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Fracture of a Carotid Stent: A Word of Caution
622
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Letters to the Editor
Fracture of a Carotid Stent: A Word of Caution From: Nicolas Diehm, MD Samuel Baum Barry T. Katzen, MD Margaret Kovacs, EdD James Benenati, MD Division of Interventional Radiology Baptist Cardiac and Vascular Institute 8900 N Kendall Dr Miami, FL 33176 (N.D., S.M, B.T.K., M.K., J.B.) Division of Clinical and Interventional Angiology and Vascular Research Swiss Cardiovascular Center Inselspital University Hospital Bern, Switzerland (N.D.) Editor: Carotid artery stent (CAS) placement with embolic protection is increasingly being regarded as a treatment alternative for patients with internal carotid artery stenosis who are at high risk for carotid endarterectomy. However, longterm results of CAS placement and detailed information of the behavior of metal stents in the carotid artery are still sparse. As the use of this technique expands and the number of reported incidences of complications related to this procedure grows, we suggest that further studies systematically assess the incidence and clinical implications of stent fractures after CAS placement. Herein, we offer additional evidence of CAS fracture and the associated restenosis at the fracture site. In June 2006, we encountered a 70-year-old woman who was referred for CAS placement for a left common and internal carotid artery stenosis. Her symptoms included transient ischemic attacks and amaurosis twice, with the last event occurring 1 week before referral. Two months earlier, she had undergone successful CAS placement in the right internal carotid artery for an 80% de novo stenosis. Her risk factors included type II diabetes mellitus, hypercholesterolemia, and hypertension. In addition, she had undergone laryngectomy and neck irradiation for laryngeal carcinoma 20 years ago. Duplex ultrasonography (US) and intraarterial digital subtraction angiography revealed a high-grade stenosis of the left common carotid artery that extended into the proximal internal carotid artery without evidence of substantial plaque formation. The patient was enrolled in the EXACT carotid stent trial. After transfemoral access was obtained, a 5— 8-mm-diameter, 40-mm-long tapered Xact carotid stent (Abbott Laboratories, Abbott Park, Illinois) was placed in the left common and internal carotid artery by using a 5-mm Emboshield (Abbott Laboratories) embolic protection device. Before stent placement, the lesion had been predilated with a 3-mm balloon. The final angiogram showed good stent expansion and excellent flow in this arterial segment. Except for periprocedural hypotension associated with the first CAS procedure that responded well to intravenous administration of neosynephrine and resolved without further sequelae, the procedures were carried out without com-
DOI: 10.1016/j.jvir.2007.12.451
April 2008
JVIR
plications. Postprocedural duplex US revealed normal flow velocities. The patient recovered uneventfully and was asymptomatic when she presented for a regular follow-up examination 1 year after the procedure, with normal carotid flow velocities. Duplex US, however, revealed a fracture at the distal portion of the stent associated with an increase in flow velocities to 236 cm/sec systolic and 51 cm/sec diastolic, corresponding to a 40%– 60% restenosis. Plain radiography confirmed the type III stent fracture (1) and showed a complete transection in the distal third of the stent deployed in the proximal internal carotid artery (Figure). Despite the fact that the patient remained asymptomatic, the fracture of a tapered nitinol stent implanted in the common and internal carotid artery 1 year after CAS placement is associated with a 40%– 60% restenosis. Stent fractures were reported to occur in the superficial femoral, tibial, renal, pulmonary, and coronary arteries. Probably caused by the paucity of systematic mid- and long-term assessments, these type of fractures in carotid stents have rarely been reported (2– 4). De Vries and colleagues (2) described a fracture of a covered carotid stent and clinical failure of endovascular treatment 7 months after implantation for a traumatic pseudoaneurysm. In addition, a recent report by Valibhoy et al (3) described a stent fracture after CAS placement for an internal carotid artery stenosis without calcification. Similar to our observations, in that case a type III stent fracture occurred 6 months after CAS placement in the noncalcified midsegment of the tapered stent implanted in the internal carotid artery. Because it was
Figure. Plain radiograph (anterior-posterior view) of the neck shows a type III fracture (arrow) of the left carotid stent in its distal third.
Volume 19
Number 4
associated with a 70% restenosis, failure of that stent necessitated its removal and carotid endarterectomy. Surdell et al (4) also reported substantial restenosis associated with stent fracture after CAS placement and complete midbody disruption in an even earlier follow-up window at 6 months. Like the femoropopliteal segment, the carotid bifurcation is located in a highly mobile part of human anatomy (5). Implantation of a carotid stent was shown to be associated with a substantial reduction of arterial compliance of the extracranial arteries. The carotid artery is only partially able to accommodate the changes in geometry that result from physiologic movements of the head, which may lead to kinking at the distal end of the stent (5). To date, there is limited information with regard to the optimal management for carotid stent fracture. Various clinical scenarios ranging from asymptomatic intimal hyperplasia to migration of stent fragments or acute thrombosis with subsequent embolic stroke are potential consequences. A fractured carotid stent was reported to be successfully removed by Valibhoy et al (3) without complications. Because our patient remained asymptomatic, and given the lack of data with regard to the safety of surgical stent removal in that particular setting, we chose a conservative approach. Although repeat stent placement in this lesion would be an option, insertion of another stent would further stiffen the carotid segment, thereby increasing the susceptibility to further stent fractures. Given the fact that reports about stent fractures associated with restenosis after CAS placement accumulate (2– 4), further studies assessing the safety of CAS placement should include assessment of stent integrity during follow-up. References 1. Jaff M, Dake M, Pompa J, Ansel G, Yoder T. Standardized evaluation and reporting of stent fractures in clinical trials of noncoronary devices. Catheter Cardiovasc Interv 2007; 70:460 – 462. 2. de Vries JP, Meijer RW, van den Berg JC, Meijer JM, van de Pavoordt ED. Stent fracture after endoluminal repair of a carotid artery pseudoaneurysm. J Endovasc Ther 2005; 12:612– 615. 3. Valibhoy AR, Mwipatayi BP, Sieunarine K. Fracture of a carotid stent: an unexpected complication. J Vasc Surg 2007; 45:603– 606. 4. Surdell D, Shaibani A, Bendok B, Eskandari MK. Fracture of a nitinol carotid artery stent that caused restenosis. J Vasc Interv Radiol 2007; 18:1297–1299. 5. Vos JA, Vos AW, Linsen MA, et al. Impact of head movements on morphology and flow in the internal carotid artery after carotid angioplasty and stenting versus endarterectomy. J Vasc Surg 2005; 41:469 – 475.
Popliteal Vein Aneurysm in Association with Inferior Vena Caval Obstruction Secondary to Hemochromatosis-Induced Hepatocellular Carcinoma From: Trevor M. Yeung, MA, MBBChir, MRCS (Eng) James Nicholson, MBBS Patrick Lintott, MD, FRCS Department of Surgery Wycombe General Hospital Queen Alexandra Rd High Wycombe HP11 2TT, United Kingdom
Letters to the Editor
•
623
Editor: A 59-year-old man with hereditary hemochromatosisinduced cirrhosis and secondary diabetes mellitus presented with recurrent superficial phlebitis of his right leg. A venous duplex examination demonstrated an incompetent saphenofemoral junction, a dilated great saphenous vein, and an incidental above-knee saccular popliteal vein aneurysm. No thrombus was identified, and venous flow was attenuated. Although the patient was advised to undergo anticoagulation immediately, he deferred warfarin treatment to commence after his holiday abroad. Upon returning home, he developed sudden onset of shortness of breath. Computed tomographic (CT) pulmonary angiography demonstrated multiple pulmonary emboli (PE). A CT venogram did not show any evidence of deep vein thrombosis (Fig 1). The patient received anticoagulation with low-molecular-weight heparin and was discharged home on warfarin. Elective surgical repair of his popliteal vein aneurysm was planned in 5 months at completion of his anticoagulation therapy. Two months after discharge, the patient developed sudden intense abdominal pain. His international normalized ratio was 4.1, hemoglobin level 11.9 g/dL (119 g/L), ferritin level normal at 231 ng/mL (231 g/L), and ␣-fetoprotein level elevated at 190.2 IU/mL. CT revealed findings consistent with a large hepatocellular carcinoma (HCC) in the left lobe of the liver that had ruptured and bled into the peritoneal cavity, and magnetic resonance (MR) imaging demonstrated tumor invading the inferior vena cava (IVC) (Figs 2–3). The patient was given vitamin K to reverse the effects of warfarin. An attempt to insert an IVC filter was abandoned when the intrahepatic IVC was found to be occluded with tumor (Fig 4). Once stabilized, the patient was discharged home with a multidisciplinary team follow-up at a tertiary referral center. While awaiting this appointment, he developed multiorgan failure and died. A subsequent postmortem examination confirmed metastatic HCC and demonstrated numerous bilateral pulmonary fibrotic scars suggestive of chronic PE. Popliteal vein aneurysms are rare—with only 117 cases being reported worldwide—and may manifest as PE or a popliteal mass or be found incidentally. To date, the largest retrospective review of popliteal vein aneurysms was performed in 25 patients; 24% manifested as PE and 76% were discovered during investigation of chronic venous disease (1). Despite the rarity of popliteal vein aneurysms, patients with PE should be investigated with lower limb venous duplex ultrasonography to identify a potential source of embolism. Surgical treatment should be offered to these patients because conservative treatment with anticoagulation can still result in recurrent PE and death (1,2). The current favored technique for saccular aneurysms like that seen in this case is tangential aneurysmectomy with lateral venorrhaphy by means of a posterior approach. Hereditary hemochromatosis is an autosomal recessive disorder in which homozygous patients develop a predisposition to iron overload. The disorder may be complicated by cirrhosis, HCC, diabetes mellitus, cardiomyopathy, and infertility (3). Phlebotomy does not reverse cirrhosis (4), and the risk of developing HCC continues despite iron removal. Patients with hereditary hemochromatosis–induced cirrhosis should be monitored for the development of HCC, but, to
DOI: 10.1016/j.jvir.2007.12.449
•
Letters to the Editor
Fracture of a Carotid Stent: A Word of Caution From: Nicolas Diehm, MD Samuel Baum Barry T. Katzen, MD Margaret Kovacs, EdD James Benenati, MD Division of Interventional Radiology Baptist Cardiac and Vascular Institute 8900 N Kendall Dr Miami, FL 33176 (N.D., S.M, B.T.K., M.K., J.B.) Division of Clinical and Interventional Angiology and Vascular Research Swiss Cardiovascular Center Inselspital University Hospital Bern, Switzerland (N.D.) Editor: Carotid artery stent (CAS) placement with embolic protection is increasingly being regarded as a treatment alternative for patients with internal carotid artery stenosis who are at high risk for carotid endarterectomy. However, longterm results of CAS placement and detailed information of the behavior of metal stents in the carotid artery are still sparse. As the use of this technique expands and the number of reported incidences of complications related to this procedure grows, we suggest that further studies systematically assess the incidence and clinical implications of stent fractures after CAS placement. Herein, we offer additional evidence of CAS fracture and the associated restenosis at the fracture site. In June 2006, we encountered a 70-year-old woman who was referred for CAS placement for a left common and internal carotid artery stenosis. Her symptoms included transient ischemic attacks and amaurosis twice, with the last event occurring 1 week before referral. Two months earlier, she had undergone successful CAS placement in the right internal carotid artery for an 80% de novo stenosis. Her risk factors included type II diabetes mellitus, hypercholesterolemia, and hypertension. In addition, she had undergone laryngectomy and neck irradiation for laryngeal carcinoma 20 years ago. Duplex ultrasonography (US) and intraarterial digital subtraction angiography revealed a high-grade stenosis of the left common carotid artery that extended into the proximal internal carotid artery without evidence of substantial plaque formation. The patient was enrolled in the EXACT carotid stent trial. After transfemoral access was obtained, a 5— 8-mm-diameter, 40-mm-long tapered Xact carotid stent (Abbott Laboratories, Abbott Park, Illinois) was placed in the left common and internal carotid artery by using a 5-mm Emboshield (Abbott Laboratories) embolic protection device. Before stent placement, the lesion had been predilated with a 3-mm balloon. The final angiogram showed good stent expansion and excellent flow in this arterial segment. Except for periprocedural hypotension associated with the first CAS procedure that responded well to intravenous administration of neosynephrine and resolved without further sequelae, the procedures were carried out without com-
DOI: 10.1016/j.jvir.2007.12.451
April 2008
JVIR
plications. Postprocedural duplex US revealed normal flow velocities. The patient recovered uneventfully and was asymptomatic when she presented for a regular follow-up examination 1 year after the procedure, with normal carotid flow velocities. Duplex US, however, revealed a fracture at the distal portion of the stent associated with an increase in flow velocities to 236 cm/sec systolic and 51 cm/sec diastolic, corresponding to a 40%– 60% restenosis. Plain radiography confirmed the type III stent fracture (1) and showed a complete transection in the distal third of the stent deployed in the proximal internal carotid artery (Figure). Despite the fact that the patient remained asymptomatic, the fracture of a tapered nitinol stent implanted in the common and internal carotid artery 1 year after CAS placement is associated with a 40%– 60% restenosis. Stent fractures were reported to occur in the superficial femoral, tibial, renal, pulmonary, and coronary arteries. Probably caused by the paucity of systematic mid- and long-term assessments, these type of fractures in carotid stents have rarely been reported (2– 4). De Vries and colleagues (2) described a fracture of a covered carotid stent and clinical failure of endovascular treatment 7 months after implantation for a traumatic pseudoaneurysm. In addition, a recent report by Valibhoy et al (3) described a stent fracture after CAS placement for an internal carotid artery stenosis without calcification. Similar to our observations, in that case a type III stent fracture occurred 6 months after CAS placement in the noncalcified midsegment of the tapered stent implanted in the internal carotid artery. Because it was
Figure. Plain radiograph (anterior-posterior view) of the neck shows a type III fracture (arrow) of the left carotid stent in its distal third.
Volume 19
Number 4
associated with a 70% restenosis, failure of that stent necessitated its removal and carotid endarterectomy. Surdell et al (4) also reported substantial restenosis associated with stent fracture after CAS placement and complete midbody disruption in an even earlier follow-up window at 6 months. Like the femoropopliteal segment, the carotid bifurcation is located in a highly mobile part of human anatomy (5). Implantation of a carotid stent was shown to be associated with a substantial reduction of arterial compliance of the extracranial arteries. The carotid artery is only partially able to accommodate the changes in geometry that result from physiologic movements of the head, which may lead to kinking at the distal end of the stent (5). To date, there is limited information with regard to the optimal management for carotid stent fracture. Various clinical scenarios ranging from asymptomatic intimal hyperplasia to migration of stent fragments or acute thrombosis with subsequent embolic stroke are potential consequences. A fractured carotid stent was reported to be successfully removed by Valibhoy et al (3) without complications. Because our patient remained asymptomatic, and given the lack of data with regard to the safety of surgical stent removal in that particular setting, we chose a conservative approach. Although repeat stent placement in this lesion would be an option, insertion of another stent would further stiffen the carotid segment, thereby increasing the susceptibility to further stent fractures. Given the fact that reports about stent fractures associated with restenosis after CAS placement accumulate (2– 4), further studies assessing the safety of CAS placement should include assessment of stent integrity during follow-up. References 1. Jaff M, Dake M, Pompa J, Ansel G, Yoder T. Standardized evaluation and reporting of stent fractures in clinical trials of noncoronary devices. Catheter Cardiovasc Interv 2007; 70:460 – 462. 2. de Vries JP, Meijer RW, van den Berg JC, Meijer JM, van de Pavoordt ED. Stent fracture after endoluminal repair of a carotid artery pseudoaneurysm. J Endovasc Ther 2005; 12:612– 615. 3. Valibhoy AR, Mwipatayi BP, Sieunarine K. Fracture of a carotid stent: an unexpected complication. J Vasc Surg 2007; 45:603– 606. 4. Surdell D, Shaibani A, Bendok B, Eskandari MK. Fracture of a nitinol carotid artery stent that caused restenosis. J Vasc Interv Radiol 2007; 18:1297–1299. 5. Vos JA, Vos AW, Linsen MA, et al. Impact of head movements on morphology and flow in the internal carotid artery after carotid angioplasty and stenting versus endarterectomy. J Vasc Surg 2005; 41:469 – 475.
Popliteal Vein Aneurysm in Association with Inferior Vena Caval Obstruction Secondary to Hemochromatosis-Induced Hepatocellular Carcinoma From: Trevor M. Yeung, MA, MBBChir, MRCS (Eng) James Nicholson, MBBS Patrick Lintott, MD, FRCS Department of Surgery Wycombe General Hospital Queen Alexandra Rd High Wycombe HP11 2TT, United Kingdom
Letters to the Editor
•
623
Editor: A 59-year-old man with hereditary hemochromatosisinduced cirrhosis and secondary diabetes mellitus presented with recurrent superficial phlebitis of his right leg. A venous duplex examination demonstrated an incompetent saphenofemoral junction, a dilated great saphenous vein, and an incidental above-knee saccular popliteal vein aneurysm. No thrombus was identified, and venous flow was attenuated. Although the patient was advised to undergo anticoagulation immediately, he deferred warfarin treatment to commence after his holiday abroad. Upon returning home, he developed sudden onset of shortness of breath. Computed tomographic (CT) pulmonary angiography demonstrated multiple pulmonary emboli (PE). A CT venogram did not show any evidence of deep vein thrombosis (Fig 1). The patient received anticoagulation with low-molecular-weight heparin and was discharged home on warfarin. Elective surgical repair of his popliteal vein aneurysm was planned in 5 months at completion of his anticoagulation therapy. Two months after discharge, the patient developed sudden intense abdominal pain. His international normalized ratio was 4.1, hemoglobin level 11.9 g/dL (119 g/L), ferritin level normal at 231 ng/mL (231 g/L), and ␣-fetoprotein level elevated at 190.2 IU/mL. CT revealed findings consistent with a large hepatocellular carcinoma (HCC) in the left lobe of the liver that had ruptured and bled into the peritoneal cavity, and magnetic resonance (MR) imaging demonstrated tumor invading the inferior vena cava (IVC) (Figs 2–3). The patient was given vitamin K to reverse the effects of warfarin. An attempt to insert an IVC filter was abandoned when the intrahepatic IVC was found to be occluded with tumor (Fig 4). Once stabilized, the patient was discharged home with a multidisciplinary team follow-up at a tertiary referral center. While awaiting this appointment, he developed multiorgan failure and died. A subsequent postmortem examination confirmed metastatic HCC and demonstrated numerous bilateral pulmonary fibrotic scars suggestive of chronic PE. Popliteal vein aneurysms are rare—with only 117 cases being reported worldwide—and may manifest as PE or a popliteal mass or be found incidentally. To date, the largest retrospective review of popliteal vein aneurysms was performed in 25 patients; 24% manifested as PE and 76% were discovered during investigation of chronic venous disease (1). Despite the rarity of popliteal vein aneurysms, patients with PE should be investigated with lower limb venous duplex ultrasonography to identify a potential source of embolism. Surgical treatment should be offered to these patients because conservative treatment with anticoagulation can still result in recurrent PE and death (1,2). The current favored technique for saccular aneurysms like that seen in this case is tangential aneurysmectomy with lateral venorrhaphy by means of a posterior approach. Hereditary hemochromatosis is an autosomal recessive disorder in which homozygous patients develop a predisposition to iron overload. The disorder may be complicated by cirrhosis, HCC, diabetes mellitus, cardiomyopathy, and infertility (3). Phlebotomy does not reverse cirrhosis (4), and the risk of developing HCC continues despite iron removal. Patients with hereditary hemochromatosis–induced cirrhosis should be monitored for the development of HCC, but, to
DOI: 10.1016/j.jvir.2007.12.449