 |
|
Long-term Risk of Stroke and Other Vascular Events in Patients With Asymptomatic Carotid Artery Stenosis
Zurab G. Nadareishvili, MD, PhD;
Peter M. Rothwell, MD, PhD;
Vadim Beletsky, MD, PhD;
Angela Pagniello, BA;
John W. Norris, MD
Arch Neurol. 2002;59:1162-1166.
ABSTRACT
| |
Context The annual risk of ischemic stroke in patients with asymptomatic carotid
artery stenosis is about 2% during the short-term (2-3 years), but the long-term
risks of stroke and other vascular events are unknown, although they may affect
surgical decision making.
Objective To evaluate the long-term risk of stroke and other vascular events in
patients with asymptomatic carotid artery stenosis.
Design Cohort study with a median follow-up of 10 years (range, 5-18 years).
Setting The teaching hospital of the University of Toronto, Toronto, Ontario.
Patients From the initial cohort of 500 patients, 106 patients with asymptomatic
carotid artery stenosis were selected because they had completed at least
5 years of follow-up.
Main Outcome Measures Ipsilateral stroke, myocardial infarction, and nonstroke vascular death.
Results The 10- and 15-year actuarial risks of ipsilateral stroke were 5.7%
(95% confidence interval [CI], 0%-12%) and 8.7% (95% CI, 1%-17%), respectively,
in patients with 0% to 49% internal carotid artery stenosis, and 9.3% (95%
CI, 1%-18%) and 16.6% (95% CI, 1%-32%) in patients with 50% to 99% internal
carotid artery stenosis. The 10- and 15-year risks of myocardial infarction
and nonstroke vascular death were 10.1% (95% CI, 4%-16%) and 24.0% (95% CI,
14%-34%). Age (P = .02), diabetes mellitus (P = .02), and internal carotid artery stenosis of 50% or
more (P = .04) were predictive of increased risks
of myocardial infarction and nonstroke vascular death. Internal carotid artery
stenosis of 50% or more did predict the risk of ipsilateral stroke (P = .003) when all 181 asymptomatic carotid arteries were
included.
Conclusions The annual stroke risk in patients with asymptomatic carotid artery
stenosis was low and remained stable during long-term follow-up. Any benefit
from carotid surgery is therefore unlikely to increase significantly with
long-term follow-up. The high long-term risks of myocardial infarction and
nonstroke vascular death suggest that prevention strategies should concentrate
on coronary risk more than stroke risk.
INTRODUCTION
CAROTID ARTERY atherosclerosis is responsible for 20% to 30% of ischemic
strokes.1 Recent prospective, randomized multicenter
trials have demonstrated the superiority of carotid endarterectomy (CEA) over
medical therapy for stroke prevention among patients with previous cerebral
ischemic events.2-3 However, the
role of CEA in asymptomatic carotid artery stenosis remains controversial,4-6 partly because of uncertainty
about the natural history of the condition with medical treatment alone.
Endarterectomy reduces the relative risk of ipsilateral stroke and death
by about 50%,7 but the absolute risk of stroke
in patients receiving medical treatment is relatively low. Most natural history
studies of asymptomatic carotid artery stenosis have reported an annual risk
of ipsilateral stroke of approximately 1% to 2%, depending on the degree of
internal carotid artery (ICA) stenosis.8-12
However, follow-up in these studies was usually only 2 to 3 years, and there
are few published data on the long-term risks. There are also very few data
on the factors that identify asymptomatic patients with a higher-than-average
risk of stroke and other vascular outcomes on long-term follow-up who might
benefit most from preventive treatment.
To provide more information about long-term risks and risk factors for
stroke and other vascular events, we studied patients with asymptomatic carotid
bruits in our neuro-Doppler laboratory from 1981 through 1999.
PATIENTS AND METHODS
PATIENTS AND STUDY DESIGN
A total of 106 patients, from an initial cohort of 500 prospectively
studied patients,13 had long-term continuous
Doppler follow-up. The study is confined to this subgroup. All patients had
annual Doppler and clinical follow-up. This included documentation of putative
risk factors for stroke (age, sex, hypertension, diabetes mellitus, and ischemic
heart disease). Medications were also recorded, although compliance was not
tested. If follow-up visits were missed, patients were telephoned and asked
about further clinical events. We recorded the following end points: ipsilateral
stroke, ipsilateral transient ischemic attack (TIA), myocardial infarction
(MI), CEA, nonstroke vascular death, and nonvascular death. All hospital records
were audited at the end of the study. We documented details of all deaths,
whenever possible, according to hospital records and autopsy reports. The
definition of nonstroke vascular death included death from MI, sudden death,
cardiac failure, ruptured aorta, and peripheral vascular disease.
CAROTID ARTERY IMAGING
Patients were examined with 2 generations of Doppler equipment. Both
were validated against catheter angiography on an annual basis.13-14
Patients enrolled in the study from 1981 through 1991 were examined with continuous-wave
carotid Doppler scanning (Dopscan 1050; Carolina Medical Inc, King, NC) using
established criteria to estimate the percentage reduction in the cross-sectional
area of the carotid arterial lumen.15 In our
laboratory, the technique has a sensitivity of 87% and a specificity of 91%
in detecting ICA stenosis of more than 30% compared with conventional angiography.13 Patients studied from 1991 through 1999 underwent
ultrasound testing using a color-coded duplex ultrasound unit (Ultramark-9;
ATL Ultrasound, Bothell, Wash), and a high degree of correlation was established
between the peak systolic velocity and angiographic measurement of ICA stenosis.14
ANALYSIS
In view of the partly retrospective nature of the clinical follow-up,
analysis of cerebrovascular outcome events was limited to stroke. Where relevant,
the number of recorded TIAs is mentioned in the results, but these events
are not included in the formal analyses.
Data were first analyzed for each patient, with each subject categorized
according to the most highly stenosed vessel. If the stenoses were identical,
the left carotid artery was chosen.7 To control
for events occurring contralateral to the patient's most highly stenosed vessel,
and to determine the relationship between plaque progression and ipsilateral
stroke, cerebrovascular outcomes for each internal carotid artery were also
analyzed separately and event rates were calculated per vessel. Previously
symptomatic (ipsilateral stroke or TIA) and/or surgically treated (CEA) arteries
were excluded from the analysis. Arteries were censored following the first
ipsilateral event (stroke or CEA), but the contralateral asymptomatic artery
was still followed.
To study the effect of baseline ICA stenosis on outcome, stenosis was
categorized as 0% to 49% or 50% to 99%. Our sample size was insufficient to
allow analysis of the degree of stenosis as a continuous variable. Plaque
progression was determined according to previously published criteria.13
Statistical analysis was performed using SPSS version 10.05 (Statistical
Product and Service Solutions Inc, Chicago, Ill). Continuous data were summarized
as mean ± SD or median (range). We used a t
test for comparison of means. In cases when normality and/or equal variance
tests failed, the Mann-Whitney test was used. Proportional differences among
the groups were evaluated with a  2 test. Event rates over
specific follow-up periods were calculated by life-table analysis. Survival
curves were calculated by Kaplan-Meier analysis of the time to the first event.
Comparison of survival curves was performed with the log-rank test.
RESULTS
One hundred six patients (44 women; mean ± SD age, 64 ±
8 years) were followed for a median of 10 years (range, 5-18 years) for a
total of 1010 patient-years of observation. At the end of the study, 1506
Doppler scans were available for analysis. All patients underwent follow-up
for 5 years, half for 10 years, 25% for 15 years, and 5% for 18 years. At
the baseline, 70% of patients had hypertension, 23% had diabetes, and 11%
were smokers.
To determine the differences between patients with complete follow-up
(n = 106) and those with incomplete follow-up (n = 394), we compared the baseline
characteristics of the 2 groups (Table 1). The mean age of patients was similar, but there were significantly
more men (P = .03) and patients with diabetes (P<.007) in the group with complete follow-up. There
were significantly fewer patients with mild (<30%) ICA stenosis but significantly
more patients with moderate (30%-74%) and severe ( 75%) stenosis in the
group with complete follow-up.
|
|
|
|
Table 1. Baseline Characteristics of Patients With and Without Complete
Follow-up*
|
|
|
ANALYSIS PER PATIENT
The maximum asymptomatic ICA stenosis was less than 30% in 25 patients,
30% to 49% in 23 patients, 50% to 69% in 23 patients, and 70% or more in 35
patients. Eleven strokes occurred during follow-up, all of which were in the
carotid territory and 10 of which were ipsilateral to the most stenosed artery.
The rate of ipsilateral stroke remained stable up to the maximum follow-up
of 18 years (Figure 1). The 10-
and 15-year actuarial risks of ipsilateral stroke were 5.7% (95% confidence
interval [CI], 0%-12%) and 8.7% (95% CI, 1%-17%), respectively, in patients
with 0% to 49% ICA stenosis and 9.3% (95% CI, 1%-18%) and 16.6% (95% CI, 1%-32%)
in patients with 50% to 99% ICA stenosis. A TIA occurred in 13 cases, of which
5 were ipsilateral to the most severe stenosis. None of the clinical risk
factors were significant predictors of ipsilateral stroke (Table 2).
|
|
|
|
Figure 1. Survival free of ipsilateral stroke
(IS) (thick line) and survival free of myocardial infarction (MI) or nonstroke
vascular death (NSVD) (thin line) in patients with asymptomatic carotid artery
stenosis.
|
|
|
|
|
|
|
Table 2. Associations Between Baseline Clinical Risk Factors and the
Main Study Outcomes Derived From Univariate Regression*
|
|
|
Seventeen patients died during follow-up, 2 from stroke and 10 from
cardiac causes, and 10 patients had an MI. The 10- and 15-year risks of MI
and nonstroke vascular death were 10.1% (95% CI, 4%-16%) and 24.0% (95% CI,
14%-34%), respectively. These risks were higher than the risk of ipsilateral
stroke (Figure 1). Nonstroke vascular
death was more common in patients with baseline maximum ICA stenosis (50%-99%)
than in those with maximum ICA stenosis (0%-49%) (log-rank = 4.3; P = .04), and there was a trend toward an increased risk of MI (log-rank
= 2.7; P = .10). The combined outcome was significantly
increased (log-rank = 4.7; P = .03).
The clinical risk factors were more predictive of MI and nonstroke vascular
death than of ipsilateral stroke (Table
2). Univariate Cox regression showed that risk of MI and nonstroke
vascular death increased with age (hazard ratio [HR], 2.07 per 10 years; P = .02), was higher in patients with diabetes (HR, 3.12; P = .02) and patients with stenosis of 50% or more (HR,
1.80; P = .04), and was nonsignificantly higher in
men (HR, 2.43; P = .09). Age (P = .01) and stenosis of 50% or more (P =
.07) were predictors of the combined end point of stroke/MI/vascular death.
ANALYSIS PER VESSEL
To increase statistical power and to take into account both carotid
arteries, data were reanalyzed calculating the end points for individual arteries.
Thirty-one previously symptomatic and/or surgically treated arteries were
excluded, leaving 181 arteries in the analysis.
There were 38 CEAs performed, and 29 of these were performed on previously
symptomatic arteries initially excluded from the analysis. Therefore, only
9 CEAs were included in our analysis; 2 arteries underwent CEA after TIAs
that occurred in asymptomatic vessels during follow-up, and the remaining
7 ICAs were surgically treated for asymptomatic carotid artery stenosis. All
9 CEAs were conducted in arteries with ICA stenosis of more than 60%. Baseline
ICA stenosis was 30% or less in 74 arteries, 30% to 49% in 34 arteries, 50%
to 69% in 30 arteries, and 70% or more in 43 arteries.
One stroke occurred contralateral to the most severely stenosed asymptomatic
ICA. Therefore, there were 11 strokes in the territory of 181 asymptomatic
carotid arteries during follow-up. The risk of stroke was significantly higher
in arteries with ICA stenosis of 50% to 99% than in those with 0% to 49% stenosis
(log-rank = 9; P = .003; Figure 2). For arteries with 50% to 99% stenosis, the 10- and 15-year
risks were 8.5% (95% CI, 1%-17%) and 18.0% (95% CI, 4%-31%), respectively.
Ipsilateral TIA occurred in the distribution of another 13 ICAs.
|
|
|
|
Figure 2. Survival free of ipsilateral stroke
(IS) distal to 181 asymptomatic carotid arteries according to the degree of
stenosis: 0% to 49% (thick line) and 50% to 99% (thin line).
|
|
|
Progression of stenosis was documented in 55 ICAs (30%), and stenosis
remained stable in 126 arteries. Overall, median baseline ICA stenosis was
35% compared with 50% at the end of follow-up (P<.001;
Mann-Whitney test). Progression of stenosis during the follow-up was not a
significant predictor of ipsilateral stroke.
COMMENT
We have shown that the long-term risk of stroke from asymptomatic stenosis
is less than 1% per year for stenoses of 50% or more and about 1% per year
for stenoses of less than 50%. These results are consistent with previous
short-term follow-up studies8-13
and show that the low risk of stroke remains constant with time. This has
important implications for surgical treatment because the marginal short-term
benefits from CEA do not change during at least the next 10 years, whereas
the long-term risks of MI and nonstroke vascular death are greater than the
risk of stroke. Management of patients with asymptomatic carotid artery stenosis
should, therefore, concentrate as much on reduction of nonstroke vascular
risk as on stroke risk.
With the exception of the degree of ipsilateral carotid artery stenosis,
baseline clinical characteristics did not predict the risk of stroke on long-term
follow-up. The difficulty of predicting the risk of stroke in patients with
asymptomatic stenosis has been noted previously.16
In contrast, and despite similarly small numbers of events, there were several
useful predictors of MI and nonstroke vascular death, including age, sex,
diabetes, and the maximum degree of asymptomatic carotid artery stenosis.
The predictive value of the severity of asymptomatic carotid artery disease
is consistent with our previous report of short-term risk.13
Plaque progression was documented in about one third of our patients.
This is higher than reported in other cohorts.17
However, progression of stenosis increases with time,18
and our rate is likely to reflect the long follow-up. In contrast to our previous
finding,13 we did not find a relationship between
plaque progression and ipsilateral stroke.
Although we consider our results valid, our study population was limited
to a subgroup of 106 patients from the initial cohort of 500.13
We selected this group because they had continuous long-term Doppler follow-up,
but this may have introduced some degree of selection bias. We cannot exclude
the possibility that the risk of stroke and other vascular events was higher
in those patients who were not followed up continuously, thereby underestimating
the long-term risk. However, baseline risk factor comparison between our cohort
and the remainder who had incomplete follow-up shows that patients with complete
follow-up were not healthier than those without it. In fact, the higher prevalence
of diabetes and the preponderance of men and more severe ICA stenoses in our
study cohort produced a bias favoring a poorer prognosis than for those with
incomplete follow-up. Therefore, it is less likely that the population of
patients without long-term follow-up had higher incidence of stroke, MI, or
vascular death.
Also, selection bias is less likely to have had a qualitative effect
on risk factor estimates, and these should be more reliable. In some cases,
clinical follow-up was obtained retrospectively, so it is possible that we
may have missed some minor strokes, which may also have caused underestimation
of the stroke risk. These 2 factors that potentially contributed to underestimation
of the stroke risk mean that, if anything, more strokes occurred than we calculated.
Although our sample size (106 patients with 181 asymptomatic stenoses) was
relatively small, and our results must be interpreted with caution, there
are currently no other data available on the long-term risks of stroke (and
other vascular events) in patients with asymptomatic carotid artery stenosis.
In the Asymptomatic Carotid Atherosclerosis Study, CEA reduced the relative
risk of ipsilateral stroke and operative death by 53% in patients with ICA
stenosis of more than 60% with 30-day operative risk of stroke and death of
less than 2.3%.7 However, not all centers achieve
this low operative risk,19-20
and negative cost-effectiveness is another important consideration.19, 21 Our data show that the annual risk
of stroke with medical treatment remains consistently low on long-term follow-up,
suggesting that any benefit from endarterectomy for asymptomatic carotid artery
stenosis is unlikely to increase dramatically with longer follow-up.
The low risk of stroke observed over many years in our patients with
asymptomatic carotid artery stenosis, in combination with the continuing long-term
risk of MI and nonstroke vascular death, challenges the value of CEA in these
patients. Any benefit from carotid surgery is unlikely to increase significantly
with long-term follow-up. The high long-term risks of MI and nonstroke vascular
death suggest that prevention strategies should concentrate on coronary risk
more than stroke risk.
AUTHOR INFORMATION
Accepted for publication January 29, 2002.
Author contributions: Study concept and design (Drs Nadareishvili, Rothwell, and Norris); acquisition
of data (Drs Nadareishvili and Beletsky and Ms Pagniello); analysis and interpretation of data (Drs Nadareishvili,
Rothwell, and Norris); drafting of the manuscript (Drs Nadareishvili, Rothwell, and Norris); critical revision of the
manuscript for important intellectual content (Drs Nadareishvili,
Rothwell, Beletsky, and Norris and Ms Pagniello); statistical expertise (Drs Nadareishvili and Rothwell and Ms Pagniello); study
supervision (Dr Norris).
Corresponding author and reprints: Zurab G. Nadareishvili, MD, PhD,
Stroke Branch, National Institute of Neurological Disorders and Stroke, National
Institutes of Health, 36 Convent Dr, Bldg 36, 4A03, Bethesda, MD 20892-4128
(e-mail: nadareishviliz{at}ninds.nih.gov).
From the Stroke Research Unit, Sunnybrook and Women's College Health
Sciences Centre, University of Toronto, Toronto, Ontario (Drs Nadareishvili,
Beletsky, and Norris and Ms Pagniello); and the Stroke Prevention Research
Unit, Department of Clinical Neurology, Radcliffe Infirmary, Oxford, United
Kingdom (Dr Rothwell). Dr Nadareishvili is now with the National Institute
of Neurological Disorders and Stroke, National Institutes of Health, Bethesda,
Md.
REFERENCES
| |
1. Timsit SG, Sacco RL, Mohr JP, et al. Early clinical differentiation of cerebral infarction from severe atherosclerotic
stenosis and cardioembolism. Stroke. 1992;23:486-491.
FREE FULL TEXT
2. European Carotid Surgery Trialists' Collaborative Group. Randomized trial of endarterectomy for recently symptomatic carotid
stenosis: final results of the MRC European Carotid Surgery Trial. Lancet. 1998;351:1379-1387.
FULL TEXT
|
ISI
| PUBMED
3. Barnett HJ, Taylor DW, Eliasziw M, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate
or severe stenosis. North American Symptomatic Carotid Endarterectomy Trial
Collaborators. N Engl J Med. 1998;339:1415-1425.
FREE FULL TEXT
4. Barnett HJ, Meldrum HE, Eliasziw M. The dilemma of surgical treatment for patients with asymptomatic carotid
disease. Ann Intern Med. 1995;123:723-725.
FREE FULL TEXT
5. Findlay JM, Tucker WS, Ferguson GG, Holness RO, Wallace MC, Wong JH. Guidelines for the use of carotid endarterectomy: current recommendations
from the Canadian Neurosurgical Society. CMAJ. 1997;157:653-659.
ABSTRACT
6. Perry JR, Szalai JP, Norris JW. Consensus against both endarterectomy and routine screening for asymptomatic
carotid artery stenosis: Canadian Stroke Consortium. Arch Neurol. 1997;54:25-28.
FREE FULL TEXT
7. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995;273:1421-1428.
FREE FULL TEXT
8. The European Carotid Surgery Trialists' Collaborative Group. Risk of stroke in the distribution of an asymptomatic carotid artery. Lancet. 1995;345:209-212.
ISI
| PUBMED
9. Norris JW, Zhu CZ, Bornstein NM, Chambers BR. Vascular risks of asymptomatic carotid stenosis. Stroke. 1991;22:1485-1490.
FREE FULL TEXT
10. Mackey AE, Abrahamowicz M, Langlois Y, et al. Outcome of asymptomatic patients with carotid disease. Asymptomatic
Cervical Bruit Study Group. Neurology. 1997;48:896-903.
FREE FULL TEXT
11. Rockman CB, Riles TS, Lamparello PJ, et al. Natural history and management of the asymptomatic, moderately stenotic
internal carotid artery. J Vasc Surg. 1997;25:423-431.
FULL TEXT
|
ISI
| PUBMED
12. Hennerici M, Hulsbomer HB, Hefter H, Lammerts D, Rautenberg W. Natural history of asymptomatic extracranial arterial disease: results
of a long-term prospective study. Brain. 1987;110:777-791.
FREE FULL TEXT
13. Chambers BR, Norris JW. Outcome in patients with asymptomatic neck bruits. N Engl J Med. 1986;315:860-865.
ABSTRACT
14. Alexandrov AV, Brodie DS, McLean A, Hamilton P, Murphy J, Burns PN. Correlation of peak systolic velocity and angiographic measurement
of carotid stenosis revisited. Stroke. 1997;28:339-342.
FREE FULL TEXT
15. Zwiebel WJ, Zagrebski JA, Crummy AB, Hirscher M. Correlation of peak Doppler frequency with lumen narrowing in carotid
stenosis. Stroke. 1982;13:386-391.
FREE FULL TEXT
16. Bock RW, Gray-Weale AC, Mock PA, et al. The natural history of asymptomatic carotid artery disease. J Vasc Surg. 1993;17:160-171.
FULL TEXT
|
ISI
| PUBMED
17. Mansour MA, Littooy FN, Watson WC, et al. Outcome of moderate carotid artery stenosis in patients who are asymptomatic. J Vasc Surg. 1999;29:217-225.
FULL TEXT
|
ISI
| PUBMED
18. Muluk SC, Muluk VS, Sugimoto H, et al. Progression of asymptomatic carotid stenosis: a natural history study
in 1004 patients. J Vasc Surg. 1999;29:208-214.
FULL TEXT
|
ISI
| PUBMED
19. Smurawska LT, Bowyer B, Rowed D, Maggisano R, Oh P, Norris JW. Changing practice and costs of carotid endarterectomy in Toronto, Canada. Stroke. 1998;29:2014-2017.
FREE FULL TEXT
20. Goldstein LB, Samsa GP, Matchar DB, Oddone EZ. Multicenter review of preoperative risk factors for endarterectomy
for asymptomatic carotid artery stenosis. Stroke. 1998;29:750-753.
FREE FULL TEXT
21. Tran C, Nadareishvili Z, Smurawska L, Oh PI, Norris JW. Decreasing costs of stroke hospitalization in Toronto. Stroke. 1999;30:185-186.
FREE FULL TEXT
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati  Twitter
What's this?
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
|
Medical (Nonsurgical) Intervention Alone Is Now Best for Prevention of Stroke Associated With Asymptomatic Severe Carotid Stenosis: Results of a Systematic Review and Analysis
Abbott
Stroke 2009;40:e573-e583.
ABSTRACT
| FULL TEXT
Atherosclerotic Peripheral Vascular Disease Symposium II: Controversies in Carotid Artery Revascularization
White et al.
Circulation 2008;118:2852-2859.
FULL TEXT
Angioplasty and Stenting of Asymptomatic Carotid Stenosis Before Cardiac Surgery: More Study Is Needed
Selim
Arch Neurol 2008;65:1672-1674.
FULL TEXT
Contemporary Management of Carotid Stenosis: Carotid Endarterectomy Is Here to Stay
Abbruzzese and Cambria
PERSPECT VASC SURG ENDOVASC THER 2007;19:248-256.
ABSTRACT
Asymptomatic Carotid Artery Stenosis and the Risk of New Vascular Events in Patients With Manifest Arterial Disease: The SMART Study
Goessens et al.
Stroke 2007;38:1470-1475.
ABSTRACT
| FULL TEXT
Suboptimal Control of Atherosclerotic Disease Risk Factors After Cardiac and Cerebrovascular Procedures
Cheng et al.
Stroke 2007;38:929-934.
ABSTRACT
| FULL TEXT
Long-Term Survival After Carotid Endarterectomy for Asymptomatic Stenosis
Kragsterman et al.
Stroke 2006;37:2886-2891.
ABSTRACT
| FULL TEXT
Primary Prevention of Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association Stroke Council: Cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: The American Academy of Neurology affirms the value of this guideline.
Goldstein et al.
Circulation 2006;113:e873-e923.
ABSTRACT
| FULL TEXT
Primary Prevention of Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association Stroke Council: Cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: The American Academy of Neurology affirms the value of this guideline.
Goldstein et al.
Stroke 2006;37:1583-1633.
ABSTRACT
| FULL TEXT
Ultrasonographic confirmation of carotid artery atheromas diagnosed via panoramic radiography
FRIEDLANDER et al.
Journal of the American Dental Association 2005;136:635-640.
ABSTRACT
| FULL TEXT
Evaluation and Management of Asymptomatic Carotid Artery Stenosis
Dodick et al.
Mayo Clin Proc. 2004;79:937-944.
ABSTRACT
Serum Chitotriosidase Activity Is Increased in Subjects With Atherosclerosis Disease
Artieda et al.
Arterioscler. Thromb. Vasc. Bio. 2003;23:1645-1652.
ABSTRACT
| FULL TEXT
Natural History of Asymptomatic Carotid Stenosis
JWatch Gastroenterology 2002;2002:11-11.
FULL TEXT
Natural History of Asymptomatic Carotid Stenosis
Journal Watch Cardiology 2002;2002:7-7.
FULL TEXT
Natural History of Asymptomatic Carotid Stenosis
JWatch General 2002;2002:5-5.
FULL TEXT
|
