(Stroke. 2000;31:376.)
© 2000 American Heart Association, Inc.
Original Contributions |
Identification of Patients at Risk for Periprocedural Neurological Deficits Associated With Carotid Angioplasty and Stenting
From the Department of Neurosurgery and Toshiba Stroke Research Center (A.I.Q., A.R.L., M.F.K.S., M.S., G.L., A.K.W., L.R.G., L.N.H.) and Department of Neurology (V.J.), School of Medicine and Biomedical Sciences, State University of New York at Buffalo, NY.
Correspondence to Adnan I. Qureshi, MD, SUNYAB Department of Neurosurgery, Millard Fillmore Hospital, 3 Gates Circle, Buffalo, NY 14209-1194. E-mail qureshi{at}acsu.buffalo.edu
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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Background and Purpose—Transient or permanent neurological deficits can occur in the periprocedural period following carotid angioplasty and stenting (CAS), presumably due to distal embolization and/or hemodynamic compromise. We performed this study to identify predictors of neurological deficits associated with carotid angioplasty and stent placement.
Methods—We reviewed medical records and angiograms in a consecutive series of patients who underwent CAS for symptomatic or asymptomatic cervical internal carotid artery stenosis from June 1996 through December 1998. Using logistic regression analysis, we evaluated the effect of demographic, clinical, intraprocedural, and angiographic risk factors on subsequent development of periprocedural neurological deficits. Periprocedural neurological deficits were defined as new or worsening transient or permanent neurological deficits that occurred during or within 48 hours of the procedure.
Results—A total of 111 patients (mean age 68.2±9.1 years) who
underwent CAS for asymptomatic (n=54) or
symptomatic (n=57) stenoses were included in this
study. A total of 14 periprocedural neurological deficits (13%) were
observed either during (n=4) or after (n=10) the procedure. Three
identified variables were independently associated with
periprocedural neurological deficits: symptomatic lesion
(OR 8.3, 95% CI 1.6 to 42.6), length of stenotic segment
11.2 mm (OR 5.2, 95% CI 1.2 to 22.5), and absence of
hypercholesterolemia (OR 5.4, 95% CI 1.4 to
20.9). Other variables, including age and degree of
stenosis (defined by NASCET criteria), were not associated with
periprocedural neurological deficits.
Conclusions—A combination of clinical and angiographic variables can be used to identify patients at risk for periprocedural neurological deficits after CAS. Such identification may help in selection of patients who may benefit from novel pharmacological and mechanical preventive approaches.
Key Words: angioplasty • carotid stenosis • cerebral ischemia, transient • stent • stroke
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Recently, carotid angioplasty and stenting (CAS) has been introduced as an alternative to carotid endarterectomy (CEA) for treatment of carotid stenosis.1 2 3 4 Temporary or permanent neurological deficits can occur during and after carotid angioplasty and stent placement. The frequency of neurological deficits has ranged from 3% to 13% in previous reports.4 5 6 7 8 Almost all of these events are ischemic in origin and related to distal embolization and/or hemodynamic compromise. Novel pharmacological9 10 11 12 13 and mechanical approaches14 15 are being introduced as adjuncts to angioplasty and stent placement to reduce the risk of these events. An important issue that needs to be addressed is the identification of patients who are at highest risk for neurological events and therefore will benefit most from use of these new preventive approaches and strategies. We performed this study to identify patients at risk for neurological events associated with carotid angioplasty and stent placement using routinely available data in a consecutive series of patients.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Patients
We reviewed the medical records of all patients who underwent carotid artery angioplasty and stent placement from June 1996 through December 1998. Our institution’s Human Investigations Committee approved the study. Patients were identified by a local registry maintained by the Department of Neurosurgery. Only patients who underwent angioplasty for cervical internal carotid artery stenosis with or without extension into bifurcation and common carotid artery were included. Patients were excluded if they had stenosis related to dissection or radiation therapy. Of 220 cases at our institution since 1995, only the most recent 120 cases performed between June 1996 and December 1998 were included, because the angiographic images were available in digital form on video tape, which allowed adequate characterization of lesion morphology.
Protocol for Angioplasty and Stent Placement
Patients were started 72 hours before the procedure on aspirin
325 mg/d, and ticlopidine 250 mg twice daily or clopidogrel 75 mg/d. On
the day of the procedure, each patient was evaluated by one of the
physicians from the endovascular team, and a complete physical and
neurological examination was documented. Each patient was given 10 mg
of decadron and 60 mg of nimodipine orally on the morning of the
procedure. All the procedures were performed under local
anesthesia. A baseline angiogram was performed, and the
lumen diameter of the stenotic and adjacent segments were
measured. An intravenous heparin bolus 5000 to 7500 U was
given to achieve activated thromboplastin time between 300 and
350 seconds. Before introduction of the balloon,
intra-arterial urokinase 100 000 to 250 000 U was infused
locally through a microcatheter if there was any subjective evidence of
local thrombosis or ulceration in the stenotic segment on
magnified biplane angiography.16 It should be noted that
the decision to use urokinase was subject to treating physician’s
preference and angiographic interpretation. Either a 9F catheter or a
7F guide sheath was advanced into the common carotid artery and placed
proximal to the stenosis. The flexible guidewire (0.14 to 0.18
inches in diameter) with angulated tip was advanced through the guide
catheter, navigated across the stenosis, and positioned in the
distal arterial segment. The vessel was predilated with a
percutaneous transluminal angioplasty balloon (PTA)
catheter placed across the stenosis. The objective of the
predilatation was to dilate the vessel just enough to allow safe
passage of the stent delivery device. After predilatation, a stent was
placed across the dilated segment over the guidewire with a stent
delivery system. The size of stent selected was determined by
evaluation and measurement of both baseline and postdilatation
angiographic studies. The type of stent was chosen according to
physician preference, lesion characteristics, and commercial
availability. A poststent dilatation of the angioplasty balloon was
performed to fully expand the stent to reference diameter. When the
inflation had been completed, a final cervical and intracranial
angiogram was obtained to confirm that the result was satisfactory and
that intracranial circulation had not been compromised. Limited
neurological examinations were performed throughout the procedure, and
a complete examination was documented at completion.
The patient was transferred to the neurointensive care unit for overnight observation. Heart and respiratory rates were continuously monitored. Blood pressure was monitored every 15 minutes. Three complete neurological examinations were documented by physicians for each patient. The first evaluation was performed before the procedure. Subsequent evaluations were performed immediately and 24 hours after the procedure. Neurological evaluations were performed every 2 hours and more frequently if necessary by the nurses in the neurointensive care unit. Any episode of neurological change detected during the nurses’ examination was further evaluated by a physician.
Data Collection
Medical records were reviewed, and the following information
was collected for each patient: age and sex; current smoking or alcohol
use; known angina pectoralis, previous myocardial infarction (MI),
coronary artery disease, hypertension, diabetes mellitus,
hypercholesterolemia (defined as serum
cholesterol >200 mg/dL or use of antilipidemic
medications), cardiac dysrhythmias, valvular heart disease,
cardiac failure, peripheral vascular disease, or renal
insufficiency; history of previous coronary bypass or
angioplasty or carotid endarterectomy; and use of
antiplatelet or other medications before admission. Any clinical
symptoms were noted and used to evaluate whether ipsilateral or
contralateral carotid artery was symptomatic. The following
details were collected for the procedure: the size and number of
balloon inflations and the size and type of stent placed. We also
recorded any new or worsening neurological deficits during or
within 48 hours of the procedure. The total period of intensive care
unit and hospital stay was recorded. Any nonneurological
complications during hospitalization were noted.
Evaluation of Angiograms
Digital subtraction angiographic images were retrospectively
collected from the digital tape storage system of our angiography unit
(Toshiba Inc). Ipsilateral and contralateral
diagnostic images of the extracranial carotid arteries and
the intracranial circulation were obtained, as well as images of the
stented artery and of the intracranial perfusion after stent placement.
The images of extracranial carotid arteries were transferred to a
computer workstation running NIH Image software
(http://rsb.info.nih.gov/NIH-IMAGE/) for subsequent measurements. One
of the investigators, who was blinded to the clinical data and outcome
of the patients, performed all the measurements. After adjusting for
magnification, the diameters of the stenosis, of the distal
internal carotid artery, and of the stented lesion were measured. The
degree of stenosis was calculated according to the NASCET
method, ie, 1-(diameter of stenosis/distal ICA diameter). This
method was chosen to ensure comparability with other
studies.17 The extension of the lesion was classified
whether it was limited to the internal carotid artery or extended into
the common carotid artery. The length of the lesion was measured, and
each lesion was classified morphologically as regular, irregular, or
irregular and ulcerated. Each of these morphological features was
further analyzed as a dichotomized variable (smooth versus
irregular with or without ulceration).
Statistical Analysis
The effects of 21 variables collected from archived patient
charts and 6 variables obtained from angiographic images were
evaluated on periprocedural neurological deficits, which were defined
as new or worsening neurological deficits during or within 48 hours
after carotid angioplasty and stent placement. The association between
continuous variables and neurological deficits was plotted to test
for linearity of the relation as suggested by Hosmer and
Lemeshow.18 Age was found to have a linear relationship
and thus included as a continuous variable. For degree of
stenosis and lesion length, a nonlinear relationship was
observed. According to the "shape" of the curve, the continuous
variable "degree of stenosis" was divided into 4
groups: 
55%, 56% through 68%, 69% through 75%, and >75%.
Lesion length was dichotomized at 11.2 mm and then entered in the
multivariate model. Systat (Version 8, SPSS Inc)
statistical software was used for all analyses. All collected
variables were initially entered into the logistic regression model
on "neurological complication" as the dependent variable.
Backward stepwise exclusion of variables was performed using a
criterion of P>0.1. After a set of significant
variables were identified, possible interactions were added to the
model and retested with backward stepwise regression. All interactions
were nonsignificant and did not remain in the model.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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A total of 120 patients underwent carotid angioplasty and stent placement from July 1996 through December 1998. Nine patients were excluded because either complete clinical (n=7) or angiographic (n=2) material was not available. A total of 111 patients (mean age 68.2±9.1 years) undergoing CAS for asymptomatic (n=54) or symptomatic stenosis (n=57) were included in the study. The frequency of periprocedural neurological deficits was similar in the excluded patients (1 of 9 patients) compared with the included patients (14 of 111 patients, P=1.0). The patients were treated with the following stents: Wallstents(Schneider; n=77), GFX(Arterial Vascular Engineering; n=1), Integra(SCIMED Boston Scientific; n=7), Smart stents(Johnson & Johnson; n=5), Palmaz (Johnson & Johnson; n=20), and combination of Wall and Palmaz stents (n=1).
Periprocedural neurological deficits occurred in 14 patients (13%) either during (n=4) or after (n=10) the procedure. Eight of 14 events occurred in the first 24 hours after the procedure, and another 2 occurred at 48 hours after the procedure. New deficits were observed in 12 patients, and 2 patients experienced worsening of preexisting deficits. Neurological deficits were referable to the hemisphere ipsilateral to the operated side in 11 patients. In the other 3 patients, neurological deficits were referable to the contralateral side. One patient had total occlusion of the carotid artery contralateral to the operated side. Another patient had high-grade carotid stenosis on the contralateral side and suffered deficits following an episode of hypotension in the postoperative period. The third patient had a previous stroke on the contralateral side and experience worsening of preexisting deficits in the postprocedural period. The deficits had resolved within 48 hours in 10 patients. At discharge, 1 patient had worsened left hemiparesis, 1 had moderate expressive aphasia with impaired fine finger movements, and the other 2 patients had mild residual weakness during hand movements. At 1-month follow-up, the deficits in 2 patients had improved. None of the new strokes was considered disabling. One patient had previous disability due to stroke that was unaffected by postprocedural worsening.
Table 2
shows the demographic and
clinical characteristics of the patients in the study.
Prophylactic intra-arterial urokinase was
administered before angioplasty in doses ranging from 100 000 IU to
250 000 IU. The frequency of periprocedural neurological deficits was
similar in patients who received prophylactic urokinase (11
of 93) and those who did not (3 of 19, P=0.6).
Table 3 shows the frequency of
periprocedural neurological deficits according to various angiographic
characteristics. The final logistic regression model consisted of 3
variables: symptomatic lesion (OR 8.3, 95% CI 1.6 to
42.6), length of stenotic segment 11.2 mm (OR 5.3, 95%
CI 1.2 to 22.5), and absence of
hypercholesterolemia (OR 5.4, 95% CI 1.4 to
20.9; Table 4). Other variables, including age, sex,
hypertension, diabetes, and smoking, did not increase the risk for
neurological complications after angioplasty and stenting. The degree
of stenosis (defined by NASCET criteria) was unrelated to
periprocedural complications.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Salient Findings of the Study
We identified 3 risk factors for periprocedural neurological deficits from a analysis of a consecutive series of patients who underwent carotid angioplasty and stent placement. These factors were presence of symptomatic ipsilateral carotid artery stenosis, long stenotic lesions (defined as
11.2 mm in this study), and absence of
hypercholesterolemia. Our study also points out
the diverse nature of postoperative neurological deficits. Most
neurological deficits (8 of 14 events) occurred in the first 24 hours
after the procedure. Four events were observed during the procedure,
and 2 others occurred at 48 hours after the procedure. The outcome of
these events was favorable, with complete resolution observed within 48
hours in 10 of 14 patients.
Risk of Periprocedural Neurological Deficits
Previous studies have documented the risk of thromboembolic events
associated with PTA alone or with stent placement. The risk of
neurological events associated with PTA alone varies from 0% to 9%,
depending on the patient population and procedural
technique.5 14 19 20 21 Theron et al14 reported
5 neurological events, related to either embolism or dissection, in 38
patients with asymptomatic carotid artery stenosis
who underwent PTA. Gil-Peralta et al5 reported 7
neurological events, related to either embolism or dissection, in a
series of 82 patients who underwent PTA. The frequency of neurological
events in patients who undergo PTA followed by stent placement ranges
from 3% to 13%.4 6 7 8 20 Mathur et al8
observed 19 neurological events in 231 patients who underwent PTA
followed by stent placement. All events were related to
thromboembolism. Henry et al6 reported 8 neurological
events among 163 patients who underwent PTA followed by stent
placement. Jordan et al7 observed 14 neurological events
in a series of 107 patients who underwent PTA followed by stent
placement. In our series, we observed a rate of 13% for periprocedural
neurological deficits with the inclusion of transient events.
Risk Factors for Periprocedural Neurological Deficits
In our study, we identified 3 variables from numerous
clinical and angiographic characteristics that identified patients at
risk for the development of periprocedural neurological deficits. These
included symptomatic lesion, absence of
hypercholesterolemia, and lesion length by
angiographic measurements. The intrinsic characteristics of the
stenotic plaque observed in symptomatic patients
predispose them to a higher risk of thromboembolic
events.22 23 This is supported by the higher risk of
periprocedural stroke observed during
endarterectomy in symptomatic patients
in NASCET and other studies compared with asymptomatic
patients in the ACAS study.24 25 26 The plaque in
symptomatic patients have a higher frequency of fissuring
as well as in situ thrombosis.22 23 Both of these
characteristics possibly contribute to increased thrombogenicity of the
stenotic segment during and after PTA and stent placement. The
relationship between periprocedural neurological deficits and absence
of hypercholesterolemia is less obvious. The
plaques in patients without
hypercholesterolemia have a low content of
lipid containing foam cells and glycosaminoglycan
deposition.27 Although most of our patients had carotid
Doppler ultrasound performed, the studies were performed at
different institutions and most reports provided only velocity
measurements. Therefore, no comments can be made regarding the
composition of plaque and its association with
hypercholesterolemia in our series. Whether
morphological characteristics of the plaque or undefined covariates in
patients who develop carotid stenosis without
hypercholesterolemia are responsible for this
paradoxical association needs to be defined in future studies. The
length of the lesion is another factor that determines the operative
manipulation required and therefore the risk of complications. Longer
lesions require longer stents and at times multiple angioplasties after
stent placement to ensure adequate dilation across the
stenosis. The postdilatation surface of longer lesions provides
a larger area of endothelial injury, dissections, and
stent struts that acts as a prothrombotic surface in the acute period
after PTA and stent placement.
Previous Study for Identification of Risk Factors
In a previous study, Mathur and coworkers8 identified
predictors of stroke in patients undergoing PTA followed by stent
placement. Age, degree of stenosis, and the length or
multiplicity of the lesions determined the stroke risk. Dependency on
the degree of the stenosis was not linear. Stenosis of
70% to 80% posed the greatest risk, whereas greater or lesser
stenoses were associated with fewer strokes. In our study,
length of lesion was observed to be associated with periprocedural
neurological deficits. Neither age nor degree of stenosis
contributed to the risk of neurological events in our study. The
outcome studied by Mathur et al8 was stroke within 1 month
of PTA and stent placement. In contrast, the outcome evaluated in our
study consisted of neurological events within the first 48 hours after
PTA and stent placement.
Potential Applications of the Predictive Scheme
We think that variables which are routinely available may be
helpful in identification of those patients who may benefit most from
novel approaches for prophylaxis of thromboembolic events. Multiple
strategies are in practice to reduce the frequency of neurological
events associated with PTA followed by stent placement. At present,
the most common regimen consists of preoperative and postoperative use
of aspirin with either ticlopidine or clopidogrel, and
intravenous heparin to prolong activated
thromboplastin time during the procedure. In our study and most of the
previously mentioned studies, both antiplatelet medication and
intraprocedural heparin were used. Novel preventive strategies, which
include both pharmacological and mechanical approaches, are undergoing
evaluation at present. These include the development of new
antiplatelet medication, such as antibodies to platelet
glycoprotein IIb/IIIa receptors.9 10 11 12 13 This is
also supplemented by improvement in stent design and delivery devices.
The high-risk group identified in our study may represent the
best candidates for such approaches.
Generalizability of the Scheme
An issue related to interpretation of our results is whether the
results are representative of PTA followed by stent
placement in other institutions. At our institution, PTA followed by
stent placement is generally reserved for patients who are poor
candidates for carotid endarterectomy, as is
evident by the high frequency of cardiac and other diseases observed in
our patient population. Decadron used to be administered preoperatively
at our institute, a practice which has been discontinued. The
antiplatelet and heparin regimens we use are similar to those in
other institutions that perform PTA and stent placement. Based on these
observations, we think that these results can be used in other patient
population as well. We have used intra-arterial urokinase
in a subset of patients16 to dissolve loose intramural
thrombi. In post hoc analysis, however, the use of
intra-arterial urokinase did not influence the risk of
neurological events. Prophylactic urokinase is no longer
being used at our institution due to availability of more effective
medications, such as glycoprotein IIb/IIIa
inhibitors.
Limitations of the Study
Because of the retrospective nature of the study, we could not
control for the exact frequency and extent of neurological
examinations. This may induce an unrecognized bias. However, because
the same physicians were involved in the care of all patients, little
variability in practice patterns is expected. We were unable to
validate the predictive value of the identified variables in a
separate set of patients owing to the small number of subjects and
observed events in this study.
Conclusions
A combination of clinical and laboratory variables can be used
to identify patients at risk for periprocedural neurological deficits.
Such identification may help in the selection of appropriate patients
who are good candidates for novel pharmacological and mechanical
preventive approaches. Prospective studies are required to validate the
predictive significance of the identified variables.
Received June 17, 1999; revision received November 18, 1999; accepted November 18, 1999.
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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 I. Linfante, J. A. Hirsch, M. Selim, G. Schlaug, L. R. Caplan, and A. S. Reddy Safety of Latest-Generation Self-expanding Stents in Patients With NASCET-Ineligible Severe Symptomatic Extracranial Internal Carotid Artery Stenosis Arch Neurol, January 1, 2004; 61(1): 39 - 43. [Abstract] [Full Text] [PDF]
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D. J. Fox Jr, C. J. Moran, D. T. Cross III, R. L. Grubb Jr, K. M. Rich, M. R. Chicoine, R. G. Dacey Jr, and C. P. Derdeyn Long-Term Outcome After Angioplasty for Symptomatic Extracranial Carotid Stenosis in Poor Surgical Candidates Stroke, December 1, 2002; 33(12): 2877 - 2880. [Abstract] [Full Text] [PDF]
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 S. Chaturvedi and R. Fessler Angioplasty and stenting for stroke prevention: Good questions that need answers Neurology, September 10, 2002; 59(5): 664 - 668. [Abstract] [Full Text] [PDF]
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G. Orlandi, S. Fanucchi, C. Fioretti, G. Acerbi, M. Puglioli, R. Padolecchia, F. Sartucci, and L. Murri Characteristics of Cerebral Microembolism During Carotid Stenting and Angioplasty Alone Arch Neurol, September 1, 2001; 58(9): 1410 - 1413. [Abstract] [Full Text] [PDF]
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G. S. Roubin, G. New, S. S. Iyer, J. J. Vitek, N. Al-Mubarak, M. W. Liu, J. Yadav, C. Gomez, and R. E. Kuntz Immediate and Late Clinical Outcomes of Carotid Artery Stenting in Patients With Symptomatic and Asymptomatic Carotid Artery Stenosis : A 5-Year Prospective Analysis Circulation, January 30, 2001; 103(4): 532 - 537. [Abstract] [Full Text] [PDF]
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A. Barth, L. Remonda, K.-O. Lovblad, G. Schroth, and R. W. Seiler Silent Cerebral Ischemia Detected by Diffusion-Weighted MRI After Carotid Endarterectomy Stroke, August 1, 2000; 31(8): 1824 - 1828. [Abstract] [Full Text] [PDF]
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