Acute No-Reflow Complicating Stenting of Severe Carotid Artery Stenosis
Presenter
Aaron E. Brice, M.D., University of Arkansas for Medical Sciences, New Haven, --
Aaron E. Brice, M.D.1, Ahmad Z Arham, M.D.2, Zain Ahmed, M.D., M.P.H., M.S.3, Yulanka Castro, MD, FSCAI4, Sameer Nagpal, M.D.2 and Carlos I. Mena-Hurtado, M.D., FSCAI5, (1)University of Arkansas for Medical Sciences, New Haven, --, (2)Yale New Haven Hospital, New Haven, CT, (3)Yale - New Haven Hospital, New Haven, CT, (4)University Hospitals Harrington Heart & Vascular Institute, Cleveland, OH, (5)Yale University, New Haven, CT
Title Acute No-Reflow Complicating Stenting of Severe Carotid Artery Stenosis Introduction Severe carotid artery stenosis poses an increased risk of stroke and may be treated effectively with percutaneous stenting by experienced operators. This case demonstrates successful recognition and management of acute no-reflow phenomenon, an uncommon and potentially devastating complication of carotid stenting utilizing distal embolic protection. Clinical Case A 73 year old man with CAD s/p CABG, left subclavian artery stenosis s/p stenting, and heparin allergy was found to have asymptomatic severe right internal carotid artery (ICA) stenosis during workup for presyncope and dizziness. On exam a loud bruit was present over the right neck. Carotid ultrasound showed a large, calcified plaque in the bulb extending into the right ICA with a peak systolic velocity (PSV) of 433 cm/s with post stenotic turbulence. After discussion with the patient shared decision was made for carotid stenting given family history of strokes and plaque morphology. He was enrolled in CREST 2 and pretreated with aspirin and clopidogrel. Right common femoral arterial access was obtained with and pigtail catheter placed in the ascending aorta where angiography showed a Type I arch and severe right ICA disease. Given his heparin allergy bivalirudin was used to achieve a therapeutic activated clotting time (ACT). A VTK catheter was engaged in the right common carotid artery (CCA). This was then exchanged for a 6-French (F) 90cm Destination sheath and selective angiography performed confirming proximal 95% ICA stenosis. Emboshield Nav6 distal embolic protection device was advanced to the distal ICA and repeat therapeutic ACT confirmed. The lesion was predilated with a 4.0x20mm compliant balloon. Then Acculink 7-10x40mm self-expanding stent was successfully deployed across the lesion. However, angiography following stent deployment showed no-reflow in the stent and right ICA. It was suspected this was due to embolization of dislodged atherosclerotic debris now occluding filter flow. Given this and potential for thrombus formation an Export catheter was immediately loaded and multiple thrombectomy runs performed in the blood column proximal to the filter. This was followed by advancing intravascular ultrasound (IVUS) catheter which showed no residual thrombus, dissection, or stent malapposition but did show a focal narrowing in the mid segment of the stent which was treated with a 5.0x20mm noncompliant balloon. The filter and contents were then recaptured by retrieval device and removed from the body. Angiography following this showed excellent flow throughout the stent and right ICA and multiple views showed intact cerebral circulation. The patient did well and discharged home the following day. Ultrasound 6 weeks later showed patent stent and no significant stenosis. Discussion In our case the high-grade lesion was friable during angioplasty which resulted in dislodgement of large debris which occluded filter pores causing loss of antegrade flow and a no-reflow phenomenon. This mechanism also referred to as pseudo no-reflow should be treated with prompt aspiration thrombectomy prior to filter collapse and retrieval to prevent massive downstream embolization of atherothrombotic material. Successful filter removal with complete restoration of flow confirms the etiology.