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(Circulation. 1995;92:1458-1464.)
© 1995 American Heart Association, Inc.
Articles |
Psychosocial Risk Factors and Nonfatal Myocardial Infarction
From the Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass (N.J.O., J.E.M., J.E.B.); the Clinical Research Section, Department of Medicine, Dartmouth-Hitchcock Medical Center, Hanover, NH (G.T.O.); and the Department of Ambulatory Care and Prevention, Harvard Medical School, Boston, Mass (J.E.B.).
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Abstract |
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Background Numerous psychosocial factors have been hypothesized to play a role in coronary heart disease. However, existing studies have yielded inconsistent results.
Methods and Results The relations between type A personality as well as suppressed versus expressed anger and risk of nonfatal myocardial infarction (MI) were studied in 340 patients and 340 age-, sex-, and community-matched control subjects. Subjects were interviewed at home to assess behavioral and medical cardiovascular risk factors, and fasting blood samples were obtained. Type A personality was associated with nonfatal MI in crude matched-pair analysis (OR, 1.57; 95% CI, 1.12 to 2.20; P=.008). Adjusting for known cardiovascular risk factors (including treated hypertension, body mass index, treated diabetes, family history of premature MI, physical activity, smoking, alcohol, total calories per day, and saturated fat) did not substantially change the magnitude of the point estimate, although the finding was no longer statistically significant (OR, 1.43; 95% CI, 0.97 to 2.09; P=.069). Further adjustment for lipids, including total cholesterol, total HDL, its subfractions (HDL2, HDL3), LDL, VLDL, and triglycerides, markedly attenuated the association (OR, 1.12; 95% CI, 0.66 to 1.90; P=.687), an effect due almost entirely to HDL cholesterol. Suppressed anger was positively but not statistically significantly associated with increased risk of MI in crude matched-pair analysis (OR, 1.33; 95% CI, 0.98 to 1.81; P=.065), in analysis adjusted for behavioral and medical cardiovascular risk factors (OR, 1.26; 95% CI, 0.89 to 1.78; P=.193), or after adjustment for lipids (OR, 1.11; 95% CI, 0.67 to 1.82; P=.695).
Conclusions These findings suggest a possible association of type A but not suppressed anger with risk of nonfatal MI that may be mediated by alterations in HDL cholesterol level. If decreases in HDL are not in the same causal pathway, then the apparent association between type A personality and risk of MI is due to confounding, principally by HDL.
Key Words: risk factors, psychosocial • myocardial infarction • coronary disease
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Introduction |
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Numerous psychosocial factors have been hypothesized to play a role in coronary heart disease (CHD). The Framingham Heart Study looked at several broad categories of these, including measures of personality type, sociocultural mobility, situational stress, and somatic strain. In this study, we evaluate two Framingham psychosocial factors: type A personality and mode of expressing anger.
Type A personality was first described by Friedman and Rosenman1 in the 1950s. They proposed that a certain group of behavioral characteristics was common in a large percentage of their patients with CHD. This group of characteristics included obsessive attempts to achieve many poorly defined goals, love of competition, a strong need for recognition and advancement, a persistent preoccupation with time and the need to get things done in a hurry, intense concentration and alertness, and high levels of "free-floating hostility." The "type A hypothesis" was first evaluated in the Western Collaborative Group Study,2 which showed that at the end of 8.5 years of follow-up, type A men were twice as likely as type B men to have suffered some manifestation of CHD, independent of other available coronary risk factors.
Although numerous retrospective and cross-sectional3 4 5 6 7 8 9 10 and several prospective11 12 13 14 epidemiological studies supported the Western Collaborative Group Study findings, other studies of high-risk populations yielded inconsistent results.15 16 17 18 19 20 21 The inability to control for important confounding variables (eg, behavioral, medical, and biochemical risk factors for CHD) was one plausible explanation for the positive findings. "Toxic" elements of personality type were also hypothesized to explain the discrepant findings. The Western Collaborative Group Study first identified two dimensions of the type A personality that were the best discriminators between case and control subjects: (1) potential for hostility and (2) anger directed outward.22 An important aspect of this dimension was identified as mode of anger expression.23 The Framingham Reaction to Anger scales categorized anger into three types: anger in, anger out, and anger discuss.11 Since the results of the Framingham Study seemed to indicate that it was the suppression or expression of anger that was important, we used the Framingham instrument to measure mode of anger expression but categorized it dichotomously as anger suppressed and anger expressed.
The Boston Area Health Study provided the opportunity to examine the relation between type A personality, mode of anger expression, and nonfatal myocardial infarction (MI) while controlling for a wide variety of behavioral, medical, and biochemical risk factors.
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Methods |
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The Boston Area Health Study is a case-control study of 340 patients with first MI and an equal number of age-, sex-, and community-matched control subjects. Case subjects were selected from admissions to the coronary or intensive care units of six suburban Boston hospitals (Emerson, Framingham Union, Leonard Morse, Mount Auburn, Newton-Wellesley, and Waltham) between January 1, 1982, and December 31, 1983. Those eligible for inclusion were white men and women <76 years of age living in the Boston area with no previous history of MI or angina pectoris.
The diagnosis of MI according to World Health Organization criteria was
confirmed from hospital records on the basis of the clinical
history accompanied by rise in creatine kinase enzyme. Permission was
sought from each admitting physician, and informed consent was obtained
from the patients in the hospital. For each case patient, a control
subject of the same sex and age (within 5 years) was selected at random
from the residents' list of the town in which the patient resided.
Specifically, the name of the patient was located in the appropriate
Massachusetts town book, and the next individual in the book of the
same sex and age, within 5 years, was selected. Because the books are
listed by addresses, the control subject was from approximately the
same neighborhood as the case patient. By these methods, a total of 340
case-control pairs were enrolled in the study,
representing participation rates of 
80% among case
patients and 60% among all control subjects, both eligible and
ineligible.
Letters of invitation were sent to potentially eligible case patients
as well as control subjects who were later contacted by telephone.
Those who agreed to participate were interviewed, usually in their
home, by one of two trained nurse interviewers 8 weeks after
hospital discharge of the case patient. Information was obtained on a
large number of coronary risk factors related specifically to
the time period before the infarction for the case patients and before
the interview for the control subjects. This information included the
subject's medical history (family history of premature MI [positive
history of MI before age 60 years in the individual's mother, father,
or siblings], history of medication for treatment of high blood
pressure, height, weight, and history of diabetes) and behavioral
factors (cigarette smoking, alcohol consumption, dietary intake, and
level of physical activity). Participants were asked their usual
occupation. Dietary intake for the year before infarction for the case
patients and the year before the interview for control subjects was
assessed by use of a self-administered food-frequency
questionnaire that has been shown to be reliable and
valid.24 A physical activity index, expressed in
kilocalories per week, was obtained by summing the results of interview
items regarding stairs climbed, blocks walked, and recreational and
leisure-time activities.25 Case patients were asked
about physical activities the week before, or for seasonal activities
the year before, the MI, and control subjects were asked about
activities in the analogous time periods preceding the interview.
Personality type was assessed by the 10 items from the Framingham type A scale. Four of these items were related to occupation. The participants were asked to answer yes or no to the following questions: (1) Have you often felt very pressed for time? (2) Has your work often stayed with you so that you were thinking about it after working hours? (3) Has your work often stretched you to the very limits of your energy and capacity? (4) Have you often felt uncertain, uncomfortable, or dissatisfied with how well you were doing at work? The other 6 items had to do with personality traits or qualities. Subjects were read the following list of traits or qualities: (1) eating too quickly, (2) having a strong need to excel (to be best) in most things, (3) usually feeling pressed for time, (4) getting quite upset when you have to wait for anything, (5) being hard-driving and competitive, and (6) being bossy or dominating. For each item, subjects were asked whether the trait described them very well, fairly well, somewhat, or not at all.
Anger was assessed according to the seven items in the Framingham Anger Scale. These items had to do with feelings and reactions when one is angry. Subjects were asked whether they usually, sometimes, or rarely/never react in the following ways when angry or annoyed: (1) try to act as though nothing has happened, (2) keep it to yourself, (3) apologize even though you are right, (4) take it out on others, (5) blame it on someone else, (6) get it off your chest, and (7) talk to a friend or relative.
Each personality type and anger item was scored, with the sign reversed where appropriate, and the values were summed. Then the control group mean for each was used as the cut point to create two nominal variables, personality type (A/B) and anger (suppressed/expressed).
Fasting blood samples were obtained from a subgroup of the case
patients (n=283) 8 weeks after hospital discharge to allow for the
stabilization of blood lipids,26 27 as well as from a
subgroup of the control subjects (n=275). Blood was drawn into 0.1%
EDTA, and plasma was obtained by centrifugation at 3000
rpm for 30 minutes at 4°C. HDL cholesterol, LDL
cholesterol, and triglyceride measurements were
performed by the Lipid Research Clinic methods.28 29
Total
and HDL cholesterol values were standardized with the Lipid
Standardization Program of the Centers for Disease Control and
Prevention. For the purposes of this study, total
cholesterol as well as cholesterol subfraction
analyses were based on the matched-pair available sample
size (n=466).
Stratified analyses were performed to control for individual risk factors by Mantel-Haenszel techniques,30 and test-based 95% CIs were calculated.31 Conditional logistic regression was used to control simultaneously for potential confounding variables. Variables chosen for inclusion in these models were known cardiovascular risk factors.
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Results |
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Table 1
presents the characteristics of case
patients and control subjects. As expected, a higher proportion of case
patients had been treated for hypertension or diabetes. Case patients
also were more likely to report a family history of premature MI and to
be physically less active. In addition, they smoked more heavily and
drank alcohol less frequently. Case patients had a higher daily caloric
intake, with a larger percent derived from saturated fat. In terms of
lipid profile, case patients had lower mean total HDL and subfractions
HDL2 and HDL3 but higher levels of LDL
and VLDL. To define personality type (A versus B) and mode of
expressing anger (suppressed versus expressed), we used the mean scores
among control subjects to define the cut points for these dichotomous
variables. A significantly larger proportion of case patients were
type A personality, whereas the higher proportion of case patients who
suppressed anger was of borderline significance.
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Table 2 presents the mean values for
cardiovascular risk factors by personality type. A
greater percentage of type A subjects were male, physically active, and
current smokers. Type A subjects were about 6 years younger on average
and consumed more calories per day. In addition, there were small and
borderline statistically significant differences in mean age- and
sex-adjusted cholesterol levels between type A and type
B subjects (1.7 mg/dL for total HDL, P=.090; 1.4 mg/dL for
HDL2, P=.060).
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With respect to anger (Table 3), those classified as
suppressive were 2 years older on average, were more likely to be
current smokers, and had higher levels of triglycerides,
but no other substantial differences were noted.
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Table 4 presents the relation between personality
type and nonfatal MI. In crude matched-pair analysis, type
A personality was associated with a statistically significant 57%
increase in risk of nonfatal MI (OR, 1.57; 95% CI, 1.12 to 2.20;
P=.008). This result was similar for men and women and,
although no longer statistically significant, varied little after
adjustment for behavioral and medical cardiovascular
risk factors, including treated hypertension, body mass index, treated
diabetes, family history of premature MI, physical activity, smoking,
alcohol intake, total calories consumed per day, and saturated fat
consumed (OR, 1.43; 95% CI, 0.97 to 2.09; P=.069). However,
this apparent increase in risk among type A subjects did not persist
after further multivariate adjustment for lipids (OR,
1.12; 95% CI, 0.66 to 1.90; P=.687). In addition, Table
4
provides the OR for personality type and nonfatal MI after adjustment
for each behavioral and medical cardiovascular risk
factor and each lipid subfraction individually. For type A, none of the
medical history or behavioral variables alone seemed to be largely
responsible for the slightly diminished effect seen in
multivariate analysis (1.57 to 1.43).
Adjustment for LDL, VLDL, and triglycerides did not
substantially change the OR either. However, when total HDL or
HDL2 was controlled for, a substantial reduction in
the OR was observed (1.57 to 1.22 and 1.57 to 1.31, respectively).
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Table 5 shows the relation between anger and nonfatal
MI. In crude matched-pair analysis, suppressed anger was
associated with a statistically nonsignificant 33% increase in risk of
nonfatal MI (OR, 1.33; 95% CI, 0.98 to 1.81; P=.065). This
effect was approximately the same after adjustment for known medical
and behavioral cardiovascular risk factors (OR, 1.26;
95% CI, 0.89 to 1.78; P=.193) and was slightly attenuated
after further multivariate adjustment for lipids (OR,
1.11; 95% CI, 0.67 to 1.82; P=.695).
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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In this case-control study, type A personality was associated with an increased risk of nonfatal MI in crude matched-pair analysis. The magnitude of this association was markedly attenuated after control for HDL cholesterol.
Four previous population-based prospective studies found an association between type A personality and risk of CHD. After 8.5 years of follow-up, the Western Collaborative Group Study found that type A personality was strongly related to CHD incidence among men 39 to 59 years old in multivariate analysis (RR=2.2 for total CHD, RR=2.10 for MI, and RR=2.5 for angina pectoris).2 In the Framingham Heart Study, type A personality was associated with total CHD and MI in multivariate analysis in men 45 to 64 years old (RR=1.8 for total CHD and RR=2.1 for MI) and with total CHD and angina pectoris in women of the same age group (RR=2.1 for total CHD and RR=3.6 for angina pectoris).11 In the Belgian-French Cooperative Heart Study,13 which studied the predictors of incidence of CHD in European male civil servants and factory workers, type A personality was a significant predictor of total CHD, MI, and sudden death (RR=1.8 for total CHD and RR=1.6 for MI and sudden death combined). In the Belgian Heart Disease Prevention Trial,14 type A personality was related to total CHD (RR=1.9), but no tests of significance or multivariate analysis results were reported. Of the population-based studies, only the Honolulu Heart Program32 and the Finnish Twin Cohort Study33 showed no association between type A personality and incidence of CHD.
Of the six studies of type A personality in high-risk people, one showed a positive relation between type A personality and CHD end points,15 one showed a negative effect,16 and three showed no relation.17 18 19 The sixth study investigated whether interventions designed to alter type A behavior lowered the risk of recurrent events among MI patients.21 There were significantly lower recurrence rates of nonfatal events among the intervention group compared with the control group (4.1% versus 10.6%).
Although some of the previous studies have controlled for total cholesterol or hypercholesterolemia, only one specifically investigated HDL cholesterol. This 1963 study,34 which compared 10 type A and 10 type B men, found that when differences in diet, weight, and physical activity were controlled for, the type A men exhibited elevations in serum levels of triglycerides and LDL and VLDL cholesterol and decreases in HDL levels (45 mg/dL for type A versus 51 mg/dL for type B). The present study raises the possibility that lowered HDL cholesterol may represent a mechanism by which type A personality increases risk of MI.
The effects of both physical and psychological stressors on cholesterol levels have been studied in the laboratory. Usually, these studies have tested the immediate effects on lipid levels of some sort of acute experimental stress, rather than the effects of chronic stress such as type A personality. Most of these studies observed increases in serum lipid levels in response to these types of stress. Several animal studies, however, have looked at the effect of chronic psychological stress on cholesterol levels. A study by Clarkson35 that investigated biological and psychosocial influences on coronary artery atherosclerosis in female monkeys showed that chronic psychological stress decreased HDL levels. In another nonhuman primate study,36 a statistically significant decrease in HDL cholesterol was observed in 24 African vervet monkeys after a year of repeated capture and venipuncture. In this study, it was also interesting that the monkeys showed a statistically significant temporary increase in HDL cholesterol after a severe hurricane, which suggests differences in the effects of acute and chronic stressors on serum lipid levels.
Several mechanisms by which psychological stress may decrease serum levels of HDL cholesterol have been hypothesized. Specifically, both norepinephrine and adrenocorticoids may diminish lipoprotein lipase activity, which in turn lowers HDL cholesterol.37 A study by Fredrikson and Blumenthal38 observed that norepinephrine excretion was greater in patients with low levels of HDL, and the authors concluded that heightened sympathetic nervous system activation, by affecting lipid levels, may be a potential CHD risk factor. Similar results have been reported by others.39 40 In another study of responses to stress in healthy type A men, plasma norepinephrine was found to be negatively correlated with HDL.41
It is known that total HDL cholesterol is inversely related
to MI. It is generally believed that for each 1-mg/dL increase in HDL
cholesterol level, there is about a 3% decrease in risk of
CHD.42 In the present study, there was a 1.7-mg/dL
difference in HDL levels between type A and type B subjects, which
would be expected to translate into an 6%, rather than 32%,
difference in risk. In a prior analysis of this data set that
investigated the roles of subfractions of HDL on risk of nonfatal MI,
it was observed that an adjusted 4.2-mg/dL difference in HDL
cholesterol resulted in a significant (P<.0001)
inverse dose-response relation; the OR for those in the highest
quartile relative to those in the lowest was 0.15.43 In a
recent prospective study of lipid levels and risk of MI, a
statistically significant age- and smoking-adjusted 4.6-mg/dL
difference in HDL levels was highly protective (RR=.38 for the highest
compared with the lowest quintile of lipid level).44
The possibility of misclassification of lipid levels for the case patients should be considered in the interpretation of the present results, as well as the results of the previously mentioned prior analysis. MI is known to affect lipid metabolism acutely.26 45 46 47 48 49 For this reason, blood specimens collected about 8 weeks after hospital discharge of the case patients were used to measure lipid levels. However, these levels could reflect behavioral and dietary changes after the infarction and not preinfarction levels. If the case patients had made dietary changes after MI that would favorably affect lipid levels, then the case patients and control subjects would be expected to have more similar lipid levels than they would have if the lipid measurements had been made before the MI. If this had happened in an extreme way, lipid levels in the case patients and control subjects might be so alike that the expected relation between lipid levels and risk of MI would not be observed. We did observe the expected relation between HDL and MI, so it is unlikely that appreciable misclassification of lipid levels due to post-MI behavioral or dietary changes was responsible for these results; however, it may partially explain how a small difference in HDL levels (1.7 mg/dL) between type A and type B individuals resulted in such a large increase in risk for type A subjects.
In addition, the lipid levels for the case patients may have been affected by postinfarction medication use, particularly treatment for elevated cholesterol and the use of thiazide diuretics or ß-blockers. We were unable to directly control for confounding by these variables because the information collected in the study referred to the year before admission to the hospital for the case patients and before the interview for the control subjects. Thus, we had no data specifically concerning the postdischarge period for the case patients. If the use of postinfarction medication unfavorably affected the lipid profile of the case patients and was independently associated with type A personality, it may have artifactually produced the observed effect through confounding.
If HDL is not in the causal pathway between type A personality and nonfatal MI, it may simply be a confounder of this association. Although controlling for possible confounders, including age, sex, weight, percent of diet from saturated fat, alcohol intake, physical activity, and smoking, did not affect this association, it is possible that some unknown confounder may be responsible for it. For example, there was a statistically significant difference in the amount of calories consumed per day between type A and type B individuals in this study. Perhaps dietary factors other than percent of diet from saturated fat that are associated independently with both type A personality and lowered HDL cholesterol are responsible for the increased risk of MI associated with type A personality in this analysis.
Suppressed anger was positively but not statistically significantly associated with MI in this study. The only other study that evaluated this hypothesis with comparable measurement of anger expression is the Framingham Heart Study, which found that "not expressing anger outwardly" predicted CHD in male white-collar workers (RR=2.20) and working women (RR=2.07) and that "not discussing anger" predicted angina in women (RR=1.71).11 Other studies23 50 that assessed which elements of the type A personality were related to coronary artery disease severity found that only "potential for hostility" and "anger in" were significantly and positively associated.
In conclusion, these findings suggest a possible association between type A personality, but not suppressed anger, and MI of a magnitude similar to that reported previously. This association persists even after adjustment for known behavioral and medical cardiovascular risk factors in multivariate analyses. The apparent increases in risk among persons with type A personality in these data may be explained largely by lower HDL levels among type A subjects. To the best of our knowledge, most previous studies of psychosocial risk factors for MI have not collected data on HDL, which has been postulated to decrease with chronic stress.35 36 If decreases in HDL are in the causal pathway—that is, if type A personality actually causes decreases in HDL—then these data are consistent with a true causal association between type A personality and risk of MI. On the other hand, if HDL is a confounder, then this variable may have artifactually produced the apparent increased risk of MI associated with type A personality that persisted after control for a large number of other behavioral, medical, and biochemical risk factors.
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Acknowledgments |
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This study was supported by research grants (HL-24423 and HL-21006) and an institutional training grant (HL-07575) from the National Heart, Lung, and Blood Institute. We are indebted to the six hospitals in the Boston area that participated in this study and to the respective collaborators: Emerson Hospital (Marvin H. Kendrick, MD), Framingham Union Hospital (Marvin Adner, MD, and Gerald Evans, MD), Leonard Morse Hospital (L. Frederick Kaplan, MD), Mount Auburn Hospital (Leonard Zir, MD), Newton-Wellesley Hospital (James Sidd, MD), and Waltham Hospital (Solomon Gabbay, MD), as well as to Charles H. Hennekens, MD, for his advice and assistance.
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Footnotes |
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Reprint requests to Dr J.E. Buring, Brigham and Women's Hospital, 900 Commonwealth Ave East, Boston, MA 02215.
Received May 24, 1994; revision received March 13, 1995; accepted March 19, 1995.
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