EP09.93: Cardiac remodelling and exercise tolerance in small for gestational age: a follow‐up cohort study from preadolescence into adolescence

To assess resting cardiovascular structure and function and exercise tolerance in adolescents born SGA. Follow-up of a perinatal cohort at tertiary university hospital in Spain of 30 adolescents born SGA (birthweight below the 10th centile) and 28 normal birthweight controls. Participants were followed from preadolescence (7-12 years of age) into adolescence (12-17 years of age). The main outcomes were resting cardiac structure and function by echocardiography, and cardiopulmonary response to incremental exercise test. While signs of cardiac remodelling and dysfunction were evident in SGA at preadolescence, no significant differences in left ventricular dimensions nor deformation could be demonstrated in SGA adolescents. During the follow-up, the SGA cohort had a significantly higher increase in LV base-to-apex length (SGA mean 17.61 ± SD 6.78 vs. controls 13.44 ± 5.12, p = 0.011), but equal increase of the LV basal diameter (p = 0.124), resulting in a similar LV sphericity at adolescent age (SGA 1.80 ± 0.14 vs. 1.77 ± 0.13, p = 0.09) in both groups. While resting cardiac function was mostly preserved in SGA adolescents, significant differences could be observed in SGA during exercise with prolonged pulmonary artery acceleration time (overall difference SGA vs controls 5.99 ms [95% CI 1.31 to 10.67], p = 0.012) and reduced tricuspid systolic myocardial peak velocity (-1.16mm [-2.23 to -0.09], p = 0.034), oxygen uptake (-0.07L/min [-0.13 to -0.005], p = 0.035), expired CO2 (-0.08L/min [-0.15 to -0.01], p = 0.033), and peak expiratory flow rate (-0.11L/s [-0.21 to -0.01], p = 0.029). Changes in cardiac shape and function, described in individuals born SGA, seem to be ameliorated in adolescence related to compensatory growth as compared to healthy controls. However, SGA adolescents had markedly reduced exercise tolerance. These results warrant further research to clarify its causes and the potential association with increased cardiovascular mortality among adults born SGA.