Abstract
ObjectivesElevated pulmonary vascular resistance occurs during the first days after birth in all newborn infants and persists in infants at risk for bronchopulmonary dysplasia (BPD).It is difficult to measure in a non-invasive fashion. We assessed the usefulness of the right ventricular index of myocardial performance (RIMP) to estimate pulmonary vascular resistance in very low birth weight infants.Study DesignProspective echocardiography on day of life (DOL) 2, 7, 14, and 28 in 121 preterm infants (median [quartiles] gestational age 28 [26]–[29] weeks, birth weight 998 [743–1225] g) of whom 36 developed BPD (oxygen supplementation at 36 postmenstrual weeks).ResultsRIMP derived by conventional pulsed Doppler technique was unrelated to heart rate or mean blood pressure. RIMP on DOL 2 was similar in infants who subsequently did (0.39 [0.33–0.55]) and did not develop BPD (0.39 [0.28–0.51], p = 0.467). RIMP declined steadily in non-BPD infants but not in BPD infants (DOL 7: 0.31[0.22–0.39] vs. 0.35[0.29–0.48], p = 0.014; DOL 14: 0.23[0.17–0.30] vs. 0.35[0.25–0.43], p<0.001; DOL 28: 0.21[0.15–0.28] vs. 0.31 [0.21–0.35], p = 0.015).ConclusionsIn preterm infants, a decline in RIMP after birth was not observed in those with incipient BPD. The pattern of RIMP measured in preterm infants is commensurate with that of pulmonary vascular resistance.
Highlights
Bronchopulmonary dysplasia (BPD) remains the most common long-term complication of very preterm birth [1]
right ventricular index of myocardial performance (RIMP) on day of life (DOL) 2 was similar in infants who subsequently did (0.39 [0.33–0.55]) and did not develop BPD (0.39 [0.28–0.51], p = 0.467)
The pattern of RIMP measured in preterm infants is commensurate with that of pulmonary vascular resistance
Summary
Bronchopulmonary dysplasia (BPD) remains the most common long-term complication of very preterm birth [1]. Premature infants at greatest risk for BPD are born before 28 weeks, during the late canalicular or saccular stage of lung development, just as the airways become juxtaposed to the pulmonary vessels. Various animal models of BPD and autopsy studies of humans who died from BPD have consistently shown a reduction in the number of small arteries and an abnormal distribution of vessels within the distal lung [5,6,7]. In addition to dysmorphic growth, the pulmonary vasculature in BPD undergoes hypertensive structural remodeling, which includes medial hypertrophy and distal muscularization of small peripheral arteries [8]. Abnormal vasoreactivity, reduced arterial number, and structural abnormalities of the vessel wall can contribute to pulmonary hypertension in BPD, leading to significant morbidity and mortality [9]. Tricuspid regurgitation to estimate RV pressure is accurate in identifying patients with chronic pulmonary hypertension in only 30% to 73% of cases [10,11]
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