**1. Introduction**

A pathological pregnancy, including preterm birth, gestational diabetes mellitus, and preeclampsia (PE), is the first gender-specific risk factor for cardiovascular disease (CVD) later in life [1]. PE, with its typical symptoms including the onset of hypertension and signs of end-organ damage, has a fourfold increase regarding the risk for long-term CVD [2]. In the last years, cardiovascular changes during a preeclamptic pregnancy and especially persistent alterations in maternal cardiac structure and function moved into the focus of scientific research [3]. It has been demonstrated that former preeclamptic women show relaxation abnormalities, diastolic dysfunction, left ventricular (LV) hypertrophy [4–6], and abnormal response to volume expansion and exercise [7–9]. In most of the studies, symptoms are rather mild and sometimes even asymptomatic. It remains unclear whether the increased risk for future CVD is related to PE or predisposing and preexisting factors [10], and thus PE represents a window to compromised future cardiovascular health. The mechanism for pathological functional and structural remodeling in the maternal heart after a pathological pregnancy is also not fully understood.

For this reason, representative animal models are of increasing importance. A well-established rodent model for PE is the rat model, whose female is transgenic for human angiotensinogen and is mated with a transgenic male for human renin. Both animals are phenotypically inconspicuous until mating. Interestingly, dams develop typical symptoms of PE such as high blood pressure and albuminuria in the last trimester of pregnancy [11,12]. In addition, placenta-induced pathology with intrauterine growth retardation [12,13], elevated sFlt-1 levels [14], and existing AT1 autoantibodies [15] are presented in this animal model. Although PE is not caused by a monocausal pathology, this model reflects appropriately the human aspects of the disease. The use of rodent models such as this will help us to understand the mechanisms of disease-related alterations in cardiac function and structure that influence maternal long-term health after a pathological pregnancy. Furthermore, potential novel preventive and therapeutic strategies can be evaluated. Nevertheless, the gap between animal models and the human disease is wide, and translational research strategies are warranted to narrow the bridge.

In this study, we tested the hypothesis of whether the transgenic rat model is suitable for the investigation of the cardiovascular burden after PE. Recently, we showed that the preeclamptic rat su ffers from hypertrophy and diastolic dysfunction [16]. Next, we compared this animal model with the systolic and the diastolic functions of the human maternal heart after a preeclamptic pregnancy. Speckle tracking echocardiography (STE), a state-of-the-art technique considered as the gold standard for early detection of cardiac dysfunction, is the current key tool for the non-invasive measurement of changes in cardiac function and structure. In this ultrasound imaging technique, the movement of heart tissue is analyzed using the naturally occurring speckle pattern in the heart muscle or in the blood. This mixture of interference patterns and natural acoustic reflections makes it possible to document the movement of the heart muscle by defining vectors and speed. These reflections are also known as speckles, which have a unique pattern for each region of the myocardium and make it possible to follow the region from one image to the next. Strain is defined as the percentage change in the dimension of an object compared to the original shape. Similarly, strain rate can be defined as the speed at which the deformation occurs. When applied to the LV, the deformation is defined by the three strains: longitudinal, circumferential, and radial. There is a systolic longitudinal and circumferential shortening and a radial thickening. Therefore, longitudinal and circumferential parameters have negative values, whereas radial parameters have positive values.

Formerly preeclamptic women were examined by STE 50 weeks after delivery and compared with age-matched controls. Transgenic rats were subjected to echocardiography and the same post processing algorithms four weeks after a preeclamptic pregnancy, which corresponds to two years in the human situation [17].
