© 1997 American Heart Association, Inc.
Articles |
Hopelessness and 4-Year Progression of Carotid Atherosclerosis
The Kuopio Ischemic Heart Disease Risk Factor Study
From the Human Population Laboratory, Public Health Institute, Berkeley, Calif (S.A.E., D.E.G.); the Human Population Laboratory, California Department of Health Services, Berkeley, Calif (G.A.K.); and the Research Institute of Public Health and Department of Community Health and General Practice, University of Kuopio, Kuopio, Finland (R.S., J.T.S.).
Correspondence to Susan A. Everson, PhD, MPH, Department of Epidemiology, School of Public Health, University of Michigan, 109 Observatory St, Ann Arbor, MI 48109-2029. E-mail severson{at}emf.net.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Abstract The importance of hope has long been recognized, whereas a lack of hope, or "giving up," is generally believed to have a negative impact on psychological well-being and physical health. Recently, hopelessness has been identified as a strong, independent predictor of cardiovascular disease morbidity and mortality in both American and Finnish populations. In this study we examined the association between high levels of hopelessness and progression of carotid atherosclerosis in participants (n=942) in the Kuopio Ischemic Heart Disease Study, a population-based study of middle-aged men from eastern Finland who underwent carotid ultrasonography at baseline and 4 years later. Men reporting high levels of hopelessness at baseline had faster progression of carotid atherosclerosis, assessed by four measures of intima-media thickening (IMT), than men reporting low to moderate levels of hopelessness. Further analyses revealed significant interactions between hopelessness and initial level of atherosclerosis, such that the effects of high hopelessness on progression were greatest among men who had baseline mean IMT values at or above the median. Moreover, progression was greatest among men reporting high levels of hopelessness at both baseline and follow-up. Traditional coronary risk factors and use of cholesterol-lowering and antihypertensive medications did not account for much variance in the observed relationships. These findings indicate that hopelessness contributes to accelerated progression of carotid atherosclerosis, particularly among men with early evidence of atherosclerosis, and that chronically high levels of hopelessness may be especially detrimental. Additional research is needed to identify the contributory pathways and/or mechanisms underlying these relationships.
Key Words: hopelessness • intima-media thickening • progression • risk factor • atherosclerosis
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
A growing body of clinical and empirical evidence1 2 3 4 5 6 supports the long-held belief that giving up hope has adverse physical and mental health consequences.7 8 9 Anda and colleagues4 recently reported that hopelessness significantly predicted fatal and nonfatal IHD after 12 years of follow-up in a cohort of more than 2800 initially healthy men and women from the National Health Examination Follow-Up Survey. Similarly, we found that a high level of hopelessness was consistently associated with increased risk for incident myocardial infarction and cardiovascular mortality, as well as other outcomes, after 6 years of follow-up in middle-aged men from eastern Finland.5 In both studies, controlling for traditional cardiovascular risk factors had relatively little impact on the observed associations between hopelessness and cardiovascular morbidity and mortality, suggesting that hopelessness operates through other, as yet unidentified, mechanisms or earlier in the causal pathway.
To better understand the relationship between hopelessness and cardiovascular disease morbidity and mortality, it may be useful to examine the influence of hopelessness earlier in the disease process, eg, in relation to progression of atherosclerosis. No prior research has addressed this issue; however, animal and human studies offer suggestive evidence that psychosocial, behavioral, and/or environmental influences may potentiate atherosclerosis.10 Accordingly, we examined the association between levels of hopelessness and 4-year progression of carotid atherosclerosis in a sample of middle-aged men participating in the KIHD study, a population-based study examining the effects of psychosocial characteristics and traditional and promising coronary risk factors on IHD and other outcomes.11 The KIHD study enabled us to examine the influence of various behavioral and biological variables on the association between hopelessness and atherosclerotic progression.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Study Population
The KIHD study is an ongoing population-based study designed to investigate previously unestablished risk factors for carotid atherosclerosis, IHD, mortality, and other outcomes among middle-aged men from the Kuopio region in eastern Finland, an area with high coronary morbidity and mortality.12 A total of 2682 42-, 48-, 54-, and 60-year-old men (82.9% of those eligible) were recruited in two cohorts. The first cohort consisted of 1166 54-year-old men (83.3% of those eligible), enrolled between March 1984 and August 1986; the second cohort included 1516 42-, 48-, 54-, and 60-year-old men (82.6% of those eligible), enrolled between August 1986 and December 1989. A total of 1229 men from the second cohort underwent ultrasound examination of the right and left carotid arteries at baseline. This group was invited to participate in a follow-up study, which was conducted between March 1991 and December 1993. Of the 1229 men who were eligible for follow-up examination, 1038 (88.2%) participated; 107 refused; 52 could not participate because of death, severe illness, or relocation; and 32 could not be contacted. Average time to follow-up was 4.2 years (range=3.8 to 5.2 years). The present study includes data from the 942 men who had complete information from the baseline and follow-up ultrasound examinations and on the measures of hopelessness and all covariates. Persons with missing data who were excluded from the present study (n=96) did not differ from participants with respect to baseline or follow-up levels of carotid atherosclerosis, although nonparticipants were slightly older (P<.002).
Baseline and Follow-up Examinations
Examinations were carried out over 2 days, 1 week apart, at both
baseline and follow-up, and consisted of a wide variety of biochemical,
physiological, anthropometric, and psychosocial
measures (see Salonen11 for complete details). Medical
history and medication use were checked during a medical examination at
both baseline and follow-up.
Hopelessness Scale
Hopelessness, defined as negative expectancies about oneself and
the future, was measured by two items from a battery of psychosocial
questionnaires administered at the baseline examination. The items were
"I feel that it is impossible to reach the goals I would like to
strive for" and "The future seems to me to be hopeless, and I
can't believe that things are changing for the better." Responses
were on a 5-point Likert scale (0, absolutely agree; 1, somewhat agree;
2, cannot say; 3, somewhat disagree; or 4, absolutely disagree). Items
were reverse-scored and summed to create a hopelessness score, with a
range of 0 to 8. Three groups were formed according to low, moderate,
or high scores on the hopelessness scale, based on meaning of the
scores and response options, as follows: 58.3% of men had low scores
(0, 1, or 2), indicating general disagreement with each of the two
statements; those with scores in the middle range of the scale (3, 4,
or 5) formed a "moderately hopeless" group (32.9%) (moderate
scores reflected a mixed response to the items); and men with high
scores (6, 7, or 8) formed a "highly hopeless" group (8.8%)
(high scores were indicative of general agreement with both
statements).
Measurement of Carotid Atherosclerosis
Extent of carotid atherosclerosis was assessed
by high-resolution B-mode ultrasonography of the right and left CCAs in
a 1.0- to 1.5-cm section at the distal end of the CCA, proximal to the
carotid bulb. Images were focused on the posterior wall of the right
and left CCA and recorded on videotape for later analysis.
Near-wall images were not obtained because of their greater measurement
variability.13 Ultrasound examinations were conducted by
one of four trained sonographers and were performed with the subject in
a supine position after a 15-minute rest.
At baseline, CCA images were obtained using a duplex ultrasound system with a 10-MHz sector transducer. At follow-up, images were obtained with a scanner equipped with a 10-MHz annular array probe.14 Wedge phantom studies of this system, calibrated against an RMI 414B tissue phantom, have demonstrated measurement precision of ±0.03 mm.14 15
Baseline and follow-up IMT measurements were made via computerized analysis of the videotaped ultrasound images using Prosound software (University of Southern California, Los Angeles, Calif). This software uses an edge-detection algorithm, specifically designed for use with ultrasound imaging,16 that allows automatic detection, tracking, and recording of the intima/lumen and media/adventitia interfaces. IMT, calculated as the mean distance between these interfaces, was estimated at approximately 100 points in both the right and left CCAs.
For the present study, four measures of IMT were used: (1) mean IMT, calculated as the mean of all IMT estimates from the right and left CCAs and considered an overall measure of the atherosclerotic process; (2) maximum IMT, the average of the points of maximum thickness from the right and left CCAs and indicative of the depth of intrusion of IMT into the lumen in this part of the CCA; (3) plaque height, the average of right and left CCA measurements of plaque height, calculated as the difference between maximum and minimum thickness, and an assessment of how steeply atherosclerotic lesions protruded into the lumen; and (4) surface roughness, a measure of variability in IMT, calculated as the SD of all IMT measurements from the right and left CCAs, and hypothesized to be a measure of sensitivity of the vessel wall to thrombus or plaque formation and hemodynamic turbulence and shear stress. Progression of atherosclerosis was estimated as follow-up minus baseline values for each of these IMT measures.
Baseline Covariates
Biological Factors
Biological risk factors included resting SBP, measured with a
random-zero sphygmomanometer and calculated as the average of four SBP
measurements obtained on the first baseline examination day (two
readings taken at minutes 10 and 15 of a 15-minute supine rest,
followed by two readings taken at minutes 5 and 10 of a 10-minute
seated rest); HDL and LDL cholesterol, separated from fresh
plasma using ultracentrifugation and precipitation and
measured enzymatically (CHOD-PAP cholesterol method,
Boehringer Mannheim, Mannheim, Germany); and BMI, calculated as
weight divided by height squared (kg/m2).
Behavioral and Education Factors
Behavioral covariates included alcohol consumption, assessed by
a questionnaire on drinking behavior over the previous 12 months and by
a 4-day instructed dietary record, and cigarette smoking, assessed
by self-report of never, former, and current smoking (pack-years).
Education was assessed by self-report of completed years of
schooling.
Medications
Use of medications for hypertension or
hyperlipidemia was assessed at baseline via
interview.
Data Analyses
To examine the association between hopelessness and progression
of atherosclerosis over 4 years, we estimated the mean
change in each measure of IMT (mean, maximum, plaque height, surface
roughness) by level of hopelessness. Because preliminary
analyses suggested a threshold effect rather than a gradient of
increasing change in IMT with increasing levels of hopelessness and
because we were specifically interested in examining the influence of
high levels of hopelessness on atherosclerotic progression, we combined
the data from the low and moderate hopelessness groups for our
analyses. Analyses were performed using the general
linear model procedure in SAS, version 6.09, installed on a Sun
SPARCstation 20. This procedure estimated least-square mean values of
IMT and performed F tests examining the effect of hopelessness on
atherosclerotic progression while simultaneously
controlling for age and other covariates in the model. In addition to
age, the initial model included adjustments for baseline IMT, zooming
depth of the ultrasound scan, sonographer, and participation in the
placebo or treatment arm of a clinical trial of
pravastatin.17
A subset of 136 KIHD participants from the present study also participated in the KAPS study, a clinical trial that showed that pravastatin effectively reduced cholesterol levels in hyperlipidemic men.17 Two dummy-coded variables representing randomization in the placebo or treatment arm of KAPS, versus nonparticipation, were included in all models; however, these covariates were nonsignificant, indicating that patients' participation in KAPS did not affect the results of this study.
To examine the influence of potential risk factors, we then calculated a second model that included all variables in the initial model plus variables representing SBP, HDL, LDL, BMI, education, cigarette smoking, alcohol consumption, and use of antihypertensive or antihyperlipidemic medications as covariates. Analyses for the four measures of IMT used in this study were conducted separately.
To determine whether the associations between hopelessness and atherosclerotic progression varied according to initial level of IMT, we then repeated the analyses, stratifying at the median level of mean IMT at baseline (0.731 mm). Finally, because it is plausible that hopelessness may have more pronounced and deleterious effects on health if it is chronic rather than acute, we repeated the analyses comparing men who reported high levels of hopelessness at both baseline and follow-up (n=49) to those reporting low to moderate levels of hopelessness at both examinations (n=627). Men who reported different levels of hopelessness at baseline and follow-up also were included in these analyses as a separate group (n=228). Thirty-eight subjects with missing data on the hopelessness scale at follow-up were excluded from these tertiary analyses.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Table 1
presents the mean
(and SD) or prevalence (%) for scores on the hopelessness scale, age,
baseline levels of IMT, and other covariates by level of
hopelessness.
|
Results from the initial models examining the influence of hopelessness on progression revealed a consistent pattern of findings across the measures of mean and maximum IMT, plaque height, and surface roughness. Compared to men with low to moderate scores on the hopelessness scale, highly hopeless men had a 19.2% greater increase in maximum IMT (+0.31 versus +0.26 mm, P<.03) and a significantly greater increase in variation of IMT along the walls of the CCA (surface roughness) (+0.03 versus +0.021 mm, P<.04). The most hopeless group also showed a 21.8% larger increase in mean IMT (+0.134 versus +0.11 mm) and a 10% greater progression in plaque height (+0.296 versus +0.269 mm) relative to those with lower hopelessness scores; however, these latter differences did not reach conventional levels of significance (P<.20). Similar results were seen after additional adjustments for biological and behavioral risk factors and medication use.
Stratifying by extent of atherosclerosis at baseline
revealed that hopelessness was related to progression of carotid
atherosclerosis only among men with baseline mean IMT
values at or above the median. Given this pattern of findings, we
recalculated the general linear models to test the interactive effects
of baseline mean IMT and hopelessness on progression. Table 2 presents the means (and SEs) for
4-year changes in mean IMT, maximum IMT, plaque height, and surface
roughness by level of hopelessness and mean IMT at baseline and the F
and P values for the interactions from both the initial and
fully adjusted models. Important interactions were identified for all
four measures of progression in the initial age-adjusted models.
Subsequent paired t tests revealed that among participants
with median or higher levels of baseline mean IMT, those reporting high
levels of hopelessness experienced significantly larger increases in
mean IMT (P<.024), maximum IMT (P<.006), plaque
height (P<.049), and surface roughness
(P<.0003) than those reporting lower levels of
hopelessness. Hopelessness was unrelated to progression in men with
less than the median level of baseline mean IMT (P>.4).
Additional adjustments for resting SBP, LDL, HDL, BMI, smoking, alcohol
consumption, education, and use of medications for hypertension and
hypercholesterolemia did not alter these
findings.
|
Table 3 presents the data from the
analyses examining the influence of chronic hopelessness on
atherosclerotic progression. Compared to men with low to moderate
levels of hopelessness at both examinations, men experiencing
chronically high levels of hopelessness had a 32.7% larger increase in
mean IMT, a 27.3% greater change in maximum IMT, and more than an 18%
larger increase in plaque height, as well as a significantly greater
increase in surface roughness of the CCA. Men whose reported level of
hopelessness differed at baseline and follow-up showed an intermediate
level of progression. Results were relatively unchanged in the models
that included adjustments for behavioral and biological risk factors
and medication use. (The models shown in Table 3 did not test the
potential interactive effects of basal level of
atherosclerosis and chronic hopelessness because the
relatively small number of chronically hopeless men did not provide
adequate power to test this interaction.)
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
This study demonstrates that a high level of hopelessness exacerbates the atherosclerotic process in middle-aged men. We observed accelerated progression in the small number of men who reported strong feelings of hopelessness at the baseline examination. The consistency of associations across measures of IMT in this study is especially noteworthy in light of the fact that less than 10% of our sample was in this highly hopeless group.
Interestingly, our analyses that examined the association
between hopelessness and atherosclerotic progression by basal level of
atherosclerosis indicated that hopelessness exerted its
effect primarily among those men with IMT levels in the upper half of
the distribution at baseline. Indeed, significant interactions between
hopelessness and baseline mean IMT were noted for all four measures of
IMT progression. This finding suggests that hopelessness exacerbates
the mechanisms that contribute to increased arterial wall
thickening but may be less important in the initial atherosclerotic
process. The lack of a cross-sectional association between reported
hopelessness and IMT values at baseline (Table 1
) is consistent
with this conclusion. Reasons why hopelessness may have fewer
atherogenic effects among men without initial thickening or be less
significant in the early stages of atherosclerosis are
unknown. The mechanisms underlying the association between hopelessness
and atherosclerotic progression remain to be identified in humans.
However, animal studies have shown that exposure to uncontrollable
stressors and learned helplessness, phenomena that can be considered
precursors to and/or correlates of hopelessness, have adverse
autonomic, neuroendocrine, and immunologic effects,18 19 20
all of which may potentiate atherogenesis.
Our observed pattern of results was consistent across the four measures of carotid atherosclerosis but strongest for the measures of maximum IMT and surface roughness. These findings indicate that hopelessness influences the overall atherosclerotic process but may be particularly pathogenic with respect to the development and/or progression of focal lesions and arterial wall roughness, thereby increasing the likelihood of plaque fissuring or rupture. Moreover, although the differential pathological and clinical significance of the four parameters of carotid atherosclerosis used in this study remain to be determined, cross-sectional data from the entire KIHD sample revealed that each 0.10-mm difference in maximum IMT was associated with an 11% increase in risk of acute myocardial infarction (P<.001).21
Our previous study showed that hopelessness was strongly and consistently related to all-cause and cause-specific mortality and incidence of cancer and myocardial infarction, independent of classic risk factors.5 These findings are consistent with the concepts of generalized resistance22 and allostatic load,23 notions that suggest that individuals in interaction with their environment develop a set of behavioral, social, psychological, and physiological adaptations that have a cumulative, generic effect on health. Hopelessness appears to be one such maladaptive, psychological response. The present study is consistent with this interpretation.
Examining the influence of long-term hopelessness on progression showed
that men who reported high levels of hopelessness at both their
baseline and follow-up examinations experienced the largest increases
in carotid atherosclerosis relative to men reporting
low to moderate hopelessness at both points in time. Men whose reported
level of hopelessness either increased or decreased during the 4 years
of follow-up showed an intermediate level of progression. This pattern
of findings suggests that long-term, pronounced feelings of
hopelessness may be particularly pathogenic. Nevertheless, our study
was not designed to examine chronicity of emotions, so our results can
only be considered suggestive. The correlation between hopelessness
scores at baseline and follow-up was .51 (P<.0001),
indicating a moderate degree of consistency in
individuals' reported sense of hopelessness across time. However, we
did not obtain information on how long respondents had experienced
feelings of hopelessness before their baseline examination. Given that
atherosclerotic lesions begin to develop early in life,24
it would be useful to gather such information in future studies to more
fully examine the impact of long-term hopelessness on the
atherosclerotic process. Additionally, given the interaction between
hopelessness and extent of atherosclerosis at baseline
identified in this study (see Table 2), it will be important to
determine whether long-term hopelessness also shows a synergistic
relationship with atherosclerosis. Our findings suggest
that sustained feelings of extreme hopelessness may be especially
atherogenic in individuals with early evidence of atherosclerotic
thickening.
The associations between hopelessness and progression of carotid atherosclerosis reported herein were relatively unchanged after adjustments for established cardiovascular disease risk factors, including HDL and LDL cholesterol levels, resting SBP, BMI, education, cigarette smoking, and alcohol consumption. This may reflect a lack of confounding by known cardiovascular risk factors, or it may be that the impact of these risk factors on disease progression was not adequately assessed because we considered only basal levels rather than changes in risk factor levels. Alternatively, it may be that the cumulative effect of these variables on atherosclerosis was taken into account by baseline level of IMT, which was a highly significant covariate in all models. It may also be the case that risk factors not measured in the present study (eg, homocysteine) or presently unidentified risk factors are contributing to the association between hopelessness and progression of carotid atherosclerosis.
The present study was conducted in middle-aged white men. It remains to be seen whether similar associations between hopelessness and progression of atherosclerosis will be evident in female or nonwhite populations and among different age groups. It will also be informative to determine whether other long- or short-term negative emotional states have similar effects on atherosclerosis or whether the findings presented here are unique to the construct of hopelessness.
In summary, the present study demonstrates that hopelessness contributes to accelerated progression of carotid atherosclerosis, particularly among men with early evidence of atherosclerosis, and that chronically high levels of hopelessness may be especially atherogenic. This study thus contributes to the growing literature1 2 3 4 5 6 25 26 27 that provides empirical support for the long-held belief that a lack of hope has adverse health effects. Future research needs to more thoroughly examine the mechanisms underlying the observed relationships and to identify the social, psychological, and physiological factors that lead to hopelessness as well as the factors that help to alleviate it.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
Supported by grant HL44199 from the National Heart, Lung, and Blood Institute and by grants from the Academy of Finland and the Finnish Ministry of Education.
Received June 17, 1996; accepted November 6, 1996.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Pettingale KW, Morris T, Greer S, Haybittle J. Mental attitudes to cancer: an additional prognostic factor. Lancet. 1985;3:750. Letter.
2. Jensen M. Psychobiological factors predicting the course of breast cancer. J Pers. 1987;55:317-342.[Medline] [Order article via Infotrieve]
3. Stein S, Linn MW, Stein EM. Psychological correlates of survival in nursing home cancer patients. Gerontologist. 1989;29:224-228.[Abstract]
4. Anda R, Williamson D, Jones D, et al. Depressed affect, hopelessness, and the risk of ischemic heart disease in a cohort of U.S. adults. Epidemiology. 1993;4:285-294.[Medline] [Order article via Infotrieve]
5.
Everson SA, Goldberg DE, Kaplan GA, et al.
Hopelessness and risk of mortality and incidence of myocardial
infarction and cancer. Psychosom Med. 1996;58:113-121.
6.
Greene SM. The relationship between depression
and hopelessness: implications for current theories of
depression. Br J Psychiatry. 1989;154:650-659.
7. Scheier MF, Carver CS. Optimism, coping, and health: assessment and implications of generalized outcome expectancies. Health Psychol. 1985;4:219-247.[Medline] [Order article via Infotrieve]
8. Snyder CR, Irving LM, Anderson JR. Hope and health. In: Snyder CR, Forsyth DR, eds. Handbook of Social and Clinical Psychology. Elmsford, NY: Pergamon Press, 1991:285-305.
9. Scheier MF, Carver CS. Effects of optimism on psychological and physical well-being: theoretical overview and empirical update. Cogn Ther Res. 1992;16:201-228.
10. Kaplan JR, Pettersson K, Manuck SB, Olsson G. Role of sympathoadrenal medullary activation in the initiation and progression of atherosclerosis. Circulation. 1991;84[suppl VI]:VI-23-VI-32.
11. Salonen JT. Is there a continuing need for longitudinal epidemiologic research? The Kuopio Ischemic Heart Disease Risk Factor Study. Ann Clin Res. 1988;20:46-50.[Medline] [Order article via Infotrieve]
12. Keys A. Seven Countries: A Multivariate Analysis of Death and Coronary Heart Disease. Cambridge, Mass: Harvard University Press, 1980.
13. Wikstrand J, Wendelhag L. Methodological considerations of ultrasound investigation of intima-media thickness and lumen diameter. J Int Med. 1994;236:555-559.[Medline] [Order article via Infotrieve]
14. Salonen R, Salonen JT. Intima-media changes in a population study: KIHD. In: Boccalon H, ed. Vascular Medicine. Amsterdam: Elsevier Science Publishers, 1993;301-304.
15. Salonen JT, Korpela H, Nyyssönen K, Salonen R. Precision and reproducibility of ultrasonographic measurement of progression of common carotid artery atherosclerosis. Lancet. 1993;341:1158-1159.
16.
Blankenhorn DH, Selzer RH, Crawford DW, et al.
Beneficial effects of colestipol-niacin therapy on the common carotid
artery: two- and four-year reduction of intima-media thickness measured
by ultrasound. Circulation. 1993;88:20-28.
17.
Salonen R, Nyyssönen K, Porkkala E, et al. Kuopio
Atherosclerosis Prevention Study (KAPS): a
population-based primary preventive trial of the effect of LDL lowering
on atherosclerotic progression in carotid and femoral arteries.
Circulation. 1995;92:1758-1764.
18. Seligman MEP, Maier SF, Solomon RL. Unpredictable and uncontrollable aversive events. In: Brush FR, ed. Aversive Conditioning and Learning. New York: Academic Press, 1971.
19. Weiss JM, Goodman PA, Losito BG, Corrigan S, Charry JM, Bailey WH. Behavioral depression produced by an uncontrollable stressor: relationship to norepinephrine, dopamine, and serotonin levels in various regions of rat brain. Brain Res Rev. 1981;3:167-205.
20. Weiss JM, Sundar S. Effects of stress on cellular immune responses in animals. In: Tasman A, Riba M, eds. Review of Psychiatry, vol 11. Washington, DC: American Psychiatric Press, 1992.
21. Salonen JT, Salonen R. Ultrasound B-mode imaging in observational studies of atherosclerotic progression. Circulation. 1993;87(suppl II):56-65.
22.
Cassel J. The contribution of the social
environment to host resistance. Am J Epidemiol. 1976;104:107-123.
23.
McEwen BS, Stellar E. Stress and the
individual. Arch Intern Med. 1993;153:2093-2101.
24.
Stary HC, Chandler AB, Dinsmore RE, et al. A definition
of advanced types of atherosclerotic lesions and a
histological classification of
atherosclerosis. Arterioscler Thromb Vasc
Biol. 1995;15:1512-1531.
25. Appels A, Falger PR, Schouten EG. Vital exhaustion as risk indicator for myocardial infarction in women. J Psychosom Res. 1993;37:881-890.[Medline] [Order article via Infotrieve]
26. Appels A, Mulder P. Fatigue and heart disease: the association between "vital exhaustion" and past, present, and future coronary heart disease. J Psychosom Res. 1989;33:727-738.[Medline] [Order article via Infotrieve]
27.
Kop WJ, Appels A, de Leon CF, Swart HB, Far FW.
Vital exhaustion predicts new cardiac events after successful
coronary angioplasty. Psychosom Med. 1994;56:281-287.
This article has been cited by other articles:
 |
|
 |
|
  M. O. Whipple, T. T. Lewis, K. Sutton-Tyrrell, K. A. Matthews, E. Barinas-Mitchell, L. H. Powell, and S. A. Everson-Rose Hopelessness, Depressive Symptoms, and Carotid Atherosclerosis in Women: The Study of Women's Health Across the Nation (SWAN) Heart Study Stroke, October 1, 2009; 40(10): 3166 - 3172. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. C. Rice, A. B. Zonderman, E. J. Metter, S. S. Najjar, and S. R. Waldstein Absence of Relation Between Depressive Symptoms and Carotid Intimal Medial Thickness in the Baltimore Longitudinal Study of Aging Psychosom Med, January 1, 2009; 71(1): 70 - 76. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Valtonen, D. E. Laaksonen, T. Tolmunen, K. Nyyssonen, H. Viinamaki, J. Kauhanen, and L. Niskanen Hopelessness -- novel facet of the metabolic syndrome in men Scand J Public Health, November 1, 2008; 36(8): 795 - 802. [Abstract] [PDF]
|
|
|
|
 |
|
 J. C. Stewart, D. L. Janicki, M. F. Muldoon, K. Sutton-Tyrrell, and T. W. Kamarck Negative Emotions and 3-Year Progression of Subclinical Atherosclerosis Arch Gen Psychiatry, February 1, 2007; 64(2): 225 - 233. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. J. Giltay, M. H. Kamphuis, S. Kalmijn, F. G. Zitman, and D. Kromhout Dispositional optimism and the risk of cardiovascular death: the zutphen elderly study. Arch Intern Med, February 27, 2006; 166(4): 431 - 436. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. E. Innes, C. Bourguignon, and A. G. Taylor Risk Indices Associated with the Insulin Resistance Syndrome, Cardiovascular Disease, and Possible Protection with Yoga: A Systematic Review J Am Board Fam Med, November 1, 2005; 18(6): 491 - 519. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Elovainio, L. Keltikangas-Jarvinen, M. Kivimaki, L. Pulkki, S. Puttonen, T. Heponiemi, M. Juonala, J. S. A. Viikari, and O. T. Raitakari Depressive Symptoms and Carotid Artery Intima-Media Thickness in Young Adults: The Cardiovascular Risk in Young Finns Study Psychosom Med, July 1, 2005; 67(4): 561 - 567. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. D. Kubzansky, K. W. Davidson, and A. Rozanski The Clinical Impact of Negative Psychological States: Expanding the Spectrum of Risk for Coronary Artery Disease Psychosom Med, May 1, 2005; 67(Supplement_1): S10 - S14. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B Wolff, H J Grabe, H Volzke, J Ludemann, C Kessler, J B Dahm, H J Freyberger, U John, and S B Felix Relation between psychological strain and carotid atherosclerosis in a general population Heart, April 1, 2005; 91(4): 460 - 464. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. A. Everson-Rose, J. S. House, and R. P. Mero Depressive Symptoms and Mortality Risk in a National Sample: Confounding Effects of Health Status Psychosom Med, November 1, 2004; 66(6): 823 - 830. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. J. Giltay, J. M. Geleijnse, F. G. Zitman, T. Hoekstra, and E. G. Schouten Dispositional Optimism and All-Cause and Cardiovascular Mortality in a Prospective Cohort of Elderly Dutch Men and Women Arch Gen Psychiatry, November 1, 2004; 61(11): 1126 - 1135. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Haatainen, A. Tanskanen, J. Kylmaa, K. Honkalampi, H. Koivumaa-Honkanen, J. Hintikka, and H. Viinamaki Ftors Associated with Hopelessness: A Population Study International Journal of Social Psychiatry, June 1, 2004; 50(2): 142 - 152. [Abstract] [PDF]
|
|
|
|
|
|
H. Tiemeier, W. van Dijck, A. Hofman, J. C. M. Witteman, T. Stijnen, and M. M. B. Breteler Relationship Between Atherosclerosis and Late-Life Depression: The Rotterdam Study Arch Gen Psychiatry, April 1, 2004; 61(4): 369 - 376. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Prescott, C. Holst, M. Gronbaek, P. Schnohr, G. Jensen, and J. Barefoot Vital exhaustion as a risk factor for ischaemic heart disease and all-cause mortality in a community sample. A prospective study of 4084 men and 5479 women in the Copenhagen City Heart Study Int. J. Epidemiol., December 1, 2003; 32(6): 990 - 997. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Steptoe and M. Marmot Burden of Psychosocial Adversity and Vulnerability in Middle Age: Associations With Biobehavioral Risk Factors and Quality of Life Psychosom Med, November 1, 2003; 65(6): 1029 - 1037. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Schwarz, H. Schachinger, R. H. Adler, and S. M. Goetz Hopelessness Is Associated With Decreased Heart Rate Variability During Championship Chess Games Psychosom Med, July 1, 2003; 65(4): 658 - 661. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Harper, J. Lynch, W.-L. Hsu, S. A Everson, M. M Hillemeier, T. E Raghunathan, J. T Salonen, and G. A Kaplan Life course socioeconomic conditions and adult psychosocial functioning Int. J. Epidemiol., April 1, 2002; 31(2): 395 - 403. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. D. Kubzansky, D. Sparrow, P. Vokonas, and I. Kawachi Is the Glass Half Empty or Half Full? A Prospective Study of Optimism and Coronary Heart Disease in the Normative Aging Study Psychosom Med, November 1, 2001; 63(6): 910 - 916. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. L. Stern, R. Dhanda, and H. P. Hazuda Hopelessness Predicts Mortality in Older Mexican and European Americans Psychosom Med, May 1, 2001; 63(3): 344 - 351. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. W. Cohen, S. Madhavan, and M. H. Alderman History of Treatment for Depression: Risk Factor for Myocardial Infarction in Hypertensive Patients Psychosom Med, March 1, 2001; 63(2): 203 - 209. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Reilly Enhancing human healing BMJ, January 20, 2001; 322(7279): 120 - 121. [Full Text]
|
|
|
|
 |
|
 S. Paterniti, M. Zureik, P. Ducimetiere, P.-J. Touboul, J.-M. Feve, and A. Alperovitch Sustained Anxiety and 4-Year Progression of Carotid Atherosclerosis Arterioscler Thromb Vasc Biol, January 1, 2001; 21(1): 136 - 141. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. C. Whiteman, I. J. Deary, and F. G. R. Fowkes Personality and Social Predictors of Atherosclerotic Progression: Edinburgh Artery Study Psychosom Med, September 1, 2000; 62(5): 703 - 714. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. A. Everson, G. A. Kaplan, D. E. Goldberg, and J. T. Salonen Hypertension Incidence Is Predicted by High Levels of Hopelessness in Finnish Men Hypertension, February 1, 2000; 35(2): 561 - 567. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Rozanski, J. A. Blumenthal, and J. Kaplan Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy Circulation, April 27, 1999; 99(16): 2192 - 2217. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. L. Gornel, D. P. Gray, R. Steele, K. Sweeney, W. D. Rosamond, L. E. Chambless, A. R. Folsom, D. Levy, and T. J. Thom Rates of Death from Coronary Heart Disease N. Engl. J. Med., March 4, 1999; 340(9): 730 - 732. [Full Text]
|
|
|
|
|
|
S. A. Everson, R. E. Roberts, D. E. Goldberg, and G. A. Kaplan Depressive Symptoms and Increased Risk of Stroke Mortality Over a 29-Year Period Arch Intern Med, May 25, 1998; 158(10): 1133 - 1138. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||