case report Treatment of complicated case with subclavia steal syndrome and stenosis of common iliac artery Bujar Gjikolli1, Besima Hadžihasanović2, Suad Jaganjac3, Edin Herceglija4, Maida Nikšić1, Amel Hadzimehmedagić5, Mirza Dilić6, Emir Solaković7, Zulejha Merhemić1, Šerif Bešlić8, Lidija Lincender9, Rame Miftari10 Neuroradiology Department, Institute of Radiology, KCU Sarajevo, Bosnia and Herzegovina, 2Muskuloskeletal Department, Institute of Radiology, KCU Sarajevo, Bosnia and Herzegovina, 3Klinikum Eilbek Hamburg, Germany, 4 Vascular Department, Institute of Radiology, KCU Sarajevo, Bosnia and Herzegovina 5Clinic for Orthopedics and Traumatoology, KCU Sarajevo, Bosnia and Herzegovina, 6Clinic for Vascular Diseases, KCU Sarajevo, Bosnia and Herzegovina, 7Clinic for Vascular Surgery, KCU Sarajevo, Bosnia and Herzegovina, 8Thoracic Department, Institute of Radiology, KCU Sarajevo, Bosnia and Herzegovina, 9Abdominal Department, Institute of Radiology, KCU Sarajevo, Bosnia and Herzegovina, 10Institute of Radiology, Nuclear Medicine Dep., UCC of Kosova, Pristhine, Republic of Kosova Background. The aim of this case report is to describe the realization of complex radiological minimally invasive interventional procedures at the Institute of Radiology in KCU Sarajevo during which we treated a very complicated case with the left subclavia steal syndrome and the stenosis of the left common iliac artery. Case report. The patient was 57 years old with previous history of ischemic lesions in brain, with occlusion of the left arteria carotis communis (ACC) and stenosis of the right arteria carotis interna (ACI), with dizziness and inability to look upward. The patient was treated first with subintimal recanalization and introduction of self-expandable stent into the left subclavia artery to compensate for the very wide remnant of the occluded artery. After four months of follow up with no change, our team attempted to treat stenosis of the right ACI but failed to do so and during this procedure in-stent restenosis in the left subclavia artery was noted. After less than two weeks we performed balloon dilatation of in-stent restenosis of a previously installed stent into the left subclavia artery. The patient underwent CT and CT angiography (CTA), colour Doppler ultrasonography (CDUS), MRI and MR angiography (MRA) before and after the procedures. Conclusions. A follow up and, if needed, a balloon dilation are necessary to prevent the re-occlusion of the previously treated subclavia artery with stenting. Key words: subclavia steal syndrome; intentional subintimal recanalisation; restenosis; balloon dilation Received 13 August 2007 Accepted 21 August 2007 Correspondence to: Bujar Gjikolli M.D., Radiologist, Institute of Radiology, University Clinical Centre of Kosova, Pristine, Kosova; E-mail: bujargjikolli@yahoo. com Introduction Subclavia steal syndrome (SSS) is a group of signs and symptoms resulting from steno-occlusive disease proximal to the origin of the vertebral artery, in which the arterial flow is reversed.1-4 It was described in 1960 for the first time, and the association between this phenomenon and neurologic symptoms was recognized in 1961.5'6' SSS refers to the retrograde vertebral artery flow associated with transient neurologic symptoms related to cerebral ischemia while subclavia steal phenomena (SSP) refer to the retrograde flow in the vertebral artery only. Stenosis or occlusion of the proximal subclavia artery causes a reversed vertebral flow with resulting decreased blood pressure in the arm distal to the steno-oc-clusive disease. A reduced blood pressure causes the ipsilateral vertebral artery blood flow alteration as a compensatory pathway through the arm, and this sign confirms subclavia disease proximal to the origin of the vertebral artery. Other potential collateral pathways include those between the external carotid artery (ECA) and the subclavia artery from occipital branches of ECA and the superior thyroid artery of ECA to the inferior thyroid artery branch of thyrocervical trunk. There are four types of subclavia steal, defined by territory from which blood is "stolen" in SSS: vertebro-vertebral, carotid-basilar, external carotid-vertebral, and carotid-subclavia.7 Based on vertebral hemodynamic changes, SSS has three defined stages: reduced antegrade vertebral flow (stage I), reversal of flow during reactive hyperemia testing of the arm (stage II), and permanent retrograde vertebral flow indicating subclavia artery occlusion (stage III).8 Arm symptoms can be provoked during arm exercise or peripheral reactive hyper-aemia, while neurological symptoms occur when compensatory flow to the subclavia artery from the vertebral artery diverts too much flow to the arm and away from brain. Neurologic symptoms result primarily from the insufficient intracranial circulation through circle of Willis mainly through the posterior communicating artery. Absence of a posterior communicating artery, extra cranial carotid artery stenosis and higher flow toward the arm can cause neurologic symptoms. The spontaneous resolution of vertebro-basilar symptoms may be related to the establishment of extra cranial collaterals to the subclavia circulation. Etiology of SSS is predominantly atherosclerotic in people older than fifty years of age. In Asians Takayasu arteritis as etiology can be seen in up to 36% of the population. Other causes of SSS include giant cell ar-teritis, tumour encasement, trauma, previous surgical procedure such as aortic stent-graft placement for thoracic dissection or aneurysm, coarctation of aorta with the obliteration of subclavia orifice, extra vascular obstruction, hypoplasia / atresia or isolation of subclavia artery with the anomalous aortic arch, vascular ring, ligation for the correction of tetralogy of Fallot or co-arcta-tion of aorta.9 The risk of stroke seems low10 but patients with SSS can be severely debilitated by arm and intracranial ischemia symptoms. As many as 15% of initially asymptomatic patients can experience vertebro-basilar transient ischemic attacks during two years of follow up.11 SSS is more frequent in males than females with incidence 1.5-2:1 while Takayasu arteritis is more common in females. SSS has a left-sided to right-sided ratio of 3-4:1 as a result of turbulence-related atherosclerosis of the acutely angled left subclavia artery. Symptoms include dizziness, unsteadiness, vertigo, vision changes, arm ischemia causing arm claudication and rest pain, focal sensory or motor loss, dysphasia, and unilateral visual disturbances. Symptoms may develop during the exercise of the upper limbs, when blood is deviated from the vertebro-basilar system to the upper limb. A reduced blood pressure with change of >20 mm Hg when compared with contra lateral arm, weak or absent radial and ulnar pulse are other signs suggesting SSS. Colour Doppler US is the preferred examination.12 CT visualizes calcifications related to atheroma. Contrast enhanced CT angiography (CTA) can visualize the degree of subclavia artery stenosis or occlusion, including other changes in the arteries; mural thrombus, ulceration, and arterial wall calcification can be evaluated. MRI and contrast enhanced 3-D MR an-giography (MRA) after localizing 2-dimen-sional time-of-flight can also confirm SSP. Phase-contrast MRA measures the vertebral artery flow direction and velocity.13-15 SSS can be treated with minimally invasive radiological procedures of percutaneous transluminal angioplasty and stenting if angioplasty fails, using balloon-expandable stents or in some cases self expandable stents.16-22 Vertebro-basilar stroke during interventional procedures is rare due to the delayed establishment of the ante grade flow in the vertebral artery after the angi-oplasty/stenting. A distal protection may be useful especially in cases with thrombosis/unstable plaque. Soman 5/5 JO ' Ex 1 «MIP nWh Collection '3 KCU5 Saraievo I 1950 Jan 01 M 11368 Acc: 2005 Nov 30 JcqTmt 14 09 25.394010 2 Additionally SSS can be treated with surgical revascularization using either synthetic graft or saphenous vein grafts. Invasive options include carotid-subclavia bypass (CSB), carotid-subclavia transposition (CST), and axillo-axillary bypass.23-26 With this presentation we would like to describe the realization of complex radiological interventional therapeutic procedures of treating subclavia steal syndrome and stenosis of the left common iliac artery, at the institute of Radiology KCUS under the supervision of a Bosnian expert Dr. Suad Jaganjac working at the Hamburg Klinik Eilbek in Germany. Case report A 57-year-old male patient had complained of multiple symptoms, including weakness, dizziness, inability to look upward, speech difficulties and difficulties in using his left hand, in the five years following cerebral vascular insult. In 2002 he was admitted to the vascular surgery hospital KCUS because of atherosclerotic changes with stenosis of arteria carotis communis (ACC) and arteria carotis Figure 1 (a, b). CT angiography (CTA) maximum intensity projection (MIP) reformats show the occlusion of the left subclavian artery and the left brachial artery receiving blood from the left vertebral artery- steal syndrome. interna (ACI) in the left side. In 2003 he was hospitalized in the clinic for cardiovascular diseases in UCC Tuzla where surgeons confirmed stenosis of the right ACI but did not intervene in the artery. The patient also complained for claudi- Figure 2 (a, b, c, d). CTA reconstructed images show the occlusion of left common carotid artery (ACC) less than 1 cm from the aortic arch with the reconstruction of left internal carotid artery (ACI) through collaterals coming from left external carotid artery (ACE). The occlusion of the left subclavia artery approximately 1 cm from its origin with its reconstruction in the level of origin of the vertebral artery and severe stenosis of right ACI in its initial part. cating pain in his legs after 20 meters of walking. He had high blood pressure and increased triglycerides in blood but was not diabetic. He quit smoking in 2002 after more than 40 years of 1-1.5 packages of cigarettes per day. Figure 3 (a, b). Colour Doppler ultrasound (CD US) showing flow in the left internal carotid artery (ACI) and ACE above the occluded left common carotid artery (ACC). In November 2005, the patient complained of ongoing symptoms and underwent CTA at our institute (Figure 1). The occlusion of left ACC and left subclavia steal syndrome was diagnosed but no interventions were performed. In December 2006 the patient was referred for CTA again and the occlusion of left ACC and left subclavia artery reconstructed through the left vertebral artery was shown. The remnant subclavia artery below the occlusion was measured at 1.11 cm. High grade stenosis of right ACI has been shown too. Left ACI was reconstructed through collaterals coming mainly through arteria carotis externa (ACE) branches (Figure 2). During discussion, the patient mentioned physicians' previous difficulties doctors had accessing his femoral artery for diagnostic digital subtraction angiography (DSA). Additional CTA of abdominal aorta and the upper part of his lower extremities confirmed mild stenosis of the right femoral artery and significant stenosis of the left common iliac artery. Additionally colour Doppler ultrasound (CD US) confirmed the changes seen in the CTA: the disturbance of the flow and the steal syndrome in the left side (Figures 3, 4). Left ACC showed maximum diameter of 6.5 mm without detectable flow while in ACI and ACE portion there was flow detectable coming from surrounding collaterals. Right ACC had maximum diameter of 7 mm with intima medial thickness of 1.3 mm with laminar flow and Peak Systolic SP S ILVAS Ml 1.2 KCUS UlEWifl 19 RdlliokHMii SSirS-W-U-29.5 3.5CIB(»Hl 1H OS «,12-3006 Ot-UWIfiPW fit Diet rCA-PS f SIOlcm/* I Rl Dist ICA-ED 45.24cm/s ' R1 t>i*t tCA-fil M2 . m Dist ICA PI 1.72 1 Rl Dist ICA-n/D SM ' —■-1 m DisL rCA- TAmnx 121 18tm/s 1 r A Figure 4 (a, b). Colour Doppler ultrasound (CD US) images showing stenosis of the initial part in the right arteria carotis interna (ACI) and its increased spectral values. Figure 5 (a, b, c, d, e). Steps of the procedure performed. Subintimal recanalization, pre stenting balloon dilation, introduction of the stent with additional balloon dilatation giving the final result and preserving the vertebral artery which fills with contrast immediately after filling the aortic arch. Figure 6 (a, b, c). Stenosis of the left iliac artery before stenting and result gained after stenting. Velocity (PSV) 91.43 cm/s and End Diastolic Velocity (EDV) 21.33 cm/s in its proximal part and turbulent flow with PSV 79.49 cm/s, EDV 32.56 cm/s in its distal part. The dorsal part of the bifurcation and the initial part of the right ACI showed partly hyperand partly hypo-echogenic plaque inside the lumen, reducing its width 3.5 mm with increase of PSV to 254.02 cm/s and EDV 45.24 cm/s. After analyzing all imaging procedures performed, we decided to offer the patient treatment of subclavia syndrome while avoiding treating the stenosis of the right ACI as the only big artery supplying his brain with blood. He agreed and the procedure was performed in January 10, 2007 at the Institute of Radiology - KCU Sarajevo. We used a left brachial approach and a hydrophilic guiding wire to perform Bolia's intentional subintimal recanalization. After reaching the aorta the guiding wire was pulled out with a goose neck snare from the introducer in the left femoral artery. Meanwhile this introducer was installed to confirm the position of the guide wire in 11 m 13 ill- U I'W a mJ .vV - s • m ft A 1 Jf i m • S # 4$ # ft * t # B Figure 7 (a, b). Diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) images show old ischemic lesions and no new ischemic lesions at all. Figure 8 (a, b). Maximum intensity projection (MIP) MR reconstructions after stenting showing position and the patency of the left subclavian and left vertebral arteries. O.OT MRC25749 Ex: 1