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There is widespread acceptance of the increased prevalence of cardiovascular disease occurring within 1 to 2 decades in women following a preeclamptic pregnancy. More recent evidence suggests that the deranged biochemical and echocardiographic findings in women do not resolve in the majority of preeclamptic women following giving birth. Many women continue to be hypertensive in the immediate postnatal period with some exhibiting occult signs of cardiac dysfunction. There is now promising evidence that with close monitoring and effective control of blood pressure control in the immediate postnatal period, women may have persistently lower blood pressures many years after stopping their medication. This review highlights the evidence that delivering effective medical care in the fourth trimester of pregnancy as a means of improving the long-term cardiovascular health of women after a preeclamptic birth.

The sFlt-1 (soluble fms-like tyrosine kinase-1), PlGF (placental growth factor), and their ratio are useful for predicting delivery because of preeclampsia in singleton pregnancies. Evidence on the utility of sFlt-1/PlGF ratio in twin pregnancies is lacking. We aimed to evaluate the predictive value of sFlt-1/PlGF ratio for delivery because of preeclampsia in twins. A retrospective data analysis of 164 twin pregnancies with suspected preeclampsia was performed. The sFlt-1/PlGF ratio, which was known to clinicians, was significantly higher in women who delivered within 1 and 2 weeks compared with those who did not (median: 98.9 and 84.2 versus 23.5 pg/mL, respectively; P P >0.100 for interaction). The area under the curve values of sFlt-1/PlGF were significantly higher than for PlGF alone (mean 0.88 and 0.88 versus 0.81 and 0.80) for predicting delivery because of preeclampsia within 1 and 2 weeks of blood sampling ( P =0.055 and 0.001, respectively). sFlt-1/PlGF ratio lower than 38 was able to rule-out delivery within 1 and 2 weeks with a negative predictive value of 98.8% and 96.4% for delivery because of preeclampsia within 1 and 2 weeks, respectively. A cutoff of 38 is applicable for ruling out delivery because of preeclampsia in twin pregnancies.

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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)

Commonly used in vitro fertilization (IVF) protocols produce pregnancies without a corpus luteum (CL), a major source of reproductive hormones. IVF pregnancies without a CL showed deficient gestational increases of central (aortic) arterial compliance (CAC) during the first trimester, and were at increased risk for developing preeclampsia. Here we investigated whether there was generalized impairment of cardiovascular adaptation in IVF pregnancies without a CL compared to pregnancies conceived spontaneously or through ovarian stimulation, which lead to 1 and > 1 CL, respectively (n=19–26 participants per cohort). Prototypical maternal cardiovascular adaptations of gestation were serially evaluated non-invasively, initially during the follicular phase before conception, 6 times in pregnancy, and then, on average, 1.6 years postpartum. The expected increases of cardiac output, left atrial dimension, peak left ventricular filling velocity in early diastole (E wave velocity), peripheral/central arterial pulse pressure ratio, and global AC, as well as decrease in augmentation index were significantly attenuated or absent during the first trimester in women who conceived without a CL, when compared to the 1 and >1 CL cohorts, which were comparable. Thereafter, these cardiovascular measures showed recovery in the 0 CL group except for E wave velocity, which remained depressed. These results provided strong support for a critical role of CL factor(s) in the transformation of the maternal cardiovascular system in early gestation. Regimens that lead to the development of a CL or replacement of missing CL factor(s) may be indicated to improve cardiovascular function and reduce preeclampsia risk in IVF pregnancies.

Fetal growth restriction and preeclampsia are both conditions of placental etiology and associated to increased risk for the long-term development of cardiovascular disease in the mother. At presentation, preeclampsia is associated with maternal global diastolic dysfunction, which is determined, at least in part, by increased afterload and myocardial stiffness. The aim of this study is to test the hypothesis that women with normotensive fetal growth-restricted pregnancies also exhibit global diastolic dysfunction. This was a prospective case-control study conducted over a 3-year period involving 29 preterm fetal growth-restricted pregnancies, 25 preeclamptic with fetal growth restriction pregnancies, and 58 matched control pregnancies. Women were assessed by conventional echocardiography and tissue Doppler imaging at diagnosis of the complication and followed-up at 12 weeks postpartum. Fetal growth-restricted pregnancies are characterized by a lower cardiac index and higher total vascular resistance index than expected for gestation. Compared with controls, fetal growth-restricted pregnancy was associated with significantly increased prevalence ( P