Abstract
Preterm birth coincides with a key developmental window of cardiac growth and maturation, and thus has the potential to influence long-term cardiac function. Individuals born preterm have structural cardiac remodelling and altered cardiac growth and function by early adulthood. The evidence linking preterm birth and cardiovascular disease in later life is mounting. Advances in the perinatal care of preterm infants, such as glucocorticoid therapy, have improved survival rates, but at what cost? This review highlights the short-term and long-term impact of preterm birth on the structure and function of the heart and focuses on the impact of antenatal and postnatal glucocorticoid treatment on the immature preterm heart.
Highlights
Preterm birth is strongly associated with adverse health outcomes in the neonatal period and in later life
This review focuses primarily on the structural and functional effects of preterm birth on the heart and the consequences of antenatal and postnatal glucocorticoids on the heart
Preterm birth is a catalyst for a unique cardiac phenotype
Summary
Preterm birth is strongly associated with adverse health outcomes in the neonatal period and in later life. Cardiomyocytes (the functional units of the heart) differentiate and mature late in gestation in preparation for the major hemodynamic transition that occurs at birth, whereby there is a marked increase in left ventricular output, systemic blood pressure, and heart rate. Cardiac development progressively transitions from hyperplastic cardiomyocyte growth to hypertrophic growth, whereby the cardiomyocytes become mature and terminally differentiated in preparation for the increased haemodynamic demand at birth [6,7,8,9]. Cardiomyocytes mostly remain mononucleated as they undergo hypertrophy and commonly respond to stimuli like haemodynamic changes or stress by DNA synthesis without karyokinesis or cytokinesis [10,19] These responses result in polyploid mononucleated cells rather than multinucleation [10,19]. In preterm-born infants, the degree of prematurity is directly related to myocardial maturity, which influences myocardial contractility and the ability to cope with the haemodynamic demands [24,25,26,27]
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