Hepatic artery thrombosis (HAT) is one of the most severe vascular complications following liver transplantation, with reported incidence ranging from 2% to 9% in adult recipients and a well‑established association with graft loss and biliary ischemic injury [1–3]. Although early diagnosis and prompt treatment might allow graft salvage, management remains challenging and no standardized therapeutic algorithm has been universally adopted [4]. Retransplantation is traditionally considered the definitive treatment; however, it is frequently limited by organ availability and by the clinical instability of affected patients [1,5]. In selected cases, surgical revascularization may be attempted, but technical feasibility and outcomes depend on timing and local vascular conditions. Over the last decade, endovascular approaches—including intra‑arterial thrombolysis, angioplasty, and stent placement—have emerged as less invasive alternatives with encouraging results in appropriately selected patients [1,4,6]. Patients undergoing liver retransplantation represent a particularly high‑risk subgroup for vascular complications owing to previous arterial manipulation, complex anatomy, and the need for alternative inflow strategies such as aorto‑hepatic reconstruction. Complications involving aorto‑hepatic conduits are uncommon but technically demanding, and published experience remains limited. Isolated reports have described endovascular management of aorto‑hepatic bypass thrombosis or conduit‑related complications [7,8]; however, data specifically addressing recurrent HAT after retransplantation in the setting of aorto‑hepatic reconstruction are exceedingly scarce. Herein, we report a complex case of recurrent HAT occurring after liver retransplantation with aorto‑hepatic reconstruction successfully managed by endovascular recanalization. This case highlights the technical considerations and clinical decision‑making process in an extremely challenging vascular scenario and underscores the potential role of endovascular therapy even in highly selected post‑transplant settings [9].

A 43‑year‑old woman with a 15‑year history of primary sclerosing cholangitis presented in October 2024 with hepatic decompensation, including elevated serum transaminases, gamma‑glutamyl transferase, and alkaline phosphatase. Imaging revealed chronic liver disease with cirrhotic nodular remodeling and progressive cholestasis. The patient underwent orthotopic liver transplantation in November 2024. Anticoagulation post‑transplant included oral acetylsalicylic acid 100 mg/day and subcutaneous heparin 4000 IU/day. On postoperative day 5, color‑Doppler ultrasound and computed tomography (CT) angiography demonstrated complete thrombosis of the hepatic artery graft; selective digital subtraction angiography (DSA) confirmed the finding (Figure 1a,b). An initial endovascular recanalization attempt was unsuccessful, due to complete graft thrombosis, and a conservative observational strategy was adopted. In the following weeks, the patient developed fever and progressive hyperbilirubinemia. CT revealed ischemic cholangiopathy with multiple intrahepatic bilomas and abscesses. Follow‑up CT in January 2025 (Figure 2a–c) revealed two large bilomas in the left and right hepatic lobes, treated with percutaneous image‑guided drainage, along with additional abscessed bilomas in segment VI. Persistent fever, right upper quadrant pain, and septic deterioration led to liver retransplantation in March 2025. During retransplantation, arterial inflow was reconstructed using a donor hepatic artery graft anastomosed to the anterior abdominal aorta. The postoperative course was initially favorable until September 2025, when follow‑up color‑Doppler ultrasound and CT angiography (Figure 3a,b) demonstrated thrombosis of the hepatic artery graft with minimal opacification of intrahepatic branches. At this stage, anticoagulation included oral acetylsalicylic acid 100 mg/day, with subcutaneous heparin 4000 IU/day added after diagnosis of recurrent graft thrombosis. Given the high surgical risk, endovascular revascularization was performed via right common femoral artery access. DSA confirmed graft occlusion (Figure 4a). Using a 0.018‑inch guidewire, successful intraluminal recanalization of the graft and intrahepatic branches was achieved. Sequential percutaneous transluminal angioplasty (PTA) (Figure 4b,c) and deployment of overlapping balloon‑expandable stents restored arterial patency. During the procedure, intravenous heparin 2500 IU was administered. Final post‑procedural DSA demonstrated technical success with complete graft revascularization (Figure 4d). Post‑procedurally, dual antiplatelet therapy with clopidogrel 75 mg/day plus acetylsalicylic acid 100 mg/day was given for 30 days, followed by acetylsalicylic acid 100 mg/day alone from day 31 onwards, which the patient is advised to continue lifelong to prevent stent thrombosis. Early post‑procedural CT two weeks after the intervention confirmed stent patency and adequate arterial perfusion. Subsequent color‑Doppler ultrasounds (Figure 5a–c) at one, two, and three months demonstrated sustained graft patency with normal arterial waveforms. At four‑month follow‑up, CT angiography (Figure 6a,b) confirmed preserved stent and hepatic arterial tree patency, with homogeneous arterial enhancement of the liver parenchyma. The patient remains asymptomatic and in excellent clinical condition at the most recent follow‑up.

HAT is a serious vascular complication following liver transplantation, associated with high rates of graft failure, biliary complications, and mortality, particularly when occurring early [10–12]. The biliary tree relies almost exclusively on arterial blood supply; thus, prolonged or complete hepatic arterial occlusion frequently results in ischemic cholangiopathy, including bile duct necrosis, biloma formation, recurrent infections, and sepsis, often necessitating retransplantation [13,14]. Early HAT is traditionally managed with urgent surgical revision or retransplantation; however, these strategies might be limited by technical complexity, poor patient condition, and donor organ availability [15]. Over the past two decades, endovascular techniques have emerged as alternative or rescue strategies, particularly in late‑onset HAT or in patients at high surgical risk [16–18]. Reported endovascular approaches include catheter‑directed thrombolysis, PTA, and stent placement, with variable technical and clinical success depending on timing, vessel anatomy, and extent of thrombosis [19]. In the present case, the initial endovascular recanalization attempt after the first liver transplantation was unsuccessful. DSA demonstrated complete thrombosis of the hepatic arterial tree, which precluded guidewire passage and restoration of antegrade flow [16,19]. The patient subsequently developed severe ischemic cholangiopathy, emphasizing the biliary system’s limited tolerance of prolonged arterial ischemia [10,18]. Following retransplantation with an aorto‑hepatic arterial reconstruction, recurrent hepatic artery graft thrombosis occurred. CT imaging revealed weak opacification of the distal intrahepatic arterial branches. This distal arterial opacification was interpreted not only as a potential predictor of technical success [15,19] but also as indicative of a partial “filtering” thrombosis, in which the lumen was not completely occluded. This residual channel allowed the guidewire to reach the downstream vascular bed, which then became the target for restoring perfusion through sequential PTA and deployment of overlapping stents. This mechanistic insight provides a physiologic explanation for the angiographic finding and highlights a hypothesis‑generating role for distal opacification in guiding endovascular intervention [15,16]. Through a right common femoral artery approach, recanalization of the hepatic artery graft was achieved using a supportive 0.018‑inch guidewire. Sequential PTA and overlapping stent deployment successfully preserved arterial patency and restored intrahepatic perfusion. This experience aligns with prior reports describing endovascular management of complex hepatic arterial complications, including aorto‑hepatic bypass thrombosis [7] and conduit‑related stenosis or pseudoaneurysm [8]. Compared with these cases, our patient represents a particularly challenging scenario due to recurrent HAT after retransplantation, emphasizing both technical originality and clinical relevance. The case also underscores the critical role of multimodality imaging—color‑Doppler ultrasound, CT angiography, and DSA—in the detection, characterization, and longitudinal monitoring of hepatic arterial complications [20]. Prompt recognition of HAT, careful assessment of distal arterial patency, and timely procedural planning are essential factors influencing both technical and clinical outcomes [21,22]. Sustained stent patency on follow‑up imaging confirmed durable arterial perfusion, avoiding further open surgical intervention. Although long‑term outcomes and optimal patient selection criteria remain to be fully defined, this case illustrates that endovascular approaches can serve as graft‑saving strategies in carefully selected patients. In particular, in the presence of partial distal perfusion, endovascular recanalization may provide a minimally invasive alternative that reduces the need for immediate retransplantation, even after complex aorto‑hepatic reconstructions [7,8,22].

Endovascular recanalization could represent a safe and effective minimally invasive alternative for managing HAT after liver transplantation, particularly when distal intrahepatic arterial flow is preserved. Careful imaging assessment, procedural planning, and timely intervention are essential to restore arterial perfusion, preserve graft patency, and achieve favorable outcomes. However, these observations are based on a single case, and broader recommendations cannot be drawn. This case illustrates that even complex post‑transplant HAT may be successfully managed with minimally invasive endovascular techniques in selected patients.