Abnormal Abdominal Aorta Hemodynamics Are Associated With Necrotizing Enterocolitis in Infants With Hypoplastic Left Heart Syndrome
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The risk of necrotizing enterocolitis (NEC) in association with congenital heart disease is highest in patients with hypoplastic left heart syndrome (HLHS). Within the HLHS population, however, risk factors for NEC remain debated. We hypothesized that some infants with HLHS have vascular changes that contribute to gut hypoperfusion independent of diastolic runoff and low cardiac output. We analyzed the abdominal aorta pulsatility index and right-ventricular function on routine preoperative and postoperative echocardiograms for all infants who underwent stage I palliation for HLHS from January 2007 to January 2012. The echocardiography findings and clinical course were compared between those with and those without an episode of NEC. Of the 61 cases reviewed, 11 (18 %) developed NEC during a mean follow-up of 3.8 ± 1.3 years. Those with NEC had a lower abdominal aorta pulsatility index compared with those without NEC both on stage I preoperative (3.38 ± 0.15 vs. 3.89 ± 0.09, p < 0.05) and postoperative echocardiograms (2.21 ± 0.28 vs. 3.05 ± 0.78, p = 0.01) despite similar ventricular function and operative risk. Abdominal aorta Doppler pulsations are lower in patients with HLHS whose clinical course is complicated by NEC. This finding suggests that the systemic vasculature in a subset of neonates with HLHS may be inherently abnormal. Further investigation is warranted to determine if this is secondary to structural changes in the mesenteric and/or systemic vasculature.
KeywordsCongenital heart disease Hypoplastic left heart syndrome Necrotizing enterocolitis
The authors thank research coordinators Mason Heywood and Anna Jolley for their assistance with data collection and organization. Study data were collected and managed using REDCap  electronic data capture tools hosted at University of Utah Center for Clinical and Transitional Sciences. The Center is supported by National Institutes of Health (NIH) funding (Grant No. CTSA 5UL1RR025764-02). Dr. Miller is supported by NIH training grant NHLBI T32 5T32HL007576-27.
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