a School of Psychology,
c Department of Epidemiology and Public Health, Queens University, Belfast BT7 1NN, Northern Ireland.
b Department of Epidemiology and Public Health, Faculty of Medicine, Strasbourg, France.
d The Toulouse MONICA Project, INSERM U558, Toulouse, France.
e The Lille MONICA Project, INSERM U508, Lille, France.
f The Coordinating Centre, U258 INSERM, Paris, France.
Abstract
Background France has a substantially lower level of premature mortality from cardiovascular diseases (CVD) relative to its comparators. Compared with Northern Ireland, France has one-half the rate, despite having a similar cardiovascular risk profile to Northern Ireland. In this prospective longitudinal study the psychosocial risk hypothesis for CVD was tested.
Method A cohort of 9758 men (7359 in France and 2399 in Northern Ireland) aged 5059 years who were initially free of any CVD were recruited. At baseline the subjects completed a psychosocial questionnaire, measuring hostility, depression, social support, and the Type A behaviour pattern. At 5-years follow-up their clinical status was determined.
Results Multivariate analysis indicated that, contrary to prediction, France had a substantially more negative psychosocial risk profile than Northern Ireland. The psychosocial risk factors were not successful at predicting at 5-years follow-up the hard clinical endpoint of definite fatal/non-fatal myocardial infarction. In the case of the softer clinical endpoint, angina pectoris/unstable angina, only depression predicted outcome with a small effect size.
Conclusion The findings provide little support for the psychosocial risk hypothesis. The psychosocial risk profile was more negative in France, the opposite of that predicted. The finding of a relationship between depression and angina may reflect a tendency for individuals who respond negatively on mood state to report more cardiac symptoms irrespective of physical disease state.
Keywords Coronary heart disease, depression, hostility, TABP, social support, France, Northern Ireland
Accepted 9 August 2002
France, despite having a diet high in saturated fats, has a significantly lower level of premature deaths from coronary heart disease (CHD) than comparable countries elsewhere.1,2 This can be illustrated by comparing France with Northern Ireland. Coronary events recorded in the MONICA study (a World Health Organization initiated multicentre, world-wide epidemiological study) indicate that in France CHD mortality in men was on average approximately one-half the rate found in Northern Ireland. Thus, per 100 000 the rates for France (Lille, Strasbourg and Toulouse, respectively) were 172, 141 and 91 versus 279in Belfast. For total coronary events (fatal and non-fatal), the respective rates were 298, 292, 233 versus 695, a 2.32.98-fold difference.3 This difference in coronary event rates between the two countries cannot be explained in terms of the classical risk factors for heart disease. Multiple logistic function scores, based on age, cigarette smoking, systolic blood pressure, total cholesterol and body mass index (BMI), which provide an estimate of predicted risk, indicated that Lille was highest (0.023), followed by Belfast (0.022) and Strasbourg (0.021), with Toulouse the lowest (0.016); certainly not a profile that could explain the higher incidence in Northern Ireland.4 In a correlational study, less than 25% of the variance in cardiovascular and ischaemic heart disease mortality in men across 35 populations in the MONICA study was explained by the three risk factors, cigarette smoking, blood pressure, and total cholesterol.5 More recent data from the MONICA study suggest that the percentage of the variability in trends in coronary event rates that are explained by trends in the major risk factors is 15% in the case of women and40% in the case of men.6
The view that the classical risk factors explained half or lessof new cardiac events and variations in incidence7 (recently questioned by Magnus and Beaglehole8) led to a considerable body of research examining putative psychosocial risk factors. There is accumulating evidence that the social environment, in particular social support (lack of it), is a factor affecting health in general,9 and cardiovascular disease (CVD) in particular.10,11 Population-based prospective studies indicate that individuals who are socially isolated are at increased risk for all-cause mortality, with social support related to survival post-myocardial infarction.12 Prospective cohort studies suggest an aetiological link between social support and CHD.13 Social support is thought to mediate the effects of stress on illness as well as directly affecting illness.9
At the personal level, several psychological traits have been identified as independent risk factors for CVD, the best known of these being the type A behaviour pattern (TABP).14 Matthews and Haynes 15 in their review of the TABP literature concluded that there was an association between TABP and cardiac mortality, the most consistent evidence coming from population-based prospective studies, but with less support from prospective studies of high-risk subjects. Booth-Kewley and Friedman16 in their (quantitative) meta-analysis of studies examining psychological variables and CHD identified TABP as one of the variables with the strongest association, although there has been a trend toward more negative findings in recent years.13,17
In recent years, hostility has been the focus of much of the psychosocial research on the aetiology of CVD.18 There is fairly substantial evidence, based on prospective studies, linking hostility to CHD.19,20 Miller, Smith, Turner, Guijarro and Hallet21 in their meta-analytical review of some 45 studies concluded that hostility was an independent (independent of other known risk factors) risk factor for all-cause mortality and for CVD mortality and morbidity.
Related to hostility is the psychological state, depression. Booth-Kewley and Friedman16 in their review of psychological variables and CVD identified depression as the variable with the greatest predictive power. In prospective longitudinal studies, depression measured at baseline has been shown to be associated with an elevated risk of myocardial infarction (MI) at follow-up;22,23 population-based case-control studies also support this link.24 Wulsin, Vaillant and Wells25 concluded from their review of the literature that there was an increased riskof death associated with depression, particularly death from unnatural causes and CVD. Glassman and Shapiro26 identified six recent community surveys that controlled for smoking, five of the studies showing a significant association between depression and ischaemic heart disease. Barrick27 recently reviewed the epidemiological evidence linking mood disorders and coronary artery disease, and concluded that mood was a covariate risk factor in the pathogenesis of the disease. She suggested that further research was needed to establish if it was a causal factor.
Given that the classical risk factors cannot account for the large differences in CHD mortality between France and Northern Ireland, and the evidence implicating TABP, hostility, depression and social support in CHD, the present study was designed to test the psychosocial hypothesis. In particular, it was hypothesized that Northern Ireland, with two to three times the rate of CHD mortality compared to France, would have higher levels of TABP, hostility and depression, and lower levels of social support, compared to France.
One final issue in the study concerns the measurement equivalence across the two countries of the instruments used to measure the psychosocial variables. In cross-cultural research such as this it cannot be assumed that instruments developed to measure particular factors in one country, when translated into the language of another country, will measure the same thing. This issue will also be addressed.
Methods
The data were collected under the aegis of the PRIME (Prospective Epidemiological Study of Myocardial Infarction) study, the methodology for which has been described in detail elsewhere.4
Subjects
A sample of 10 593 men, aged 5059 years, were recruited between 1991 and 1994 in four centres, namely Lille (n = 2627), Strasbourg (n = 2611) and Toulouse (n = 2610) in France, and Belfast (n = 2745) in Northern Ireland. A 5-year follow-up has been completed on these men. At screening, 9758 subjects were found to be free of CHD, based on clinical and historical evidence. The findings reported here are based on this cohort of initially disease free men, except for the measurement model that was based on the total sample.
Instruments
Type A behaviour pattern was measured with the Framingham scale,28 which has predicted angina-related CHD in both men and women over 8-,29 10-,30 14-31 and 20-year periods.32 Although this is a ten-item measure, Haynes in a personal communication with Chesney33 had suggested that four items could be dropped. It was the shorter, six-item scale that was used. Factor analysis of the six items indicates that two latent factors are measured by the scale, these being hard-driving competitiveness (four items, e.g. Having a strong need to excel in most things) and impatience (two items, e.g. I get upset when I have to wait for something).34 Hostility was measured with items taken from the Cook-Medley Hostility Scale.35 It has been argued that the core element in this 50-item scale is a cynical distrust of others, this being the first factor extracted in the exploratory factor analysis by Greenglass and Julkunen.36 The seven items selected centred on this construct (e.g. Most people inwardly dislike putting themselves out to help other people). Depression was measured with a nine-item modification of the Welsh depression sub-scale derived from the Minnesota Multiphasic Personality Inventory,37 the items reflecting negative perceptions of life and the self (e.g. I feel helpless). Social support was measured with four items recommended for use in the World Health Organization MONICA study,38 these items assessing the number of relatives and friends available (e.g. How many relatives do you have that you feel close to?). The items in the four measures, competitiveness, impatience, hostility and depression, were scored 0 and 1, giving a range of scores of 04, 02, 014 and 018, respectively. Each item of social support was measured on a scale 07, giving a range of scores 028. The alpha coefficients (based on the present sample) were acceptably high for competitiveness (0.68), hostility (0.77), depression (0.74) and social support (0.84), but low in the case of impatience (0.27), reflecting the fact that there were only two items in the scale.
Procedure
Initially, a confirmatory factor analysis, using the programme LISREL,39 was carried out on the Belfast data. This was done to determine the quality of the measurement model. In a confirmatory factor analysis a measurement model is first specified; that is, the number of latent factors are identified, together with a specification of the observed items loading on each factor. This model is then tested against the observed data, with various measures provided indicating goodness-of-fit. Having established a satisfactory measurement model with the Belfast data, the equivalence of this model was then tested in the three French centres, again using confirmatory factor analysis. When testing goodness-of-fit it is usual to report the 2 value, with a non-significant
2 indicating a good fit. However, with large sample sizes, such as those in the present study, the increased statistical power means that
2 will be large even when the model is only trivially false.40 Browne and Cudeck41 suggest using the root mean square error of approximation (RMSEA), which is an analysis of residuals, smaller values indicating a better fit. They suggest that RMSEA values < 0.05 indicate a close fit, with values between 0.05 and 0.08 indicating a reasonable fit.
Analyses
The data were analysed using multivariate analysis of variance (Manova), Pearson correlations, and logistic regression with the statistical package SPSS.42 Manova was chosen as the dependent measures were correlated. With large samples sizes, as in the present study, quite trivial differences can reach statistical significance. Therefore effect sizes (the degree to which the phenomenon is present in the population) are reported as appropriate. Cohen43 has suggested that the values corresponding to small, medium, and large effect sizes for eta squared (2, the proportion of the variance accounted for by population membership) are 0.01, 0.06, and 0.14. Similarly, for correlations Cohen suggests r values of 0.10, 0.30, and 0.50.
Results
Measurement model
The confirmatory factor analysis on the Belfast data indicated that the five factor model, competitiveness, impatience, hostility, depression and social support, fitted the data well (RMSEA = 0.034). The five factor model with 26 items was then tested on each of the three French centres, again using confirmatory factor analysis, with each of the analyses indicating a good fit (RMSEA: Strasbourg = 0.037, Toulouse = 0.037, Lille = 0.038). Examination of the values (Table 1
), an indication of the covariation between the latent factors (and thus interpretable as the percentage of shared variance between any two latent factors), shows that the two TABP factors, competitiveness and impatience, are highly associated (0.72). Impatience is quite strongly associated with hostility (0.39) and depression (0.38), and to a lesser extent with social support (-0.19). Competitiveness, however, only has a modest association with hostility (0.18), and none with depression (-0.04) and social support (0.00). Hostility and depression are strongly associated (0.43), with both negatively associated with social support (-0.35 and 0.31, respectively).
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Correlations between the medical, behavioural and psychosocial variables
There were a number of statistically significant correlations between the two sets of variables, a function in good part of the very large sample size (Table 4). Accepting Cohens43 definition of a small effect size (r = 0.10, i.e. 1% of the variance), only three of the significant correlations reach this size. Thus, higher levels of hostility are associated with a larger waist/hip ratio (r = 0.155) and BMI (r = 0.102), with impatience also associated with a larger BMI (r = 0.142).
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Discussion
The reasons for the relatively low rates of premature mortality from CHD in France compared to comparable countries elsewhere remain unclear, although Law and Wald have suggested that this may reflect a time lag effect.44 They suggest that France adopted a high fat diet more recently than other countries such as Britain, and that, given that there is a time lag between a rise in serum cholesterol and its expression in heart disease, the lower French CHD mortality rate may be a function of this lag. However, this remains a hypothesis. Recent data from the MONICA study suggest that the classical risk factors cannot account for the greater part of the wide variation in CHD mortality in different countries5,6 Recent data from the PRIME study support this, for the two- to threefold difference in CHD mortality between Northern Ireland and France cannot be explained in terms of differences in the classical risk factor profile of the two countries.4 The analyses reported here indicate a slightly riskier lipid profile in Northern Ireland compared to France, but otherwise in respect of the other risk factors the picture is not dissimilar in the two countries with some positive features in Northern Ireland. Given the relative failure of the classical risk factors to account for variations in CHD mortality between the two countries, are the psychosocial risk factors any better at accounting for the variations in mortality? The simple answer, based on the present data, is no. Not only does the psychosocial risk profile not explain the differences in CHD mortality between Northern Ireland and France, it is in fact the opposite of that predicted. The French sample scores higher on hostility, competitiveness and impatience, and lower on social support compared to the Northern Ireland sample, with depression at similar levels in the two countries. Overall, the psychosocial risk profile for France is substantially worse compared to Northern Ireland, as indicated by the effect size (2 = 0.174).
These unexpected results cannot be explained by reference to the measurement model. The confirmatory factor analyses indicate that the same latent factors are being measured in the four populations. Hostility is measured with the same items that defined the first factor extracted from the exploratory factor analysis of the full Cooke-Medley hostility scale by Greenglass and Julkunen.36 They labelled this factor cynicism. Barefoot, Dodge, Peterson, Dahlstrom and Williams45 also identified this cynicism factor, and found that it, together with two other factors (hostile affect and aggressive responding), was a better predictor of all-cause mortality than the complete, 50-item hostility scale (the sample was too small to analyse by cause of death, but half of the deaths were from CHD). The seven items of the hostility scale are the same as seven of the eight comprising the cynical distrust scale used by Everson et al.46 which predicted both all-cause mortality and cardiovascular mortality over a 9-year follow-up period. In the case of TABP, this was measured with the six items recommended by Haynes33 based on her analyses of the Framingham data. However, rather than having one score based on the six items, two scores were used. This is justified given that, although the two latent factors, competitiveness and impatience, covary strongly ( = 0.72), they are not measuring the same thing. Price47 suggested that impatience might mediate any pathogenic effect via its connection with hostility. In the present study the Framingham factor impatience covaries quite strongly with hostility (
= 0.39) and depression (
= 0.38), whereas the other Framingham factor, competitiveness, has a much weaker relationship with hostility (
= 0.18) and is not related to depression (
= -0.04). In the case of social support it has been argued that people high in cynicism would be low in social support,36 and there is evidence supporting this.48 This is the case in the present study, with a negative co-variation between hostility and social support (
= -0.35). One might also expect social support and depression to co-vary negatively, which is the case (
= -0.31). Thus, it might reasonably be concluded that the measurement element of the study is satisfactory, and that hostility, social support, depression and the two elements of the Framingham TABP (competitiveness and impatience) are being validly measured in the two countries. The finding that the French and the Northern Irish have similar levels of depression is also unexpected. It is known that depression and hostility are related,49 with substantial covariation between the two latent factors in the present study (43%). Given that the French score substantially higher than the Northern Irish on hostility then it might be expected that the French would also score higher on depression, but they do not.
In regard to the prediction of clinical endpoints with the psychosocial factors, here there was little in the way of success. The psychosocial factors did not predict the hard clinical endpoint, death from MI or definite non-fatal MI. In regard to the softer endpoint, angina, this did produce a highly significant 2, with depression and to a lesser extent hostility related to outcome. If the focus is solely on the level of significance (P = 0.006) this would be taken as a substantial finding. However, with large sample sizes highly significant P-values do not necessarily indicate large effects. Inspection of the partial correlations indicates an r = 0.099 for depression, and r = -0.051 for hostility. The partial correlation for depression thus equates to what Cohen43 calls a small effect size. As Cohen has pointed out small does not necessarily mean trivial within a large population. Nonetheless, the association remains only modest. In the case of hostility the partial correlation does not reach the small effect size (and is also negative, i.e. it is having a slight positive effect). It is also possible that the findings are artefactual. In a study of subjectively perceived stress and heart disease,50 a relationship was found between stress and reported symptoms of heart disease but not with objective indices of disease. The authors suggested that individuals who have a tendency to respond negatively on measures of stress may also have a tendency to over-report cardiac symptoms. This may account for the relationship between depression and angina found in the present study; negative emotions having been found to predict the reporting of somatic complaints but not actual disease.51
The study thus provides little support for the psychosocial hypothesis. The expression of the psychosocial risk factors in the two populations does not accord with the different incidence of CVD in France and Northern Ireland. Nor were the psychosocial factors successful in predicting actual coronary disease (MI). It is possible, but yet to be proven, that the differences in rates of cardiac events, fatal and non-fatal, between the two countries reflects differences in protective factors, in particular the anti-oxidant hypothesis, with diet the major factor.52 Also, the more proactive approach to the treatment of cardiovascular risk factors in France compared to Northern Ireland may play a role in preventing cardiac events, but this also has yet to be proven.3
Acknowledgements
We are indebted to Dr Brendan Bunting of the University of Ulster, for the courses on LISREL that he has run over the years, and his willingness to discuss and illuminate the complexities of structural equation modelling. The PRIME study is organized under an agreement between INSERM and the Merck, Sharpe and Dohme-Chibret laboratory, with the following participating laboratories. The Strasbourg MONICA Project, Department of Epidemiology and Public Health, Faculty of Medicine, Strasbourg, France (D Arveiler, B Haas). The Toulouse MONICA Project, INSERM U558, Toulouse, France (J Ferrieres, JB Ruidavets). The Lille MONICA Project, INSERM U508, Lille, France (P Amouyel, M Montaye). The Departments of Epidemiology and Public Health,a Medicineb and Psychology,c The Queens University of Belfast, Belfast, Northern Ireland (AE Evans,a E McCrum,a CP Salters,a J Yarnell,a D McMaster,b DH Sykesc). Department of Atherosclerosis, SERLIA-INSERM UR545, Lille, France (G Luc, JM Bard, JC Fruchart). The Laboratory of Haematology, La Timone Hospital, Marseilles, France (I Juhan-Vague). The Laboratory of Endocrinology, INSERM U326, Toulouse, France (B Perret). The Vitamin Research Unit, The University of Bern, Bern, Switzerland (F Gey). The DNA Bank, Service Commun n° 7 INSERM U525, Paris, France (F Cambien). The Coordinating Centre, U258 INSERM, Paris, France (P Ducimetiere, PY Scarabin, A Bingham).
KEY MESSAGES
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