© 2001 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
Sustained Anxiety and 4-Year Progression of Carotid Atherosclerosis
From the National Institute of Health and Medical Research (INSERM), Unit 360 (S.P., A.A.), Unit 258 (M.Z., P.D.), Centre de Diagnostic et de Prévention Neurovasculaire (P.-J.T.), and Centre d’Examen EVA-INSERM (J.-M.F.), Nantes, France.
Correspondence to Dr Sabrina Paterniti, INSERM U360 Hôpital de la Salpêtrière, 84 bd. de l’Hôpital, 75651 Paris Cedex 13, France. E-mail paternit{at}chups.jussieu.fr
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Abstract—Several studies have shown that anxiety disorders are associated with a higher risk of coronary artery disease. However, the relationship between anxiety disorders and atherosclerosis has been studied to a lesser extent. The goal of this study was to examine whether high and stable trait anxiety was associated with the progression of atherosclerosis. The study group consisted of 726 subjects (297 men and 429 women), aged 59 to 71 years, recruited from the electoral rolls of the city of Nantes. The subjects had no history of coronary artery disease at baseline evaluation and or at the 2-year follow-up. Two follow-up examinations were conducted 2 and 4 years after the baseline evaluation. Trait anxiety was evaluated by means of the French translation of the Spielberger Inventory (a 20-item trait inventory, form X-2). The "sustained anxiety" group consisted of men and women with the highest Spielberger Inventory scores at baseline and at the 2-year follow-up examination. Each ultrasound examination included measurement of intima-media thickness and the sites of plaque in the extracranial carotid arteries. Men with sustained anxiety showed a higher 4-year increase of common carotid intima-media thickness than did men without sustained anxiety (adjusted means 0.08 versus 0.04 mm, respectively; P=0.05) and a higher risk of 4-year plaque occurrence (adjusted OR 3.5, 95% CI 1.4 to 8.5). Among women, sustained anxiety was associated with a higher 4-year increase of common carotid intima-media thickness (0.07 versus 0.04 for women with versus women without sustained anxiety, respectively; P=0.07). These results suggest that chronically high levels of anxiety may contribute to accelerating the evolution of carotid atherosclerosis.
Key Words: trait anxiety • carotid arteries • atherosclerosis • longitudinal studies
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Introduction |
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Personality traits, such as type A behavior,1 2 anger,3 hostility,4 5 and hopelessness,6 7 are associated with a higher risk of coronary heart disease and of fatal or nonfatal myocardial infarction. Recent studies have shown that these personality traits are also associated with the progression of carotid atherosclerosis, measured by angiography8 9 10 or ultrasonography.11 12 13 14 15
Similarly, anxiety is also associated with a higher risk of coronary artery disease. Phobic anxiety, generalized anxiety, panic disorder, and worry are predictors of myocardial infarction and/or cardiac death,16 17 18 19 20 21 yet their association with direct measures of atherosclerosis has been studied to a lesser extent. Tennant and Langeluddecke22 suggested in a preliminary study that trait anxiety was a correlate of atherosclerosis, but they failed to confirm their data in a larger study conducted on 90 patients undergoing coronary angiography.23 Matthews et al24 found that baseline trait anxiety measured with the Spielberger Inventory scale did not predict average carotid intima-media-thickness (IMT) scores 10 years later in a group of 200 healthy postmenopausal women. In the same study, measures of trait anger and anger-in (a tendency to suppress anger) were associated with higher carotid IMT.
Anxious symptomatology is associated with reduced heart rate variability25 26 and reduction in vagal control of the heart.27 28 Several studies have found that reduction in the vagal control of heart rate is associated with increased cardiac mortality.29 30 Decreased heart rate variability, which is an important index of vagal function, has also been shown to be a strong predictor of fatal outcome after myocardial infarction.31 32 Given these findings, such pathophysiological situations may contribute to explaining the susceptibility of persons with high anxiety levels to sudden cardiac death. On the other hand, high blood pressure33 and anxiety-associated habits34 35 of some anxious patients (eg, smoking and alcohol use) increase the risk of the progression of atherosclerosis.
Because it is plausible that chronic rather than acute anxiety may have more pronounced effects on the progression of atherosclerosis, the authors examined whether stable trait anxiety is predictive of the progression of atherosclerosis.
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Methods |
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Study Group
The Etude sur le Vieillissiment Artériel (EVA) Study is an ongoing longitudinal study on cognitive and vascular aging conducted in the city of Nantes (western France). The study group consisted of 1389 volunteers, born between 1922 and 1932, recruited from the electoral rolls of the city of Nantes. The study protocol was approved by the Ethics Committee of Bicêtre University Hospital, and written consent was given by all participants. The group was invited to participate in 2 follow-up examinations, which were conducted 2 and 4 years after the baseline evaluation. The Spielberger Inventory was not administered to 275 subjects who were enrolled in the first 6 months of the EVA Study, because a definitive decision about measuring anxiety was taken after the study had begun. Because the presence of coronary heart disease may increase anxiety symptoms, 61 men and 51 women who reported angina or myocardial infarction at baseline or 2-year follow-up examination were excluded from further analyses. Of the 1029 remaining subjects, 859 were followed up 2 and 4 years after baseline. The present study examines data from the 726 subjects (297 men and 429 women) who had completed data from baseline and follow-up ultrasound examinations as well as data for anxiety and covariate measures.
Persons who were included in the present study, compared with those not included, had lower anxiety scores (38.4 versus 40.6, respectively; P<0.001) and lower body mass index (BMI 25.3 versus 26.0, respectively; P<0.001) and took psychotropic drugs less often (19.2% versus 27.3%, respectively; P<0.004). The 2 groups did not differ significantly for baseline common carotid artery (CCA)-IMT, plaque presence, and other covariates.
Interview and Measures
During the baseline visit, which took place between
June 1991 and July 1993, a structured questionnaire including items on
sociodemographic characteristics, smoking, alcohol consumption, medical
history, and current medication use was administered to participants by
a member of the study team. Medical examination included blood
sampling, ultrasound examination of carotid arteries, and 1-hour
cognitive testing. Mean weekly alcohol intake (in milliliters of pure
ethanol) was estimated from a detailed description of alcoholic
beverage consumption during a typical week, including the quantity and
frequency of use.
Each subject was asked whether he/she had suffered from any of 6 specified common diseases (myocardial infarction, angina, stroke, hypercholesterolemia, hypertension, and diabetes) and/or from any other chronic medical conditions. All drugs used over the month preceding the examination were noted.
Weight and height were measured. BMI was computed as weight (kilograms) divided by height squared (in meters squared). Two separate measures of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were taken after a 10-minute pause with an automatic blood pressure monitor. Means of 2 measures of SBP and DBP were used for this analysis. Pulse pressure (PP) was defined as the difference between SBP and DBP. Blood samples were drawn between 8:00 and 9:00 AM after a 12-hour fast. Total cholesterol assay was performed by using the PAP enzymatic cholesterol kit, supplied by Biomérieux.36
Anxiety Measures
Trait anxiety was evaluated by means of the French
translation of the 20-item Spielberger Inventory (form
X-2).37 The Spielberger
Inventory provides a measure of relatively stable dispositional aspects
of anxiety. The items are rated from 1 to 4 in terms of frequency
categories (almost never, sometimes, often, and almost always). In the
present study, intraclass correlation coefficients between the 2
anxiety measures were 0.70 (men) and 0.76 (women). These findings are
similar to those of
Spielberger.38 Internal
consistency of the Spielberger Inventory was high
(standardized Cronbach’s 
=0.82 and 0.85 for men and women,
respectively). The stability of the Spielberger Inventory has been
confirmed in longitudinal
studies39 and in
anxiety-provoking
situations.40 Early
psychometric studies conducted in adult and elderly people have
provided support for the difference between trait and state anxiety,
discriminant validity, and test-retest reliability of the Spielberger
Inventory.41 42
The Spielberger Inventory was mailed to the participants
3 weeks before the examination. The instrument was administered to
subjects at baseline and at 2-year follow-up.
Ultrasonography
Ultrasound examinations at baseline, 2-year
follow-up, and 4-year follow-up were performed by use of the Aloka
SSD-650, with a transducer frequency of 7.5 MHz. This system provides
an axial resolution of 0.30 mm. Acquisition, processing, and
storage of B-mode images were computer-assisted with software specially
designed for longitudinal studies
(EUREQUA).43
Details of the protocol have been described elsewhere.44 45 Each examination that was included involved scanning of the CCAs, of the carotid bifurcation, and of the origin (first 2-cm) of the internal carotid arteries. All measurements were made by the sonographer at the time of examination (online). The IMT was measured on the far wall of the mid and distal CCA as the distance between the lumen-intima interface and the media-adventitia interface by use of an automated edge-detection algorithm. One transversal and 2 longitudinal measurements of IMT were completed on the right and left CCAs at a site free of any discrete plaques; the means of the 4 right and left longitudinal CCA-IMT measurements were analyzed.
The near and far walls of arterial segments were
scanned longitudinally and transversally to assess the presence of
plaques. Plaque presence was defined as localized echo structures
encroaching the vessel lumen for which distance between the
media-adventitia interface and the internal side of the lesion was
1 mm.
The same sonographers performed baseline, 2-year, and 4-year
follow-up examinations for 76% of the subjects. Reproducibility of the
scanning and reading procedures has been reported
elsewhere.43 45
Briefly, random subsamples of images of CCAs, of the carotid
bifurcations, and of the origin (first 2-cm) of the internal carotid
arteries recorded by the 4 sonographers were sent for measurements
to a single expert sonographer (P.-J.T.) who was not aware of the
measurement results obtained at the EVA Center. Agreement between the 2
readings of CCA-IMT was good (correlation 0.82, coefficient of
variation 9.1%, mean±SD absolute difference 0.06±0.06 mm). The
coefficients for agreement between the 2 readings of plaque
presence were 0.86 for longitudinal views and 0.91 for transverse
views.
Statistical Analysis
Descriptive and analytic statistics were performed
with the use of SAS (release 6.12, SAS Statistical
Institute).
Because of sex differences, separate analyses were performed for each sex.
The "sustained anxiety" group consisted of men and women with Spielberger Inventory scores in the highest decile of the sex-specific distribution at baseline and at the 2-year follow-up examination. The lower limit of the decile was 41 and 49 for men and women, respectively. Men and women who did not satisfy this criterion were classified in the "no sustained anxiety group."
To examine the progression of
atherosclerosis, change in mean longitudinal CCA-IMT
was estimated by subtracting baseline CCA-IMT from 4-year follow-up
CCA-IMT. The occurrence of carotid plaques during the follow-up (at
2-year examination or/and at 4-year examination) was defined as the
occurrence of 1 plaque in previously normal segments and/or the
occurrence of new plaques in segments that previously had
plaques.
Covariates considered were baseline age, BMI, alcohol (daily alcohol use, expressed in milliliters of pure ethanol; scored as 0 for nonusers), and tobacco use (smoker, exsmoker, and nonsmoker), cholesterol measures, and antihypertensive, lipid-lowering, and psychotropic drug use.
In a previous study, we found that PP is a better predictor of CCA-IMT than is SBP alone or mean blood pressure.44 Therefore, PP rather than blood pressure was used in multivariate analyses.
For longitudinal analyses of the relation between sustained anxiety and CCA-IMT change or plaque occurrence, the mean value between baseline and 2-year examination was used for quantitative covariates (PP, BMI, alcohol, and cholesterol); medication use was considered at baseline and/or 2-year follow-up.
Associations between sustained anxiety scores and the
covariates were assessed by ANOVA and 
2
test.
ANCOVAs were performed to examine the effect of sustained anxiety on CCA-IMT progression while simultaneously controlling for covariates and baseline CCA-IMT. Logistic regression models were then used to calculate the odds ratio (OR) of plaque occurrence by level of sustained anxiety, controlling for covariates and plaque presence at baseline.
Statistical significance was set at a value of P=0.05 (2-tailed test).
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Baseline Association Between Risk Factors and Sustained Anxiety
Table 1
presents the mean±SD or
prevalence of Spielberger scale scores, age, baseline levels of
CCA-IMT, and other covariates by level of sustained anxiety in men and
women. Men and women with or without sustained anxiety did not differ
on covariates, except for psychotropic drug use.
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Among subjects using antihypertensive drugs, 44.2% took ß-blockers, 36.6% took ACE inhibitors, and 14.0% took calcium inhibitors. Fibrates (74.0%) and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (21.9%) were the most prescribed lipid-lowering drugs. The most represented classes of psychotropic drugs were anxiolytics (61.9%), hypnotics (28.8%), and antidepressants (19.4%). Half of hypnotics and almost all anxiolytics were benzodiazepines; most of antidepressants were serotonin-reuptake inhibitors.
Sustained Anxiety and 4-Year Progression of
CCA-IMT
No significant differences were found when baseline
CCA-IMT was compared in men with and in men without sustained anxiety
(mean±SD 0.70±0.14 versus 0.69±0.13, respectively;
P=0.61). Women with sustained
anxiety had lower baseline CCA-IMT than did women without sustained
anxiety (mean±SD 0.62±0.09 versus 0.65±0.09, respectively;
P=0.05). These differences did
not change when covariates were adjusted.
Models examining the influence of high and stable levels of
trait anxiety on the progression of CCA-IMT showed a consistent
pattern in men and women
(Table 2). In both sexes, sustained anxiety was associated
with a 2-fold increase of CCA-IMT.
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Sustained Anxiety and Plaque Occurrence Between
Baseline and 4-Year Follow-Up
No significant differences were found when the
percentages of subjects with or without sustained anxiety were compared
for the presence of plaque at baseline (men, 34.5% versus 23.2%,
P=0.18; women, 14.9% versus
16.5%, P=0.78).
Anxious men had an increased risk of plaque occurrence
(Table 2
). Among men without plaque at baseline, 34 of 205
(16.6%) nonanxious men developed 1 new plaque at follow-up versus 7
of 19 (36.8%) anxious men (unadjusted OR 2.9, 95% CI 1.1 to 8.0;
P=0.04). Among men with at
least 1 plaque at baseline, 18 of 52 (34.6%) nonanxious men developed
new plaques at follow-up versus 5 of 8 (62.5%) anxious men (unadjusted
OR 3.1, 95% CI 0.7 to 14.7;
P=0.14).
Among women, no consistent association between anxiety and plaque occurrence was found.
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Discussion |
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The present study shows that men with high and stable levels of trait anxiety have a greater increase of CCA-IMT and a more important risk of plaque occurrence. In women, high anxiety levels were associated with greater CCA-IMT but not with higher risk of plaque occurrence. There are few studies examining plaque occurrence in women. Similar to our results, Matthews et al15 found an association between hostility and IMT in women but failed to show any association with plaque scores. There was no clear explanation for the different association between anxiety and plaque in men and women. It is possible that anxiety interacts with sex-related risk or protective factors that modify the effects of anxiety on plaque formation.
Kubzanski et al20 found that worrying, which is an important component of anxiety, was a risk factor for myocardial infarction. Other studies did not confirm this association but reported an association between anxiety and sudden cardiac death, suggesting that mechanisms different from atherosclerosis (like alterations in vagal control) may be responsible for cardiac mortality in anxious patients.16 18 Kawachi et al19 did not find any significant association between anxiety and cardiac events; the duration of the follow-up (32 years) may explain the negative finding.
In the present study, repeated measures of trait anxiety allowed a definition of sustained anxiety. This offers several advantages when the relationship between anxiety and the progression of atherosclerosis is examined. First, 2 measures provide a more reliable score of trait anxiety, helping to avoid misclassification bias. Second, high stable trait anxiety is more likely to have an impact on the progression of atherosclerosis, which takes place over time. The results of the present study concur with those from a recent study by Everson et al,14 in which men who reported high levels of hopelessness at baseline and follow-up examinations showed the highest increase in carotid atherosclerosis compared with men reporting low to moderate hopelessness at both points in time.
The EVA Study is based on a homogeneous cohort of volunteers who are, by design, in a narrow age range. They have higher educational levels, higher income, better cognitive functioning, and less physical disabilities than the French general population of the same age range. People with high physical or mental morbidity, such as high anxiety, advanced atherosclerosis, or both, have probably not been included. This selection limited the power of cross-sectional analyses. The power of longitudinal analyses was higher, allowing us to detect the effect of sustained anxiety on carotid measures in the relatively short term. This phenomenon, ie, finding no cross-sectional relationship but strong longitudinal association, was observed in the analysis of the other EVA Study data and in other population-based studies.46 47
Atherosclerosis in the carotid arteries may be considered to be a marker of generalized atherosclerosis of the arteries, including coronary arteries.48 49 As such, the association between sustained anxiety and carotid atherosclerosis is consistent with the reported association between chronic anxiety disorders and cardiovascular events.
One possible explanation for the association between anxiety and the progression of atherosclerosis is that cardiovascular problems may produce anxiety. This is not a likely explanation for the present results, inasmuch as subjects reporting angina or myocardial infarction were excluded from further analyses. The association may be also be due to the confounding effects of high blood pressure, smoking, and alcohol use. Multivariate analyses, however, allowed for controlling of the possible confounding effects of these factors. Other unknown or unmeasured factors, such as physical exercise or diet, may be involved in the relationship between anxiety and the progression of atherosclerosis. Anxiety is associated with sympathetic activation, which has been suggested to alter endothelial integrity50 51 ; this effect could contribute to the progression of arteriosclerosis. Anxious patients may have sympathetic nervous system hyperreactivity.52 This tendency to exhibit exaggerated heart rate and blood pressure responses to behavioral stimuli is associated with a more rapid progression of atherosclerosis.15 53 54 Recent studies suggest that psychological/behavioral factors, such as depression, hostility, and anxiety, are associated with diminished autonomic control of the heart, which may induce a higher blood pressure variability, with effects on the coronary endothelium and plaque formation.55
The present study suffers from some limitations. First, 29% of the initial population was not followed up or had missing values. Nevertheless, because they did not differ significantly for initial levels of IMT and plaque presence, an important bias is not probable. Second, no clinical diagnosis of anxiety disorders was performed. As such, it was not possible to examine whether the observed association was due to anxiety disorders, to high (yet nonpathological) levels of anxious traits, or to both. Finally, variability of the measures of anxiety may have classification bias as a consequence. We considered the subjects with high scores at both baseline and the 2-year follow-up as anxious subjects. In this manner, we excluded from our definition subjects with acute and transient anxiety. On the other hand, we perhaps excluded some subjects habitually anxious but with an occasional low anxiety score. However, the intraclass coefficient correlation between baseline and the 2-year follow-up scores of the Spielberger Inventory was relatively high in the present study.
In conclusion, the present study, conducted in a large community-based cohort, suggests that sustained anxiety is a risk factor for the progression of carotid atherosclerosis, especially in men. Follow-up of the cohort will allow for the examining of the relationship between sustained anxiety and vascular events. Further studies involving the pathophysiological mechanisms that could be involved in this association may have important implications, inasmuch as trait anxiety, or its consequences, may be easier to modify than personality characteristics.
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Acknowledgments |
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The EVA Study was supported by the Merck Sharp and Dhome-Chibret Co and EISAI (France). Dr Sabrina Paterniti was supported by a postdoctoral grant from INSERM. We are grateful to C. Delanoë and E. Marceteau for their technical support.
Received January 18, 2000; accepted September 4, 2000.
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