Radiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Published online before print September 28, 2005, 10.1148/radiol.2372041620
This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
2372041620v1
237/2/620    most recent
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yoon, W.
Right arrow Articles by Kang, H. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yoon, W.
Right arrow Articles by Kang, H. K.
(Radiology 2005;237:620-626.)
© RSNA, 2005

Neuroradiology

Symptomatic Middle Cerebral Artery Stenosis Treated with Intracranial Angioplasty: Experience in 32 Patients1

Woong Yoon, MD, Jeong Jin Seo, MD, Ki Hyun Cho, MD, Myeong Kyu Kim, MD, Byeong Chae Kim, MD, Man Seok Park, MD, Tae Sun Kim, MD, Jae Kyu Kim, MD and Heoung Keun Kang, MD

1 From the Departments of Radiology (W.Y., J.J.S., J.K.K., H.K.K.), Neurology (K.H.C., M.K.K., B.C.K., M.S.P.), and Neurosurgery (T.S.K.), Chonnam National University Hospital, Chonnam National University Medical School, 8 Hak-dong, Dong-ku, Gwangju 501-757, South Korea. Received September 20, 2004; revision requested November 24; revision received December 13; accepted January 14, 2005. Address correspondence to W.Y. (e-mail: radyoon{at}cnuh.com).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
PURPOSE: To retrospectively review the outcome after angioplasty in patients with symptomatic, high-grade middle cerebral artery (MCA) stenosis refractory to medical therapy.

MATERIALS AND METHODS: Institutional review board approval to perform angioplasty procedures for MCA stenosis was obtained, and written informed consent was obtained from each patient or the patient's family. Institutional review board approval was also obtained for the retrospective review of patients' data. The institutional review board waived the need for informed consent for this retrospective analysis.Thirty-two consecutive patients (18 men, 14 women; median age, 55 years) with symptomatic MCA stenosis greater than 70% underwent angioplasty between June 1994 and July 2003. The indication for angioplasty was recurrent transient ischemic attack (TIA) refractory to antithrombotic therapy in 24 patients and acute ischemic stroke in eight. Patient records were retrospectively reviewed for angiographic findings, periprocedural complications, and follow-up data.

RESULTS: Angioplasty reduced the degree of stenosis to less than 50% in 29 of 32 patients (91%). There were two major complications during angioplasty: acute occlusion of the treated MCA and vascular rupture that resulted in death. Thus, the risk of disabling stroke or death was 6% (two of 32 patients), and the mortality rate was 3% (one of 32 patients). The rate of periprocedural TIA was 19% (six of 32 patients). Five patients had asymptomatic intimal dissection. During the follow-up period, which ranged from 5 to 92 months (median, 20 months), TIA occurred in one patient in whom the results of angioplasty were suboptimal. The remaining 29 patients did not experience further ischemic events attributable to the treated MCA stenosis during the follow-up period. Asymptomatic restenosis occurred in one of five patients in whom data from follow-up angiography were available.

CONCLUSION: MCA angioplasty resulted in a low recurrence rate of ischemic symptoms during long-term follow-up.

© RSNA, 2005


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Patients with atherosclerotic middle cerebral artery (MCA) stenosis are at high risk of further ischemic events despite medical treatment. The rate of cerebral ischemic events after first strokes per year in patients with symptomatic MCA stenosis is approximately 8%–21% (1–3). The treatment of patients with intracranial stenosis has empirically consisted of antithrombotic therapy and the reduction of vascular risk factors. The best therapy, however, has yet to be determined (4,5). Thijs and Albers (6) reported that 51.7% of patients with intracranial stenosis in whom antithrombotic therapy had failed had recurrent TIA and/or stroke or death, with a median time to recurrence of 36 days. This high subsequent stroke rate necessitates more effective treatment methods for the secondary prevention of further ischemic events in patients with symptomatic intracranial stenosis. The results of a prospective, randomized, multicenter study (7) showed that extracranial-intracranial bypass surgery did not reduce the risk of ischemic stroke in comparison with aspirin therapy in patients with occlusive disease in the intracranial carotid artery or MCA.

With advances in device technology, intracranial angioplasty has emerged as a potential therapeutic option. At present, intracranial angioplasty is usually performed in patients with symptomatic intracranial internal carotid or vertebrobasilar arteries (8–17). The reports of intracranial angioplasty for symptomatic MCA stenosis remain insufficient, and most series have been limited in terms of the small number of MCA cases included or because of the lack of long-term follow-up. The purpose of our study, therefore, was to retrospectively review the outcome after angioplasty in 32 patients with symptomatic high-grade MCA stenoses refractory to medical therapy.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 References
 
Patients
Between June 1994 and July 2003, 48 patients underwent intracranial balloon angioplasty for the treatment of stenoses or occlusions in the MCA at our institution. Of these patients, those who underwent MCA angioplasty for the treatment of acute cardiogenic embolic occlusion (n = 11) or vasospasm after subarachnoid hemorrhage (n = 2) were excluded from the study. Patients with a clinically significant tandem stenosis in the extracranial or intracranial internal carotid artery and MCA (n = 2) and those with atherosclerotic stenosis in the M2 segment of the MCA (n = 1) were also excluded. The remaining 32 patients who had had transient ischemic attacks (TIAs) or strokes attributed to clinically significant atherosclerotic stenosis of the M1 segment of the MCA were included in this study. All 32 patients had at least 70% luminal narrowing in the MCA at catheter angiography. There were 18 men and 14 women aged 36–75 years (median age, 55 years). Patients had had either a recurrent TIA that occurred during maximum antiplatelet treatment (n = 24) or a nondisabling acute ischemic stroke (n = 8). The antiplatelet regimen used in patients with recurrent TIAs was a combination treatment with 100–325 mg per day of aspirin plus 250 mg per day of ticlopidine or 75 mg per day of clopidogrel. All eight patients with acute ischemic stroke underwent magnetic resonance (MR) imaging before (n = 5) or after (n = 3) angioplasty. At diffusion-weighted MR imaging, acute infarction was classified as cortical, territorial, and subcortical (18). Subcortical infarcts were subdivided into deep perforator, border zone, superficial perforator, and combined subcortical infarcts according to the classification system of Bogousslavsky and Regli (19).

Our institutional review board approved the angioplasty procedure for MCA stenosis, and written informed consent was obtained from each patient or the patient's family. Approval from the institutional review board was also obtained for the retrospective review of patients' data. The institutional review board waived the need for informed consent for this retrospective analysis.

Procedures
All angiographic procedures and angioplasty were performed by one of two radiologists with 3 years (W.Y.) and 7 years (J.K.K.) of experience in neurovascular intervention. The patients received 325 mg of aspirin daily for at least 3 days before the procedure. A bolus of 3000–5000 U of heparin was given intravenously at the beginning of the procedure in all patients. All endovascular procedures were performed with the patient under local anesthesia. Complete diagnostic cerebral angiography was performed in each patient. The degree of MCA stenosis (S), expressed as a percentage, was measured by comparing the diameter of the vessel at the site of greatest stenosis (Dsten) with the normal diameter of the vessel just distal to the stenosis (Ddist), as follows: S = [1 – (Dsten/Ddist)] · 100 (20). Until 1999, vessel diameter was measured with software provided with the digital subtraction angiography equipment (Angiostar; Siemens Medical Systems, Erlangen, Germany) used for angiography. After that time, the measurement was derived from angiographic images obtained with biplane digital subtraction angiography equipment (Advantx LCN+; GE Medical Systems, Milwaukee, Wis) by using reference markers of known size applied to each patient's head.

A 6-F guiding catheter was inserted into the cervical portion of the internal carotid artery over an exchange wire. Since 2002 (from patient 17 to patient 32), abciximab (Reopro; Eli Lilly, Indianapolis, Ind) was given as a 0.25 mg per kilogram of body weight intravenous bolus along with heparin just after placement of the guiding catheter. The first 30 patients were treated with Stealth angioplasty balloons (Target Therapeutics, Fremont, Calif), and the last two patients were treated with coronary balloons (HayatePro; Terumo, Tokyo, Japan). With use of road mapping, the stenosis in the MCA was crossed with a 0.014-inch micro-guidewire and a balloon angioplasty catheter was introduced across the stenosis. The micro-guidewire was subsequently replaced by an occlusion valve wire when Stealth balloons were used. The size of the balloon catheter used was determined according to the size of the adjacent artery just distal to the stenosis. Until 1996 (for patients 1–5), the diameter of the balloon catheter was approximated to the diameter of the normal vessel and the balloon catheter was inflated for less than 30 seconds with a pressure of 6–8 atm (0.6–0.8 nm). Since 1997 (for patients 6–32), the diameter of the balloon was chosen to be 0.5 mm smaller than that of the normal vessel just distal to the stenosis. The balloon was inflated slowly with a screw-type pressure inflation device at 2–4 atm (0.2–0.4 nm) for 30–60 seconds up to two times. Follow-up angiography was performed by means of a guiding catheter after the procedure, and the degree of residual stenosis was recorded. Technical success was defined as a residual stenosis of less than 50% on follow-up angiograms without any serious complications (eg, vessel rupture, acute thrombotic occlusion of the MCA).

Postprocedural Management
After the procedure, a complete neurologic examination was performed in each patient by one of three neurologists (K.H.C., M.K.K., or B.C.K.). The arterial sheath was removed, and hemostasis was achieved with manual compression. Heparin was infused intravenously for 12–24 hours after the procedure. Antiplatelet medication was administered as it had been before the procedure. The National Institutes of Health Stroke Scale (NIHSS) score was recorded before treatment, 24 hours after treatment, and on the day of discharge.

After discharge, patients received daily doses of 325 mg of aspirin and 250 mg of ticlopidine or 75 mg of clopidogrel. Aspirin was administered for at least 1 year; ticlopidine or clopidogrel was discontinued after 3 months. All patients were followed up at regular intervals of 1–3 months in the outpatient clinic at our institution. Symptom recurrence was defined as cerebral ischemic events (eg, TIA or stroke) in the territory that angioplasty was performed during the follow-up period. In patients who initially had acute ischemic stroke, clinical outcomes were measured 3 months after the procedure with use of the modified Rankin scale. Restenosis was evaluated with catheter angiography or transcranial Doppler ultrasonography (US). Results of follow-up catheter angiography were available in five patients after 15–33 months (median, 19 months) (Fig 1). There was no specific indication for follow-up angiography in these patients. Baseline transcranial Doppler US examinations were performed before angioplasty in 27 patients. Follow-up transcranial Doppler US examinations were performed more than two times, usually at 3 months and 1 year after angioplasty, in 24 patients. Restenosis was defined as an increase in mean flow velocity of more than 30 cm/sec between two consecutive transcranial Doppler US examinations (2,21) or as an increase in the degree of residual stenosis measured on follow-up catheter angiograms. Follow-up information was obtained with chart review and/or telephone interview by one of two authors (W.Y. or J.J.S.).



View larger version (198K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 1a. Angiograms obtained in 36-year-old man with acute ischemic stroke. (a) Posteroanterior left internal carotid angiogram shows focal high-grade stenosis (arrow) in proximal M1 segment of left MCA. (b) Posteroanterior angiogram obtained immediately after angioplasty shows good patency of dilated segment with no residual stenosis. (c) Follow-up angiogram obtained 20 months after angioplasty shows no restenosis of original proximal M1 segment of the MCA, although minimal narrowing (arrow) is suggested more distally beyond the temporal branch. The patient remained asymptomatic.

 


View larger version (212K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 1b. Angiograms obtained in 36-year-old man with acute ischemic stroke. (a) Posteroanterior left internal carotid angiogram shows focal high-grade stenosis (arrow) in proximal M1 segment of left MCA. (b) Posteroanterior angiogram obtained immediately after angioplasty shows good patency of dilated segment with no residual stenosis. (c) Follow-up angiogram obtained 20 months after angioplasty shows no restenosis of original proximal M1 segment of the MCA, although minimal narrowing (arrow) is suggested more distally beyond the temporal branch. The patient remained asymptomatic.

 


View larger version (204K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 1c. Angiograms obtained in 36-year-old man with acute ischemic stroke. (a) Posteroanterior left internal carotid angiogram shows focal high-grade stenosis (arrow) in proximal M1 segment of left MCA. (b) Posteroanterior angiogram obtained immediately after angioplasty shows good patency of dilated segment with no residual stenosis. (c) Follow-up angiogram obtained 20 months after angioplasty shows no restenosis of original proximal M1 segment of the MCA, although minimal narrowing (arrow) is suggested more distally beyond the temporal branch. The patient remained asymptomatic.

 

   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 References
 
The results of MCA angioplasty and the clinical follow-up data are shown in Table 1. The degrees of stenosis before the procedure ranged from 70% to 95% (median, 90%), whereas the degree of residual stenosis after the procedure ranged from 0% to 60% (median, 10%). Intracranial angioplasty for symptomatic MCA stenosis was technically successful in 29 of 32 patients (91%). There were three technical failures, including two major complications. In a patient with eccentric stenosis of 80% in the M1 portion of the MCA (patient 23), a postprocedural angiogram revealed 60% residual stenosis after angioplasty despite the balloon being inflated twice for a total of 60 seconds. Additional dilation was not performed because of the potential risk of arterial rupture. Major complications included one vessel rupture and one vessel occlusion. One patient with a long and severe (95% narrowing) stenotic segment in the distal M1 portion of the MCA (patient 5) had an arterial rupture that resulted in massive subarachnoid hemorrhage and death. Another patient with a long and severe stenosis (patient 11) had an acute thrombotic occlusion of the MCA after angioplasty. The occluded segment was partially opened after intraarterial thrombolysis with urokinase, but permanent stroke remained (modified Rankin score of 1 at 3 months). Thus, the procedure-related stroke or death rate was 6% (two of 32 patients), and the mortality rate was 3% (one of 32 patients).


View this table:
[in this window]
[in a new window]

  		TABLE 1. Summary of Patient Data

 
Minor Periprocedural Complications
The periprocedural TIA rate was 19% (six of 32 patients): One patient had TIA associated with intimal dissection that was revealed on the postangioplasty angiogram, and five patients experienced TIA only. Five patients had a procedure-related small intimal dissection, which did not compromise the blood flow, without neurologic worsening or sequelae (Fig 2). Groin hematoma developed in four patients and was successfully managed with conservative treatment. None of the patients had retroperitoneal hemorrhage or femoral artery pseudoaneurysm.



View larger version (227K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 2a. Angiograms obtained in 50-year-old man with TIA. (a) Posteroanterior left internal carotid angiogram shows focal high-grade stenosis (arrow) in M1 segment of left MCA. (b) Posteroanterior angiogram obtained immediately after angioplasty shows patent M1 segment with mild residual stenosis and a newly developed intimal dissection (arrows).

 


View larger version (221K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 2b. Angiograms obtained in 50-year-old man with TIA. (a) Posteroanterior left internal carotid angiogram shows focal high-grade stenosis (arrow) in M1 segment of left MCA. (b) Posteroanterior angiogram obtained immediately after angioplasty shows patent M1 segment with mild residual stenosis and a newly developed intimal dissection (arrows).

 
Patients with Recurrent TIA before Angioplasty
Before undergoing angioplasty, 24 of 32 patients had recurrent TIA despite receiving antithrombotic therapy. Two patients with major complications were excluded from follow-up. The remaining 22 patients were monitored for 5–92 months. During the follow-up period, ipsilateral, nonfatal ischemic stroke attributable to the MCA stenosis for which angioplasty was performed occurred 5 months after treatment in one patient in whom angioplasty was unsuccessful (patient 23). In this patient, diffusion-weighted MR imaging performed 1 day after stroke depicted combined subcortical infarcts. Follow-up for this patient was discontinued. The remaining 21 patients who initially had TIA did not have any further cerebral ischemic events attributed to MCA treatment during the follow-up period. During the follow-up period, one patient (patient 4) developed acute infarction in the territory of the vertebrobasilar arteries. Another two patients (patients 6 and 18) had acute coronary syndrome; both patients underwent coronary angioplasty. None of the patients died during the follow-up period.

Patients with Acute Ischemic Stroke before Angioplasty
Eight patients had an acute, nonfatal ischemic stroke before MCA angioplasty. The results of angioplasty in these patients are given in Table 2. Of these eight patients, five had an acute infarction in the ipsilateral MCA territory 4–8 weeks before angioplasty. Acute infarction was diagnosed on the basis of the findings seen on diffusion-weighted MR images obtained within 7 days of symptom onset. All five patients had subcortical infarcts; three (patients 1, 20, and 21) had deep perforator infarcts, one (patient 13) had superficial perforator infarcts, and one (patient 17) had combined subcortical infarcts. These patients underwent scheduled angiography and subsequent angioplasty after antithrombotic therapy. The NIHSS scores in these patients ranged from 1 to 9 (median, 8.5) before the procedure. Three of these five patients showed neurologic improvement, and their NIHSS scores 24 hours after treatment ranged from 1 to 6. Substantial improvements in motor weakness contributed to the decreased NIHSS score in these three patients. Two patients were neurologically unchanged after the procedure. All five patients had good clinical outcomes at 3 months: Three patients had a modified Rankin score of 0, and two had a score of 1.


View this table:
[in this window]
[in a new window]

  		TABLE 2. Outcomes of Intracranial Angioplasty in Eight Patients with Acute Ischemic Stroke

 
Of eight patients with acute ischemic stroke, three presented within 6 hours of ictus and showed progressive neurologic deficit during observation. These patients underwent emergent angiography and subsequent angioplasty. In these patients, cerebral angiograms revealed only focal atherosclerotic stenosis in the MCA, without any angiographic findings indicative of cardiogenic embolism or arterial dissection in the cerebral vasculature. These patients underwent emergent angioplasty only; intraarterial thrombolysis, which is considered an initial treatment in patients with acute ischemic stroke within 6 hours of symptom onset, was not performed. The patients showed marked neurologic improvement after angioplasty—their NIHSS scores were 8–17 just before the procedure and 1–4 24 hours after treatment. These three patients underwent follow-up MR imaging within 1 week after angioplasty, and MR images showed deep perforator subcortical infarcts. Each of these three patients had a good clinical outcome at 3 months: Two patients had a modified Rankin score of 0, and one patient had a score of 1. All eight patients were monitored for 17–64 months. During this follow-up period, none of the eight patients who initially presented with symptoms of acute ischemic stroke had further ischemic stroke or TIA in the territory of the treated MCA.

Angiographic Follow-up
Images from follow-up catheter angiography were available in five patients. The results of follow-up angiography are shown in Table 3. In one patient (patient 9) who had residual stenosis of 10% just after angioplasty, the degree of stenosis increased to 30% on angiograms obtained 33 months after angioplasty. This patient, however, did not have any ischemic symptoms during follow-up. No restenosis occurred in the remaining four patients. Thus, the symptomatic restenosis rate was 0% in five patients who underwent follow-up angiography. Twenty-four patients underwent serial transcranial Doppler US more than two times during the follow-up period. No patients in whom follow-up transcranial Doppler US data were available showed restenosis at transcranial Doppler US.


View this table:
[in this window]
[in a new window]

  		TABLE 3. Results of Follow-up Angiography in Five Patients

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
References
 
In the extracranial-intracranial bypass study (7), patients with MCA stenosis who underwent bypass surgery fared considerably worse than did those in the medical (aspirin therapy) group. This was consistent with the progression of a stenosed MCA to occlusion accompanied by an early ischemic stroke, whereas the bypass was widely patent (7). It was suggested that bypass decreases the pressure gradient across the MCA stenosis, thereby precipitating thrombosis to occlusion and resulting in stroke due to blockage of perforators (7,22).

Patients with MCA stenosis are at high risk of further ischemic events despite medical treatment. In the extracranial-intracranial bypass study group, patients with stenosis in the MCA who received medical treatment had an annual stroke rate of 8%–10% (1). Arenillas et al (2) reported an annual ischemic event rate of 9.1% in 40 patients with symptomatic MCA stenosis who were receiving antiplatelet or anticoagulation agents. Wong et al (3) reported a recurrent ischemic event rate of 10.5% at 6 months after first stroke in 143 Asian patients with MCA occlusive disease detected at transcranial Doppler US. Recently, the Warfarin-Aspirin Symptomatic Intracranial Disease Study (23) was prematurely terminated owing to the high end-point results (ischemic stroke or brain hemorrhage) with both agents and the confirmed increased bleeding with warfarin. As a result of that study, the 1-year rate of stroke in the territory of the symptomatic intracranial stenosis was 11%–12% with medical therapy with either warfarin or aspirin (M. I. Chimowitz, written communication, December 2004). The results of these studies demonstrate the need for more effective treatment—other than drug therapy—for the prevention of future stroke. More invasive revascularization procedures, such as angioplasty and stent placement, may prove to be alternative methods in patients with intracranial atherosclerosis who are at high risk for stroke.

Results of previous studies have indicated that intracranial angioplasty may reduce the rate of further stroke in patients with intracranial atherosclerosis. Results of a retrospective study involving 23 patients (14), including three with MCA lesions, showed that the annual stroke rate was 3.2% in the region of the treated artery after intracranial angioplasty. Mori et al (12) reported a cumulative stroke risk of 8% 1 year after angioplasty in 12 patients with focal (5 mm or less in length) intracranial stenosis, including five with MCA stenosis. Alazzaz et al (16) reported their results in 15 patients, including five with MCA lesions, with a follow-up period of 1 month to 2 years in which two patients developed recurrent ischemic symptoms at 1 month and at 2 years. In the present study, 29 of 32 patients did not have further cerebral ischemic events attributed to MCA treatment during a follow-up period of 10–92 months (median, 20 months). On the basis of our results, we believe that intracranial angioplasty for symptomatic MCA stenosis refractory to drug therapy can be a promising alternative for reducing the risk of further TIA or stroke if it can be performed safely.

Intracranial angioplasty for the treatment of atherosclerotic stenosis has been associated with potential periprocedural risks, including arterial dissection, arterial rupture, and acute thrombotic occlusion. The major periprocedural complication rate associated with intracranial angioplasty has been reported to be 0%–50% in the literature (8–11,13–17). Connors and Wojak (15) described an overall periprocedural stroke or death rate of 7.1% (three strokes and two deaths) in 70 patients who underwent intracranial angioplasty for anterior and posterior circulation. Marks et al (14) reported one MCA rupture among 23 patients, including three with MCA stenosis, for a mortality rate of 4.3%. Alazzaz et al (16) reported a 13% stroke rate and no mortality in 15 patients, including five with MCA lesions. Recently, Gupta et al (17) reported a major complication rate of 50%, including 39% of cases that were hemorrhagic complications (17% intracranial and 22% extracranial), in 18 patients who underwent intracranial angioplasty for the treatment of impending stroke and neurologic instability. An aggressive combination of various antithrombotics, anticoagulants, and thrombolytics was mainly responsible for the high rate of hemorrhagic complications in that series of patients.

In the present study, two major complications, including one death, occurred during angioplasty. In one patient with a 95% diffuse stenosis in the distal M1 segment, angioplasty was performed with a 3-mm balloon and resulted in fatal rupture of that segment. Several factors—the large size of the balloon used, rapid inflation, and a long, high-grade stenosis—probably contributed to this arterial rupture. To avoid this event, extremely slow inflation with a screw-type inflation device is mandatory. The following is a brief description of our current angioplasty technique, which is especially focused on the prevention of vessel rupture: The balloon catheter is very slowly inflated for 30 seconds to 1 atm (0.1 nm), with monitoring of the pressure gauge on the inflation device; another 30 seconds are needed for holding on the pressure. Thus, the entire inflation time will be 4 minutes if the balloon catheter is inflated to 4 atm (0.4 nm). The balloon pressure should not exceed 6 atm (0.6 nm) and is usually in the range of 4–6 atm (0.4–0.6 nm). In addition, according to recommendations made by Connors and Wojak (15), the balloon is always undersized; the diameter of the balloon should always be 0.5 mm less than that of the normal vessel just distal to the stenosis.

Recently, several investigators reported the technical feasibility and safety of intracranial stent placement for the treatment of intracranial atherosclerotic stenosis (24–26). In comparison with intracranial angioplasty, stent placement theoretically can minimize the risk of acute vessel occlusion from dissection and decrease restenosis resulting from the recoil of atherosclerotic vessels. Intracranial stent placement, however, has potential hazards, such as arterial rupture, in-stent thrombosis, malposition of the stent, or the inability to pass the stent to the appropriate location. Furthermore, the reported complication rate of intracranial stent placement is high, especially in the MCA. In a retrospective study of intracranial stent placement in 12 patients because of symptomatic MCA stenosis, Kim et al (25) reported a major complication rate of 33%—including two vessel ruptures and two thromboembolic complications—and a mortality rate of 8.3%. In a relatively large series of primary stent placement, Jiang et al (26) used a coronary balloon stent in 40 patients with MCA stenosis and reported a procedural complication rate of 10%—including one acute vessel occlusion and three subarachnoid hemorrhages—and a mortality rate of 2.5%. In addition, data from long-term follow-up after intracranial stent placement are lacking to date.

Our study had several limitations. First, the rates of periprocedural TIA and stroke in this study may not reflect those of current state-of-the-art practices because the technique of angioplasty (with regard to balloon sizing, dilation pressure, and inflation time) has evolved during the 9-year study period. The rate of procedure-related complications in this study would be minimized if current techniques were used. In addition, only those patients who were treated in the last half of the study received a bolus of abciximab, a platelet glycoprotein IIb/IIIa receptor inhibitor that is currently considered effective for preventing acute thrombosis associated with neurovascular procedures. Another limitation of this study was that the follow-up imaging to evaluate restenosis was not perfect. Catheter angiography, which is a standard of reference, was performed in only a small number of patients. Although transcranial Doppler US was performed for follow-up in a large number of patients, it has several disadvantages in the diagnosis of MCA stenosis: The diagnostic transcranial Doppler US criteria for identifying MCA stenosis are variable, and concomitant stenoses in other cerebral arteries may cause over- or underestimation of the degree of MCA stenosis (27).

In conclusion, MCA angioplasty resulted in a low rate of recurrence of ischemic symptoms at follow-up in patients with symptomatic MCA stenosis refractory to medical therapy.


   FOOTNOTES
 

Abbreviations: MCA = middle cerebral artery • NIHSS = National Institutes of Health Stroke Scale • TIA = transient ischemic attack

Authors stated no financial relationship to disclose.

Author contributions: Guarantor of integrity of entire study, W.Y.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; approval of final version of submitted manuscript, all authors; literature research, W.Y.; clinical studies, all authors; statistical analysis, W.Y.; and manuscript editing, W.Y., J.J.S., K.H.C., H.K.K.


   References
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

  1. Bogousslavsky J, Barnett HJ, Fox AJ, Hachinski VC, Taylor W. Atherosclerotic disease of the middle cerebral artery. Stroke 1986;17:1112–1120.[Abstract/Free Full Text]
  2. Arenillas JF, Molina CA, Montaner J, et al. Progression and clinical recurrence of symptomatic middle cerebral artery stenosis: a long-term follow-up transcranial Doppler ultrasound study. Stroke 2001;32:2898–2904.[Abstract/Free Full Text]
  3. Wong KS, Li H, Lam WW, et al. Progression of middle cerebral artery occlusive disease and its relationship with further vascular events after stroke. Stroke 2002;33:532–536.[Abstract/Free Full Text]
  4. Chaturvedi S, Fessler R. Angioplasty and stenting for stroke prevention. Neurology 2002;59:664–668.[Abstract/Free Full Text]
  5. Chaturvedi S, Caplan LR. Angioplasty for intracranial atherosclerosis: is the treatment worse than the disease? Neurology 2003;61:1647–1648.
  6. Thijs VN, Albers GW. Symptomatic intracranial atherosclerosis: outcome of patients who fail antithrombotic therapy. Neurology 2000;55:490–497.[Abstract/Free Full Text]
  7. The EC/IC Bypass Study Group. Failure of extracranial-intracranial arterial bypass to reduce the risk of ischemic stroke. N Engl J Med 1985;313:1191–1200.[Abstract]
  8. Clark WM, Barnwell SL, Nesbit G, et al. Safety and efficacy of percutaneous transluminal angioplasty for intracranial atherosclerotic stenosis. Stroke 1995;26:1200–1204.[Abstract/Free Full Text]
  9. Touho H. Percutaneous transluminal angioplasty in the treatment of atherosclerotic disease of the anterior cerebral circulation and hemodynamic evaluation. J Neurosurg 1995;82:953–960.[Medline]
  10. McKenzie JD, Wallace RC, Dean BL, et al. Preliminary results of intracranial angioplasty for vascular stenosis caused by atherosclerosis and vasculitis. AJNR Am J Neuroradiol 1996;17:263–268.[Abstract]
  11. Takis C, Kwan ES, Pessin MS, Jacobs DH, Caplan LR. Intracranial angioplasty: experience and complications. AJNR Am J Neuroradiol 1997;18:1661–1668.[Abstract]
  12. Mori T, Fukuoka M, Kazita K, Mori K. Follow-up study after intracranial percutaneous transluminal cerebral balloon angioplasty. AJNR Am J Neuroradiol 1998;19:1525–1533.[Abstract]
  13. Suh DC, Sung KB, Cho YS, et al. Transluminal angioplasty for middle cerebral artery stenosis in patients with acute ischemic stroke. AJNR Am J Neuroradiol 1999;20:553–558.[Abstract/Free Full Text]
  14. Marks MP, Marcellus M, Norbash AM, et al. Outcome of angioplasty for atherosclerotic intracranial stenosis. Stroke 1999;30:1065–1069.[Abstract/Free Full Text]
  15. Connors JJ, Wojak JC. Percutaneous transluminal angioplasty for intracranial atherosclerotic lesions: evolution of technique and short-term results. J Neurosurg 1999;91:415–423.[Medline]
  16. Alazzaz A, Thornton J, Aletich VA, et al. Intracranial percutaneous transluminal angioplasty for arteriosclerotic stenosis. Arch Neurol 2000;57:1625–1630.[Abstract/Free Full Text]
  17. Gupta R, Schmacher HC, Mangla S, et al. Urgent endovascular revascularization for symptomatic intracranial atherosclerotic stenosis. Neurology 2003;61:1729–1735.[Abstract/Free Full Text]
  18. Ringelstein EB, Biniek R, Weiller C, et al. Type and extent of hemispheric brain infarctions and clinical outcome in early and delayed middle cerebral artery recanalization. Neurology 1992;42:289–298.[Abstract/Free Full Text]
  19. Bogousslavsky J, Regli F. Centrum ovale infarcts: subcortical infarction in the superficial territory of the middle cerebral artery. Neurology 1992;42:1992–1998.[Abstract/Free Full Text]
  20. The Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) Study Group. Prognosis of patients with symptomatic vertebral or basilar artery stenosis. Stroke 1998;29:1389–1392.
  21. Ley-Pozo J, Ringelstein EB. Noninvasive detection of occlusive disease of the carotid siphon and middle cerebral artery. Ann Neurol 1990;28:640–647.[CrossRef][Medline]
  22. Awad I, Furlan AJ, Little JR. Changes in intracranial stenotic lesions after extracranial-intracranial bypass surgery. J Neurosurg 1984;60:771–776.[Medline]
  23. Chimowitz MI, Lynn MJ, Howlett-Smith H, et al. Comparison of warfarin and aspirin for symptomatic intracranial stenosis. N Engl J Med 2005;352:1305–1316.[Abstract/Free Full Text]
  24. de Rochemont Rdu M, Turowski B, Buchkremer M, et al. Recurrent symptomatic high-grade intracranial stenoses: safety and efficacy of undersized stents—initial experience. Radiology 2004;231:45–49.[Abstract/Free Full Text]
  25. Kim JK, Ahn JY, Lee BH, et al. Elective stenting for symptomatic middle cerebral artery stenosis presenting as transient ischemic deficits or stroke attacks: short-term arteriographical and clinical outcome. J Neurol Neurosurg Psychiatry 2004;75:847–851.[Abstract/Free Full Text]
  26. Jiang WJ, Wang YJ, Du B, et al. Stenting of symptomatic M1 stenosis of middle cerebral artery: an initial experience of 40 patients. Stroke 2004;35:1375–1380.[Abstract/Free Full Text]
  27. Bang OY, Cho JH, Han BI, Joo IS, Kim DI, Huh K. Transcranial Doppler findings in middle cerebral arterial occlusive disease in relation to degree of stenosis and presence of concomitant stenoses. J Clin Ultrasound 2003;31:142–151.[CrossRef][Medline]



This article has been cited by other articles:


Home page
 StrokeHome page
M. Mazighi, J. S. Yadav, and A. Abou-Chebl
Durability of Endovascular Therapy for Symptomatic Intracranial Atherosclerosis
Stroke, June 1, 2008; 39(6): 1766 - 1769.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Neuroradiol.Home page
D.C. Suh, J.K. Kim, J.W. Choi, B.S. Choi, H.W. Pyun, Y.J. Choi, M.-H. Kim, H.R. Yang, H.I. Ha, S.J. Kim, et al.
Intracranial Stenting of Severe Symptomatic Intracranial Stenosis: Results of 100 Consecutive Patients
AJNR Am. J. Neuroradiol., April 1, 2008; 29(4): 781 - 785.
[Abstract] [Full Text] [PDF]

Home page
 RadiologyHome page
W.-J. Jiang, B. Du, T. W. Leung, X.-T. Xu, M. Jin, and K.-H. Dong
Symptomatic Intracranial Stenosis: Cerebrovascular Complications from Elective Stent Placement
Radiology, April 1, 2007; 243(1): 188 - 197.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
2372041620v1
237/2/620    most recent
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yoon, W.
Right arrow Articles by Kang, H. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yoon, W.
Right arrow Articles by Kang, H. K.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
RADIOLOGY RADIOGRAPHICS RSNA JOURNALS ONLINE