Abstract

Introduction: In preeclampsia, symptoms like high blood pressure and albuminuria are caused by a state of anti-angiogenic and immune imbalance resulting in endothelial dysfunction. The evaluation of smaller vessels is a challenge, but clinically of increasing importance. Objective: We want to examine whether the increased risk for postpartum maternal cardiovascular disease after preeclamptic pregnancy is resultant from microvascular changes in connection with the structural remodelling processes. Methods: We compared echo data from a human cohort with data from our transgenic animal model (hAGTxhRen) after preeclamptic pregnancy. In addition, we investigated cardiac changes in gene (qPCR) and protein expression levels (ELISA, IHC staining) in maternal rats, as well as alterations in microvascular 3D remodeling using LSFM and Micro CT. Results: We were able to show that the echo changes in our transgenic rat model are comparable to human data. Basic parameters like ejection fraction (human 0,91; animal 0,86), end-systolic volume (human 1,26; animal 1,22) or heart rate (human 1,13; animal 1,16) are altered at the end of pregnancy in same direction. Also markers of hypertrophy like relative wall thickness (human 1,19; animal 1,21) are changed. With the help of speckle trackle analysis, a more sensitive method to detect subclinical changes in hearts functionality, both groups show a reduction of global longitudinal strain (human 0,75; animal 0,6) and strain rate (human 0,81; animal 0,73). The microvasculature and entire vascular network has been visualized so far only in cleared mouse brains and partially in adult mouse hearts. Here, we present the 3D network of lectin-labeled blood vessels in cleared adult rat hearts with the analysis of cardiac small vessels with regard to branching points, vessel length and up to a diameter of 6μm. Discussion: Preeclampsia leads to a weakened functionality in postpartum hearts, in a human cohort as well as in our transgenic animal model. Studies are underway to quantify coronary microvascular pathology as a possible missing link between preeclampsia and higher risk for further cardiovascular disease. (values show postpartum change compared to non-pregnant)

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