‐1 and TNF‐α, have been shown to play a role in cardiac dysfunction and the structural abnormalities seen during PE, however, the mechanisms remain unclear. Therefore, it is important to utilise an appropriate model of PE to assess cardiac function and investigate mechanisms of cardiac dysfunction, such as the Reduced Uterine Perfusion Pressure (RUPP) model, where silver clips are placed on the abdominal aorta and branches of the ovarian arteries to induce placental ischemia. We have previously reported that the RUPP model has many of the characteristics seen in women with PE. The aim of this study was to assess cardiac structure and function in RUPP rats during pregnancy and post‐partum to discern any similarities to the human condition. A normal pregnant (NP, n =8) and RUPP ( n =8) group was included in this study. The RUPP group underwent surgery on gestational day (GD) 14 for placement of silver clips. Both the NP and RUPP rats had carotid catheters placed on GD 18, and all initial blood pressure and echocardiography measurements were made on GD 19. A second echocardiography analysis was performed 3 months post‐partum. The RUPP group had significantly increased mean arterial pressure compared to the NP group on GD 19 (123 ± 3 vs. 97 ± 2 mmHg, P<0.01). RUPP hearts also showed reductions in ejection fraction (60 ± 2 vs. 78 ± 2 %, P<0.01) and fractional shortening (46 ± 3 vs. 56 ± 1 %, P=0.05), in addition to cardiac hypertrophy (0.97 ± 0.04 vs.0.91 ± 0.02 g, P=0.02). Interestingly, systolic dysfunction was persistent post‐partum in RUPP hearts, where ejection fraction (67 ± 3 vs.76 ± 2 %, P<0.01) and fractional shortening (50 ± 5 vs. 56 ± 2 %, P=0.05) remained impaired. In conclusion, cardiac dysfunction is present in the RUPP model during pregnancy and post‐partum. Therefore, this model could be useful in understanding the mechanisms which underpin the cardiac structural and functional abnormalities seen in PE patients. Support or Funding Information This study was funded by the NIH (HL51971).