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Published on: January 27, 2023
Serial Assessment of Cardiac Function and Pulmonary Hemodynamics in Infants With Down Syndrome
Aisling Smith1, Neidin Bussmann1, Colm Breatnach1
1Department of Neonatology, Rotunda Hospital, Dublin, Ireland.
Insights
Infants with Down syndrome (DS) show impaired heart function and higher pulmonary pressures compared to controls over two years. These findings highlight cardiorespiratory risks in DS, regardless of congenital heart disease.
Area of Science:
- Pediatric Cardiology
- Neonatology
- Genetics
Background:
- Limited longitudinal data exists on cardiopulmonary hemodynamics in infants with Down syndrome (DS) beyond the neonatal period.
- Down syndrome is associated with increased risk of congenital heart disease (CHD) and potential cardiorespiratory complications.
Purpose of the Study:
- To investigate the longitudinal evolution of biventricular function and pulmonary pressures in infants with DS over the first two years of life.
- To determine if these changes occur independently of the presence of congenital heart disease (CHD).
Main Methods:
- A prospective observational cohort study involving 70 infants with DS (48 with CHD, 22 without) and 60 controls.
- Serial echocardiograms were performed at birth, 6 months, 1 year, and 2 years to assess biventricular systolic and diastolic function using deformation analysis.
- Pulmonary vascular resistance was evaluated using pulmonary artery acceleration time and left ventricular eccentricity index.
Main Results:
- Infants with DS exhibited smaller left and right ventricular lengths and reduced systolic strain compared to controls over the two-year period.
- Pulmonary artery acceleration time was consistently lower in the DS group, indicating elevated pulmonary vascular resistance.
- No significant differences in cardiac function or pulmonary pressures were observed between DS infants with and without CHD.
Conclusions:
- Infants with Down syndrome demonstrate impaired myocardial function and elevated pulmonary vascular resistance during the first two years of life.
- These maturational deficits in cardiorespiratory function are present in infants with DS, irrespective of congenital heart disease.
- The findings offer crucial insights into the pathophysiology underlying cardiorespiratory morbidity in the DS population.
Background:
There is a dearth of longitudinal data describing the evolution of cardiopulmonary hemodynamics in infants with Down syndrome (DS) beyond infancy. We hypothesized that babies with DS, independent of the presence of congenital heart disease (CHD), demonstrate biventricular systolic and diastolic impairment and sustained elevation of pulmonary pressures compared with controls over the first 2 years of age.
Methods:
This was a prospective observational cohort study of 70 infants with DS (48 with CHD and 22 without CHD) and 60 controls carried out in 3 tertiary neonatal intensive care units in Dublin, Ireland. Infants with DS with and without CHD and non-DS controls underwent serial echocardiograms at birth, 6 months, 1 year, and 2 years of age to assess biventricular systolic and diastolic function using deformation analysis. Pulmonary vascular resistance was assessed using pulmonary artery acceleration time and left ventricular (LV) eccentricity index.
Results:
Infants with DS exhibited smaller LV (birth: 27 ± 4 vs 31 ± 2 mm, P < .01; 2 years: 43 ± 5 vs 48 ± 4 mm, P < .01) and right ventricular (birth: 28 ± 3 vs 31 ± 2 mm, P < .01; 2 years: 40 ± 4 vs 44 ± 3 mm, P < .01) lengths and lower LV (birth: -19% ± 3% vs -22% ± 2%, P < .01; 2 years: -24% ± 2% vs -26% ± 2%, P < .01) and right ventricular (birth: -19% ± 4% vs -22% ± 3%, P < .01; 2 years: -29% ± 6% vs -33% ± 4%, P < .01) systolic strain over the 2-year period. Pulmonary artery acceleration time was lower in the DS group throughout the study period (birth: 44 ± 10 vs 62 ± 14 ms, P < .01; 2 years 71 ± 12 vs 83 ± 11 ms, P < .01). No differences were observed between DS infants with and without CHD (all P > .05).
Conclusions:
Infants with DS exhibit impaired maturational changes in myocardial function and pulmonary vascular resistance. Such novel findings provide valuable insights into the pathophysiology affecting cardiorespiratory morbidity in this population.
