Ventricular–arterial coupling is preserved in prematurely born 11-year-old children but calls for life-long prevention of hemodynamic deterioration

Ventricular–arterial coupling (VAC) is preserved in prematurely born 11-year-old children but calls for life-long prevention of hemodynamic deterioration, the article is very interesting as early low weight birth infants were analyzed at 11 years matched with controls with birth weight less than 1000 g. The study empathizes cardiac and arterial remodeling in those infants as the case groups showed higher SBP and DBP, lower left ventricular (LV) end-diastolic and end-systolic dimensions, and lower LV mass. Cardiac output was 0.38 l/min lower in cases, who also had higher arterial resistance and augmentation ratio. VAC did not differ between groups (P = 0.48). Lower LV end-diastolic and end-systolic dimensions, and 9.2 g [95% confidence interval (CI) 3.7–14.6] lower LV mass. LV volumes and mass correlated with body size without significant between-group differences (P ≥ 0.12). Cardiac output was 0.38 l/min lower in cases, who also had higher arterial resistance and augmentation ratio. The tension–time index was 231 mmHg ms (95% CI 128–335) higher in cases. Ea and Ees were higher in cases (0.40 and 0.65 but VAC did not differ between groups (P = 0.48). This study is very interesting as follow-up was performed at 11 years of age, demonstrating that fetuses with low birth weight share an increased SBP and DBP, confirming many studies that evaluated in-utero and after birth low-weight fetuses and infants. Several authors reported fetal adaptation in the womb as a consequence of reduced intrauterine space or placental limitation, and, in fact, some fetuses thought to be growth retarded are, in retrospect, found to be constitutionally small [1,2]. Intima–media thickness is actually considered to be one of the earliest morphological markers of plaque formation and atherosclerosis in intrauterine growth restriction (IUGR) fetuses and neonates [3–5]. Microscopic observation of abdominal aortic walls of stillbirth IUGR fetuses, in fact, confirmed that there is intima thickening and the presence of inflammatory elements, such as macrophages, activated endothelial cells and fibroblastoid cells, indicating that IUGR is a potential marker of atherosclerosis development and may be associated with an increased risk of adult-onset diseases [4–6]. Using high-resolution ultrasound to study aorta intima media thickness (aIMT), Skilton et al. reported that it was significantly higher in IUGR than in according for gestational age newborns and found this value an accurate, feasible and sensitive marker of atherosclerosis risk. As no confounding factors connected to childhood and adulthood was implicated, aIMT appeared to delineate fetal contribution to later cardiovascular disease [7]. Koklu et al.[7] in 2007 evaluated the potential use of aIMT to study high-risk neonates and concluded that it can help to identify precocious asymptomatic vascular dysfunction in IUGR newborns. Cosmi et al.[8] assessed aIMT in IUGR fetuses and in the same infants after a mean follow-up of 18 months and found that values were inversely related EFW and still present at the end of follow-up. Consistent with the finding that atherosclerosis first begins to develop in the aortic intima; it is possible that IUGR and Doppler abnormalities are correlated to altered vascular function causing possible endothelial damage, responsible for high blood pressure in infants [9–10]. According several authors, children with IUGR have abnormal cardiac morphology, subclinical cardiac longitudinal dysfunction and hypertension, all of which increase linearly with the severity of growth restriction. In conclusion, this study is of particular interest, despite limits are sampling very low-birth-weight preterm infants and not correlating to Doppler anomalies. ACKNOWLEDGEMENTS Conflicts of interest There are no conflicts of interest.