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Is Type A Behavior Really a Trigger for Coronary Heart Disease Events?

From the Department of Epidemiology (J.E.J.G., P.C.E.), Statistics and Public Health, University of Wales College of Medicine, Cardiff; Department of Epidemiology and Public Health (P.M.S., J.W.G.Y.), Queens University, Belfast; and Department of Psychiatry (S.A.S.), Queen Mary College, London

Address reprint requests to: Dr JEJ Gallacher, Department of Epidemiology, Statistics and Public Health, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN UK. Email: Gallacher{at}cf.ac.uk

	ABSTRACT

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OBJECTIVE: The purpose of this study was to compare chronic with acute mechanisms by which Type A might predict incident coronary heart disease (CHD).

METHOD: The study included 2394 men aged 50 to 64 years who were assessed for CHD, Type A behavior, and CHD risk factors. Type A was assessed using the Jenkins Activity Survey (JAS), the Bortner scale, and the Framingham scale. Further examinations were completed at 5 and 9 years for incident CHD.

RESULTS: After 9 years, there was no increased risk of CHD associated with any Type A score. Nevertheless, high Bortner scores were associated with increased risk of incident CHD at 5 years and high JAS and Bortner scores were associated with a decreased risk between 5 and 9 years. Further analysis of Type A scores on time to first coronary event found strong inverse associations for all type A scores (JAS = 205 -0.49 months to first event, 95% CI = -0.20, -0.78, p = .001) (Bortner = 176 -0.27 months; 95% CI = -0.10, -0.44; p = .002) (Framingham = 0.44 -0.0011 months; 95% CI = -0.0002, -0.0019; p = .01).

CONCLUSIONS: The data show Type A is a strong predictor of when incident coronary heart disease (or coronary event) will occur rather than if it will occur. These findings suggest that Type A increases exposure to potential triggers, rather than materially affecting the process of atherosclerosis.

Key Words: coronary disease • Type A behavior • trigger hypothesis • atherosclerosis • stress • psychosocial factors

Abbreviations: CHD = coronary heart disease;; ECG = electrocardiogram;; JAS scale = Jenkins Activity Survey scale;; WHO = World Health Organization;; MI = myocardial infarction;

	INTRODUCTION

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For over a decade, the description of Type A behavior having a "topsy-turvy" career retains a prophetic quality (1). Although the initial balance of opinion has been in favor of an association with incident coronary heart disease (CHD) (2–4) sufficient negative findings have subsequently been reported (5–9) to limit satisfaction with the hypothesis (10).

Since these early studies, the conceptual focus has shifted to redefining the etiological component of the type A construct in terms of hostility/anger. Nevertheless, both predictive (11–16) and null findings (17–23) are still reported. There remains, therefore, scepticism concerning the role of stress related variables as predictors of CHD (24, 25)

Alternatively, the hypothesis could be re-examined. Although both chronic and acute mechanisms have always been implicated (26), emphasis has been given to the former. Analyses have focused, therefore, on Type A as an independent contributor to atherosclerosis. By way of contrast, an acute mechanism suggests Type A increases exposure to circumstances inducing extreme cardiovascular activity, precipitating a coronary event. This may be characterized as the "trigger" hypothesis. This study compares evidence for these contrasting mechanisms.

	METHOD

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Study Population and Survey Methods
The design of the Caerphilly Study has been described elsewhere (27, 28). The original cohort of 2512 men aged 45 to 59 years was recruited between 1979 and 1983, and since then, they have been re-examined at roughly 5-year intervals. The men who are the subject of this report are those seen at the first re-examination between 1984 and 1988, when they were aged 50 to 64 years. Men of the same age who had moved into the geographically defined area since the original recruitment were also considered eligible. A total sample, therefore, of 2884 men was identified.

Each phase comprised a detailed medical examination and lifestyle history. Measurements included blood pressure, smoking habit and alcohol consumption, social class, employment status, and the London School of Hygiene and Tropical Medicine chest pain questionnaire (a standard instrument for assessing angina pectoris and possible MI) (29). A full 12-lead ECG was recorded. The men were invited to return, fasting, to an early-morning clinic where a blood sample was taken. Among many other variables, cholesterol was estimated (30). Informed consent was obtained for all subjects.

To provide data on comparability, type A behavior was assessed using the Jenkins Activity Survey (JAS), Bortner, and Framingham Type A scales. The JAS Type A scale is a self administered 21-item subset of the full JAS (31). The Bortner Type A scale has 14 items and uses bipolar analogue response scales (32). The Framingham Type A scale is interviewer administered and has 10 items (33).

Follow-up and Incident CHD
Follow-up occurred at 5 and 9 years. All men were flagged with the National Health Service central registry and death certificates coded to ICD 410 to 414 were used as the definition of fatal CHD. The chest pain questionnaire and Hospital Activity Analysis (a record for each hospital admission of demographics, diagnosis, procedures, and duration of stay) of all men admitted to local hospitals with a diagnosis of ICD 410 to 414 were used as a basis for a search of the hospital notes for events meeting standard World Health Organization (WHO) criteria for acute myocardial infarction (MI) (34). Finally the appearance on any follow-up ECG of major or moderate Q waves (Minnesota codes 1–1-any, or 1–2-1 to 1–2-5 or 1–2-7) when there were no Q waves (1–1-any, 1–2-any or 1–3-any) on the baseline ECG was taken as evidence that a nonfatal MI had occurred during the follow-up period. Incident CHD was defined as the occurrence of any of the three categories of CHD.

Statistical Methods
Type A scores were treated as continuous variables in all analyses. Logarithmic transformation of the Type A scores made no material difference to the results which are, therefore, presented in natural units. For associations with CHD risk factors and with time to incident CHD, formal analyses were by multiple linear regression. For associations with incident CHD, multiple logistic regression was used with the occurrence or not of incident CHD as the dependent variable.

Men with evidence of ischemia at baseline were not excluded (35). Thirty-one percent of this population sample had some evidence of ischemia as judged by the chest pain questionnaire or the ECG. A substantial proportion of this latter group would be asymptomatic. Exclusion of men with evidence of ischemia, among whom 50% of the incident events occurred, was not deemed satisfactory. Instead measures of angina, history of severe chest pain and ECG ischemia were included as covariates in the analysis. However, the analyses were repeated excluding men with previous CHD.

	RESULTS

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Of the defined population, 2398 (83%) were examined. Of these, 2360 completed the JAS, 2330 completed the Bortner, and 2373 completed the Framingham scale. Of the 2398 men, 161 (6.7%) developed CHD up to the time of the first follow-up at 5 years, whereas 282 (11.8%) had developed CHD by the second follow-up at 9 years.

The distribution of each Type A scale score was unimodal. The JAS showed a positive skew (mean = 179.2, SD = 73.3, median = 162), the Bortner was normally distributed (mean = 163.8, SD = 41.3, median = 165) and the Framingham score also showed a positive skew (mean = 0.371, SD = 0.214, median = 0.333). Pearson correlation coefficients between Type A scales were between r = 0.5 and r = 0.6 suggesting communality rather than homogeneity between scales.

All three Type A scores were higher in social classes I and II and lower in unemployed and retired men as well as in older men (Table 1). Type A score was highest in men smoking 25 or more cigarettes daily. Pearson correlation showed all Type A scores were slightly inversely associated with systolic pressure (r = -0.090 JAS, -0.061 Bortner, -0.084 Framingham) and positively associated with total cholesterol (r = 0.047 JAS, 0.047 Bortner, 0.032 Framingham). The JAS and Bortner were also associated with alcohol consumption (r = 0.043 JAS, 0.047 Bortner). These associations were slight with statistical significance being achieved due to large numbers.

View larger version (19K): [in this window] [in a new window]   Fig. 1. Type A score according to time of first CHD event for the entire cohort and for men without CHD at baseline. All men, —; CHD-free at baseline, - - -.

The magnitude of the regression coefficient is slightly increased if adjustment is made for age, social class, employment status, smoking, alcohol consumption systolic pressure, cholesterol, height and weight both for the cohort as a whole (JAS = 292-0.566 months to first event; 95% CI: -0.264, -0.869; r² = 0.1; p = .0001) (Bortner = 225-0.348 months to first event; 95% CI: -0.181, -0.515; r² = 0.15; p = .0001) (Framingham = 0.643-0.00136 months to first event; 95% CI: 0.000, -0.002; r² = 0.08; p = .002) and for men without CHD at baseline (JAS = 210-0.828 months to first event; 95% CI: -0.312, -1.343; r² = 0.2; p = .002) (Bortner = 192-0.402 months to first event; 95% CI; -0.138, -0.665; r² = 0.23; p = .003) (Framingham = 0.238-0.00203 months to first event; 95% CI: -0.001, -0.003; r² = 0.16; p = .004) as well as for men with CHD at baseline (JAS = 379-0.34 months to first event; 95% CI: -0.716, 0.041; r² = 0.13; p = .08) (Bortner = 274-0.316 months to first event; 95% CI: -0.087, -0.545; r² = 0.13; p = .007) (Framingham = 0.955-0.0009 months to first event; 95% CI = -0.002, 0.000; r² = 0.13; p = .08).

	DISCUSSION

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There are two principal findings from this study. First, over 9 years, there is no difference in Type A scores between those who suffer a coronary event and those who do not. This was found regardless of Type A questionnaire and adjustment for a variety of standard CHD risk factors. The second finding is that among those who do suffer an event, Type A score is strongly associated with the timing of the event. This was found regardless of Type A questionnaire, age, social class, employment status, smoking, alcohol consumption, or evidence of ischemia at baseline.

It is not unreasonable to see the results at 9 years reflecting a balancing of random effects between the two follow-up periods. This explanation is inadequate insofar as it does not account for the very strong and consistent association between each Type A score and time to first coronary event.

It may be that Type A has a predictive "shelf life" and that in the present study the shelf life was the relatively short span of 0 to 5 years. Other studies have shown what can be interpreted as a shelf life effect (36, 37). A shelf life is not necessarily a criticism of psychosocial data. It is unlikely that psychosocial factors will not change over time. This is particularly true of Type A with its known decline with age. Consequently, the validity of point-time psychosocial measurements must be considered to reduce over time and the secular trend of psychosocial associations is a central research interest. Nevertheless, the shelf life explanation does not take account of the inversion of the association between 5and 9 years of follow-up.

In this study, the association of Type A with incident CHD does not predict whether, but when. For men, who for reasons other than Type A were going to have a heart attack, when this attack occurred was predicted by Type A score. Of the suggestions considered, only this explains why Type A score was lower in men with incident CHD between years 5 and 9. Consistent with this view is the observation that the associations of Type A with time to first event were strengthened when men with previous CHD were excluded ie, a coronary event reduces subsequent exposure to triggers. That surviving a coronary event may change subsequent behavior, and hence exposure to behavioral risk factors, is not a new suggestion (38) and quite apart from any patient-generated change, standard cardiac counseling, which would be available to almost all MI survivors, has been shown to reduce Type A behavior by about 10% (39). Why a reduction in Type A should affect the strength of the association depends on the mechanism involved. If chronic atherosclerosis were postulated then little or no reduction in risk might be anticipated as only the rate of atherogenesis would be affected and risk from existing plaque levels would be maintained. If, however, a trigger mechanism is considered the subsequent avoidance of triggers, either deliberately or fortuitously due to incapacity, would immediately reduce subsequent risk.

Exploring this explanation requires some care. First of all, it must be made clear that this is not a test of an a priori hypothesis but a presentation of an unexpected but very clear, consistent and robust trend. Second, the data set have limitations in that 27 men, those with ECG-defined MI only, were excluded from the analysis, because the timing of their coronary event was indeterminate. The mean Type A scores of this small group, however, were in the middle of the range and would not materially affect the results. It is unlikely that assessment procedures were flawed as WHO criteria were used in the assessment of incident CHD and standard Type A assessment techniques were used. It could be argued that the Type A assessment procedures, being questionnaires rather than interview based under estimate hostility. This is a reasonable criticism in that an audio or video structured interview may be more sensitive to different facets of Type A behavior including hostility. However, this adds, rather than detracts, from the potential interest of the present findings because it suggests that psychosocial factors other than hostility may also be implicated in the etiology of CHD.

Considering that Type A does not predict whether a coronary event will occur, it is unlikely that Type A, as measured by these questionnaires, is involved in the underlying process of atherosclerosis. That Type A predicts when a coronary event will occur, however, suggests that these Type A scores predict exposure to the provocation of an event. The predictive power shown by Type A in these data are not great. It should be borne in mind, however, that Type A behavior would not be the only predictor of time of event, and that Type A score would be a surrogate for likely exposure to a trigger rather than the trigger itself. Nevertheless, a strong indication is given of a potentially important mechanism. Extreme emotional events including episodes of anger have been shown to be closely associated chronologically with the occurrence of coronary and ischemic events (40–45). This conclusion is consistent with the known characteristics of Type A behavior. The more extreme the expression of hostility, the more frequent will be exposure to circumstances provoking extreme cardiovascular response. This will produce greatest risk in men with already unhealthy arteries and lead to any trigger effect being confounded with atherosclerosis in a cross sectional analysis, such as in a case series (46). Entertaining a trigger hypothesis also gives opportunity to re-consider time urgency as a predictor of CHD. Although hostility has emerged as the preferred predictive component of type A, recent evidence suggests time urgency may also be operating (47). As with hostility, the more extreme the expression of time urgency, the more frequent will be the exposure to cardiovascular provocation. We provide a hypothesis, therefore, by which time urgency and hostility might predict a coronary event independent of any direct effect on atherosclerosis.

That all three Type A scores were predictive of timing of CHD event can be viewed variously. It may be that all three questionnaires are vulnerable to the same confounding factor and the association is a statistical artifact. The likelihood of this cannot be assessed from these data. Alternatively, they may each be measuring something in common which is predictive of the timing of a CHD event. Observation of each Type A scale shows items reflecting time urgency and hostility but it cannot be assumed that these are the predictive items. Of interest would be an item and factor analysis of the Type A scales but this is not straightforward due to the very different scoring systems used and is beyond the scope of this article.

The possibility of Type A precipitating exposure to triggers does not preclude Type A being associated with increased risk factor levels at times of crisis (48), nor does it preclude an exaggerated physiological response by Type A (49). Neither does it follow that hostility, assessed more directly, perhaps by Type A structured interview, would not be related to an atherosclerotic process. Indeed, in this same cohort suppressed anger has been shown to predict incident CHD at 9 years (16). It does suggest, however, that it is primarily through exposure and response to what is perceived to be a crisis rather than the gradual but relentless hardening of arteries that Type A, as measured in this study, increases CHD risk.

Acknowledging a trigger function of Type A, and providing a means to test it, offers an opportunity to re-visit the wealth of Type A data already available. The failure of long-term follow-up studies to confirm short-term associations potentially has an explanation that makes sense of the initial findings (20, 21). It may also provide an explanation for the enigmatic suggestion from at least one large study that Type A score may be protective (30)! Finally, it offers a key to understanding reports of successful secondary prevention that suggests survival may be related to avoidance of triggers rather than reduced atherosclerosis (39).

Of particular interest is whether these findings can be replicated. Analyses of Type A score on time-to-first event could be conducted on many extant data sets. Only then will we be in a position to consider with confidence whether Type A acts as a trigger for coronary events.

Received for publication December 28, 2001.

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