Hepatic Artery Dissection Treated With a Rapamycin-Coated Stent: Report of a Case With 1-Year Angiographic Follow-up

Introduction

Hepatic artery dissection is an uncommon clinical event with few reported cases in the literature. Although rare, most reported dissections have occurred in the setting of intra-arterial hepatic artery chemotherapy or as a complication of liver transplant.^1–3 Treatment strategies have included surgery and, more recently, percutaneous balloon angioplasty (PTA) with adjunctive bare-metal stents.^1,2,4,5 Improved endovascular technology has led the way to greater success in treating complex arterial disease. Drug-eluting stents (DES), specifically, have proven efficacious in reducing coronary in-stent stenosis from neointimal hyperplasia.^6,7 This report describes successful treatment and midterm angiographic follow-up of a hepatic artery dissection with a DES.

Case Report

A 55-year-old female with panvascular disease, diabetes mellitus and tobacco abuse presented with reoccuring abdominal pain, emesis and weight loss. The patient's medical history was complex and dated back to the late 1990’s. She initially was evaluated for angina and lower extremity rest pain. Treatment included angioplasty of the coronary and iliac arteries. In 1999, the patient developed abdominal pain and weight loss. Subsequent evaluation disclosed an occluded inferior mesenteric artery and a proximally occluded superior mesenteric artery. The celiac artery was patent and the pancreatic duodenal collateral was present, but it was determined by vascular surgeons to be insufficient in preventing symptoms. The patient underwent open surgical grafting to the superior mesenteric (SMA) with resolution of the abdominal pain and weight gain. In March 2002, the patient began to experience recurrent epigastric pain with nausea and emesis. Repeat mesenteric angiography revealed a patent bypass to the SMA along with a new 95% stenosis of the celiac artery. Though the graft appeared to have a 40-50% stenosis, no significant pressure gradient was evident utilizing a 4 Fr multi-purpose diagnostic catheter. The celiac artery stenosis was treated with percutaneous angioplasty and adjunctive stent placement with resolution of the patient’s symptoms. The celiac artery was sized with quantitative angiography, and a balloon expandable stent was placed with a 7 mm balloon. The patient did well until February of 2003, when abdominal symptoms recurred. Nonvascular gastrointestinal pathology was evaluated and ruled out. Elective visceral angiography revealed a patent bypass to the SMA, but restenosis of the celiac artery stent. The celiac artery was accessed with a 6 Fr JR 4.0 Cordis Guiding Catheter (Cordis Corporation, Miami Lakes, Florida) via the right femoral artery. Balloon angioplasty with a 7.0 X 15 mm (chosen to be the same size as the celiac artery) Viatrac balloon (Guidant Corporation, Indianapolis, Indiana) of the celiac artery restenosis led to a flow-limiting arterial dissection of the hepatic artery. This theoretically could have been due to the distal balloon inadvertently extending into the hepatic artery during balloon inflation, a wire dissection or an extension from the celiac angioplasty. A 3.5 X 18 mm Cypher® (Cordis Endovascular, Warren, New Jersey) stent was placed across the dissection and deployed. Less than 5% residual stenosis was noted. The patient's post procedure course was unremarkable and she was discharged the day of the procedure. The patient presented for regular followup 1-month post procedure with resolution of her abdominal symptoms. In November 2004, the patient developed recurrent angina. She underwent coronary angiography and was found to have left anterior descending coronary artery (LAD) and right coronary arter (RCA) stenoses amenable to intervention. At that time, selective celiac artery angiography was completed to visualize the mesenteric and hepatic arteries, and evaluate patency. The hepatic artery stent demonstrated patency 14 months post-Cypher stent implantation.

Discussion

Limited information on hepatic artery dissection can be found in the literature. Generally, arterial dissections most commonly occurred in the renal, intracranial, coronary or pulmonary arteries.^8–10 These dissections can be caused by atherosclerosis, trauma, fibromuscular dysplasia, connective tissue disease and as in this case, iatrogenic.^11–14 Visceral arterial dissection, although more rare, commonly occurred in the superior mesenteric artery.¹⁵ Infrequent case reports have documented splenic artery, gastric artery, and hepatic artery dissections.¹⁶ Hepatic artery dissection has been recognized as a complication of intra-arterial hepatic chemotherapy or liver transplant.^1,2,3 Experience with this vascular lesion suggests that 64–71% will spontaneously recanalize after one month.^{17, 18} However, when complete arterial occlusion results from dissection, recanulization is rare. Carmody and Sniderman treated two post indwelling chemotherapeutic catheter-induced hepatic artery dissections with a Palmaz® stent (Cordis Endovascular) and a Wallstent® (Boston Scientific, Maple Grove, MN).¹ Angiographic follow-up on the Palmaz stent showed moderate stenosis requiring angioplasty after three months. The Wallstent-treated lesion did not produce clinical symptoms attributable to stenosis after 39 months; however, no angiographic follow-up was ever performed. Ogata et al. treated a chemotherapeutic in-dwelling catheter-induced hepatic artery dissection with Palmaz stent.² Digital subtraction angiography showed adequate patency after 6 months. In this case, the patient originally presented with typical symptoms of visceral artery ischemia. However, typically a patient only needs to have one of the three main visceral vessels to be patent to allow for adequate organ perfusion. Prior to our evaluations, the patient had successful relief from her symptoms by a surgical bypass to the SMA. The relief of symptoms certainly suggests that the pancreatic duodenal collateral bed, though present, was not adequate for shared perfusion. Treatment of the celiac stent restenosis led to significant hepatic artery dissection. Given the risk of vessel closure, the lesion required intervention. Following balloon dilation, deployment of the coronary stent was deemed appropriate in order to maintain patency. Recent advances in endovascular technology have fostered greater success in treating complex coronary artery lesions. Coronary artery DES have been shown to decrease in-stent restenosis in the coronary vasculature.^6,7 Since visceral stents are difficult to evaluate for the development of restenosis, a DES was used empirically, extrapolating the potential for benefit from the coronary bed to the hepatic artery. Additionally, patency of that stent was demonstrated at 14 months. This case is significant because, as far as is known, no other study has deployed a DES in a visceral artery. Although uncommon, hepatic artery dissections have long-term sequela with an incidence of restenosis and recurrent interventions. Though a non-DES could have been utilized, we chose to use one. The effectiveness of using DES to treat hepatic lesions is unknown and potential drawbacks are possible. Coronary stents have lower radial strength and would not be as good of a choice for aorto-ostial lesions. No clinical trial data is available to show safety and efficacy in mesenteric vessels and routine use may not be advisable until more clinical data is available. This would especially be true in patients that may not be advisable to prevent sten thrombosis. However, due to the low incidence of mesenteric vessel ischemia, the role of this technology in treating the hepatic artery, or other visceral arteries needs, may be better evaluated at the present time in the renal vascular bed.

Correspondence: garyansel@aol.com