Splenic Artery Embolization Reverses Non-Occlusive Hepatic Artery Hypoperfusion Syndrome by Enhancing the Hepatic Arterial Buffer Response - 11/04/26

Doi : 10.1016/j.liver.2026.100347

Dustin G Roberts ¹, Jonas Kruse ¹, Arjun B Ranade ¹, Fady M Kaldas ², Edward W Lee ^1,², Vivy T Cusumano ³, Lucas R Cusumano ^1,^⁎

¹ David Geffen School of Medicine at University of California, Division of Vascular & Interventional Radiology, Los Angeles CA

² David Geffen School of Medicine at University of California, Department of Liver Transplantation, Los Angeles CA

³ David Geffen School of Medicine at University of California, Division of Digestive Diseases, Los Angeles CA

^⁎ Corresponding author: Lucas Cusumano MD MPH. (310) 301-6800, 757 Westwood Plaza, Los Angeles, CA. 757 Westwood Plaza Los Angeles CA

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HIGHLIGHTS

•	Non-occlusive hepatic artery hypoperfusion syndrome (NOHAHS) represents a maladaptive hepatic arterial buffer response (HABR) driven by increased intrahepatic arterial resistance and relative portal hyperperfusion.
•	Reciprocal hemodynamic changes imposed by SAE resulted in marked enhancement of the HABR, evidenced by a >2-fold increase in the hepatic artery–to–portal vein flow ratio (HAF:PVF).
•	Hemodynamic improvements translate into sustained clinical benefit, with significant improvements in serum bilirubin and albumin up to 12 months post-intervention.
•	SAE is an effective and generally safe treatment for NOHAHS, though more aggressive embolization in patients with markedly enlarged splenic vasculature may increase complication risk.

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ABSTRACT

Purpose

: Nonocclusive hepatic artery hypoperfusion syndrome (NOHAHS)—formerly splenic artery steal syndrome—is an underrecognized complication following liver transplantation characterized by arterial insufficiency despite hepatic artery patency. The pathogenesis is driven by maladaptation of the hepatic arterial buffer response (HABR) rather than true steal. This study evaluates the hemodynamic and clinical sequelae of splenic artery embolization (SAE) for NOHAHS.

Methods

: Twelve patients with graft dysfunction without an alternative cause, patent hepatic artery with elevated resistive index (RI) or slow end-diastolic flow, and dominant splenic circulation were included in this single-center retrospective study. Hemodynamic parameters were calculated using Doppler-derived flow measurements, including hepatic artery flow (HAF), portal vein flow (PVF), and HAF:PVF buffer ratios. Hepatic function biomarkers were assessed up to 12 months post-SAE.

Results

SAE significantly improved HAF (mean HAF: 91.0 ± 58.0 to 162.4 ± 133.4 mL/min; RI: 0.79 ± 0.10 to 0.72 ± 0.09; P<0.01) while simultaneously reducing PVF (mean PVF: 1,768.5 ± 824.4 to 1,021.6 ± 520.0 mL/min; P<0.01), resulting in a 2.7-fold increase in the buffer ratio (HAF:PVF ratio: 0.068 to 0.190; P<0.01). Sustained improvements in serum bilirubin and albumin were observed after SAE (P<0.05). Procedure-related complications included two cases of non-occlusive splenic vein thrombosis and one splenic abscess.

Conclusion

: SAE enhances the HABR via reciprocal modulation of hepatic artery and portal vein inflow to improve graft function in NOHAHS. These findings strengthen the HABR theory of graft inflow modulation and support the effectiveness of SAE as a treatment for NOHAHS in the post-transplant period.

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KEYWORDS : Hepatic arterial buffer response, non-occlusive hepatic artery hypoperfusion syndrome, splenic artery steal syndrome, splenic artery embolization

Abbreviations : CTA, EDV, GRWR, HA, hepatic arterial buffer response, HAF, MPVV, NOHAHS, OLT, PHP, PSV, PV, PVF, RI, SpA, SAE, SASS, SpV