The cardiopulmonary transition at birth is a critical physiological process requiring coordinated cardiovascular adaptation to meet the increased circulatory demands of extrauterine life. This transition may be compromised in infants affected by suboptimal fetal growth, such as in infants born small for gestational age (SGA) or classified with fetal growth restriction (FGR). Suboptimal fetal growth often arises from reduced oxygen and nutrient supply, leading to prioritised perfusion of crucial organs and subsequent cardiac and arterial remodelling. These cardiovascular adaptations, while necessary for fetal survival, may persist postnatally and increase the risk of an impaired cardiovascular transition at birth. Altered echocardiographic function and cardiac injury biomarkers are often detectable in this population during the early postnatal period, indicating underlying myocardial stress and a predisposition to an impaired transition. FGR and/or SGA neonates often exhibit impaired diastolic function, reflecting impaired myocardial relaxation and reduced compliance, and systolic dysfunction, including a reduced capacity to increase left ventricular output over time. Additionally, elevated pulmonary vascular resistance contributes to an increased risk of respiratory morbidity. Emerging preclinical data suggest that these adaptations may impede the neonate's ability to respond to perinatal stressors, thus increasing the risk of adverse outcomes. Understanding the multifaceted nature of cardiovascular dysfunction in FGR and/or SGA infants during the perinatal period is essential to improving their long-term outcomes, thus reducing the risk of cardiovascular disease later in life.
Azman et al. (Mon,) studied this question.