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Intracranial Atherosclerotic Disease

DOI: 10.4061/2011/282845

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Intracranial atherosclerotic disease (ICAD) is the most common proximate mechanism of ischemic stroke worldwide. Approximately half of those affected are Asians. For diagnosis of ICAD, intra-arterial angiography is the gold standard to identify extent of stenosis. However, noninvasive techniques including transcranial ultrasound and MRA are now emerging as reliable modalities to exclude moderate to severe (50%–99%) stenosis. Little is known about measures for primary prevention of the disease. In terms of secondary prevention of stroke due to intracranial atherosclerotic stenosis, aspirin continues to be the preferred antiplatelet agent although clopidogrel along with aspirin has shown promise in the acute phase. Among Asians, cilostazol has shown a favorable effect on symptomatic stenosis and is of benefit in terms of fewer bleeds. Moreover, aggressive risk factor management alone and in combination with dual antiplatelets been shown to be most effective in this group of patients. Interventional trials on intracranial atherosclerotic stenosis have so far only been carried out among Caucasians and have not yielded consistent results. Since the Asian population is known to be preferentially effected, focused trials need to be performed to establish treatment modalities that are most effective in this population. 1. Introduction 1.1. Epidemiology Intracranial atherosclerotic stenosis of the major arteries (intracranial internal carotid artery, middle cerebral artery, vertebral artery, and basilar artery) is the most common proximate mechanism of ischemic stroke worldwide [1]. It causes 30% to 50% of strokes in Asians [2] and 8% to 10% of strokes in North American Caucasians [3]. Intracranial atherosclerotic disease, ICAD, defined as atherosclerosis of the large arteries at the base of the brain, preferentially affects Asians, Hispanics, Far East Asians, and Blacks as compared to carotid bifurcation disease [3–6]. Also, about 20%–45% of non-Caucasians with large artery disease have combined extracranial and intracranial lesions [7–10]. The prevalence of atherosclerotic stenosis by subtype and race is further reported in Table 1. Table 1: Prevalence of intracranial atherosclerotic disease/extracranial atherosclerotic disease by race. 2. Predisposing Factors for ICAD in Susceptible Populations 2.1. Racial Associations Sacco et al. [3] found no difference between races in the proportion of patients with extracranial atherosclerotic stroke, while intracranial atherosclerosis was seen more frequently in African American and Hispanic subjects than in Caucasian

References

[1]  P. B. Gorelick, K. S. Wong, H. J. Bae, and D. K. Pandey, “Large artery intracranial occlusive disease: a large worldwide burden but a relatively neglected frontier,” Stroke, vol. 39, no. 8, pp. 2396–2399, 2008.
[2]  L. K. Wong, “Global burden of intracranial atherosclerosis,” International Journal of Stroke, vol. 1, no. 3, pp. 158–159, 2006.
[3]  R. L. Sacco, D. Kargman, Q. Gu, and M. C. Zamanillo, “Race-ethnicity and determinants of intracranial atherosclerotic cerebral infarction: the Northern Manhattan Stroke Study,” Stroke, vol. 26, no. 1, pp. 14–20, 1995.
[4]  L. R. Caplan, P. B. Gorelick, and D. B. Hier, “Race, sex and occlusive cerebrovascular disease: a review,” Stroke, vol. 17, no. 4, pp. 648–655, 1986.
[5]  K. Nishimaru, L. C. McHenry Jr., and J. F. Toole, “Cerebral angiographic and clinical differences in carotid system transient ischemic attacks between American Caucasian and Japanese patients,” Stroke, vol. 15, no. 1, pp. 56–59, 1984.
[6]  E. Feldmann, N. Daneault, E. Kwan et al., “Chinese-white differences in the distribution of occlusive cerebrovascular disease,” Neurology, vol. 40, no. 10, pp. 1541–1545, 1990.
[7]  P. McGarry, L. A. Solberg, M. A. Guzman, and J. P. Strong, “Cerebral atherosclerosis in New Orleans. Comparisons of lesions by age, sex, and race,” Laboratory Investigation, vol. 52, no. 5, pp. 533–539, 1985.
[8]  M. T. Garcia-Rondon and Y. Reyes-Iglesias, “Cerebral angiographic findings and risk factor profile in a hispanic male population,” Annals of Neurology, vol. 42, p. 440, 1997.
[9]  S. Y. Leung, T. H. K. Ng, S. T. Yuen, I. J. Lauder, and F. C. S. Ho, “Pattern of cerebral atherosclerosis in Hong Kong Chinese: severity in intracranial and extracranial vessels,” Stroke, vol. 24, no. 6, pp. 779–786, 1993.
[10]  S. J. Lee, S. J. Cho, H. S. Moon et al., “Combined extracranial and intracranial atherosclerosis in Korean patients,” Archives of Neurology, vol. 60, no. 11, pp. 1561–1564, 2003.
[11]  M. Moussouttas, L. Aguilar, K. Fuentes et al., “Cerebrovascular disease among patients from the Indian subcontinent,” Neurology, vol. 67, no. 5, pp. 894–896, 2006.
[12]  D. A. de Silva, F.-P. Woon, M.-P. Lee, C. P. L. H. Chen, H.-M. Chang, and M.-C. Wong, “South Asian patients with ischemic stroke: intracranial large arteries are the predominant site of disease,” Stroke, vol. 38, no. 9, pp. 2592–2594, 2007.
[13]  R. J. Wityk, D. Lehman, M. Klag, J. Coresh, H. Ahn, and B. Litt, “Race and sex differences in the distribution of cerebral atherosclerosis,” Stroke, vol. 27, no. 11, pp. 1974–1980, 1996.
[14]  Y. N. Huang, S. Gao, S. W. Li et al., “Vascular lesions in Chinese patients with transient ischemic attacks,” Neurology, vol. 48, no. 2, pp. 524–525, 1997.
[15]  Y. D. Kim, H. Y. Choi, H. J. Cho et al., “Increasing frequency and burden of cerebral artery atherosclerosis in Korean stroke patients,” Yonsei Medical Journal, vol. 51, no. 3, pp. 318–325, 2010.
[16]  N. C. Suwanwela and A. Chutinetr, “Risk factors for atherosclerosis of cervicocerebral arteries: intracranial versus extracranial,” Neuroepidemiology, vol. 22, no. 1, pp. 37–40, 2003.
[17]  S. P. Waddy, G. Cotsonis, M. J. Lynn et al., “Racial differences in vascular risk factors and outcomes of patients with intracranial atherosclerotic arterial stenosis,” Stroke, vol. 40, no. 3, pp. 719–725, 2009.
[18]  T. Uehara, M. Tabuchi, T. Hayashi, H. Kurogane, and A. Yamadori, “Asymptomatic occlusive lesions of carotid and intracranial arteries in Japanese patients with ischemic heart disease: evaluation by brain magnetic resonance angiography,” Stroke, vol. 27, no. 3, pp. 393–397, 1996.
[19]  L. A. Solberg and P. A. McGarry, “Cerebral atherosclerosis in Negroes and Caucasians,” Atherosclerosis, vol. 16, no. 2, pp. 141–154, 1972.
[20]  W. Mak, T. S. Cheng, K. H. Chan, R. T. F. Cheung, and S. L. Ho, “A possible explanation for the racial difference in distribution of large-arterial cerebrovascular disease: ancestral European settlers evolved genetic resistance to atherosclerosis, but confined to the intracranial arteries,” Medical Hypotheses, vol. 65, no. 4, pp. 637–648, 2005.
[21]  K. Asplund, “Antioxidant vitamins in the prevention of cardiovascular disease: a systematic review,” Journal of Internal Medicine, vol. 251, no. 5, pp. 372–392, 2002.
[22]  D. P. Vivekananthan, M. S. Penn, S. K. Sapp, et al., “Use of antioxidant vitamins for the prevention of cardiovascular disease: metaanalysis of randomized trials,” The Lancet, vol. 361, no. 9374, pp. 2017–2023, 2003.
[23]  J. Moossy, “Development of cerebral atherosclerosis in various age groups,” Neurology, vol. 9, pp. 569–574, 1959.
[24]  A. Elbaz and P. Amarenco, “Genetic susceptibility and ischemic stroke,” Current Opinion in Neurology, vol. 12, no. 1, pp. 47–55, 1999.
[25]  A. Hassan and H. S. Markus, “Genetics and ischaemic stroke,” Brain, vol. 123, pp. 1784–1812, 2000.
[26]  F. J. Carr, M. W. McBride, H. V. O. Carswell et al., “Genetic aspects of stroke: human and experimental studies,” Journal of Cerebral Blood Flow and Metabolism, vol. 22, no. 7, pp. 767–773, 2002.
[27]  S. Kunitz, C. Gross, A. Heyman, et al., “The pilot stroke data bank: definition, design, and data,” Stroke, vol. 15, no. 4, pp. 740–746, 1984.
[28]  I. Holme, S. C. Enger, A. Helgeland, et al., “Risk factors and raised atherosclerotic lesions in coronary and cerebral arteries. Statistical analysis from the Oslo study,” Arteriosclerosis, vol. 1, no. 4, pp. 250–256, 1981.
[29]  P. B. Gorelick, L. R. Caplan, D. B. Hier, S. L. Parker, and D. Patel, “Racial differences in the distribution of anterior circulation occlusive disease,” Neurology, vol. 34, no. 1, pp. 54–59, 1984.
[30]  O. Y. Bang, J. W. Kim, J. H. Lee et al., “Association of the metabolic syndrome with intracranial atherosclerotic stroke,” Neurology, vol. 65, no. 2, pp. 296–298, 2005.
[31]  F. Rincon, R. L. Sacco, G. Kranwinkel, et al., “Incidence and risk factors of intracranial atherosclerotic stroke: the Northern Manhattan Stroke Study,” Cerebrovascular Diseases, vol. 28, no. 1, pp. 65–71, 2009.
[32]  T. N. Turan, A. A. Makki, S. Tsappidi et al., “Risk factors associated with severity and location of intracranial arterial stenosis,” Stroke, vol. 41, no. 8, pp. 1636–1640, 2010.
[33]  K. S. Wong, S. Gao, Y. L. Chan et al., “Mechanisms of acute cerebral infarctions in patients with middle cerebral artery stenosis: a diffusion-weighted imaging and microemboli monitoring study,” Annals of Neurology, vol. 52, no. 1, pp. 74–81, 2002.
[34]  A. E. Baird, K. O. L?vblad, G. Schlaug, R. R. Edelman, and S. Warach, “Multiple acute stroke syndrome: marker of embolic disease?” Neurology, vol. 54, no. 3, pp. 674–678, 2000.
[35]  J. Bogousslavsky and F. Regli, “Borderzone infarctions distal to internal carotid artery occlusion: prognostic implications,” Annals of Neurology, vol. 20, no. 3, pp. 346–350, 1986.
[36]  M. del Sette, M. Eliasziw, J. Y. Streifler, V. C. Hachinski, A. J. Fox, and H. J. Barnett, “Internal borderzone infarction: a marker for severe stenosis in patients with symptomatic internal carotid artery disease,” Stroke, vol. 31, no. 3, pp. 631–636, 2000.
[37]  L. R. Caplan, “Intracranial branch atheromatous disease: a neglected, understudied, and underused concept,” Neurology, vol. 39, no. 9, pp. 1246–1250, 1989.
[38]  H. P. Adams, H. C. Damasio, S. F. Putman, and A. R. Damasio, “Middle cerebral artery occlusion as a cause of isolated subcortical infarction,” Stroke, vol. 14, no. 6, pp. 948–952, 1983.
[39]  C. M. Fisher, “Capsular infarcts. the underlying vascular lesions,” Archives of Neurology, vol. 36, no. 2, pp. 65–73, 1979.
[40]  D. K. Lee, J. S. Kim, S. U. Kwon, S.-H. Yoo, and D.-W. Kang, “Lesion patterns and stroke mechanism in atherosclerotic middle cerebral artery disease: early diffusion-weighted imaging study,” Stroke, vol. 36, no. 12, pp. 2583–2588, 2005.
[41]  L. C. Turtzo, R. F. Gottesman, and R. H. Llinas, “Diffusion-weighted imaging showing “Pearls” predicts large-vessel disease as stroke etiology,” Cerebrovascular Diseases, vol. 28, no. 1, pp. 49–54, 2009.
[42]  H. Yamauchi, R. Nish, T. Higashi, S. Kagawa, and H. Fukuyama, “Hemodynamic compromise as a cause of internal border-zone infarction and cortical neuronal damage in atherosclerotic middle cerebral artery disease,” Stroke, vol. 40, no. 12, pp. 3730–3735, 2009.
[43]  C. P. Derdeyn, W. J. Powers, and R. L. Grubb Jr., “Hemodynamic effects of middle cerebral artery stenosis and occlusion,” American Journal of Neuroradiology, vol. 19, no. 8, pp. 1463–1469, 1998.
[44]  D. W. Kang, J. A. Chalela, M. A. Ezzeddine, and S. Warach, “Association of ischemic lesion patterns on early diffusion-weighted imaging with TOAST stroke subtypes,” Archives of Neurology, vol. 60, no. 12, pp. 1730–1734, 2003.
[45]  J. Bogousslavsky, “Double infarction in one cerebral hemisphere,” Annals of Neurology, vol. 30, no. 1, pp. 12–18, 1991.
[46]  P. T. Akins, T. K. Pilgram, D. T. Cross III, and C. J. Moran, “Natural history of stenosis from intracranial atherosclerosis by serial angiography,” Stroke, vol. 29, no. 2, pp. 433–438, 1998.
[47]  S. U. Kwon, Y. J. Cho, J. S. Koo, et al., “Cilostazol prevents the progression of the symptomatic intracranial arterial stenosis: the multicenter double-blind placebo-controlled trial of cilostazol symptomatic intracranial arterial stenosis,” Stroke, vol. 36, no. 4, pp. 782–786, 2005.
[48]  S. U. Kwon, D. W. Kang, J. M. Park, et al., “Trial of efficacy and safety of cilostazol on the progression of symptomatic intracranial stenosis comparing clopidogrel: trial of cilostazol in symptomatic intracranial stenosis-2 (TOSS-2),” Cerebrovascular Diseases, vol. 27, supplement 6, pp. 10–11, 2009.
[49]  M. I. Chimowitz, M. J. Lynn, H. Howlett-Smith et al., “Comparison of warfarin and aspirin for symptomatic intracranial arterial stenosis,” The New England Journal of Medicine, vol. 352, no. 13, pp. 1305–1316, 2005.
[50]  S. E. Kasner, M. I. Chimowitz, M. J. Lynn et al., “Predictors of ischemic stroke in the territory of a symptomatic intracranial arterial stenosis,” Circulation, vol. 113, no. 4, pp. 555–563, 2006.
[51]  M. Mazighi, R. Tanasescu, X. Ducrocq et al., “Prospective study of symptomatic atherothrombotic intracranial stenoses: the GESICA study,” Neurology, vol. 66, no. 8, pp. 1187–1191, 2006.
[52]  D. S. Liebeskind, G. A. Cotsonis, J. L. Saver, et al., “Collateral dramatically alter stroke risk in intracranial atherosclerosis,” Annals of Neurology, vol. 69, no. 6, pp. 963–974, 2011.
[53]  J. T. Fifi, P. M. Meyers, S. D. Lavine et al., “Complications of modern diagnostic cerebral angiography in an academic medical center,” Journal of Vascular and Interventional Radiology, vol. 20, no. 4, pp. 442–447, 2009.
[54]  S. M. Debrey, H. Yu, J. K. Lynch, et al., “Diagnostic accuracy of magnetic resonance angiography for internal carotid artery disease: a systematic review and meta-analysis,” Stroke, vol. 39, no. 8, pp. 2237–2248, 2008.
[55]  J. E. Heiserman, B. P. Drayer, P. J. Keller, et al., “Intracranial vascular stenosis and occlusion: evaluation with three-dimensional time-of-flight MR angiography,” Radiology, vol. 185, no. 3, pp. 667–673, 1992.
[56]  Y. Korogi, M. Takahashi, N. Mabuchi et al., “Intracranial vascular stenosis and occlusion: diagnostic accuracy of three-dimensional, fourier transform, time-of-flight MR angiography,” Radiology, vol. 193, no. 1, pp. 187–193, 1994.
[57]  C. G. Choi, D. H. Lee, J. H. Lee et al., “Detection of intracranial atherosclerotic steno-occlusive disease with 3D time-of-flight magnetic resonance angiography with sensitivity encoding at 3T,” American Journal of Neuroradiology, vol. 28, no. 3, pp. 439–446, 2007.
[58]  J. F. Arenillas, “Intracranial atherosclerosis: current concepts,” Stroke, vol. 42, supplement 1, pp. S20–S23, 2011.
[59]  S. Bash, J. P. Villablanca, R. Jahan et al., “Intracranial vascular stenosis and occlusive disease: evaluation with CT angiography, MR angiography, and digital subtraction angiography,” American Journal of Neuroradiology, vol. 26, no. 5, pp. 1012–1021, 2005.
[60]  E. Feldmann, J. L. Wilterdink, A. Kosinski et al., “The stroke outcomes and neuroimaging of intracranial atherosclerosis (SONIA) trial,” Neurology, vol. 68, no. 24, pp. 2099–2106, 2007.
[61]  G. Fürst, A. Saleh, F. Wenserski et al., “Reliability and validity of noninvasive imaging of internal carotid artery pseudo-occlusion,” Stroke, vol. 30, no. 7, pp. 1444–1449, 1999.
[62]  A. M. Demchuk, I. Christou, T. H. Wein et al., “Accuracy and criteria for localizing arterial occlusion with transcranial doppler,” Journal of Neuroimaging, vol. 10, no. 1, pp. 1–12, 2000.
[63]  International Stroke Trial Collaborative Group, “The International Stroke Trial (IST): a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke,” The Lancet, vol. 349, no. 9065, pp. 1569–1581, 1997.
[64]  Z.-M. Chen, “CAST: randomised placebo-controlled trial of early aspirin use in 20,000 patients with acute ischaemic stroke,” The Lancet, vol. 349, no. 9066, pp. 1641–1649, 1997.
[65]  S. E. Kasner, M. J. Lynn, M. I. Chimowitz, et al., “Warfarin aspirin symptomatic intracranial disease (WASID) trial investigators. Warfarin vs aspirin for symptomatic intracranial stenosis: subgroup analyses from WASID,” Neurology, vol. 67, no. 7, pp. 1275–1278, 2006.
[66]  H. C. Diener, L. Cunha, C. Forbes, J. Sivenius, P. Smets, and A. Lowenthal, “European stroke prevention study 2. Dipyridamole and acetylsalicylic acid in the secondary prevention of stroke,” Journal of the Neurological Sciences, vol. 143, no. 1-2, pp. 1–13, 1996.
[67]  CAPRIE Steering Committee, “A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE),” The Lancet, vol. 348, no. 9038, pp. 1329–1339, 1996.
[68]  R. L. Sacco, H. C. Diener, S. Yusuf, et al., “Aspirin and extended-release dipyridamole versus clopidogrel for recurrent stroke,” The New England Journal of Medicine, vol. 359, no. 12, pp. 1238–1251, 2008.
[69]  R. J. Adams, G. Albers, M. J. Alberts, et al., “Update to the AHA/ASA recommendations for the prevention of stroke in patients with stroke and transient ischemic attack,” Stroke, vol. 39, no. 5, pp. 1647–1652, 2008.
[70]  K. Wong, C. Chen, J. Fu et al., “Clopidogrel plus aspirin versus aspirin alone for reducing embolisation in patients with acute symptomatic cerebral or carotid artery stenosis (CLAIR study): a randomised, open-label, blinded-endpoint trial,” The Lancet Neurology, vol. 9, no. 5, pp. 489–497, 2010.
[71]  Y. Huang, Y. Cheng, J. Wu et al., “Cilostazol as an alternative to aspirin after ischaemic stroke: a randomised, double-blind, pilot study,” The Lancet Neurology, vol. 7, no. 6, pp. 494–499, 2008.
[72]  Y. Shinohara, Y. Katayama, S. Uchiyama et al., “Cilostazol for prevention of secondary stroke (CSPS 2): an aspirin-controlled, double-blind, randomised non-inferiority trial,” The Lancet Neurology, vol. 9, no. 10, pp. 959–968, 2010.
[73]  S. Chaturvedi, T. N. Turan, M. J. Lynn et al., “Risk factor status and vascular events in patients with symptomatic intracranial stenosis,” Neurology, vol. 69, no. 22, pp. 2063–2068, 2007.
[74]  T. N. Turan, G. Cotsonis, M. J. Lynn, S. Chaturvedi, and M. Chimowitz, “Relationship between blood pressure and stroke recurrence in patients with intracranial arterial stenosis,” Circulation, vol. 115, no. 23, pp. 2969–2975, 2007.
[75]  P. Amarenco, J. Bogousslavsky, A. Callahan III, et al., “High-dose atorvastatin after stroke or transient ischemic attack,” The New England Journal of Medicine, vol. 355, no. 6, pp. 549–559, 2006.
[76]  B. Ovbiagele, J. L. Saver, M. J. Lynn, and M. Chimowitz, “Impact of metabolic syndrome on prognosis of symptomatic intracranial atherostenosis,” Neurology, vol. 66, no. 9, pp. 1344–1349, 2006.
[77]  T. M. Sundt Jr., H. C. Smith, J. K. Campbell, et al., “Transluminal angioplasty for basilar artery stenosis,” Mayo Clinic Proceedings, vol. 55, no. 11, pp. 673–680, 1980.
[78]  T. N. Turan, C. P. Derdeyn, D. Fiorella, and M. I. Chimowitz, “Treatment of atherosclerotic intracranial arterial stenosis,” Stroke, vol. 40, no. 6, pp. 2257–2261, 2009.
[79]  M. P. Marks, J. C. Wojak, F. Al-Ali et al., “Angioplasty for symptomatic intracranial stenosis: clinical outcome,” Stroke, vol. 37, no. 4, pp. 1016–1020, 2006.
[80]  M. Hartmann and O. Jansen, “Angioplasty and stenting of intracranial stenosis,” Current Opinion in Neurology, vol. 18, no. 1, pp. 39–45, 2005.
[81]  SSYLVIA Study Investigators, “Stenting of symptomatic atherosclerotic lesions in the vertebral or intracranial arteries (SSYLVIA): study results,” Stroke, vol. 35, no. 6, pp. 1388–1392, 2004.
[82]  A. Bose, M. Hartmann, H. Henkes et al., “A novel, self-expanding, nitinol stent in medically refractory intracranial atherosclerotic stenoses: the wingspan study,” Stroke, vol. 38, no. 5, pp. 1531–1537, 2007.
[83]  O. O. Zaidat, R. Klucznik, M. J. Alexander et al., “The NIH registry on use of the wingspan stent for symptomatic 70–99% intracranial arterial stenosis,” Neurology, vol. 70, no. 17, pp. 1518–1524, 2008.
[84]  A. I. Qureshi, J. F. Kirmani, H. M. Hussein, et al., “Early and intermediate-term outcomes with drug-eluting stents in high-risk patients with symptomatic intracranial stenosis,” Neurosurgery, vol. 59, no. 5, pp. 1044–1051, 2006.
[85]  R. Gupta, F. Al-Ali, A. J. Thomas et al., “Safety, feasibility, and short-term follow-up of drug-eluting stent placement in the intracranial and extracranial circulation,” Stroke, vol. 37, no. 10, pp. 2562–2566, 2006.
[86]  F. Siddiq, G. Vazquez, M. Z. Memon et al., “Comparison of primary angioplasty with stent placement for treating symptomatic intracranial atherosclerotic diseases: a multicenter study,” Stroke, vol. 39, no. 9, pp. 2505–2510, 2008.
[87]  F. Siddiq, M. Z. Memon, G. Vazquez, A. Safdar, and A. I. Qureshi, “Comparison between primary angioplasty and stent placement for symptomatic intracranial atherosclerotic disease: meta-analysis of case series,” Neurosurgery, vol. 65, no. 6, pp. 1024–1033, 2009.
[88]  A. L. Jarvis, M. Chimowitz, M. J. Lynn, et al., “Outcome of patients with 50–99% intracranial stenosis and TIA or stroke on antithrombotic therapy treated medically vs. stenting,” in Proceedings of the 60th Annual Meeting of the American Academy of Neurology, Chicago, Ill, USA, April 2008.
[89]  C. P. Derdeyn and M. I. Chimowitz, “Angioplasty and stenting for atherosclerotic intracranial stenosis: rationale for a randomized clinical trial,” Neuroimaging Clinics of North America, vol. 17, no. 3, pp. 355–363, 2007.
[90]  K. Dmyterko Jr., “SAMMPRIS trial halted after high risk of stroke/death found,” Industry News, April 2011.
[91]  R. L. Grubb Jr., W. J. Powers, C. P. Derdeyn, H. P. Adams Jr., and W. R. Clarke, “The carotid occlusion surgery study,” Neurosurgical Focus, vol. 14, no. 3, p. e9, 2003.
[92]  S. Mizumura, J. Nakagawara, M. Takahashi et al., “Three-dimensional display in staging hemodynamic brain ischemia for JET study: objective evaluation using SEE analysis and 3D-SSP display,” Annals of Nuclear Medicine, vol. 18, no. 1, pp. 13–21, 2004.
[93]  W.-J. Jiang, X.-T. Xu, M. Jin, B. Du, K.-H. Dong, and J.-P. Dai, “Apollo stent for symptomatic atherosclerotic intracranial stenosis: study results,” American Journal of Neuroradiology, vol. 28, no. 5, pp. 830–834, 2007.
[94]  W. Kurre, J. Berkefeld, M. Sitzer, T. Neumann-Haefelin, and R. du Mesnil de Rochemont, “Treatment of symptomatic high-grade intracranial stenoses with the balloon-expandable Pharos stent: initial experience,” Neuroradiology, vol. 50, no. 8, pp. 701–708, 2008.
[95]  The EC/IC Bypass Study Group, “Failure of extracranial-intracranial arterial bypass to reduce the risk of ischemic Stroke. Results of an international randomized trial,” The New England Journal of Medicine, vol. 313, no. 19, pp. 1191–1200, 1985.

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