Abstract
Background
Previous studies have shown that prematurity leads to altered right ventricular (RV) geometry and performance with persistent impairments in RV systolic function in young adulthood. It is unknown to what extent pulmonary physiology impacts these findings.
Purpose
To better quantify known alterations in RV morphology and function in preterm-born young adults and to determine to what extent these changes are influenced by the pulmonary circulation.
Methods
A total of 101 normotensive preterm-born (n=47, mean gestational age 32.8±3.2 weeks) and term-born (n=54) young adults were recruited. Echocardiography and cardiovascular magnetic resonance (CMR) imaging were performed to characterise RV morphology, RV function, pulmonary hemodynamics and RV-pulmonary arterial vascular (PA) coupling. CMR cine images were used to create a 3D computational atlas of the RV geometry and principal component analysis was undertaken to identify the key modes of shape variation. Spirometry was performed to assess lung function.
Results
RV CMR revealed a higher absolute and indexed RV mass (P<0.05) and lower ejection fraction (54.90±5.17 versus 57.48±4.39%, P=0.008) in young adults born preterm. RV end-diastolic areas and volumes for CMR and echocardiography were lower in preterm-born compared to term-born young adults (P≤0.001). Principal component analysis of the computational atlas defined the anatomical modes of the RV geometry, with mode 1 accounting for 25.3% of the population variance. Preterm and term cohorts showed significant differences (P<0.001) in mode 1, which represented a smaller and shorter RV cavity in the preterm group (Figure 1). Measurements of RV function by echocardiography, including RV fractional area of change (FAC) and tricuspid annular plane systolic excursion (TAPSE), were lower in preterm-born compared to term-born adults (P<0.05). Despite lower pulmonary artery acceleration times (PAAT) in those born preterm (141.1±15.1 versus 159.2±21.6msec, P<0.001), indicating increased pulmonary vascular resistance, the RV remained coupled to its pulmonary circulation (TAPSE/PAAT: 0.13±0.02 versus 0.14±0.03m/sec, P=0.153). Reduced RV performance in preterm-born individuals remained significant when adjusting for pulmonary function parameters (P<0.05).
Conclusions
Multimodality cardiac imaging demonstrated that moderately preterm-born young adults exhibit structural and functional RV alterations, independent of lung physiology. Their RV remains hemodynamically coupled to its pulmonary circulation despite higher RV afterload, lower RV function and altered morphology.
Figure 1. Statistical shape model of the RV
Funding Acknowledgement
Type of funding source: Foundation. Main funding source(s): British Heart Foundation
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