Affiliations: [a] Department of Pediatrics, Division of Neonatology, University of Iowa, Iowa City, IA, USA
| [b] Department of Pediatrics, Neonatal-Perinatal Medicine Section, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA
| [c] Department of Pediatrics, Division of Pediatric Infectious Disease, University of Iowa, Iowa City, IA, USA
| [d] Department of Internal Medicine, University of Iowa, Iowa City, IA, USA
Correspondence:
[*]
Address for correspondence: Amy H. Stanford, MD, 200 Hawkins Drive, 8809 JPP Iowa City, IA, 52242, USA. Tel.: +1 319 353 7030; E-mail: amy-stanford@uiowa.edu.
Abstract: BACKGROUND:
Pulmonary vascular disease (PVD) is a major determinant of both morbidity and mortality in extremely low birth weight infants. It is biologically plausible that postnatal cytomegalovirus (pCMV) infection may lead to PVD in premature infants secondary to pneumonitis or via derangement of pulmonary vascular development directly through endothelial dysfunction. Uncertainty remains, however, regarding thresholds for intervention in premature infants with cardiorespiratory instability and presumed CMV infection likely secondary to the limited understanding of the natural history of the disease. METHODS/RESULTS:
We describe four cases of premature infants with clinical and echocardiography features of PVD, in the setting of postnatally acquired CMV. All patients had atypical PVD trajectories, refractory to vasodilator treatment, which improved after initiation of CMV treatment. CONCLUSION:
We highlight the need to consider postnatally acquired CMV infection in patients with PVD non-responsive to standard pulmonary vasodilator therapies or disease severity which is out of proportion of the usual clinical trajectory. Treatment of extremely premature infants with CMV-associated PVD may have positive impact on cardiorespiratory health, although duration of therapy remains uncertain.
