Key result
Experimental models fail to fully capture the complex link between preeclampsia and subsequent heart failure.
Why the study?
Preeclampsia pathophysiology remains poorly understood due to variable disease manifestation in animal models, despite increasing the risk of subsequent cardiovascular disease including myocardial infarction and HF.
There is a critical need for advanced, human-based 3D models to adequately study the complex progression from preeclampsia to long-term cardiovascular disease.
Current models limit translation of preeclampsia-CVD links into practice; leaves open the need for advanced human-based systems.
Preeclampsia is a multifactorial cardiovascular disorder diagnosed after 20 weeks of gestation, and is the leading cause of death for both mothers and babies in pregnancy. The pathophysiology remains poorly understood due to the variability and unpredictability of disease manifestation when studied in animal models. After preeclampsia, both mothers and offspring have a higher risk of cardiovascular disease (CVD), including myocardial infarction or heart attack and heart failure (HF). Myocardial infarction is an acute myocardial damage that can be treated through reperfusion; however, this therapeutic approach leads to ischemic/reperfusion injury (IRI), often leading to HF. In this review, we compared the current in vivo, in vitro and ex vivo model systems used to study preeclampsia, IRI and HF. Future studies aiming at evaluating CVD in preeclampsia patients could benefit from novel models that better mimic the complex scenario described in this article.
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Ming et al. (2021) conducted a review in Preeclampsia and Cardiovascular Disease. Experimental disease models (in vivo, in vitro, ex vivo) was evaluated. Current experimental models fail to fully replicate the complex pathophysiology linking preeclampsia with the subsequent development of cardiovascular diseases such as heart failure.
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