Clinical Investigations
Pediatric Echocardiography
Association of Gestational Age at Birth With Left Cardiac Dimensions at Near-Term Corrected Age Among Extremely Preterm Infants

https://doi.org/10.1016/j.echo.2023.04.003Get rights and content

Highlights

  • We compared echocardiography of 102 infants born <26 weeks to that of 103 infants ≥26 weeks.

  • At around 36 weeks, left-sided dimensions were smaller in infants born earlier.

  • Gestational age at birth was inversely proportional to LV EDV.

Background

Remodeling and altered ventricular geometry have been described in adults born preterm. Although they seem to have an adverse cardiac phenotype, the impact of various degrees of prematurity on cardiac development has been scarcely reported. In this study, we evaluated the impact of gestational age (GA) at birth on cardiac dimensions and function at near-term age among extremely preterm infants.

Methods

This is a retrospective single-center cohort study of infants born at <29 weeks of GA between 2015 and 2019. Infants with available clinically acquired echocardiography between 34 and 43 weeks were included. Two groups were investigated: those born <26 weeks and those born ≥26 weeks. All measurements were done by an expert masked to clinical data using the raw images. The primary outcome was measurements of cardiac dimensions and function based on GA group. Secondary outcomes were the association between cardiac dimensions and postnatal steroid exposure and with increments of GA at birth.

Results

A total of 205 infants were included (<26 weeks, n = 102; ≥26 weeks, n = 103). At time of echocardiography, weight (2.4 ± 0.5 vs 2.5 ± 0.5 kg, P = .86) and age (37.2 ± 1.6 vs 37.1 ± 1.9 weeks, P = .74) were similar between groups. There was no difference in metrics of right-sided dimensions and function. However, left-sided dimensions were decreased in infants born <26 weeks, including systolic left ventricle (LV) diameter (1.06 ± 0.20 cm vs 1.12 ± 0.18 cm, P = .02), diastolic LV length (2.85 ± 0.37 vs 3.02 ± 0.57 cm, P = .02), and estimated LV end-diastolic volume (5.36 ± 1.69 vs 6.01 ± 1.79 mL, P = .02).

Conclusions

In our cohort of very immature infants, birth at the extreme of prematurity was associated with smaller left cardiac dimensions around 36 weeks of corrected age. Future longitudinal prospective studies should evaluate further the impact of prematurity on LV development and performance and their long-term clinical impact.

Introduction

Advances in neonatal care have contributed to a significantly increased survival rate of infants born at the extremes of prematurity.1 Many pre- and postnatal factors, such as preeclampsia, chorioamnionitis, and postnatal treatments and complications, may have short- and long-term impact on cardiac development and function.

Extremely preterm infants are often exposed to suboptimal nutrition, chronic inflammation, persistence of shunts, hormonal imbalances, occurrence of early- or late-onset sepsis, and necrotizing enterocolitis. Both evolving and established bronchopulmonary dysplasia (BPD) are associated with the occurrence of pulmonary vascular disease, which may adversely impact heart-lung interactions. In fact, infants with BPD and with established pulmonary hypertension (PH) can develop right ventricular (RV) failure and have increased mortality rates.2, 3, 4 Alterations in left ventricular (LV) and RV geometry have been described in adults born preterm.5, 6, 7, 8, 9, 10 It may be that those same alterations in geometry are present in early infancy and linked to complications known to exist in premature infants. Thus, abnormal postnatal cardiac development may influence lifelong cardiovascular health and persist in adulthood.5, 6, 7 Unfortunately, the impact of various degrees of prematurity on cardiac development has been scarcely reported, and it is unclear whether anomalies could be detected as early as near-term corrected age. Therefore, the aim of this study was to investigate cardiac development in the extremely preterm population (birth at <29 weeks of gestational age [GA]) and explore whether a greater degree of prematurity (birth at <26 weeks of GA) would be associated with a more profound change in cardiac dimensions and function at near-term corrected age.

Section snippets

Materials and Methods

A single-center retrospective cohort study was conducted in preterm infants born at <29 weeks of GA admitted to our institution between February 2015 and September 2019. Infants were included if alive and with an echocardiography acquired for clinical indications between 34 and 426/7 weeks of postmenstrual age (PMA). Infants with major congenital anomalies (except for an interatrial shunt, a small ventricular septal defect, or a patent ductus arteriosus [PDA]) or genetic syndromes, as well as

Results

A total of 385 infants born at <29 weeks of GA were identified, and 205 met the inclusion criteria (Figure 1). Of these, 102 infants were born at <26 weeks of GA and 103 infants were born at ≥26 weeks of GA. Demographic and clinical characteristics are described in Table 1. As expected, infants born at <26 weeks of GA were more often exposed to surfactant and mechanical ventilation and had higher rates of late-onset sepsis. These infants had a higher frequency of BPD (but not severe BPD) and

Discussion

In this retrospective cohort study, a detailed and comprehensive analysis of cardiac dimensions and function was performed in a large population of extremely preterm infants. Interestingly, in those born at <26 weeks of GA, a smaller LV EDV, shorter LV length, and smaller left atrial diameter were observed at around 36 weeks of PMA (Figure 2). To our knowledge, this is the first report describing an association between extreme immaturity and a decrease in left-sided cardiac dimensions at such

Conclusion

In a contemporary cohort of premature infants born at <29 weeks of GA and assessed by echocardiography around 36 weeks of corrected age, smaller left cardiac dimensions (LV EDV, LV length, and left atrium diameter) were found in those born at <26 weeks of GA. These findings could be a step toward better understanding the pathophysiology of cardiac development in prematurity. Our findings need to be confirmed by prospective studies including a larger sample size over a longitudinal prolonged

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    Conflicts of Interest: None.

    This work was funded by the Pilot Grant by the Department of Pediatrics of McGill University, the Just for Kids Foundation, and the Montreal Children’s Hospital Foundation.

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