Cath Lab Digest

Introduction
Radiation-induced vasculitis (RIV) is a well-documented complication in patients with a history of previous head and neck or mediastinal radiation. Cardiac valves and ostial location lesions of the epicardial coronary arteries are the more common sites of injury.¹ However, areas distant to the heart have also been shown to undergo changes after radiation-induced therapy. These areas are not limited to but include the carotid, vertebral and less commonly, the subclavian arteries. Treatment of RIV has included percutaneous intervention, surgical and medical therapy.² We present a patient with prior mantle and mediastinal radiation who presented with vertebral basilar insufficiency and left arm claudication.

Case Report
A 52-year-old female was found to have an isolated cervical node on routine physical exam and was subsequently diagnosed with non-Hodgkins lymphoma. She underwent successful mantle and mediastinal radiation. Shortly thereafter, she developed anginal symptoms, and further evaluation revealed a critical ostial left main stenosis. Given lack of traditional cardiac risk factors and history of radiation therapy, the diagnosis of coronary-induced fibrosis from RIV was made. The patient underwent coronary artery bypass with a left internal mammary artery (LIMA) conduit to the left anterior descending artery (LAD) and a radial graft to the left circumflex artery. Due to technical issues, the LIMA became atretic and ultimately occluded. Due to unstable anginal symptoms, the patient underwent successful unprotected percutaneous coronary intervention (PCI) of the left main artery.

One year later, the patient complained of intermittent dizziness and left arm claudication. A physical exam revealed a loud bruit over her left subclavian artery (LSCA) and blood pressure discrepancy between upper extremity pressures. An angiography was performed with a presumptive diagnosis of subclavian steal syndrome. The angiography revealed a critical left vertebral artery (LVA) ostial stenosis and a significant LSCA stenosis with a 30 mmHg trans-stenotic gradient after the origin of the LVA 9 (Figure 1). (Please ask author if “LVA 9” is correct). The patient was referred for percutaneous intervention.

Procedure
A 6 Fr Shuttle Sheath (Cook, Inc., Bloomington, IN) was used to engage the proximal LSCA. Initially, the LVA was wired with a Filter Wire Ex distal protection device (Boston Scientific Corporation, Maple Grove, MN). Next, a 5 Fr angled taper glide catheter (Terumo Medical Corporation, Somerset, NJ) was placed across the LSCA stenosis over an 0.035” angled glidewire (Terumo). The glidewire was removed and a BMW 0.014” wire (Guidant Corporation, Santa Clara, CA) was advanced into the left axillary artery (Figure 2).

At this time, sequential balloon inflations were performed with a 4 x 30mm Crossail balloon (Guidant Corp.)) in the LVA and a 5 x 20mm Savvy balloon (Cordis Endovascular, Warren, NJ) in the LSCA. Next, V-stenting technique was used to treat the stenoses. A 5 x 15 Herculink stent (Guidant Corp.) was placed into the LVA and a 6 x 18 Herculink was placed into the LSCA. Post dilation of the LVA stent was performed with a 6 x 2 Savvy balloon. Final angiography demonstrated wide patency of both treated arterial segments (Figure 4).
The patient tolerated the procedure well and there were no complications. The patient was discharged the following day on ASA and clopidogrel therapy.

Discussion
This case represents an unusual presentation of a rare condition. Though more commonly seen involving cardiac valves and epicardial coronary arteries, radiation-induced vascular injury may occur anywhere in the field of exposure. It is unclear whether radiation injury causes direct fibrosis or causes molecular and genetic changes that lead to the development of early atherosclerosis. Certain cytokines and growth factors, such as TGF-beta1 and IL-1 beta, may stimulate radiation-induced endothelial proliferation, fibroblast proliferation, collagen deposition and fibrosis leading to advanced lesions of atherosclerosis.²

One study that evaluated revascularization procedures performed for radiation-induced supra-aortic trunk disease found that the mean interval between irradiation and arterial revascularization was 15.2 years.³ This is considerably longer than our patient who presented with symptomatic multi-vessel vascular disease within 5 years of her therapy. It is unclear whether larger dosing or choice of anti-proliferative agent may have played a role in her rapid disease progression.

In the same study of 92 stenotic or occlusive lesions identified in 64 patients, 26 had lesions involving the LSCA with 15 requiring a revascularization procedure, noting the high incidence of symptomatic disease in this vascular territory. The incidence of vertebral artery involvement was not included.