Autograft Enlargement After the Ross Procedure in Pediatric Patients: Somatic Growth or Pathologic Dilatation?
Purpose of ReviewPulmonary autograft autotransplantation represents a popular surgical approach for pediatric patients requiring aortic valve replacement due to the potential for autograft enlargement to accommodate somatic growth. Nevertheless, autograft dilatation and the subsequent need for reintervention are quite common. Published data suggest that autograft enlargement may result from pathological passive remodeling rather than active somatic growth and vice versa. The present review serves to comprehensively evaluate available evidence related to the fate of the pulmonary autograft after the Ross procedure as it relates to the etiology, risk factors and patterns of autograft failure.ResultsStudies present conflicting results supporting both pathological dilation and active somatic growth. Primary factors impacting the successful remodeling of the autograft include native aortic and pulmonary valve anatomy, medical history, concomitant procedures, perioperative management, age at the time of surgery, and the surgical technique used for the Ross procedure.ConclusionAutograft enlargement after the pediatric Ross operation may result from either somatic growth or passive dilation or a combination of both factors. Distinguishing between the two primary etiologies of autograft enlargement depends upon meticulous patient selection and a surgical strategy precisely tailored to individual anatomy and risk.
Authors
- Scott D. Olson (ORCID: https://orcid.org/0000-0001-8032-3755)
- Alexander Mills (ORCID: https://orcid.org/0000-0001-6265-7073)
- IOANNIS ZOUPAS
Institutions
- Memorial Hermann (US)
- The University of Texas Health Science Center at Houston (US)
Publication Details
- Journal
- World Journal for Pediatric and Congenital Heart Surgery
- Published
- 2026-01-14
- DOI
- https://doi.org/10.1177/21501351251400224
- Primary Topic
- Aortic Disease and Treatment Approaches
- Type
- article
- Field-Weighted Citation Impact
- 0.00