Figure 6.

Schematic representation of the evolution from placentation and maternal vascular adaptation to the clinical end stage of (A) normal pregnancy, (B) normal pregnancy with cardiac signs of volume overload, (C) early-onset preeclampsia, (D) crossover late-onset preeclampsia (type I), and (E) high-output late-onset preeclampsia (type II). A: The normal remodeling of the spiral arteries is followed by the normal expansion of the body water volume in an uncomplicated pregnancy. B: The same situation as in panel A, but the woman presents at term with echocardiographic signs of volume overload [113]. C: Shallow spiral artery dilatation, presenting already in the first trimester with signs of endothelial activation and vascular hypertonia, followed by the suboptimal expansion of the plasma volume, and resulting in early-onset preeclampsia and poor fetal growth [39]. D: The normal remodeling of the spiral arteries is followed by the normal expansion of the body water volume with subsequent secondary endothelial activation, resulting in crossover from a high volume/low resistance to a low volume/high resistance circulation, eventually presenting as late-onset preeclampsia type I [38]. E: The normal remodeling of the spiral arteries is followed by the normal expansion of the body water volume in women with high intra-abdominal pressure, resulting in high-output late-onset preeclampsia type II [37].