Preeclampsia is a long-term cardiovascular risk factor for the mother and possibly the offspring. Preeclampsia and cardiovascular diseases share common pathophysiological features, including endothelial dysfunction. We explored whether endothelial function, measured noninvasively, as well as circulating biomarkers reflecting lipid metabolism, angiogenesis, and inflammation, differed in paired mothers and offspring 5 to 8 years after delivery. Twenty-six mother and child pairs after pregnancies complicated by preeclampsia were compared with 17 mother and child pairs after uncomplicated pregnancies. In addition, we assessed whether concentrations of maternal circulating biomarkers at delivery predicted findings 5 to 8 years postpartum. We also included an assessment of early onset preeclampsia and specifically addressed the effects of small for gestational age. Endothelial function was significantly reduced in both mothers and children after preeclampsia when combined with a small-for-gestational-age infant compared with mothers and children after pregnancies without a small-for-gestational-age infant (mothers: P<0.001; children: P<0.05). Postpartum maternal soluble fms-like tyrosine kinase 1 (P=0.05) and high-sensitivity C-reactive protein (P=0.02) were elevated in the preeclampsia group compared with controls. High concentrations of these maternal biomarkers both at delivery and 5 to 8 years postpartum were also more frequent in preeclampsia compared with controls (P<0.05). The novelty of our study is the parallel finding of reduced endothelial function in mother and child pairs 5 to 8 years after small-for-gestational-age preeclamptic pregnancies, accompanied by increased inflammatory and antiangiogenic maternal biomarkers. This finding supports the concept of transgenerational risk of cardiovascular disease after preeclampsia.

The function of the heart was studied in 20 asphyxiated term neonates by measuring the longitudinal peak systolic strain and peak systolic strain rate by tissue Doppler in 18 segments of the heart on days 1, 2, and 3 of life. The fractional shortening was assessed at each examination as well. Measurements were compared against measurements in 48 healthy term neonates examined by the same protocol. The function of the heart was lower in the asphyxiated neonates - peak systolic strain (mean (95% confidence interval) -19.4% (-20.4, -18.5), peak systolic strain rate -1.65 (-1.74, -1.56) per second) than in the healthy term neonates (peak systolic strain -21.7% (-22.3, -21.0), peak systolic strain rate -1.78 (-1.84, -1.74) per second; p < 0.001). Fractional shortening was similar in the asphyxiated (29.2% (26.8, 31.5)) and healthy term neonates (29.0% (27.9, 30.1); p = 0.874). The peak systolic strain differed significantly between the asphyxiated and healthy term neonates for the left basal and right basal groups of segments (p < 0.05) but not for the left apical, right apical, septum apical, or septum basal groups of segments. The peak systolic strain rate differed significantly only for the septum apical group of segments. The differences were largest on the second day of life. Measurements were similar in asphyxiated neonates with elevated and normal cardiac troponin T levels. The peak systolic strain and strain rate were in this study more sensitive indices than fractional shortening for assessing the reduced myocardial function in asphyxiated term neonates.