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Scepter C Scepter XC ®
®
REDEFINING DELIVERABILITY, VERSATILITY AND CONTROL MicroVention has developed two occlusion balloon catheters. Scepter C® compliant balloon is designed for reliable vessel occlusion yet conforms to vessel anatomy. Scepter XC® x-tra compliant balloon conforms to extremely complex anatomies where neck coverage is more challenging. Used with
Nursing Neurology Engineering Cardiology Find out more at www.sagepub.com/social
For more information or a product demonstration, contact your local MicroVention representative. MICROVENTION, Scepter C, Scepter XC and Headway are registered trademarks of MicroVention, Inc. Scientific and clinical data related to this document are on file at MicroVention, Inc. Refer to Instructions for Use, contraindications and warnings for additional information. Federal (USA) law restricts this device for sale by or on the order of a physician. © 2015 MicroVention, Inc. 5/15
MicroVention, Inc. Worldwide Headquarters 1311 Valencia Avenue Tustin, California 92780, USA MicroVention UK Limited MicroVention Europe, S.A.R.L. MicroVention Deutschland GmbH Web
PH +1.714.247.8000
PH +44 (0) 191 258 6777 PH +33 (1) 39 21 77 46 PH +49 211 210 798-0 microvention.com
Original Article
Early middle cerebral artery stenosis following stent-assisted thrombectomy
Interventional Neuroradiology 2015, Vol. 21(3) 337–340 ! The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1591019915581947 ine.sagepub.com
Su¨ha Akpınar and Gu¨liz Yılmaz
Abstract Stent-assisted thrombectomy (SAT) is an extensively used endovascular treatment method for stroke in which the thrombectomy stents come into direct contact with the vascular intimal surface and entrap the thrombus causing the arterial occlusion. Although there are a few studies that demonstrate that the vessel wall changes in the arteries where stroke intervention is performed, we observed progressive stenosis in early follow-up imaging studies in a case. We present a middle cerebral artery (MCA) stroke patient who had four repetitive stent passes during SAT and developed distal MCA stenosis 2 months after SAT at the control magnetic resonance angiography (MRA). Inclusion of early follow-up MRA studies would be helpful in defining the silent vascular changes in patients who have undergone repetitive SAT.
Keywords Magnetic resonance angiography, middle cerebral artery, stenosis, stent-assisted thrombectomy
Introduction Stent-assisted thrombectomy (SAT) has dramatically changed the course of stroke patients, and is used extensively for endovascular stroke treatment especially in large vessel occlusions. Its efficacy is the early recanalization of the occluded artery and total removal of the thrombus. It is well known that any repeated insult on the intimal surface of the artery can result in various degrees of intimal hyperplasia.1,2 However, it is not yet clarified whether this close intimal contact of the thrombectomy stents, especially with repeated stent passes, gives rise to high-grade vascular stenosis on early follow-ups. We present a patient with middle cerebral artery (MCA) stenosis which occurred 2 months after a neurointerventional procedure, who had undergone four repeated SAT passes.
Case A 65-year-old female patient was brought to the emergency department with the complaints of transient attacks of right-sided hemiparesis and aphasia which progressed to stroke in 6 hours. The patient was examined by magnetic resonance imaging (MRI) which showed total occlusion of the left MCA M1 segment with diffusion restriction at the left MCA territory. There was non-stenotic, non-ulcerated calcified plaque at the common carotid artery bifurcation on computed tomography angiography (CTA). Further questioning revealed a history of chronic cardiac atrial fibrillation, and the etiology was presumed cardioembolic
according to the Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification. Hence she underwent neuroendovascular treatment, where a 8Fr Balloon guiding catheter (Corail, Balt, France) was inserted into the distal part of the cervical internal carotid artery (ICA). We reached the occlusion site with a Transend 14 microguidwire (Stryker, USA) and Rebar 2.8 mm (ev3, Covidien, USA) microcatheter, and performed repeated SAT with a 5 30 mm Solitaire (ev3, Covidien, USA) stent. There was no dissection initially at the ICA, which was confirmed by the first two runs on digital subtraction angiography (DSA). Due to the repeated to and fro movement of the inflated balloon guiding the catheter during the thrombectomy procedure, a focal 1 cm-long ICA dissection occurred at the distal cervical segment of the ICA, which did not cause any flow disturbance. After the fourth SAT, we were able to recanalize the MCA M1 segment with a result of thrombolysis in cerebral infarction (TICI) score of 3. The left MCA segments and branches were normal in size at the final control runs (Figure 1a and b). The patient’s hemiplegia significantly resolved and her speech returned to normal in the following days. As she had the local dissection at the distal cervical
Department of Radiology, Faculty of Medicine, Near East University, Nicosia, Turkey Corresponding author: Gu¨liz Yılmaz, Department of Radiology, Faculty of Medicine, Near East University Hospital, Nicosia, 922000 Turkey. Email: [email protected]
338
Interventional Neuroradiology 21(3)
Figure 1. (a) Digital subtraction angiography scan demonstrates left middle cerebral artery M1 segment occlusion and the dissection at the cervical internal carotid artery. (b) Digital subtraction angiography scan of left middle cerebral artery recanalization after stentassisted thrombectomy with normal diameter.
segment of the ICA, a low dose of fraxiparine (low molecular weight heparin) 2 0.4 ml (3800 IU) was administered and no bleeding was observed on susceptibility weighted images on MRI. She did not have any additional symptoms and her clinical status had improved at follow-up. At the seventh day before discharge the proximal ICA lumen was found almost occluded on color Doppler ultrasound, and total occlusion was confirmed at the distal segments of the ICA with CTA and 3D time of flight MR angiography (MRA) (Figure 2). Although the patient was on coumadin treatment, the distal dissection flap at the ICA distal cervical segment had progressed downwards to the ICA orifice and occluded it. The patient was planned to have a control MRA 6–8 weeks later to evaluate the recanalization of the dissected segment. On her 8-week control MRA, in addition to the previous ICA occlusion, focal stenosis at the left MCA distal M1 segment was observed where multiple stent passes had been performed. Although the MCA distal segment was initially normal after the intervention, progression to high-grade (70–75%) stenosis was confirmed at the 6-month control CTA (Figure 3(a–c)). After the recognition of MCA M1 segment stenosis, the patient was put on coumadin and clopidogrel therapy. She is still asymptomatic although the stenosis had progressed to high-grade stenosis, and she is receiving the same treatment regimen.
Discussion Stent-assisted thrombectomy has changed the survival rates of stroke patients, with early and efficient recanalization rates of occluded vessels. We prefer to use large-sized stents, especially in large-vessel occlusions, to entrap the thrombus, which is usually a hard plaque in embolic patients, and to recanalize the occlusion site without distal migration of the thrombus. For the Solitaire AB/FR stents, a 4 15/20 mm stent is advised
Figure 2. First-week control cranial magnetic resonance angiography scan shows left ICA occlusion with normal MCA M1 segment.
for vessels 2–4 mm in diameter and a 6 20/30 mm stent for vessels 3–5.5 mm in diameter.3 In our case, the diameter of the M1 segment was 3.0–3.2 mm, measured by CTA, which indicates a stent can be used between 4 and 6 mm in diameter. Repeated SAT is necessary in persistent occlusion cases, which increases the risk of intimal injury due to the stents being in direct contact with the intimal surface, which is also supported in animal model studies.2,4 Vessel wall imaging studies early after medical and interventional stroke treatment showed vessel wall reaction at the stroke site in almost all of the interventionally treated
Akpınar and Yılmaz
339
Figure 3. (a) Eighth week control contrast-enhanced cranial magnetic resonance angiography axial MIP scan with early distal middle cerebral artery stenosis. (b) Six-month cranial magnetic resonance angiography scan and (c) Computed tomography angiography scan shows left middle cerebral artery M1 segment stenosis progression to high-grade stenosis (arrow).
patient group, whereas 50% of the medically treated stroke patients had a vessel wall reaction, defined as wall thickening and enhancement.5 However, it is not stated in this study how these vessel wall reactions proceeded over time. The appearance of early onset vascular stenosis in previously normal-looking arterial lumen has not been stated as a complication in follow-up studies.6 In our series of 34 SAT with an average of 2.5 stent passes, only one case, who had undergone four consecutive passes, had MRA 2 months later, to examine the dissection that took place at the ICA cervical segment. In addition to the ICA occlusion, MCA stenosis was observed which was assumed normal in DSA, MRA and CTA studies before and early after SAT. It is well known that any insult on the vascular intimal surface may cause intimal hyperplasia, and it cannot be determined how serious this may become in time.2,7 However, repeated thrombectomy passes performed at persistent occlusions give rise to repeated contact of the stent with the arterial intimal surface. This may cause intimal reaction which has early and late effects and can be exaggerated according to the rate of injury.1,2 According to animal model studies and vessel wall evaluation with MRI, intimal injury may occur without early imaging findings.4,5 Although the presence of vascular injury on the endovascularly treated arterial segments has been studied, stenosis was not
identified in the early period after SAT with early reports.5 Kurre et al. declared asymptomatic de novo stenosis on DSA controls, as 3.4% out of 117 territories in different thrombectomy applications, which were more frequent in patients who had vasospasm during the procedure.7 They reported a total of four cases of de novo stenosis and one occlusion. All cases were asymptomatic and the majority were significantly stenosed already at follow-up (40%, 60%, 70% and 70%, respectively). Solitaire stent was used in two cases in whom 70% stenosis was observed at the vertebral artery (VA) and MCA M2 segment. Although the mean follow-up period was 107 days in their study, VA stenosis was observed on day 222 and the M2 stenosis was observed at day 154 control DSA. In our case M1 distal segment stenosis was observed as early as 63 days follow-up, progressing to 70–75% high-grade stenosis under anticoagulation treatment. We did not observe vasospasm during the procedure in our case, and follow-up studies were done with MRA instead of DSA. Control MRA done at the eighth week revealed early MCA stenosis findings, which were more prominent at 6 months on CTA. These non-invasive modalities accurately identified the progression of the vascular stenosis. The reasons for cerebrovascular stenosis can be atherosclerosis, vascular dissection or vasculitis.7–9
340 Our patient had no stenosis or atherosclerosis on the MCA vessel wall before and early after the thrombectomy on DSA, MRA and CTA studies. Atherosclerosis may be a reason for stenosis in the long run, but studies undertaken to expose the rate of progression of atherosclerosis in an already diseased vessel showed that its rate of increase is greatest in the first 2 years, at 0.2–0.3 mm per year in coronaries, which are the most vulnerable vessels in the body.10 Hence the progression of atherosclerosis cannot be supported as the reason for stenosis in our case. On the control MRI and CTA soon after the thrombectomy there was no sign of dissection at the MCA wall, and the patient’s laboratory tests for vasculitis were also normal. According to the etiology of stroke, patients usually receive antiplatelet treatment after the intervention. Similarly, double antiplatelet treatment is preferred in cerebrovascular stenosis according to the latest guidelines.8 The patient was put on coumadin for the dissection follow-up, and clopidogrel was added to the coumadin treatment after the onset of MCA de novo stenosis. We assumed that the medical treatment after the stroke intervention masked the clinical symptoms that may arise due to the MCA stenosis in the long run, as the patient was asymptomatic during this period. Depending on the post-interventional period, when de novo stenosis is noticed in patients who have undergone SAT, antiplatelet treatment should be continued as advised in cerebrovascular stenosis. Stent-assisted thrombectomy is the method of choice in stroke treatment, with fast and effective recanalization rates. Besides, it is not emphasized in large series whether critical stenosis may arise in patients who have undergone SAT, especially with repeated stent passes, on the early follow-ups. Large series with screening imaging modalities would be helpful to identify the effects of the thrombectomy stents on the vascular intima. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Conflict of interest None declared.
Interventional Neuroradiology 21(3) References 1. Subbotin VM. Analysis of arterial intimal hyperplasia: Review and hypothesis. Theor Biol Med Model 2007; 4: 41. 2. Gory B, Bresson D, Kessler I, et al. Histopathologic evaluation of arterial wall response to 5 neurovascular mechanical thrombectomy devices in a swine model. Am J Neuroradiol 2013; 34: 2192–2198. 3. Mordasini P, Zubler C, Schroth G, et al. Thrombectomy for acute ischemic stroke treatment: A review. EJMINT Invited Review. 2012; 1238000077. Epub 21 September 2012. 4. Nogueira R, Levy EI, Gounis M, et al. The Trevo device: Preclinical data of a novel stroke thrombectomy device in two different animal models of arterial thrombo-occlusive disease. J Neurointerv Surg 2012; 4: 295–300. 5. Power S, Matouk C, Casaubon LK, et al. Vessel wall magnetic resonance imaging in acute ischemic stroke. Effects of embolism and mechanical thrombectomy on the arterial wall. Stroke 2014; 45: 2330–2334. 6. van der Kolk AG, Zwanenburg JJM, Brundel M, et al. Intracranial vessel wall imaging at 7.0-T MRI. Stroke 2011; 42: 2478–2484. 7. Kurre W, Pe´rez MA, Horvath D, et al. Does mechanical thrombectomy in acute embolic stroke have long-term side effects on intracranial vessels? An angiographic follow-up study. Cardiovasc Intervent Radiol 2013; 36: 629–636. 8. Lee VH. Medical management of intracranial atherosclerotic stenosis. Open Atherosclerosis Thromb J 2010; 3: 16–23. 9. Komotar RJ, Kellner CP, Raper DM, et al. Update on the natural history of intracranial atherosclerotic disease: A critical review. World J Radiol 2010; 2: 166–171. 10. Vos J, de Feyter PJ, Kingmaf JH, et al. Evolution of coronary atherosclerosis in patients with mild coronary artery disease studied by serial quantitative coronary angiography at 2 and 4 years follow-up. Eur Heart J 1997; 18: 1081–1089.
Connect with SAGE Facebook “f ” Logo
CMYK / .eps
Facebook “f ” Logo
CMYK / .eps
Channels feature news, current research, podcasts, free content, and announcements from your favorite SAGE journals.
Health
Scepter C Scepter XC ®
®
REDEFINING DELIVERABILITY, VERSATILITY AND CONTROL MicroVention has developed two occlusion balloon catheters. Scepter C® compliant balloon is designed for reliable vessel occlusion yet conforms to vessel anatomy. Scepter XC® x-tra compliant balloon conforms to extremely complex anatomies where neck coverage is more challenging. Used with
Nursing Neurology Engineering Cardiology Find out more at www.sagepub.com/social
For more information or a product demonstration, contact your local MicroVention representative. MICROVENTION, Scepter C, Scepter XC and Headway are registered trademarks of MicroVention, Inc. Scientific and clinical data related to this document are on file at MicroVention, Inc. Refer to Instructions for Use, contraindications and warnings for additional information. Federal (USA) law restricts this device for sale by or on the order of a physician. © 2015 MicroVention, Inc. 5/15
MicroVention, Inc. Worldwide Headquarters 1311 Valencia Avenue Tustin, California 92780, USA MicroVention UK Limited MicroVention Europe, S.A.R.L. MicroVention Deutschland GmbH Web
PH +1.714.247.8000
PH +44 (0) 191 258 6777 PH +33 (1) 39 21 77 46 PH +49 211 210 798-0 microvention.com
Original Article
Early middle cerebral artery stenosis following stent-assisted thrombectomy
Interventional Neuroradiology 2015, Vol. 21(3) 337–340 ! The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1591019915581947 ine.sagepub.com
Su¨ha Akpınar and Gu¨liz Yılmaz
Abstract Stent-assisted thrombectomy (SAT) is an extensively used endovascular treatment method for stroke in which the thrombectomy stents come into direct contact with the vascular intimal surface and entrap the thrombus causing the arterial occlusion. Although there are a few studies that demonstrate that the vessel wall changes in the arteries where stroke intervention is performed, we observed progressive stenosis in early follow-up imaging studies in a case. We present a middle cerebral artery (MCA) stroke patient who had four repetitive stent passes during SAT and developed distal MCA stenosis 2 months after SAT at the control magnetic resonance angiography (MRA). Inclusion of early follow-up MRA studies would be helpful in defining the silent vascular changes in patients who have undergone repetitive SAT.
Keywords Magnetic resonance angiography, middle cerebral artery, stenosis, stent-assisted thrombectomy
Introduction Stent-assisted thrombectomy (SAT) has dramatically changed the course of stroke patients, and is used extensively for endovascular stroke treatment especially in large vessel occlusions. Its efficacy is the early recanalization of the occluded artery and total removal of the thrombus. It is well known that any repeated insult on the intimal surface of the artery can result in various degrees of intimal hyperplasia.1,2 However, it is not yet clarified whether this close intimal contact of the thrombectomy stents, especially with repeated stent passes, gives rise to high-grade vascular stenosis on early follow-ups. We present a patient with middle cerebral artery (MCA) stenosis which occurred 2 months after a neurointerventional procedure, who had undergone four repeated SAT passes.
Case A 65-year-old female patient was brought to the emergency department with the complaints of transient attacks of right-sided hemiparesis and aphasia which progressed to stroke in 6 hours. The patient was examined by magnetic resonance imaging (MRI) which showed total occlusion of the left MCA M1 segment with diffusion restriction at the left MCA territory. There was non-stenotic, non-ulcerated calcified plaque at the common carotid artery bifurcation on computed tomography angiography (CTA). Further questioning revealed a history of chronic cardiac atrial fibrillation, and the etiology was presumed cardioembolic
according to the Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification. Hence she underwent neuroendovascular treatment, where a 8Fr Balloon guiding catheter (Corail, Balt, France) was inserted into the distal part of the cervical internal carotid artery (ICA). We reached the occlusion site with a Transend 14 microguidwire (Stryker, USA) and Rebar 2.8 mm (ev3, Covidien, USA) microcatheter, and performed repeated SAT with a 5 30 mm Solitaire (ev3, Covidien, USA) stent. There was no dissection initially at the ICA, which was confirmed by the first two runs on digital subtraction angiography (DSA). Due to the repeated to and fro movement of the inflated balloon guiding the catheter during the thrombectomy procedure, a focal 1 cm-long ICA dissection occurred at the distal cervical segment of the ICA, which did not cause any flow disturbance. After the fourth SAT, we were able to recanalize the MCA M1 segment with a result of thrombolysis in cerebral infarction (TICI) score of 3. The left MCA segments and branches were normal in size at the final control runs (Figure 1a and b). The patient’s hemiplegia significantly resolved and her speech returned to normal in the following days. As she had the local dissection at the distal cervical
Department of Radiology, Faculty of Medicine, Near East University, Nicosia, Turkey Corresponding author: Gu¨liz Yılmaz, Department of Radiology, Faculty of Medicine, Near East University Hospital, Nicosia, 922000 Turkey. Email: [email protected]
338
Interventional Neuroradiology 21(3)
Figure 1. (a) Digital subtraction angiography scan demonstrates left middle cerebral artery M1 segment occlusion and the dissection at the cervical internal carotid artery. (b) Digital subtraction angiography scan of left middle cerebral artery recanalization after stentassisted thrombectomy with normal diameter.
segment of the ICA, a low dose of fraxiparine (low molecular weight heparin) 2 0.4 ml (3800 IU) was administered and no bleeding was observed on susceptibility weighted images on MRI. She did not have any additional symptoms and her clinical status had improved at follow-up. At the seventh day before discharge the proximal ICA lumen was found almost occluded on color Doppler ultrasound, and total occlusion was confirmed at the distal segments of the ICA with CTA and 3D time of flight MR angiography (MRA) (Figure 2). Although the patient was on coumadin treatment, the distal dissection flap at the ICA distal cervical segment had progressed downwards to the ICA orifice and occluded it. The patient was planned to have a control MRA 6–8 weeks later to evaluate the recanalization of the dissected segment. On her 8-week control MRA, in addition to the previous ICA occlusion, focal stenosis at the left MCA distal M1 segment was observed where multiple stent passes had been performed. Although the MCA distal segment was initially normal after the intervention, progression to high-grade (70–75%) stenosis was confirmed at the 6-month control CTA (Figure 3(a–c)). After the recognition of MCA M1 segment stenosis, the patient was put on coumadin and clopidogrel therapy. She is still asymptomatic although the stenosis had progressed to high-grade stenosis, and she is receiving the same treatment regimen.
Discussion Stent-assisted thrombectomy has changed the survival rates of stroke patients, with early and efficient recanalization rates of occluded vessels. We prefer to use large-sized stents, especially in large-vessel occlusions, to entrap the thrombus, which is usually a hard plaque in embolic patients, and to recanalize the occlusion site without distal migration of the thrombus. For the Solitaire AB/FR stents, a 4 15/20 mm stent is advised
Figure 2. First-week control cranial magnetic resonance angiography scan shows left ICA occlusion with normal MCA M1 segment.
for vessels 2–4 mm in diameter and a 6 20/30 mm stent for vessels 3–5.5 mm in diameter.3 In our case, the diameter of the M1 segment was 3.0–3.2 mm, measured by CTA, which indicates a stent can be used between 4 and 6 mm in diameter. Repeated SAT is necessary in persistent occlusion cases, which increases the risk of intimal injury due to the stents being in direct contact with the intimal surface, which is also supported in animal model studies.2,4 Vessel wall imaging studies early after medical and interventional stroke treatment showed vessel wall reaction at the stroke site in almost all of the interventionally treated
Akpınar and Yılmaz
339
Figure 3. (a) Eighth week control contrast-enhanced cranial magnetic resonance angiography axial MIP scan with early distal middle cerebral artery stenosis. (b) Six-month cranial magnetic resonance angiography scan and (c) Computed tomography angiography scan shows left middle cerebral artery M1 segment stenosis progression to high-grade stenosis (arrow).
patient group, whereas 50% of the medically treated stroke patients had a vessel wall reaction, defined as wall thickening and enhancement.5 However, it is not stated in this study how these vessel wall reactions proceeded over time. The appearance of early onset vascular stenosis in previously normal-looking arterial lumen has not been stated as a complication in follow-up studies.6 In our series of 34 SAT with an average of 2.5 stent passes, only one case, who had undergone four consecutive passes, had MRA 2 months later, to examine the dissection that took place at the ICA cervical segment. In addition to the ICA occlusion, MCA stenosis was observed which was assumed normal in DSA, MRA and CTA studies before and early after SAT. It is well known that any insult on the vascular intimal surface may cause intimal hyperplasia, and it cannot be determined how serious this may become in time.2,7 However, repeated thrombectomy passes performed at persistent occlusions give rise to repeated contact of the stent with the arterial intimal surface. This may cause intimal reaction which has early and late effects and can be exaggerated according to the rate of injury.1,2 According to animal model studies and vessel wall evaluation with MRI, intimal injury may occur without early imaging findings.4,5 Although the presence of vascular injury on the endovascularly treated arterial segments has been studied, stenosis was not
identified in the early period after SAT with early reports.5 Kurre et al. declared asymptomatic de novo stenosis on DSA controls, as 3.4% out of 117 territories in different thrombectomy applications, which were more frequent in patients who had vasospasm during the procedure.7 They reported a total of four cases of de novo stenosis and one occlusion. All cases were asymptomatic and the majority were significantly stenosed already at follow-up (40%, 60%, 70% and 70%, respectively). Solitaire stent was used in two cases in whom 70% stenosis was observed at the vertebral artery (VA) and MCA M2 segment. Although the mean follow-up period was 107 days in their study, VA stenosis was observed on day 222 and the M2 stenosis was observed at day 154 control DSA. In our case M1 distal segment stenosis was observed as early as 63 days follow-up, progressing to 70–75% high-grade stenosis under anticoagulation treatment. We did not observe vasospasm during the procedure in our case, and follow-up studies were done with MRA instead of DSA. Control MRA done at the eighth week revealed early MCA stenosis findings, which were more prominent at 6 months on CTA. These non-invasive modalities accurately identified the progression of the vascular stenosis. The reasons for cerebrovascular stenosis can be atherosclerosis, vascular dissection or vasculitis.7–9
340 Our patient had no stenosis or atherosclerosis on the MCA vessel wall before and early after the thrombectomy on DSA, MRA and CTA studies. Atherosclerosis may be a reason for stenosis in the long run, but studies undertaken to expose the rate of progression of atherosclerosis in an already diseased vessel showed that its rate of increase is greatest in the first 2 years, at 0.2–0.3 mm per year in coronaries, which are the most vulnerable vessels in the body.10 Hence the progression of atherosclerosis cannot be supported as the reason for stenosis in our case. On the control MRI and CTA soon after the thrombectomy there was no sign of dissection at the MCA wall, and the patient’s laboratory tests for vasculitis were also normal. According to the etiology of stroke, patients usually receive antiplatelet treatment after the intervention. Similarly, double antiplatelet treatment is preferred in cerebrovascular stenosis according to the latest guidelines.8 The patient was put on coumadin for the dissection follow-up, and clopidogrel was added to the coumadin treatment after the onset of MCA de novo stenosis. We assumed that the medical treatment after the stroke intervention masked the clinical symptoms that may arise due to the MCA stenosis in the long run, as the patient was asymptomatic during this period. Depending on the post-interventional period, when de novo stenosis is noticed in patients who have undergone SAT, antiplatelet treatment should be continued as advised in cerebrovascular stenosis. Stent-assisted thrombectomy is the method of choice in stroke treatment, with fast and effective recanalization rates. Besides, it is not emphasized in large series whether critical stenosis may arise in patients who have undergone SAT, especially with repeated stent passes, on the early follow-ups. Large series with screening imaging modalities would be helpful to identify the effects of the thrombectomy stents on the vascular intima. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Conflict of interest None declared.
Interventional Neuroradiology 21(3) References 1. Subbotin VM. Analysis of arterial intimal hyperplasia: Review and hypothesis. Theor Biol Med Model 2007; 4: 41. 2. Gory B, Bresson D, Kessler I, et al. Histopathologic evaluation of arterial wall response to 5 neurovascular mechanical thrombectomy devices in a swine model. Am J Neuroradiol 2013; 34: 2192–2198. 3. Mordasini P, Zubler C, Schroth G, et al. Thrombectomy for acute ischemic stroke treatment: A review. EJMINT Invited Review. 2012; 1238000077. Epub 21 September 2012. 4. Nogueira R, Levy EI, Gounis M, et al. The Trevo device: Preclinical data of a novel stroke thrombectomy device in two different animal models of arterial thrombo-occlusive disease. J Neurointerv Surg 2012; 4: 295–300. 5. Power S, Matouk C, Casaubon LK, et al. Vessel wall magnetic resonance imaging in acute ischemic stroke. Effects of embolism and mechanical thrombectomy on the arterial wall. Stroke 2014; 45: 2330–2334. 6. van der Kolk AG, Zwanenburg JJM, Brundel M, et al. Intracranial vessel wall imaging at 7.0-T MRI. Stroke 2011; 42: 2478–2484. 7. Kurre W, Pe´rez MA, Horvath D, et al. Does mechanical thrombectomy in acute embolic stroke have long-term side effects on intracranial vessels? An angiographic follow-up study. Cardiovasc Intervent Radiol 2013; 36: 629–636. 8. Lee VH. Medical management of intracranial atherosclerotic stenosis. Open Atherosclerosis Thromb J 2010; 3: 16–23. 9. Komotar RJ, Kellner CP, Raper DM, et al. Update on the natural history of intracranial atherosclerotic disease: A critical review. World J Radiol 2010; 2: 166–171. 10. Vos J, de Feyter PJ, Kingmaf JH, et al. Evolution of coronary atherosclerosis in patients with mild coronary artery disease studied by serial quantitative coronary angiography at 2 and 4 years follow-up. Eur Heart J 1997; 18: 1081–1089.
