Abstract P203: Microvascular Imaging As Early Predictor For Cardiac Dysfunction After Preeclampsia

Abstract

Preeclampsia (PE), the most common pregnancy disease, is the main cause for maternal and fetal mortality and morbidity worldwide. The disease is characterized by a sudden increase in blood pressure in combination with signs of end organ damage, e.g. proteinuria and the underlying mechanisms are poorly understood. Immune dysregulation and endothelial dysfunction are important pathomechanisms leading to PE, we hypothesize that anti-angiogenesis and dysregulation of microvascular perfusion postpartum lead to the increased cardiovascular risk in later life. In addition, we will test if the examination of retinal vessels can be used as a diagnostic window for early risk prediction of cardiovascular alterations. In a well-established transgenic rat model for PE, we performed speckle tracking echocardiography, immunostaining, RNA sequencing and small vessel imaging by micro-computed tomography of the heart and the eyes in former preeclamptic rats (PEpp) and healthy controls (WTpp). A reduction of cardiac vessels (AUC 0-200 μm: WTpp 77.19±4.64 vs. PEpp 62.59±2.72) in combination with an increase of small vessels in the retina (AUC 0-50 μm: WTpp 52.89±1.47 vs. PEpp 59.54±1.09) is shown postpartum. Data from echocardiography (Global longitudinal strain: WTpp -22.03±2.47 % vs. PEpp -14.50±1.80 %) and histological staining (CD31: WTpp 292.7±30.9 per fov vs. PEpp 219.0±10.5 per fov) support the hypothesis of persistent cardiovascular alterations after PE. Performing RNAseq, 65 genes were found to be permanently altered in the left ventricle of the heart of preeclamptic rats compared to 4 genes in controls. In the retinal tissue, 39 genes in PEpp and no genes in WTpp were identified postpartum compared to never pregnant animals (adjusted p-value < 0.05,