Abstract 271: Evidence of Arterial Stiffness in Young Adult Women Born Extremely Preterm (<29 weeks).

Background: Epidemiological studies reported that preterm infants have increased arterial systemic blood pressure in adulthood. We have recently shown in an animal model that premature vascular aging could be involved in this process. Aim: To assess biophysical properties (arterial stiffness) of the aorta as early signs of a vascular aging process in young adult women born extremely preterm. Methods: We studied 4 women (aged 24±1 years) born extremely preterm (26.1±0.5 weeks, 803±58 grams) in the absence of any significant medical or psychiatric co-morbidity. Subjects were compared to 6 control women born at term (40.6±0.8 weeks, 32518±139 grams) matched for age. The aortic diameters, the pulse wave transit time around the aortic arch and the ascending aortic peak flow were measured with echo-Doppler and the blood pressure recorded. Pulse wave velocity, aortic input impedance (Zi), characteristic impedance (Zc), arterial pressure-strain elastic modulus (Ep), and arterial wall stiffness index (βSI) were calculated. Results: Preterm women had slightly but not significantly increased arterial systolic blood pressure compared to young women born term (111±6 vs. 104±2 mmHg, p=0.23). Diastolic and mean arterial blood pressure were similar (62±4 vs. 61±3, p=0.84 and 77±4 vs. 75±3 mmHg, p=0.73 respectively). Pulse wave velocity did not differ between groups (3.6±0.6 vs. 3.2±0.2 m/sec, p=0.53). βSI and Ep, direct indices of central arterial rigidity, were not significantly different between preterm women compared to controls (4.9±2.1 vs. 3.7±0.4, p=0.46 and 58±24 vs. 42±4 kPa, p=0.38 respectively). Zc and Zi, indices of the resistance to ejection to blood flow, were increased compared to controls (134±21 vs. 105±9, p=0.18 and 185±8 vs. 152±10, p -5 , respectively). Conclusions: This first series of results suggest that women who were born very preterm present indices of arterial rigidity compared to term controls. This alteration of the vascular tree could be a patho-physiological mechanism linking prematurity to adult cardiovascular diseases.