Introduction: Chronic lung disease (CLD) of prematurity can exert significant load to the right ventricle (RV), but the long-term consequences on RV-pulmonary vascular (PV) coupling is not well known. The RV-PV coupling can be characterized by the RV length-force relationship (tricuspid annular plane systolic excursion [TAPSE] vs. generated pulmonary artery systolic pressure [PASP]). Pulmonary artery acceleration time [PAAT] provides a validated estimate of PASP in infants.
Hypothesis: We hypothesize that the length-force relationship (TAPSE vs. PAAT), as a non-invasive index of the RV-PA coupling, is diminished in preterm-born compared to term-born infants at one year of age.
Methods: In a prospective study of 80 extreme preterm infants (< 29 weeks gestation at birth) enrolled through the Prematurity and Respiratory Outcomes Program (NHLBI U01 HL101794), TAPSE (cm) for RV length shortening and PAAT (msec) to estimate PASP for generated force (RV afterload ) were measured and compared to those in 40 age- and weight- matched term-born healthy infants at one year of age. TAPSE x PAAT was calculated to develop length-force relationship as an index of RV-PA coupling. Chronic lung disease (CLD), defined as the need for any respiratory support at 36 weeks post-menstrual age, was diagnosed in 49 preterm infants (61%).
Results: All preterm infants had significantly lower TAPSE x PAAT index than term-born infants [mean (standard deviation), 164 ± 23 vs. 120 ± 35 cm*ms, p < 0.01]. Preterm-born infants with CLD had lower TAPSE x PAAT than those without CLD [148 ± 35 vs. 101 ± 19 cm*ms, p< 0.01),] (Figure). Data analysis included adjustment for gestational age, body surface area at one year, and heart rate.
Conclusions: Preterm-born infants exhibit abnormal RV-PV coupling at one year of age, irrespective of neonatal lung disease status, suggesting it as a distinct pathology. Persistence of RV-PV axis dysfunction beyond infancy warrants long-term follow-up for risk stratification.