J Neurosurg 76:520-523, 1992
Resolution of petrous internal carotid artery stenosis after transluminal angioplasty Case report ROBF~RT C. ROSTOMIIA', M.D., MaRc R. MAYBERG, M.D., Josr:Pn M. ESKRIDGE, M.D., ROBERT GOODKIN, M.D., AND H. RICHARD WINN, M , D .
Departments ~?fNeurological Surgery and Radiology, University of Washington, Seattle Veterans /l[kfirs Medical Center, Seattle, H/ashington u.- Percutaneous transluminal angioplasty is commonly used for treatment of peripheral vascular disease, but only recently has it been applied to craniocervical lesions. The successful use of perculaneous transluminal angioplasty for treatment of an isolated high-grade stenosis of the petrous internal carotid artery is described in a patient with progressive ischemic symptoms despite maximum medical management. At his 2-year followup examination, the patient remained asymptomatic with angiographic evidence of progressive resolution of the stenofic lesion and indirect evidence of improved hemispheric blood flow ipsilateral to the lesion. Percutaneous transluminal angioplasty may provide an effective means of treatment for selective intracranial atherosclerotic stenosis. KEY WORDS 9 angioplasty transient ischemic attack
p
9 internal carotid artery
ERCUTANEOUS transluminal angioplasty has only recently been utilized for dilatation of stenotic lesions involving the supra-aortic vessels. Advances in catheter technology have reduced morbidity from distal embolism and have enabled cannulation of smaller distal intracranial vessels. Successful percutaneous transluminal angioplasty dilatation has been reported for basilar and vertebral stenoses,' ''-~'22extracranial carotid lesionsy 3-2s and vasospasm after subarachnoid hemorrhage (SAH); U~ however, there are few reported cases of percutaneous transluminal angioplasty for atherosderotic stenoses of the pelrous or intraeranial portion of the internal carotid avery (ICA) or distal cerebral vessels.~~8 l ntracranial ICA stenosis due to atherosclerosis has been associated with significant stroke and mortality rates, particularly if the lesion is symptomatic or exists in tandem with extracranial ICA stenosis) .j4 Although extracranial-to-intracranial artery bypass procedures have been utilized previously for these lesions, a randomized prospective trial demonstrated no benefit for this procedure. 6 We report the use of percutaneous transluminal angioplasty as an interventional option for treatment of a symptomatic left intrapetrous ICA stenosis. At 2 years 520
9
ischemia
9 atherosclerosis
9
postdilatation, the patient remained asymptomatic and angiographic studies demonstrated progressive improvement of the stenosis, displaying evidence of increased perfusion in the distribution of the original lesion. While intracranial ICA stenosis signifies advanced systemic atherosclerotic vascular disease and an overall poor prognosis, T M a select group of patients with stable systemic disease and symptoms referable to a surgically inaccessible ICA lesion may benefit from percutaneous transluminal angioplasty. Case Report
This 68-year-old man presented to the Seattle Veterans Affairs Medical Center in June, 1988, with a 12month history, of progressive transient cerebral and retinal ischemia relating to the left ICA circulation. These spells included multiple episodes of transient numbness and weakness in the right arm, dysarthria, and left monocular blindness lasting minutes to hours. Examination. Neurological examination showed normal function between episodes. Carotid artery, duplex examination revealed decreased flow through the left cervical ICA without focal stenosis, consistent with J. Neurosurg. / Vo&me 76 / March, 1992
Transluminal angioplasty
FIG. 1. Preoperativeleft carotid artery angiograms, lateral (left) and anterior (right) views, showing high-grade stenosis (arrows) in the petrous portion of the internal carotid artery (ICA). Note that filling from the left ICA is limited to the left middle cerebral artery territory.
a distal flow-restrictive lesion. Cerebral angiographic studies demonstrated a focal 95% stenosis of the left intrapetrous ICA, which filled the left middle cerebral artery (MCA) territory only (Fig. 1). Computerized tomography scans revealed a left thalamic infarct of indeterminate age. Echocardiography did not identify a potential source for cerebral emboli. Transient ischemic episodes became increasingly frequent, involving both the left middle cerebral and the retinal circulations. Anticoagulation therapy with heparin or warfarin did not significantly reduce the frequency of ischemic episodes. Operation. On July, 26, 1988, percutaneous transluminal angioplasty of the left petrous ICA was performed. After administration of 10,000 U heparin, the Iesion was dilated in stages. Under routine fluoroscopic guidance, 3- and 4-ram angioplasty balloons* were sequentially inserted via a transfemoral approach. Total balloon inflation time was less than 1 minute. Stenosis was reduced from 95% to less than 40% (Fig. 2). Immediately following angioplasty, the patient was maintained on systemic heparin, which was then changed to warfarin anticoagulation therapy for 6 weeks. Postoperative Course. In the 2 years since percutaneous transluminal angioplasty, the patient has remained asymptomatic on a low-dose aspirin regimen. Serial carotid artery duplex and transcranial Doppler ultrasound (TDC) evaluations show normal blood flow through the extracranial and intracranial ICA on the left. Because sequential carotid artery duplex examinations revealed rapid progression of a right cervical ICA stenosis from 1% to 99% over a 10-month period, repeat angiographic studies were performed in June, 1990. Compared to those made immediately after percutaneous transluminal angioplasty, the new angio* Angioplasty balloons manufactured by ACS, Temecula, California.
J. Neurosurg. / Volume 76 /March, 1992
FIG. 2. Postoperativeleft carotid artery angiogram, lateral projection, immediately after angioplasty demonstrating reduction in stenosis (arrow) from 95% to less than 40%.
grams demonstrated improvement of the previously dilated left petrous carotid artery stenosis from about 40% to 20%, with remodeling at the angioplasty site; the left anterior cerebral artery was now shown to be filling from the left ICA (Fig. 3). Discussion
Both symptomatic and asymptomatic intracranial ICA stenoses (with and without tandem cervical ICA stenosis) have been associated with a high rate of morbidity and mortality from stroke and myocardial infarction?'t5 In these studies, stroke and transient ischemic attacks had a higher incidence in the territory of the intracranial ICA lesion. Tandem intracranial and extracranial stenoses have been associated with a higher
FIG. 3. Postoperative internal carotid artery (ICA) angiograms, lateral (left) and anterior (right) views, 2 years after angioplasty demonstrating a further increase in vessel caliber from 40% to 20% stenosis (arrows). The left ICA now fills both the middle cerebralartery and the anterior cerebralartery distributions. 521
R. C. Rostomily, et al. risk for ischemic events than has intracranial stenosis alone. 14The severity of intracranial stenosis in patients treated surgically for carotid bifurcation disease does not appear to influence the incidence of immediate or delayed ischemic symptoms following endarterectomy) 9'2~ Therefore, carotid endarterectomy has been advocated as the initial treatment in symptomatic tandem lesions. The report of a case in which ICA siphon stenosis resolved after carotid endarterectomy for tandem stenosis underscores the rationale for this approachJ However, in the absence of effective surgical measures, therapeutic options are limited for patients with isolated symptomatic intracranial ICA lesions who fail conservative medical treatment. The present report describes the successful use of percutaneous transluminal angioplasty for treatment of isolated symptomatic intracranial ICA stenosis with a 2-year symptom-free follow-up period and angiographic confirmation of a progressively resolving lesion. To our knowledge, only two case reports have described the use of percutaneous transluminal angioplasty for symptomatic atheromatous intracranial ICA lesions] 6'~s In one case, clinical improvement in ischemic symptoms was noted after angioplasty of a cavernous carotid artery lesion, 16 but no angiographic follow-up study was provided. A recent case report described the percutaneous transluminal angioplasty of a symptomatic atheromatous MCA stenosis with evidence of clinical and hemodynamic improvement, despite early anglographic evidence of restenosis) s In the present case, repeat angiographic studies revealed evidence of improved hemodynamic status in the left ICA distribution in response to progressive stenosis of the contralateral ICA, and showed an enlarged caliber of the previously dilated pe~rous carotid artery segment. The introduction of percutaneous transluminal angioplasty in 1964 by Dotter and Judkins s provided a noninvasive alternative for the treatment of occlusive vascular disease. Although primarily used for distal lower-extremity and coronary stenoses, percutaneous transluminal angioplasty has only recently been advocated for use on the extracranial and intracranial vasculature. 9,jl'~6,~s'2~-25 In symptomatic vasospasm after SAH, this procedure has been shown to provide longstanding increases in vessel caliber as demonstrated by angiography L~~ and by decreased TCD velocity) 'j~ However, its potential efficacy and the natural history of intracranial atheromatous lesions dilated by percutaneous transluminal angioplasty can only be inferred from experience with other vascular territories. In coronary vessels, percutaneous transluminal angioplasty has been associated with acute occlusion rates of 2% to 4% and delayed restenosis in up to 30% of cases, usually within the first 6 months] 2'~7Certain risk factors for restenosis, such as stenosis location at vessel angulations, have been identified and may be helpful in considering candidates for future cerebral percutaneous transluminal angioplasty. 7,~2Dilatation of coronary vessels by this procedure is considered to be me522
diated by "plaque-splitting, '~3"~7which then allows for stretching of the media and adventitia. Fisher, etal., ~ analyzed atherosclerotic changes in human cerebral vasculature at autopsy, and showed a predilection for stenosis in the carotid siphon with flat, often calcified, atheromatous plaques. Whether these atheromatous changes in intracranial vessels would respond to percutaneous transluminal angioplasty through a mechanism similar to that shown for coronary vessels is unknown. Currently, only preliminary experimental work has been performed with this procedure on normal intracranial vessels in animals. 2 Advances in catheter technology have reduced the risks of distal embolism during percutaneous transluminal angioplasty; nevertheless, greater experience is needed to confirm the safety and efficacy of this procedure in preventing stroke related to a stenotic lesion of the intracranial ICA. Subsequent to the case presented here, we have performed angioplasty on four patients with assorted intracranial (three cases) and extracranial carotid artery (one case) lesions, with only one complication of an asymptomatie ICA dissection, which healed. In two of these four patients, angioplasty was unsuccessful due to the technical limitations of the catheter. The advent of a new Food and Drug Administration-approved microcathetert should facilitate safe cannulation of distal intracranial vessels. Patient selection will also play an important role in the success of future attempts at percutaneous transluminal angioplasty for intracranial atherosclerotic disease. The selection process may be facilitated by cerebral blood flow estimates and assessments of circulatory reserve to confirm a hemodynamically significant lesion prior to percutaneous transluminal angioplasty. Followup blood flow studies could then be correlated with clinical and angiographically determined changes to characterize the factors that influence outcome. Further experimental work and analysis of pathological material may hello to establish whether clinical improvement is based on increased vessel caliber and concomitant hemodynamic changes alone or whether an alteration of plaque morphology occurs, which reduces embolic risk as well. This report establishes the potential application of percutaneous transluminal angioplasty for the treatment of isolated symptomatic focal intracranial ICA stenosis in a patient who failed medical therapy. In a similar group of patients at high risk for stroke, percutaneous transluminal angioplasty may provide long-standing maintenance of adequate vessel caliber with a concomitant improvement in hemodynamic status. References
1. BracardS, Picard L, Marchal JC, et al: Role ofangioplasty in the treatment of symptomatic vascular spasm occurring in the post-operativecourse of intracranial ruptured aneurysms. J Neuroradiol 17:6-19, 1990 1"Microcathetermanufactured by Target Therapeutics, Los Angeles, California. J. Neurosurg. / Volume 76/March, 1992
Transluminal angioplasty 2. Chavez L, Takahashi A, Yoshimoto T, el al: Morphological changes in normal canine basilar arteries after transluminal angioplasty. Neurol Res 12:12-16, 1990 3. Craig DR, Meguro K, Watridge C, et at: lntracranial internal carotid artery stenosis. Stroke 13:825-828, 1982 4, Day AL, Rhoton AL, Quisling RG: Resolving siphon stenosis following endarterectomy. Stroke 11:278-281, 1980 5. Dotter CT, Judkins MP: Transluminal treatment of arteriosclerotic obstruction. Description of a new technic and a preliminary report of its application. Circulation 30:654-670, 1964 6. The EC/IC Bypass Study Group: Failure of extracranialintracranial arterial bypass to reduce the risk of ischemic stroke. Results of an international randomized trial. N Engl3 Med 313:1191-1200, 1985 7. Ellis SG, Roubin GS, King SB II1, et al: Importance of stenosis morphology in the estimation of restenosis risk after elective percutaneous transluminal coronary angioplasty. Am 3 Cardio163:30-34, 1989 8. Fisher CM, Gore I, Okabe N, et al: Atherosclerosis of the carotid and vertebral arteries - - extracranial and intracranial. 3 Neuropathol Exp Neuro124:455-476, 1965 9. Hasso AN, Bird CR, Zinke DE, et ah Fibromuscular dysplasia of the internal carotid artery. Percutaneous transluminal angioplasty. AJR 136:955-960, 198 I 10. Higashida RT, Halbach VV, Cahan LD, et al: Transluminal angioplasty for treatment of intracranial arterial vasospasm J Neurosurg 71:648-653, 1989 11. Higashida RT, Hieshima GB, Tsai FY, et al: Transluminal angioplasty of the vertebral and basilar artery. AJNR 8:745-749, 1987 12. Liu MW, Roubin GS, King SB III: Restenosis after coronary angioplasty. Potential biologic determinants and the role of intimal hyperplasia. Circolatlon 79: 1374-1387, 1989 13. Lyon RT, Zarins CK, Lu CT, et al: Vessel, plaque, and lumen morphology after transluminal balloon angioplasty. Quantitative study in distended human arteries. Arteriosclerosis 7:306-314, 1987 14, Marzewski DJ, Furlan AJ, St Louis P, et al: Intracranial internal carotid artery stenosis: long-term prognosis. Stroke 13:821-824, 1982 15. Newell DW, Eskridge JM, Mayberg MR, et al: Angioplasty for the treatment of symptomatic vasospasm following subarachnoid hemorrhage. J Neurosurg 71: 654-660, 1989
J. Neurosurg. / Volume 76/March, 1992
16. O'leary DH, Clouse ME: Percutaneous transluminal angioplasty for the cavernous carotid artery for recurrent ischemia. AJNR 5:644-645, 1984 17. Pathology of coronary angioplasty (review). Lancet 2: 423-424, 1989 18. Purdy PD, Devous MD St, Unwin DH, et al: Angioplasty of an atherosclerotic middle cerebral artery associated with improvement in regional cerebral blood flow. AJNR 11:878-880, 1990 19. Roederer GO, Langlois YE, Chan ARW, et al: Is siphon disease important in predicting outcome of carotid endarterectomy? Arch Surg 118:1177-1181, 1983 20. Schuler J J, Flanigan DP, Lira LT, et al: The effect of carotid siphon stenosis on stroke rate, death, and relief of symptoms following elective carotid endarterectomy. Surgery 92:1058-1067, 1982 21. Sundt TM Jr, Smith HC, Campbell JK, et al: Transluminal angioplasty for basilar artery stenosis. Mayo Clin Proc 55:673-680, 1980 22. Theron J, Courtheoux P, Henriet JP, et al: Angioplasty of supraaortic arteries. J Neuroradiol 11:187-200, 1984 23. Theron J, Raymond J, Casasco A, et al: Percutaneous angioplasty of atherosclerotic and postsurgical slenosis of carotid arteries. AJNR 8:495-500, 1987 24. Tsai FY, Matovich V, Hieshima G, et al: Percutaneous transluminal angioplasty of the carotid artery. AJNR 7: 349-358, 1986 25. Wiggli U, Gratzl O: Transluminal angioplasty of stenotic carotid arteries: case reports and protocol. AJNR 4: 793-795, 1983 26. Zubkov YN, Nikiforov BM, Shustin VA: Balloon catheter technique of dilatation of constricted cerebral arteries after aneurysmal SAH. Acta Nenroehir 70:65-79, 1984
Manuscript received April 15, 1991. Accepted in final form July 16, 1991. This work was supported by National Institute of Neurological Disorders and Stroke Award NESA-T32-NS07144 to Dr. Rostomily and Clinical Investigator Development Award NS1191 and National Institutes of Health Grant HL44458 to Dr. Mayberg. Address reprint requests to: Marc R. Mayberg, M.D., Department of Neurological Surgery, RI-20, University of Washington Medical Center, 1959 Northeast Pacific, Seattle, Washington 19891.
523
Resolution of petrous internal carotid artery stenosis after transluminal angioplasty Case report ROBF~RT C. ROSTOMIIA', M.D., MaRc R. MAYBERG, M.D., Josr:Pn M. ESKRIDGE, M.D., ROBERT GOODKIN, M.D., AND H. RICHARD WINN, M , D .
Departments ~?fNeurological Surgery and Radiology, University of Washington, Seattle Veterans /l[kfirs Medical Center, Seattle, H/ashington u.- Percutaneous transluminal angioplasty is commonly used for treatment of peripheral vascular disease, but only recently has it been applied to craniocervical lesions. The successful use of perculaneous transluminal angioplasty for treatment of an isolated high-grade stenosis of the petrous internal carotid artery is described in a patient with progressive ischemic symptoms despite maximum medical management. At his 2-year followup examination, the patient remained asymptomatic with angiographic evidence of progressive resolution of the stenofic lesion and indirect evidence of improved hemispheric blood flow ipsilateral to the lesion. Percutaneous transluminal angioplasty may provide an effective means of treatment for selective intracranial atherosclerotic stenosis. KEY WORDS 9 angioplasty transient ischemic attack
p
9 internal carotid artery
ERCUTANEOUS transluminal angioplasty has only recently been utilized for dilatation of stenotic lesions involving the supra-aortic vessels. Advances in catheter technology have reduced morbidity from distal embolism and have enabled cannulation of smaller distal intracranial vessels. Successful percutaneous transluminal angioplasty dilatation has been reported for basilar and vertebral stenoses,' ''-~'22extracranial carotid lesionsy 3-2s and vasospasm after subarachnoid hemorrhage (SAH); U~ however, there are few reported cases of percutaneous transluminal angioplasty for atherosderotic stenoses of the pelrous or intraeranial portion of the internal carotid avery (ICA) or distal cerebral vessels.~~8 l ntracranial ICA stenosis due to atherosclerosis has been associated with significant stroke and mortality rates, particularly if the lesion is symptomatic or exists in tandem with extracranial ICA stenosis) .j4 Although extracranial-to-intracranial artery bypass procedures have been utilized previously for these lesions, a randomized prospective trial demonstrated no benefit for this procedure. 6 We report the use of percutaneous transluminal angioplasty as an interventional option for treatment of a symptomatic left intrapetrous ICA stenosis. At 2 years 520
9
ischemia
9 atherosclerosis
9
postdilatation, the patient remained asymptomatic and angiographic studies demonstrated progressive improvement of the stenosis, displaying evidence of increased perfusion in the distribution of the original lesion. While intracranial ICA stenosis signifies advanced systemic atherosclerotic vascular disease and an overall poor prognosis, T M a select group of patients with stable systemic disease and symptoms referable to a surgically inaccessible ICA lesion may benefit from percutaneous transluminal angioplasty. Case Report
This 68-year-old man presented to the Seattle Veterans Affairs Medical Center in June, 1988, with a 12month history, of progressive transient cerebral and retinal ischemia relating to the left ICA circulation. These spells included multiple episodes of transient numbness and weakness in the right arm, dysarthria, and left monocular blindness lasting minutes to hours. Examination. Neurological examination showed normal function between episodes. Carotid artery, duplex examination revealed decreased flow through the left cervical ICA without focal stenosis, consistent with J. Neurosurg. / Vo&me 76 / March, 1992
Transluminal angioplasty
FIG. 1. Preoperativeleft carotid artery angiograms, lateral (left) and anterior (right) views, showing high-grade stenosis (arrows) in the petrous portion of the internal carotid artery (ICA). Note that filling from the left ICA is limited to the left middle cerebral artery territory.
a distal flow-restrictive lesion. Cerebral angiographic studies demonstrated a focal 95% stenosis of the left intrapetrous ICA, which filled the left middle cerebral artery (MCA) territory only (Fig. 1). Computerized tomography scans revealed a left thalamic infarct of indeterminate age. Echocardiography did not identify a potential source for cerebral emboli. Transient ischemic episodes became increasingly frequent, involving both the left middle cerebral and the retinal circulations. Anticoagulation therapy with heparin or warfarin did not significantly reduce the frequency of ischemic episodes. Operation. On July, 26, 1988, percutaneous transluminal angioplasty of the left petrous ICA was performed. After administration of 10,000 U heparin, the Iesion was dilated in stages. Under routine fluoroscopic guidance, 3- and 4-ram angioplasty balloons* were sequentially inserted via a transfemoral approach. Total balloon inflation time was less than 1 minute. Stenosis was reduced from 95% to less than 40% (Fig. 2). Immediately following angioplasty, the patient was maintained on systemic heparin, which was then changed to warfarin anticoagulation therapy for 6 weeks. Postoperative Course. In the 2 years since percutaneous transluminal angioplasty, the patient has remained asymptomatic on a low-dose aspirin regimen. Serial carotid artery duplex and transcranial Doppler ultrasound (TDC) evaluations show normal blood flow through the extracranial and intracranial ICA on the left. Because sequential carotid artery duplex examinations revealed rapid progression of a right cervical ICA stenosis from 1% to 99% over a 10-month period, repeat angiographic studies were performed in June, 1990. Compared to those made immediately after percutaneous transluminal angioplasty, the new angio* Angioplasty balloons manufactured by ACS, Temecula, California.
J. Neurosurg. / Volume 76 /March, 1992
FIG. 2. Postoperativeleft carotid artery angiogram, lateral projection, immediately after angioplasty demonstrating reduction in stenosis (arrow) from 95% to less than 40%.
grams demonstrated improvement of the previously dilated left petrous carotid artery stenosis from about 40% to 20%, with remodeling at the angioplasty site; the left anterior cerebral artery was now shown to be filling from the left ICA (Fig. 3). Discussion
Both symptomatic and asymptomatic intracranial ICA stenoses (with and without tandem cervical ICA stenosis) have been associated with a high rate of morbidity and mortality from stroke and myocardial infarction?'t5 In these studies, stroke and transient ischemic attacks had a higher incidence in the territory of the intracranial ICA lesion. Tandem intracranial and extracranial stenoses have been associated with a higher
FIG. 3. Postoperative internal carotid artery (ICA) angiograms, lateral (left) and anterior (right) views, 2 years after angioplasty demonstrating a further increase in vessel caliber from 40% to 20% stenosis (arrows). The left ICA now fills both the middle cerebralartery and the anterior cerebralartery distributions. 521
R. C. Rostomily, et al. risk for ischemic events than has intracranial stenosis alone. 14The severity of intracranial stenosis in patients treated surgically for carotid bifurcation disease does not appear to influence the incidence of immediate or delayed ischemic symptoms following endarterectomy) 9'2~ Therefore, carotid endarterectomy has been advocated as the initial treatment in symptomatic tandem lesions. The report of a case in which ICA siphon stenosis resolved after carotid endarterectomy for tandem stenosis underscores the rationale for this approachJ However, in the absence of effective surgical measures, therapeutic options are limited for patients with isolated symptomatic intracranial ICA lesions who fail conservative medical treatment. The present report describes the successful use of percutaneous transluminal angioplasty for treatment of isolated symptomatic intracranial ICA stenosis with a 2-year symptom-free follow-up period and angiographic confirmation of a progressively resolving lesion. To our knowledge, only two case reports have described the use of percutaneous transluminal angioplasty for symptomatic atheromatous intracranial ICA lesions] 6'~s In one case, clinical improvement in ischemic symptoms was noted after angioplasty of a cavernous carotid artery lesion, 16 but no angiographic follow-up study was provided. A recent case report described the percutaneous transluminal angioplasty of a symptomatic atheromatous MCA stenosis with evidence of clinical and hemodynamic improvement, despite early anglographic evidence of restenosis) s In the present case, repeat angiographic studies revealed evidence of improved hemodynamic status in the left ICA distribution in response to progressive stenosis of the contralateral ICA, and showed an enlarged caliber of the previously dilated pe~rous carotid artery segment. The introduction of percutaneous transluminal angioplasty in 1964 by Dotter and Judkins s provided a noninvasive alternative for the treatment of occlusive vascular disease. Although primarily used for distal lower-extremity and coronary stenoses, percutaneous transluminal angioplasty has only recently been advocated for use on the extracranial and intracranial vasculature. 9,jl'~6,~s'2~-25 In symptomatic vasospasm after SAH, this procedure has been shown to provide longstanding increases in vessel caliber as demonstrated by angiography L~~ and by decreased TCD velocity) 'j~ However, its potential efficacy and the natural history of intracranial atheromatous lesions dilated by percutaneous transluminal angioplasty can only be inferred from experience with other vascular territories. In coronary vessels, percutaneous transluminal angioplasty has been associated with acute occlusion rates of 2% to 4% and delayed restenosis in up to 30% of cases, usually within the first 6 months] 2'~7Certain risk factors for restenosis, such as stenosis location at vessel angulations, have been identified and may be helpful in considering candidates for future cerebral percutaneous transluminal angioplasty. 7,~2Dilatation of coronary vessels by this procedure is considered to be me522
diated by "plaque-splitting, '~3"~7which then allows for stretching of the media and adventitia. Fisher, etal., ~ analyzed atherosclerotic changes in human cerebral vasculature at autopsy, and showed a predilection for stenosis in the carotid siphon with flat, often calcified, atheromatous plaques. Whether these atheromatous changes in intracranial vessels would respond to percutaneous transluminal angioplasty through a mechanism similar to that shown for coronary vessels is unknown. Currently, only preliminary experimental work has been performed with this procedure on normal intracranial vessels in animals. 2 Advances in catheter technology have reduced the risks of distal embolism during percutaneous transluminal angioplasty; nevertheless, greater experience is needed to confirm the safety and efficacy of this procedure in preventing stroke related to a stenotic lesion of the intracranial ICA. Subsequent to the case presented here, we have performed angioplasty on four patients with assorted intracranial (three cases) and extracranial carotid artery (one case) lesions, with only one complication of an asymptomatie ICA dissection, which healed. In two of these four patients, angioplasty was unsuccessful due to the technical limitations of the catheter. The advent of a new Food and Drug Administration-approved microcathetert should facilitate safe cannulation of distal intracranial vessels. Patient selection will also play an important role in the success of future attempts at percutaneous transluminal angioplasty for intracranial atherosclerotic disease. The selection process may be facilitated by cerebral blood flow estimates and assessments of circulatory reserve to confirm a hemodynamically significant lesion prior to percutaneous transluminal angioplasty. Followup blood flow studies could then be correlated with clinical and angiographically determined changes to characterize the factors that influence outcome. Further experimental work and analysis of pathological material may hello to establish whether clinical improvement is based on increased vessel caliber and concomitant hemodynamic changes alone or whether an alteration of plaque morphology occurs, which reduces embolic risk as well. This report establishes the potential application of percutaneous transluminal angioplasty for the treatment of isolated symptomatic focal intracranial ICA stenosis in a patient who failed medical therapy. In a similar group of patients at high risk for stroke, percutaneous transluminal angioplasty may provide long-standing maintenance of adequate vessel caliber with a concomitant improvement in hemodynamic status. References
1. BracardS, Picard L, Marchal JC, et al: Role ofangioplasty in the treatment of symptomatic vascular spasm occurring in the post-operativecourse of intracranial ruptured aneurysms. J Neuroradiol 17:6-19, 1990 1"Microcathetermanufactured by Target Therapeutics, Los Angeles, California. J. Neurosurg. / Volume 76/March, 1992
Transluminal angioplasty 2. Chavez L, Takahashi A, Yoshimoto T, el al: Morphological changes in normal canine basilar arteries after transluminal angioplasty. Neurol Res 12:12-16, 1990 3. Craig DR, Meguro K, Watridge C, et at: lntracranial internal carotid artery stenosis. Stroke 13:825-828, 1982 4, Day AL, Rhoton AL, Quisling RG: Resolving siphon stenosis following endarterectomy. Stroke 11:278-281, 1980 5. Dotter CT, Judkins MP: Transluminal treatment of arteriosclerotic obstruction. Description of a new technic and a preliminary report of its application. Circulation 30:654-670, 1964 6. The EC/IC Bypass Study Group: Failure of extracranialintracranial arterial bypass to reduce the risk of ischemic stroke. Results of an international randomized trial. N Engl3 Med 313:1191-1200, 1985 7. Ellis SG, Roubin GS, King SB II1, et al: Importance of stenosis morphology in the estimation of restenosis risk after elective percutaneous transluminal coronary angioplasty. Am 3 Cardio163:30-34, 1989 8. Fisher CM, Gore I, Okabe N, et al: Atherosclerosis of the carotid and vertebral arteries - - extracranial and intracranial. 3 Neuropathol Exp Neuro124:455-476, 1965 9. Hasso AN, Bird CR, Zinke DE, et ah Fibromuscular dysplasia of the internal carotid artery. Percutaneous transluminal angioplasty. AJR 136:955-960, 198 I 10. Higashida RT, Halbach VV, Cahan LD, et al: Transluminal angioplasty for treatment of intracranial arterial vasospasm J Neurosurg 71:648-653, 1989 11. Higashida RT, Hieshima GB, Tsai FY, et al: Transluminal angioplasty of the vertebral and basilar artery. AJNR 8:745-749, 1987 12. Liu MW, Roubin GS, King SB III: Restenosis after coronary angioplasty. Potential biologic determinants and the role of intimal hyperplasia. Circolatlon 79: 1374-1387, 1989 13. Lyon RT, Zarins CK, Lu CT, et al: Vessel, plaque, and lumen morphology after transluminal balloon angioplasty. Quantitative study in distended human arteries. Arteriosclerosis 7:306-314, 1987 14, Marzewski DJ, Furlan AJ, St Louis P, et al: Intracranial internal carotid artery stenosis: long-term prognosis. Stroke 13:821-824, 1982 15. Newell DW, Eskridge JM, Mayberg MR, et al: Angioplasty for the treatment of symptomatic vasospasm following subarachnoid hemorrhage. J Neurosurg 71: 654-660, 1989
J. Neurosurg. / Volume 76/March, 1992
16. O'leary DH, Clouse ME: Percutaneous transluminal angioplasty for the cavernous carotid artery for recurrent ischemia. AJNR 5:644-645, 1984 17. Pathology of coronary angioplasty (review). Lancet 2: 423-424, 1989 18. Purdy PD, Devous MD St, Unwin DH, et al: Angioplasty of an atherosclerotic middle cerebral artery associated with improvement in regional cerebral blood flow. AJNR 11:878-880, 1990 19. Roederer GO, Langlois YE, Chan ARW, et al: Is siphon disease important in predicting outcome of carotid endarterectomy? Arch Surg 118:1177-1181, 1983 20. Schuler J J, Flanigan DP, Lira LT, et al: The effect of carotid siphon stenosis on stroke rate, death, and relief of symptoms following elective carotid endarterectomy. Surgery 92:1058-1067, 1982 21. Sundt TM Jr, Smith HC, Campbell JK, et al: Transluminal angioplasty for basilar artery stenosis. Mayo Clin Proc 55:673-680, 1980 22. Theron J, Courtheoux P, Henriet JP, et al: Angioplasty of supraaortic arteries. J Neuroradiol 11:187-200, 1984 23. Theron J, Raymond J, Casasco A, et al: Percutaneous angioplasty of atherosclerotic and postsurgical slenosis of carotid arteries. AJNR 8:495-500, 1987 24. Tsai FY, Matovich V, Hieshima G, et al: Percutaneous transluminal angioplasty of the carotid artery. AJNR 7: 349-358, 1986 25. Wiggli U, Gratzl O: Transluminal angioplasty of stenotic carotid arteries: case reports and protocol. AJNR 4: 793-795, 1983 26. Zubkov YN, Nikiforov BM, Shustin VA: Balloon catheter technique of dilatation of constricted cerebral arteries after aneurysmal SAH. Acta Nenroehir 70:65-79, 1984
Manuscript received April 15, 1991. Accepted in final form July 16, 1991. This work was supported by National Institute of Neurological Disorders and Stroke Award NESA-T32-NS07144 to Dr. Rostomily and Clinical Investigator Development Award NS1191 and National Institutes of Health Grant HL44458 to Dr. Mayberg. Address reprint requests to: Marc R. Mayberg, M.D., Department of Neurological Surgery, RI-20, University of Washington Medical Center, 1959 Northeast Pacific, Seattle, Washington 19891.
523
