AJR Your Link to CME
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
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 Google Scholar
Google Scholar
Right arrow Articles by Kantarci, F.
Right arrow Articles by Islak, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kantarci, F.
Right arrow Articles by Islak, C.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
DOI:10.2214/AJR.05.0452
AJR 2006; 187:779-787
© American Roentgen Ray Society


Clinical Observations

Follow-Up of Extracranial Vertebral Artery Stents with Doppler Sonography

Fatih Kantarci1, Ismail Mihmanli1, Mehmet Sait Albayram2, Hakan Barutca1, Fatih Gulsen1, Naci Kocer2 and Civan Islak2

1 Department of Radiology, Division of Ultrasonography, Cerrahpasa Medical Faculty, Istanbul University, Kocamustafapasa 34300, Istanbul, Turkey.
2 Department of Radiology, Division of Neuroradiology, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey.

Received March 15, 2005; accepted after revision May 9, 2005.

 
Part of this article was presented at the 2004 EUROSON Congress, Zagreb, Croatia.

Address correspondence to I. Mihmanli (mihmanli{at}yahoo.com).


Abstract
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
OBJECTIVE. The objective of our study was to determine the Doppler sonography findings suggestive of restenosis in the follow-up of patients treated by stent placement in the extracranial vertebral artery.

CONCLUSION. Follow-up of vertebral artery stents with Doppler sonography may be performed by direct insonation of the stent or by indirect measurements from the V2 segment (the part of the vertebral artery that courses within the intervertebral foramina). The V2 segment Doppler sonography measurements may guide future examinations and provide essential information regarding the proximally deployed stent.

Keywords: angioplasty • arteriosclerosis • Doppler sonography • hemodynamics • stenosis • stents • vascular imaging • vertebral artery


Introduction
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
A growing group of studies is suggesting that endovascular intervention, with percutaneous transluminal angioplasty (PTA) and stenting, is a safe and effective treatment for extracranial vertebral artery atherosclerotic stenosis, especially at the vertebral artery origin [1-15]. The results of primary stenting procedures are promising and suggest considerably lower restenosis rates (< 50%). Secondary endovascular interventions for early (thrombosis) and late (restenosis) complications of stent deployment may be performed, and they may further increase the patency rates [9-12]. As with the carotid artery stenting procedures, follow-up of patients after vertebral artery stenting is crucial in the early detection of restenosis before complete occlusion develops [9, 14].

The gold standard for the follow-up of carotid and vertebral artery stenting procedures is angiography. However, their invasive nature and their use of radiation do not allow frequent angiographic examinations in these patients. Rather, angiography is generally performed at the end of the first year after stent deployment or in patients who are symptomatic [1-15]. On the other hand, Doppler sonography, a noninvasive and radiation-free imaging tool, has been favored in recent years as a screening method for the follow-up of carotid artery stents [16-23]. Doppler sonography has provided considerable knowledge and follow-up data on carotid artery stents. Because the number of vertebral artery stenting procedures is considerably less than the number of carotid artery stenting procedures, the outcome of vertebral artery stenting using angiography or Doppler sonography is less well understood. Furthermore, the details of the Doppler sonography examinations have not been provided in a limited number of reports [1-15].

The aim of this study is to report our experience with the Doppler sonography follow-up of extracranial vertebral artery stenoses treated by primary stent placement. We discuss the findings suggestive of restenosis and the limitations of Doppler sonography in the follow-up of extracranial vertebral artery stents.


Materials and Methods
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Patients
We retrospectively reviewed the records of 12 consecutive patients who underwent endovascular stent placement for atherosclerotic disease of the extracranial portion of the vertebral artery between February 2001 and November 2004. Ten patients were men and two were women. The mean age of the patients was 62.2 years (range, 48-77 years).

The indications for stent placement were posterior circulation ischemia that was refractory to medical treatment. All patients had severe (3 70%) stenosis of the extracranial portion of the vertebral artery on angiographic examination. The stenoses ranged from 70% to 95% (mean, 85.7%).

Locations of the Lesions
Nine patients had isolated unilateral vertebral artery origin stenoses. One patient had bilateral vertebral artery origin stenoses, two patients had unilateral vertebral artery origin and concomitant stenoses (70%) in the ipsilateral vertebral artery V2 segment (the part of the vertebral artery that courses within the intervertebral foramina). One patient had unilateral stenosis in the V1 segment (the part of the vertebral artery from the origin of the subclavian artery to the point at which it enters the transverse foramina). In all, 12 patients had 15 extracranial vertebral artery stenoses. None of the vertebral arteries was originating from the aorta. Concomitant lesions in the carotid and contralateral vertebral arteries were present in 11 patients. Of the patients with unilateral extracranial vertebral artery stenoses, four had contralateral vertebral artery occlusion and two had contralateral vertebral artery hypoplasia. Contralateral vertebral artery origin stenosis (= 50%) was present in two patients.

Procedure
All procedures were performed via percutaneous transfemoral access with the patient under local anesthesia. During the procedure, the patients received 5,000 IU of heparin, administered IV, to achieve an activated clotting time of more than 200 seconds. In each case, the procedure started with four-vessel cerebral angiography. Thereafter, a 7- to 8-French 100-cm-long guiding catheter was used to reach the lesions at the vertebral artery. By using the sheath or guiding catheter in a road map or overlay technique, the lesion was visualized. After crossing the lesion with a guidewire, balloon expandable stents were deployed. Balloon angioplasty with appropriate balloon size was performed when necessary before stent implantation. Finally, a control angiogram was obtained from the stented segment and intracranial circulation of the treated vessel. The patients were monitored in the neurosurgical ward.

Doppler Sonography Technique
All vertebral artery Doppler examinations were performed by the same experienced radiologist using a high-resolution sonographic system (Sonoline Elegra or Antares, Siemens Medical Solutions) using 4-7.5- and 4-9-MHz broadband linear array transducers. Gain and velocity settings of the color Doppler unit were adjusted to ensure that all examinations were technically adequate. Data on Doppler waveforms and velocities were obtained with an angle of insonation of 60° or less.

The first step of the examination included the successful identification of the origin of the vertebral artery and the deployed stent. This was achieved by identification of the V2 segment. A color Doppler map was then used to follow the vertebral artery caudally at the V1 segment. The stent was evaluated on gray-scale and color Doppler sonography for the obvious presence of in-stent neointimal hyperplasia and luminal narrowing when the previously mentioned technique was successful in identifying the stent at the vertebral artery origin. If neointimal hyperplasia or luminal narrowing was seen, the peak systolic velocity in the stent was measured.

The second step of the examination included the Doppler readings from the V2 segment. Measurements were taken in the C6-C5, C5-C4, and C4-C3 vertebral interspaces, and the mean of these measurements was calculated. The sonographic scanner is supported with proper software for direct and automatic calculation of the hemodynamic parameters based on spectral Doppler waveforms provided that there are three consecutive clear waveforms at the strip at each vertebral interspace. Spectral waveforms were both manually and automatically traced on the strip. The automatic trace measurements were verified by manual calculations of the Doppler indexes. The reported indexes by automatic trace of the machine were reasonable, and therefore the results of the automatic trace measurements were used in the study.

The peak systolic velocity, end diastolic velocity, resistive index, acceleration time, absolute acceleration, and blood flow volume were calculated. Acceleration time was defined as the rise time for the first systolic peak, and absolute acceleration was defined as change in velocity divided by change in time during the rise for the first systolic peak. Blood flow volume calculations were performed using the following formula:

Formula
where d = diameter. The time averaged mean velocity is the intensity-weighted mean velocity integrated over time, obtained with a sample volume that covers the entire vessel diameter. The diameter of the vessel for blood flow volume was measured perpendicular to the course of the vessel using gray-scale imaging.


Figure 1
View larger version (172K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 1A 76-year-old woman with ischemic posterior circulation. Digital subtraction angiogram (DSA) of right vertebral artery (arrowhead) at anteroposterior projection reveals 75% stenosis (arrow) at vertebral artery origin. SCA = subclavian artery.

 


Figure 2
View larger version (163K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 1B 76-year-old woman with ischemic posterior circulation. Follow-up DSA, anteroposterior projection, immediately after stent deployment shows total dilatation (arrow) of stenosis. SCA = subclavian artery, arrowhead indicates vertebral artery.

 


Figure 3
View larger version (100K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 1C 76-year-old woman with ischemic posterior circulation. Immediate poststenting spectral Doppler sonogram from V2 segment of vertebral artery reveals peak systolic velocity of 57 cm/s, resistive index of 0.74, acceleration time of 60 milliseconds, absolute acceleration of 466 cm/s2, and blood flow volume of 174 mL/min.

 


Figure 4
View larger version (73K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 1D 76-year-old woman with ischemic posterior circulation. Blood flow volume on first-year follow-up spectral Doppler sonogram preceeding follow-up angiogram shows peak systolic velocity of 67 cm/s, resistive index of 0.76, acceleration time of 60 milliseconds, absolute acceleration of 516 cm/s2, and blood flow volume of 194 mL/min.

 
Follow-Up
Patients were discharged from the neurosurgical ward after the procedure when their neurologic condition was determined to be stable. Postoperatively, the patients received an oral 300-mg dose of clopidogrel (Plavix, Bristol-Myers Squibb/Sanofi Pharmaceuticals) followed by a daily oral dose of 75 mg. Aspirin was also administered in daily doses of 325 mg.


Figure 5
View larger version (76K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 1E 76-year-old woman with ischemic posterior circulation. First-year follow-up color Doppler sonogram provides direct evaluation and reveals normal color flow in stent (arrow). SCA = subclavian artery.

 


Figure 6
View larger version (167K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 1F 76-year-old woman with ischemic posterior circulation. First-year follow-up vertebral artery (arrowhead) DSA in left anterior oblique projection shows good filling of stent lumen (arrow) with contrast material. No intimal hyperplasia is seen. SCA = subclavian artery.

 
Clinical, Doppler sonography, and angiographic examinations were used in the follow-up. Our follow-up protocol included Doppler sonography within 24 hours after stent deployment. During the first year, we performed clinical follow-up at 3-month intervals. Each patient was examined also by Doppler sonography at every clinical follow-up examination. Angiographic follow-up was scheduled at the end of the first year after stent deployment. However, if Doppler sonography showed neointimal hyperplasia in the stent lumen, angiography was scheduled immediately. Restenosis was defined as 50% or more luminal narrowing on angiographic examination.


Results
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Endovascular Procedures
Fourteen of 15 extracranial vertebral artery stenoses were successfully treated by endovascular stent implantation. One patient with concomitant origin and V2 segment stenosis was treated only by stent implantation to the origin of the vertebral artery. The V2 segment stenosis of this patient could not be stented because of the tortuosity of the vertebral artery. Overall, the primary success rate of the technique was 93% (14/15). A second stent was implanted because of angiographically confirmed 50% restenosis in one patient 4 months after the first stenting procedure. This patient had recurrence of his symptoms after the initial stent placement. No patients developed immediate major complications such as thrombosis or vertebral artery dissection after stent deployment. Age, sex, side, and location of the vertebral artery stenosis, degree of stenosis on angiography, and follow-up angiography results are given in Table 1.


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

 
TABLE 1: Patient Characteristics and Angiographic Results Before and After Stenting

 

Clinical Follow-Up
The follow-up duration was 13-47 months (mean, 23.3 months). In two patients, new neurologic complications developed immediately after stent deployment. One patient had severe vertigo after vertebral artery stent deployment that resolved completely on the third day of clinical follow-up. In the other patient with concomitant internal carotid artery stenting, hyperperfusion syndrome developed after the stenting of the internal carotid artery. No new neurologic symptoms developed in these patients regarding the posterior circulation on follow-up. One patient had hypoesthesia on the left side. Another patient with bilateral internal carotid artery occlusion had depression and aphasia before the vertebral artery stenting procedure. No new neurologic symptoms occurred in these patients after stent deployment. In four patients in whom angiography disclosed restenosis of more than 50%, clinical follow-up revealed recurrence of symptoms in only one patient. In this symptomatic patient, the vertebral artery was restented 4 months after the initial stent deployment. The patient was symptom-free after the second stent implantation. The remaining patients were symptom-free on clinical follow-up.

Doppler Sonography Follow-Up
Doppler sonography revealed angiographically confirmed restenosis in four of 14 vertebral artery stents. Doppler sonography was not suggestive of restenosis in 10 stents (Figs. 1A, 1B, 1C, 1D, 1E, and 1F).

Technical success—Stents were implanted in 12 vertebral artery origins, one V1 segment, and one V2 segment (total, 14 stents). Of the origin stents, eight were adequately insonated on Doppler sonography (8/12, 67%). Four vertebral artery origin stents (three left-side and one right-side) could not be insonated on Doppler sonography because of the deep thoracic location of the vertebral artery or the short neck of the patient. The stents in the V1 and V2 segments were successfully identified. Overall, the stents at the extracranial portion of the vertebral arteries were successfully evaluated in 71% of the patients.

The V2 segments at each level (C6-C5, C5-C4, and C4-C3 interspaces) were adequately insonated in all of the vertebral arteries except one (93.3%). In one patient with a vertebral artery origin stent and V2 segment stenosis that could not be stented, only the C5-C4 vertebral interspace was adequately examined; remaining parts of the V2 segment and the origin of the vertebral artery could not be examined because of degenerative disease of the cervical vertebrae. Interestingly, this segment was the level of the V2 segment stenosis, and increased velocity was obtained from this region. The Doppler sonography examination in this patient was not used in follow-up because the examination was limited to a short segment of the vertebral artery.


Figure 7
View larger version (150K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 2A 55-year-old man with ischemic posterior circulation. Digital subtraction angiogram (DSA), anteroposterior projection, reveals 95% stenosis at vertebral artery origin (arrow). Note that vertebral artery (arrowhead) filling is poor distal to stenosis. SCA = subclavian artery.

 


Figure 8
View larger version (147K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 2B 55-year-old man with ischemic posterior circulation. Immediate follow-up DSA after stent deployment reveals total dilatation of stenotic segment (arrow) and good filling of vertebral artery (arrowhead). SCA = subclavian artery.

 


Figure 9
View larger version (128K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 2C 55-year-old man with ischemic posterior circulation. Immediate poststenting spectral Doppler sonogram from V2 segment of vertebral artery reveals peak systolic velocity of 58 cm/s, resistive index of 0.69, acceleration time of 65 milliseconds, absolute acceleration of 430 cm/s2, and blood flow volume of 177 mL/min.

 


Figure 10
View larger version (92K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 2D 55-year-old man with ischemic posterior circulation. Follow-up color Doppler sonogram of vertebral artery origin 9 months after stent deployment shows intimal hyperplasia (arrow), luminal narrowing, and color flow disturbance in stent.

 


Figure 11
View larger version (98K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 2E 55-year-old man with ischemic posterior circulation. Spectral Doppler sonogram from this segment reveals jet flow (peak systolic velocity, 295 cm/s).

 


Figure 12
View larger version (70K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 2F 55-year-old man with ischemic posterior circulation. V2 segment spectral analysis depicts decrease of peak systolic velocity (42 cm/s), resistive index (0.54), and blood flow volume (106 mL/min) when compared with immediate poststenting examination. Acceleration time is 50 milliseconds and absolute acceleration is 380 cm/s2.

 


Figure 13
View larger version (168K):
[in this window]
[in a new window]
[as a PowerPoint slide]
 
Fig. 2G 55-year-old man with ischemic posterior circulation. 9-month follow-up DSA immediately after Doppler follow-up examination confirms significant (50%) restenosis (large arrow) in stent. SCA = subclavian artery, arrowhead indicates vertebral artery, small arrows indicate stent struts.

 
Direct evaluation of the stent—Ten of the extracranial vertebral artery stents (eight origin, one V1 segment, and one V2 segment stents) were adequately insonated and evaluated by gray-scale and Doppler sonography. In three patients, restenosis was suggested by the presence of neointimal hyperplasia on gray-scale and color Doppler sonography. Of these patients, one had the stents at the vertebral artery origin and V2 segment (restenosis present only in the vertebral artery origin stent), one at the vertebral artery origin (Figs. 2A, 2B, 2C, 2D, 2E, 2F, and 2G), and the third at the V1 segment. Spectral Doppler sonography revealed jet flow at the origin and the V1 segments, respectively. These patients were at the fourth, ninth, and sixth month of clinical follow-up, respectively. In one patient with vertebral artery origin stenosis, in whom angiography revealed more than 50% restenosis, the origin of the vertebral artery could not be insonated by Doppler sonography.

V2 segment measurements—In patients with angiographically confirmed restenosis, retrospective evaluation of the V2 segment at Doppler sonography showed a more than 20% decrease of peak systolic velocity, more than 15% decrease of resistive index, and more than 30% decrease of blood flow volume between the immediate poststenting Doppler sonography examination and the Doppler sonography examination preceding the follow-up angiography. An acceleration time of more than 70 milliseconds (tardus waveform) was observed in two of these patients on follow-up. In the remaining two patients with angiographically proven restenosis, the acceleration time was less than 70 milliseconds. The absolute acceleration measurements were less than 300 cm/s2 in three patients and 380 cm/s2 in one patient on follow-up. In patients without restenosis, no patient exhibited a significant change in peak systolic velocity, resistive index, absolute acceleration, acceleration time, or blood flow volume except one. This patient showed a 16% decrease in resistive index on the Doppler sonography examination preceding the follow-up angiography, and the peak systolic velocity and blood flow volume were not significantly decreased. This patient had bilateral internal carotid artery occlusion and the brain was supplied primarily by the vertebral arteries, which may explain the decrease in the resistive index. The findings on immediate (within 24 hours) poststenting Doppler sonography; findings on Doppler sonography just before follow-up angiography; and the percentage of change in peak systolic velocity, resistive index, acceleration time, absolute acceleration, and blood flow volume for each patient are given in Table 2.


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

 
TABLE 2: Immediate Poststenting and Follow-Up Doppler Sonography Findings at Vertebral Artery Origin and V2 Segment

 


Discussion
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Percutaneous transluminal angioplasty (PTA) is now a well-established therapeutic alternative to surgical reconstruction of proximal vertebral artery stenoses and it seems to be relatively safe [1-15]. Restenosis after angioplasty without stenting is a cause of midterm failure of vertebral angioplasty in atherosclerotic disease. Primary reinforcement of the vessel wall with a stent may improve the immediate and long-term outcomes of proximal vertebral artery PTA. Although the restenosis rate in primary stenting procedures is less frequent than with PTA alone, it is still a major concern in the follow-up. The rate of restenosis after endovascular treatment of vertebral artery stenosis varies among series. Some studies have reported a low incidence of restenosis [9-12], whereas others have reported restenosis rates in as many as 50% of patients [14, 15].

The leading event in stent restenosis is neointimal hyperplasia, which is a pathophysiologic process separate from atherosclerosis [24, 25]. Neointimal hyperplasia develops through the processes of thrombus, deposition, inflammation, smooth muscle cell and fibroblast migration, and cellular proliferation [25]. Studies on coronary artery stenting procedures have shown that stent endothelialization is not complete by 1 month [25]. At 3 months, stent coverage by the endothelium is complete, with a developing neointima. Later, at 10 months, atherosclerotic plaque may occur at stent sites, manifested by foam cells and cholesterol crystals [25]. Lal et al. [26], in their study on carotid artery stenting, stated that most recurrent stenoses (≥ 40%) occurred within 18 months of intervention (in 60% of patients), and most clinically significant recurrent stenoses (≥ 80%) occurred within 15 months. Chakhtoura et al. [27] reported in-stent restenosis at a mean interval of 13 ± 7 months (range, 6-21 months) after the original carotid artery stenting procedure. On the basis of the results of these studies, we may state that restenosis usually occurs within the first year after stent deployment. Therefore, meticulous follow-up of patients with coronary, carotid, and vertebral artery stenting during the first year after stent deployment is crucial.

Although the gold standard for follow-up is angiography, its invasive nature and the use of radiation do not allow a frequent angiographic examination in these patients. A noninvasive, easily reproducible, accessible, and effective technique is required for the follow-up. Doppler sonography allows a more frequent examination to be performed, and it was successfully used in the follow-up of carotid artery stents [16-23]. Other imaging techniques, such as CT or MR angiography, may also be used in the follow-up [28, 29]. However, Doppler sonography provides essential information regarding hemodynamics and the flow character of the vessel. Also, it is safe, inexpensive, and noninvasive. It has the advantage of providing more frequent examinations using a method that does not require radiation, especially during the critical first year of follow-up, when restenosis most frequently occurs. On the other hand, Doppler sonography cannot replace the angiographic examination in the follow-up; rather, it may be used as a screening method. On the basis of our follow-up data on Doppler sonography, restenosis was detected before the first-year follow-up angiogram in three of four patients (one patient at the fourth month, one at the sixth month, and one patient at the ninth month).

It is possible to insonate the V1 and V2 segments of the vertebral artery on Doppler sonography with relative ease in most patients [30-32]. However, appropriate sonographic examination of the V1 segment is hampered by technical limitations and the confounding effect of anatomic variations. When Doppler sonography alone is used, the V1 segment, and especially the origin of the vertebral artery on the right and left sides, cannot be insonated in 6-14% and 24-40% of patients, respectively [33-35]. In our study, we could not examine the vertebral artery origin stents in one third (4/12) of the vertebral artery origin stenose. Therefore, measurements based solely on the direct insonation of the origin stent may restrict follow-up by Doppler sonography.

Once an origin stent is sufficiently insonated by Doppler sonography, the neointimal hyperplasia causing luminal narrowing may be adequately visualized. In three of four cases of angiographically confirmed restenosis (two origin stents, one V1 segment stent), we were able to directly insonate the deployed stent and show the neointimal hyperplasia in the stent. In one patient, however, we were not able to insonate the vertebral artery origin stent, and Doppler sonography failed to show neointimal hyperplasia and luminal narrowing.

The V2 segment of the vertebral artery can almost always be insonated by Doppler sonography [30]. Therefore, the V2 segment stents may be examined better than the origin stent and the V1 segment stents on sonographic examination. The V2 segment and one V1 segment stents were adequately examined in our study.

Because of the inherent confounding effects mentioned previously in the examination of the origin of the vertebral arteries and the stents deployed at the origin, we searched for other Doppler sonography parameters that might be useful in follow-up. Although the V2 segment measurements on Doppler sonography are restricted, it is a good approach because of its feasibility, short examination time, and accuracy [30-32]. The V2 segment measurements may provide indirect information about the origin of the vertebral artery and generally include measurement of peak systolic velocity, resistive index, blood flow volume, acceleration time, and absolute acceleration.

Significant stenosis of the first segment of the vertebral artery is generally reflected as a low-amplitude (decreased peak systolic velocity), tardus-parvus waveform because of a reduced-volume flow distal to the stenosis, with an abnormally low resistive index (< 0.50) at the intertransverse segment. A tardus-parvus waveform is usually reflected by an acceleration time of more than 70 milliseconds and an absolute acceleration of less than 300 cm/s2. Blood flow volume measurements may be used for quantitative assessment of the vertebrobasilar circulation [36, 37].

Some studies discuss the establishment of reference values for vertebral artery blood flow volume [36, 37]; however, the association of vertebrobasilar ischemia and vertebral artery blood flow volume has not been definitely established [37]. In our study, we assessed the change in blood flow volume on follow-up Doppler sonography examinations. Based on the V2 segment measurements, we cannot compute with certainty the amount of stenosis at a more proximal location; we can only assume that there might be a disorder involving the proximal segments of the vertebral artery. However, if we know the vertebral artery flow at the distal segments of a stented artery immediately after stent deployment, we may monitor the hemodynamic changes over time.

In our study, we observed a significant decrease of peak systolic velocity (> 20%), resistive index (> 15%), and blood flow volume (> 30%) on follow-up Doppler sonography when compared with the immediate poststenting measurements in patients having more than 50% in-stent restenosis. A tardus-parvus waveform was observed in two patients and a parvus waveform in one patient with in-stent restenosis. The spectral waveform was normal in one patient with recurrent stenosis. Concomitant carotid artery stenotic or occlusive disease may have affected the changes in acceleration time and absolute acceleration of vertebral arteries in our patients with in-stent restenosis. Also, changes in acceleration time and absolute acceleration will reliably identify only stenoses greater than 70% diameter reduction [38]. Because the use of only one Doppler sonography parameter may cause misdiagnosis, we suggest the use of all Doppler sonography parameters in the follow-up.

In patients without restenosis on follow-up angiography, no significant change in peak systolic velocity, resistive index, acceleration time, absolute acceleration, or blood flow volume was noted except for a decrease of resistive index in one patient. This patient had bilateral internal carotid artery occlusion, and the brain was supplied primarily by the vertebral arteries. The decrease of more than 15% in resistive index on follow-up in this patient may be explained by the increased blood flow volume (14% increase on follow-up). Nevertheless, new prospective studies are needed to achieve more accurate threshold values for change in peak systolic velocity, resistive index, and blood flow volume in the V2 segment.

The major drawback of our study was the limited number of patients we studied. However, as previously noticed, vertebral artery stenting procedures are not as commonly performed as carotid artery stenting procedures. Several stent coatings have been tested, either experimentally or clinically, including heparin, silicon carbide, gold, polymers with and without drug elution, and radioactive coatings [39]. Promising results in these studies might increase the use of stents in extracranial vertebral artery atherosclerotic stenoses in the future.

In conclusion, follow-up of extracranial vertebral artery stenting procedures may be performed by direct visualization of the stent lumen or indirectly by V2 segment measurements. When the stents deployed to the origin of the vertebral artery cannot be insonated on Doppler sonography, indirect information from the V2 segment of the vertebral artery can be obtained that might also suggest recurrent stenosis. The key point in the V2 segment examination is the immediate poststenting Doppler sonography evaluation, which may be a guide for future measurements. However, further prospective studies are necessary to define the exact hemodynamic changes associated with in-stent restenosis at the V2 segment of the vertebral artery.


References
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 

  1. Motarjeme A, Keifer JW, Zuska AJ. Percutaneous transluminal angioplasty of the vertebral arteries. Radiology1981; 139:715 -717[Abstract/Free Full Text]
  2. Imparato AM, Riles TS, Kim GE. Cervical vertebral angioplasty for brain stem ischemia. Surgery 1981;90 : 842-852[Medline]
  3. Higashida RT, Tsai FY, Halbach VV, et al. Transluminal angioplasty for atherosclerotic disease of the vertebral and basilar arteries. J Neurosurg 1993;78 : 192-198[Medline]
  4. Bruckmann H, Ringelstein EB, Buchner H, Zeumer H. Percutaneous transluminal angioplasty of the vertebral artery: a therapeutic alternative to operative reconstruction of proximal vertebral artery stenoses. J Neurol 1986; 233:336 -339[CrossRef][Medline]
  5. Higashida RT, Hieshima GB, Tsai FY, Halbach VV, Norman D, Newton TH. Transluminal angioplasty of the vertebral and basilar artery. AJNR 1987; 8:745 -749[Abstract]
  6. Storey GS, Marks MP, Dake M, Norbash AM, Steinberg GK. Vertebral artery stenting following percutaneous transluminal angioplasty. J Neurosurg 1996; 84:883 -887[Medline]
  7. Feldman RL, Rubin JJ, Kuykendall RC. Use of coronary Palmaz-Schatz stent in the percutaneous treatment of vertebral artery stenoses. Cathet Cardiovasc Diagn 1996;38 : 312-315[CrossRef][Medline]
  8. Malek AM, Higashida RT, Phatouros CC, et al. Treatment of posterior circulation ischemia with extracranial percutaneous balloon angioplasty and stent placement. Stroke 1999;30 : 2073-2085[Abstract/Free Full Text]
  9. Chastain HD II, Campbell MS, Iyer S, et al. Extracranial vertebral artery stent placement: in-hospital and follow-up results. J Neurosurg 1999; 91:547 -552[Medline]
  10. Jenkins JS, White CJ, Ramee SR, et al. Vertebral artery stenting. Cathet Cardiovasc Interv 2001;54 : 1-5[CrossRef][Medline]
  11. Mukherjee D, Roffi M, Kapadia SR, et al. Percutaneous intervention for symptomatic vertebral artery stenosis using coronary stents. J Invasive Cardiol 2001; 13:363 -366[Medline]
  12. Piotin M, Spelle L, Martin J-B, et al. Percutaneous transluminal angioplasty and stenting of the proximal vertebral artery for symptomatic stenosis. AJNR 2000;21 : 727-731[Abstract/Free Full Text]
  13. Rocha-Singh K. Vertebral artery stenting: ready for prime time? Cathet Cardiovasc Interv 2001;54 : 6-7[CrossRef][Medline]
  14. Albuquerque FC, Fiorella D, Han P, Spetzler RF, McDougall CG. A reappraisal of angioplasty and stenting for the treatment of vertebral origin stenosis. Neurosurgery 2003;53 : 607-616[CrossRef][Medline]
  15. SSYLVIA Study Investigators. Stenting of Symptomatic Atherosclerotic Lesions in the Vertebral or Intracranial Arteries (SSYLVIA): study results. Stroke 2004;35 : 1388-1392[Abstract/Free Full Text]
  16. Christiaans MH, Ernst JM, Suttorp MJ, et al. Antonius Carotid Endarterectomy, Angioplasty, and Stenting Study Group. Restenosis after carotid angioplasty and stenting: a follow-up study with duplex ultrasonography. Eur J Vasc Endovasc Surg2003; 26:141 -144[CrossRef][Medline]
  17. Ringer AJ, German JW, Guterman LR, Hopkins LN. Follow-up of stented carotid arteries by Doppler ultrasound. Neurosurgery2002; 51:639 -643[CrossRef][Medline]
  18. Robbin ML, Lockhart ME, Weber TM, et al. Carotid artery stents: early and intermediate follow-up with Doppler US. Radiology 1997;205 : 749-756[Abstract/Free Full Text]
  19. Lee VS, Hertzberg BS, Kliewer MA, Carroll BA. Assessment of stenosis: implications of variability of Doppler measurements in normal-appearing carotid arteries. Radiology1999; 212:493 -498[Abstract/Free Full Text]
  20. Maleux G, Bernaerts P, Thijs V, et al. Extracranial carotid artery stenting in surgically high-risk patients using the Carotid Wallstent endoprosthesis: midterm clinical and ultrasound follow-up results. Cardiovasc Intervent Radiol 2003;26 : 340-346[CrossRef][Medline]
  21. Polak JF. Duplex sonography: can it be used to evaluate carotid artery stents? Radiology 1997;205 : 649-650[Free Full Text]
  22. Lal BK, Hobson RW 2nd, Goldstein J, Chakhtoura EY, Duran WN. Carotid artery stenting: is there a need to revise ultrasound velocity criteria? J Vasc Surg 2004;39 : 58-66[CrossRef][Medline]
  23. Griewing B, Brassel F, von Smekal U, Al Ahmar MT, Kessler C. Carotid artery stenting in patients at surgical high risk: clinical and ultrasound findings. Cerebrovasc Dis2000; 10:44 -48[CrossRef][Medline]
  24. Wakhloo AK, Tio FO, Lieber BB, Schellhammer F, Graf M, Hopkins LN. Self-expanding nitinol stents in canine vertebral arteries: hemodynamics and tissue response. AJNR 1995;16 : 1043-1051[Abstract]
  25. Schwartz RS, Henry TD. Pathophysiology of coronary artery restenosis. Rev Cardiovasc Med 2002;3 [suppl 5]: S4-S9[Medline]
  26. Lal BK, Hobson RW 2nd, Goldstein J, et al. In-stent recurrent stenosis after carotid artery stenting: life table analysis and clinical relevance. J Vasc Surg 2003;38 : 1162-1168[CrossRef][Medline]
  27. Chakhtoura EY, Hobson RW 2nd, Goldstein J, et al. In-stent restenosis after carotid angioplasty-stenting: incidence and management. J Vasc Surg 2001;33 : 220-225[CrossRef][Medline]
  28. Alvarez-Linera J, Benito-Leon J, Escribano J, Campollo J, Gesto R. Prospective evaluation of carotid artery stenosis: elliptic centric contrast-enhanced MR angiography and spiral CT angiography compared with digital subtraction angiography. AJNR2003; 24:1012 -1019[Abstract/Free Full Text]
  29. Leclerc X, Gauvrit JY, Pruvo JP. Usefulness of CT angiography with volume rendering after carotid angioplasty and stenting. AJR 2000; 174:820 -822[Free Full Text]
  30. Nicolau C, Gilabert R, Chamorro A, Vazquez F, Bargallo N, Bru C. Doppler sonography of the intertransverse segment of the vertebral artery. J Ultrasound Med 2000;19 : 47-53[Abstract]
  31. Ries S, Steinke W, Devuyst G, et al. Power Doppler imaging and color Doppler flow imaging for the evaluation of normal and pathological vertebral arteries. J Neuroimaging 1998;8 : 71-74[Medline]
  32. Buckenham TM, Wright IA. Ultrasound of the extracranial vertebral artery. Br J Radiol 2004;77 : 15-20[Abstract/Free Full Text]
  33. Trattnig S, Matula C, Karnel F, Daha K, Tschabitscher M, Schwaighofer B. Difficulties in examination of the origin of the vertebral artery by duplex and colour-coded Doppler sonography: anatomical considerations. Neuroradiology 1993;35 : 296-299[CrossRef][Medline]
  34. Bartels E, Fuchs HH, Flugel KA. Duplex ultrasonography of vertebral arteries: examination, technique, normal values, and clinical applications. Angiology 1992;43 : 169-180[Medline]
  35. Touboul PJ, Bousser MG, LaPlane D, Castaigne P. Duplex scanning of normal vertebral arteries. Stroke 1986;17 : 921-923[Abstract/Free Full Text]
  36. Kizilkilic O, Hurcan C, Mihmanli I, Oguzkurt L, Yildirim T, Tercan F. Color Doppler analysis of vertebral arteries: correlative study with angiographic data. J Ultrasound Med 2004;23 : 1483-1491[Abstract/Free Full Text]
  37. Seidel E, Eicke BM, Tetternborn B, Krummenauer F. Reference values for vertebral artery flow volume by duplex sonography in young and elderly adults. Stroke 1999;30 : 2692-2696[Abstract/Free Full Text]
  38. Dubbins PA. The kidney. In: Allan PL, Dubbins PA, Pozniak MA, McDicken WN, eds. Clinical Doppler ultrasound. London, England: Churchill Livingstone, 2000:169 -190
  39. Windecker S, Mayer I, De Pasquale G, et al. Stent coating with titanium-nitric-oxide for reduction of neointimal hyperplasia. Circulation 2001;104 : 928-933[Abstract/Free Full Text]

Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?



This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
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 Google Scholar
Google Scholar
Right arrow Articles by Kantarci, F.
Right arrow Articles by Islak, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kantarci, F.
Right arrow Articles by Islak, C.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS