(Stroke. 2000;31:1871.)
© 2000 American Heart Association, Inc.
Original Contributions |
Prediction of Mortality by Ultrasound Screening of a General Population for Carotid Stenosis
The Tromsø Study
From the Institutes of Community Medicine (O.J., K.H.B., E.B.M., E.S.-B., E.A.) and Clinical Medicine (O.J., E.B.M.), University of Tromsø, Tromsø, Norway.
Correspondence to Oddmund Joakimsen, Institute of Community Medicine, University of Tromsø, N-9037 Tromsø, Norway. E-mail Oddmund.Joakimsen{at}ism.uit.no
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Abstract |
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Background and Purpose—The extensive use of ultrasound examination of carotid arteries has revealed stenosis in many asymptomatic subjects, and clinical studies have shown that carotid stenosis is a risk factor for cardiovascular disease and death. However, information on stenosis as detected in a general population and its relation to mortality is scarce. The purpose of this population-based study was to assess whether carotid stenosis is a predictor of death.
Methods—In 1994 to 1995, 248 subjects with suspected carotid stenosis were identified among 6727 men and women 25 to 84 years of age who were examined with ultrasound. These subjects and 496 age- and sex-matched control subjects were followed up for 4.2 years, and the number and causes of deaths were registered.
Results—The unadjusted relative risk for death was 2.72 (95% CI, 1.57 to 4.75) for subjects with stenosis compared with control subjects. Adjusting for cardiovascular risk factors increased the relative risk to 3.47 (95% CI, 1.47 to 8.19). The adjusted relative risk in persons with stenosis and no cardiovascular disease or diabetes was 5.66 (95% CI, 1.53 to 20.90), which was higher than in subjects with stenosis and self-reported disease (1.79; 95% CI, 0.75 to 4.27). There was a dose-response relationship between degree of stenosis and risk of death (P=0.002 for linear trend). Carotid stenosis was a stronger predictor of death than self-reported cardiovascular disease or diabetes.
Conclusions—Carotid stenosis is a strong and independent predictor of death.
Key Words: : carotid stenosis • mortality • population-based studies • ultrasonography
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Introduction |
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The use of ultrasound examinations of carotid arteries in clinical practice, clinical trials, and population health surveys has identified many persons with asymptomatic carotid stenosis. In some studies in which patients are referred to ultrasound examinations on various clinical indications, carotid stenosis has been shown to be a significant predictor of death.1 2 3 Randomized clinical trials designed for comparison of surgery and medical treatment as the most appropriate treatment for carotid stenosis have found that both symptomatic4 5 and asymptomatic6 subjects with stenosis are at high risk of cerebral stroke and cardiovascular death.
In contrast, only 2 population-based studies7 8 have
examined the relationship between carotid stenosis and
mortality. Both studies included elderly (
65 years) subjects only,
and 1 included men only.8 The purpose of this
population-based study of 6727 male and female subjects ranging from 25
to 84 years of age, revealing 248 cases of suspected carotid
stenosis, was to assess whether carotid stenosis, as
detected by ultrasound examination of a general population, is a
predictor of death.
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Subjects and Methods |
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Population
In 1994 to 1995, a population health survey was conducted in the municipality of Tromsø, Norway, by the University of Tromsø in cooperation with the National Health Screening Service. The study comprised 2 screening visits 4 to 12 weeks apart. All inhabitants in the municipality >24 years of age were invited to the first visit, and all subjects 55 to 74 years of age and 5% random samples in the other 5-year age groups were invited to both visits. In addition, 307 men 45 to 54 years of age were invited because they had participated in an intervention study in a previous survey of the Tromsø Study; therefore, the sample size for these age groups was higher than 5%. The protocol for the first visit was similar to the previous surveys in this population9 and included standardized measurements of height, weight, blood pressure, nonfasting serum lipids, and fibrinogen. Blood pressure and nonfasting serum lipids were remeasured at the second visit, which also included ultrasonographic examination of the right carotid artery. A total of 3323 men and 3404 women, 79% of those eligible, attended both visits and were examined with ultrasound. The letter of invitation contained questions on previous myocardial infarction or stroke, prevalent angina pectoris or diabetes mellitus (yes/no), treated hypertension (never/previously/currently), and cigarette smoking. The questionnaire was checked for logical inconsistencies at the examination. The study was approved by the Regional Committee for Medical Research Ethics, and written consent was obtained from all participants.
Cardiovascular Risk Factors
Height and weight were measured in participants wearing light
clothing without shoes; body mass index (BMI) was calculated as weight
in kilograms divided by the square of height in meters. Blood pressure
was recorded in a separate, quiet room by a specially trained
nurse. An automatic device (Dinamap Vital Signs Monitor) was used.
Serum cholesterol and triglycerides were
analyzed by standard enzymatic methods, and fibrinogen was
measured with the PT-Fibrinogen reagent (Instrumentation Laboratory).
The serum analyses were performed at the Department of Clinical
Chemistry, Tromsø University Hospital.
Ultrasonography
The ultrasound methods have been described in detail
previously.10 Briefly, high-resolution B-mode
ultrasonography was performed with an ultrasound scanner (Acuson Xp10
128, ART upgraded) equipped with a linear-array transducer. The common,
internal, and external carotid arteries were identified by combining
B-mode (7 MHz) and color-Doppler/pulsed-wave Doppler (5-MHz)
ultrasound. We attempted to identify and record atherosclerotic
plaques from 6 sites of the carotid artery: the near and far walls of
the internal carotid artery, the bifurcation segment of the common
carotid artery, ie, the distal part of the common carotid artery, and
the common carotid artery from the bifurcation and downstream to the
supraclavicular region. A random sample of 784 subjects was examined on
both right and left carotid arteries to provide information about
bilateral carotid stenosis. A carotid artery was defined as
being stenotic if 1 or both of the 2 criteria were met. For the
hemodynamic criterion to be met, peak systolic
velocity at the tightest, stenotic part (PSVs) had to be 0.2
m/s higher than peak systolic velocity at the point of
reference (PSVr) or 0.1 m/s higher if the stenosis was
located at the carotid bifurcation or the bulb of the internal carotid
artery. The distal part of the internal carotid artery was used as the
point of reference. For the structural criterion to be met, plaque had
to cause 35% reduction in lumen diameter on a longitudinal B-mode
scan. The degree of stenosis was calculated by the peak
systolic velocity ratio method: (1-PSVr/PSVs)x100%. Complete
occlusion of the carotid artery was graded as 100% stenosis.
Three sonographers screened the subjects: one was a neurologist (O.J.)
with 10 years’ experience in ultrasound examination of the carotid
artery; the second was a physician (E.S.-B.); and the third was a
specially trained technician. A 2-month training protocol was completed
before the survey started. A reproducibility study on plaque occurrence
found that between- and within-sonographer agreement was substantial,
with 
values of 0.72 (95% CI, 0.60 to 0.84) and 0.76
(95% CI, 0.63 to 0.89), respectively.10
Cases With Carotid Stenosis and Control Subjects
For each case with suspected stenosis, 2 control
subjects were randomly drawn among subjects who did not have
stenosis. The cases and control subjects were matched by age
(±2 years), sex, date of examination, and living area within the
municipality (rural or urban areas).
All persons with suspected stenosis and 1 of the 2 control
subjects in each triplet were referred to the outpatient clinic at
Department of Neurology, University Hospital, Tromsø, for clinical
examination and ultrasonographic reevaluation and reclassification. All
examinations were performed by 2 experienced neurologists (O.J.,
E.B.M.). A flow chart of the selection procedures is shown in Figure 1
.
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The subjects were followed from the date at screening or at ultrasound reclassification to December 1, 1998, or to the date of death. Deceased subjects were identified by linkage to the National Population Register, and details of all deaths were documented whenever possible by hospital records and autopsy reports.
The reproducibility on the grading of stenosis at
reclassification was satisfactory, with a mean absolute difference
between sonographers of 10.8%.11 The values for
agreement on categories of stenosis dichotomized at various
cutoff points (50%, 60%, and 70% stenosis) were 0.57 (95%
CI, 0.33 to 0.81), 0.66 (95% CI, 0.4 to 0.91), and 0.79 (95% CI, 0.54
to 1.00), respectively.11
Statistical Analysis
Differences between cases and control subjects in mean values of
baseline cardiovascular risk factors were tested for
statistical significance by use of 2-way ANOVA with match number of
triplets (1 to 248) and stenosis (yes/no) as factors.
Differences in proportions were tested by 
2
tests and Fisher’s exact test (2 tail). The Kaplan-Meier method was
used to calculate survival for the groups, and the log-rank test was
used to test the difference in survival between the groups. Death rates
were calculated as the number of deaths by person-years of observation
(time to death or censoring). Unadjusted relative risks were estimated
by calculation of ratios of mortality rates. Cox proportional-hazards
regression model was used to estimate the influence of carotid
stenosis on death adjusted for risk factors. Stratified
analyses were used in analyzing the matched triplets (1 case
and 2 control subjects) adjusted for smoking, BMI, systolic
blood pressure, total and HDL cholesterol,
triglycerides, and fibrinogen.
To test whether there was a dose-response relationship between degree of carotid stenosis and mortality, the subjects were categorized in 5 groups according to degree of stenosis on the basis of findings at the ultrasound reclassification at the outpatient clinic: (1) subjects without carotid stenosis (reference group), (2) those with <45% stenosis, (3) those with stenosis between 45% and 74%, (4) those with stenosis between 75% and 99%, and (5) those with 100% stenosis (ie, occlusion). The strength of the dose-response relationship was expressed by probability values for linear trend in the Cox regression model. When bilateral stenoses were present, the measures from the tightest stenosis of the 2 sides were used in the calculation of degree of stenosis.
Two-sided values of P<0.05 were considered statistically significant. The SAS software package version 6.12 was used.12
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Results |
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A total of 248 subjects with suspected carotid stenosis at the screening and 496 matched control subjects were included in the analysis of screening results (analysis A, Figure 1
). There was a male predominance (61.3%) (Table 1). Cases had higher levels of
systolic blood pressure, total cholesterol, and
triglycerides and were more likely to smoke, be treated for
hypertension, and have a history of cardiovascular
disease (CVD). There was no significant difference between cases and
control subjects with regard to BMI, HDL cholesterol,
diastolic blood pressure, and the prevalence of diabetes
mellitus.
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The follow-up time until death or the censoring date of December 1, 1998, lasted up to 4.2 years. The mean observation time was 3.6 years (median, 3.8 years) for cases and 3.8 years (median, 3.8 years) for control subjects.
Table 2 shows that among the 248 cases,
30 persons (12.1%) died during the observation time compared with 23
deaths (4.6%) among the 496 control subjects. In cases, the death rate
was 3.35 per 100 person-years compared with 1.23 per 100 person-years
in control subjects, giving a relative risk of 2.72 (95% CI, 1.57 to
4.75). After adjustment for baseline cardiovascular
risk factors, the relative risk increased to 3.47 (95% CI, 1.47 to
8.19). The relative risk of death for cases with stenosis was
greater in persons without CVD or diabetes (3.08) than in persons who
reported CVD or diabetes (1.79) (Table 2). After
multivariate adjustment, the relative risk for death
associated with stenosis became higher, especially among
persons without CVD or diabetes (5.66). Table 2 also shows that
the death rate was similar in cases with stenosis who did not
have CVD or diabetes (3.14 deaths per 100 person-years) and in cases
with stenosis who also had CVD or diabetes (3.61 deaths per 100
person-years). The log-rank test showed significant statistical
difference between the survival curves for those with and without
carotid stenosis (P=0.0002) (Figure 2). The difference was significant both
in men (P=0.007) and in women (P=005).
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CVD was the main cause of death in both control subjects and cases
(Table 3). However, death resulting from
CVD was more common among subjects with stenosis than in
control subjects. The absolute risk of death from ischemic
cerebral stroke was small, even among subjects with
stenosis.
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Table 4 shows mortality for the subjects
reexamined at the outpatient clinic (n=477), reclassified with regard
to presence of stenosis, and categorized according to degree of
stenosis (analysis B, Figure 1). The death rates
and unadjusted and adjusted relative risks for death increased by
increasing degree of stenosis (Table 4). Thus,
unadjusted and adjusted relative risks for death increased to 7.47
(95% CI, 2.53 to 20.49) and 5.50 (95% CI, 1.63 to 18.52) among those
with occlusion (P=0.002 for linear trend), indicating a
significant dose-response of carotid atherosclerosis on
mortality. Among the 237 subjects who had stenosis, the
adjusted relative risk for death per 10% increment of degree of
stenosis was 1.20 (95% CI, 1.03 to 1.41) (data not shown).
Death was significantly (P=0.04) associated with CVD or
diabetes regardless of status of stenosis. No additional
information was achieved when the analyses were stratified by
sex.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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This study shows that carotid stenosis is a strong and independent predictor of death. Cases with stenosis who reported CVD or diabetes had only a slightly higher death rate than those with stenosis who did not report CVD or diabetes, which means that prevalent CVD or diabetes did not add much to the risk of death in subjects with carotid stenosis. The higher relative risk associated with stenosis in subjects without clinical disease (3.08) compared with cases with stenosis who reported prevalent CVD or diabetes (1.79) is due to the low death rate among stenosis-free control subjects without clinical disease. The multivariate adjusted relative risk for death associated with stenosis is particularly strong for subjects who reported no prevalent CVD or diabetes (5.66). At the screening, 214 subjects reported CVD or diabetes (22 deaths), and 530 subjects reported no such diseases (31 deaths).
There was a dose-response relationship between degree of stenosis and risk of death. The highest relative risk appeared among the 19 persons who had carotid occlusion (6 of them had no CVD or diabetes) with a death rate of 9.7 per 100 person-years. This implies that as many as 30% of these subjects died during follow-up compared with 4.5% of subjects without stenosis. Advanced carotid atherosclerosis therefore seems to be a strong predictor of death also in the absence of clinical disease. Only 55% of the 60 cases with >70% stenosis reported coronary disease, previous stroke, or diabetes mellitus. The death rate for the 33 cases with clinical disease and with >70% stenosis was 8.1 compared with 7.8 per 100 person-years in the 27 subjects without such diseases (data not shown).
CVD was the cause of death in 80% of cases with stenosis compared with 43.5% in those without stenosis. In the group with stenosis, 6.7% died of an ipsilateral ischemic stroke. Most died of coronary heart disease. Several other studies have found that carotid stenosis is a stronger predictor of cardiac death than death caused by cerebral stroke.1 2 3 13 This is also in line with ultrasound and autopsy studies showing that the presence and extent of carotid atherosclerosis correlate well with atherosclerosis elsewhere in the circulation, including the coronary arteries.14 15 16
Subjects with carotid stenosis were offered annual clinical and ultrasound follow-up, whereas control subjects were examined only at study entry. Those cases who disclosed early symptoms or signs consistent with heart or cerebrovascular disease were given medical advice or therapy or were referred for further investigations and treatment. This may have resulted in a lower mortality rate among cases, thus causing an underrating of the relative risk for death in those with stenosis compared with stenosis-free control subjects.
To the best of our knowledge, only 2 studies have previously evaluated
whether carotid stenosis, as detected by ultrasound screening
of a general population, is a predictor of death. In the
Cardiovascular Health Study (CHS),7 5114
men and women 65 years of age were examined by ultrasound and
classified according to degree of stenosis. The unadjusted
relative risk for death among subjects with stenosis compared
with those without stenosis (ie, those without carotid
atherosclerotic plaques) was slightly higher and the adjusted relative
risk was lower compared with our findings. The mean age in our study
was 6 years younger than in CHS, and the participation rate was higher
in our study, 79% versus 57% in CHS. The higher age in CHS may have
contributed to the lower adjusted relative risk estimates compared with
the results of our study. Similar to our findings, the CHS
investigators found that death rates were highest among subjects with
carotid occlusion and that carotid stenosis was a better
predictor of death than self-reported CVD.
In a smaller Swedish study on 10-year mortality among 68-year-old men,17 the annual death rate among subjects with carotid stenosis (n=117) was higher than in those without stenosis (relative risk, 1.45; P=0.03). However, the association disappeared after adjustment for other risk factors. In a later publication,8 those investigators found that this higher relative risk for death was present only among those men who did not suffer from ischemic heart disease at baseline. The lower relative risk for death in that study compared with our results may be due to higher cardiovascular morbidity (eg, 42.3% had prevalent ischemic heart disease compared with 24.0% of those who reported coronary disease in our population >67 years of age) and male sex.
An association between carotid stenosis and death has been found in clinical studies.1 3 However, different inclusion criteria in population-based and clinical studies make comparisons difficult. In general, patients referred to ultrasound laboratories on clinical indications supposedly have more active clinical disease and consequently higher risk of death.
In a population-based study from Framingham,13 the presence of neck bruit, a clinical finding that is highly correlated with carotid stenosis, was associated with a 1.7-fold-higher relative risk of death in men (P<0.05) and a 1.9-fold-higher risk in women (P<0.01). Wiebers et al,2 in another population-based study, found the relative risk of death by neck bruit to be 2.2.
Prompted by the recently reported beneficial effect of endarterectomy in patients with asymptomatic carotid stenosis,6 the value of screening for asymptomatic carotid stenosis has been discussed. It has been found that ultrasound screening for carotid stenosis is not cost-effective regarding carotid endarterectomy.18 19 Any benefit from regular screening, however, is not restricted to only a possible impact on stroke incidence caused by carotid endarterectomy. Most people with carotid stenosis die from coronary heart disease and not from stroke,1 2 3 7 13 17 as also shown in the present study. The main consequence of ultrasound screening of a general population is that subjects with high risk for coronary disease will be identified. Medical intervention as part of preventive strategies may therefore save as many from disease and death as carotid endarterectomy. Our results are not an argument for routine screening of general populations to detect carotid stenosis. That is hardly a cost-effective procedure. The main purpose of our study was to use ultrasonographic measurements as part of the study of CVD origin. However, many subjects will incidentally have asymptomatic carotid stenosis disclosed by ultrasound examinations performed as part of scientific studies or on clinical indications. We therefore believe that knowing the risk of death in such subjects must be of interest.
This study has shown that the presence of carotid stenosis as detected by ultrasound screening of a general population is a strong predictor of death, stronger than self-reported CVD or diabetes. The relative risk for death is particularly strong for subjects with stenosis who reported no prevalent CVD or diabetes. There is a dose-response relationship between degree of carotid stenosis and death. Subjects with carotid stenosis should be treated as high-risk subjects and offered clinical follow-up to lower cardiovascular risk factor levels and to recognize early clinical signs of CVD for further diagnostic and therapeutic interventions.
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Acknowledgments |
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This study was supported by grants from the Norwegian Research Council and was conducted in collaboration with the National Health Screening Service, Oslo, Norway.
Received December 29, 1999; revision received April 14, 2000; accepted May 5, 2000.
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