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Anger in Young Men and Subsequent Premature Cardiovascular Disease
The Precursors Study
Patricia P. Chang, MD, MHS;
Daniel E. Ford, MD, MPH;
Lucy A. Meoni, ScM;
Nae-Yuh Wang, PhD;
Michael J. Klag, MD, MPH
Arch Intern Med. 2002;162:901-906.
ABSTRACT
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Background Anger can trigger myocardial ischemia and may be an independent risk
factor for coronary heart disease, but its effect on early compared with late
onset of disease is unclear.
Methods We performed a prospective study of 1055 men followed up for 32 to 48
years to examine the risk of premature and total cardiovascular disease (CVD)
associated with anger responses to stress during early adult life. Highest
level of anger was defined as a self-report of all 3 possible anger reactions
to stress (expressed or concealed anger, gripe sessions, and irritability)
on a checklist questionnaire administered in medical school. Premature disease
was defined as events before age 55 years.
Results During a median follow-up period of 36 years, 205 men developed CVD
(cumulative incidence at 76 years, 34.5%), of whom 77 men developed premature
disease (cumulative incidence before 55 years, 7.9%). The highest level of
anger was associated with an increased risk of premature CVD (adjusted relative
risk, 3.1; 95% confidence interval, 1.1-8.6), including premature coronary
heart disease (relative risk, 3.5; 95% confidence interval, 1.1-11.8) and
premature myocardial infarction (relative risk, 6.4; 95% confidence interval,
1.8-22.3), compared with lower levels of anger. When CVD events after age
55 years were included, there was no longer a statistically significant association
between anger and CVD.
Conclusion High level of anger in response to stress in young men is associated
with an increased risk of subsequent premature CVD, particularly myocardial
infarction.
INTRODUCTION
DESPITE EFFECTIVE therapies and preventive efforts, coronary heart disease
(CHD) remains the primary cause of morbidity and mortality, with 15% of CHD
deaths occurring before age 65 years.1 Anger
and hostility have been related to an increased risk of cardiovascular disease.2-5 The association
of anger with heart disease may be mediated acutely through catecholamine
release and increased cardiovascular reactivity.6-7
Chronically, anger may influence risk through established cardiac risk factors,
such as hypertension or depression.8-9
Secondary prevention programs designed to reduce stress and anger in persons
with CHD show a decreased incidence of recurrent ischemic events.10 If confirmed, these findings would provide strong
evidence that the association between anger and CHD is causal.
Most prospective studies of the effect of anger on CHD have focused
on middle-aged or older populations.11-19
Only 2 studies have prospectively assessed the risk of CHD associated with
anger in young adults: a study of male medical students followed up for 25
years showed that higher levels of anger were associated with an increased
incidence of CHD,20 whereas another study of
college men followed up for 33 years found no such relationship.21
Such studies assume that anger is a trait that remains constant over time
and affects CHD incidence uniformly throughout follow-up. In these studies,
change in expression of anger at younger vs older ages was not accounted for,
and no distinction was made between early vs late onset of disease. Because
some cardiovascular disease (CVD) risk factors are more prevalent at older
ages, anger may play a lesser role in CHD at older ages.
The Johns Hopkins Precursors Study, a longitudinal study of 1337 medical
students initiated by Caroline Bedell Thomas, MD, in 1946, affords the unique
opportunity to study prospectively the long-term relationship of anger responses
in young adulthood to cardiovascular health before and after middle age and
to adjust for confounding factors at baseline and over time. We postulated
that the risk of CVD, particularly premature disease, during follow-up would
be greater in individuals who reported more anger reactions to stressful situations
at baseline.
SUBJECTS AND METHODS
STUDY POPULATION
While they were in medical school, participants in the Johns Hopkins
Precursors Study underwent a standardized medical examination and completed
questionnaires about their personal and family history, health status, health
behaviors, and reaction to stress.22-23
The cohort has been followed up after graduation by annual mailed questionnaires,
with an average response rate of 90% over every 5-year period. Vital status
of nonrespondents was ascertained by telephoning them, contacting family members,
scanning obituaries, and systematically searching the National Death Index
(last search in 1997). Vital status is known for more than 99% of the cohort.
Self-reports of measures of personal health and disease by this cohort have
been extremely accurate.24 It was not customary
to obtain informed consent during the period in which the baseline data were
collected. After the Joint Committee on Clinical Investigation was established
at our institution, the follow-up protocol was reviewed and approved.
The study sample originally consisted of 1337 members of the graduating
classes of 1948 to 1964. Excluded from this analysis were the small number
of women (n = 121), those who did not answer the questions about anger reactions
to stress in medical school (n = 133), those who reported CVD before graduation
(n = 2), and those who died in medical school or were unavailable for follow-up
(n = 26), leaving 1055 men for analysis.
MEASURES OF ANGER
Information on reactions to stress was obtained by means of the Habits
of Nervous Tension Questionnaire (HNT).22 In
response to the question, "Whenever you find yourself in situations of undue
pressure or stress, how do you usually react?" respondents could check any
of 27 items. After factor analysis and  correlation matrix determination,
3 items were defined as indicating anger: "expressed or concealed anger,"
"irritability," and "gripe sessions."25 The
HNT was readministered as part of the 1992 questionnaire, a mean of 43 years
after graduation. Although only 3 men reported all 3 anger items at baseline
and in 1992, responses to the anger items remained clustered together at both
assessments. Consequently, the same anger construct was identified in both
assessments.26
The validity of the anger measure was supported by its association with
the Multidimensional Anger Inventory questionnaire27
completed by 700 men (84.8% of those alive) in 1988. Anger at baseline was
significantly correlated with total Multidimensional Anger Inventory score
and Anger-In, Anger-Arousal, Hostile Outlook, and Range of Anger-Eliciting
Situations factor-derived scales; the correlation coefficients ranged from
0.10 (P = .007) on the Hostile Outlook factor to
0.18 (P<.001) on the total Multidimensional Anger
Inventory score. Men with all 3 anger responses in medical school who completed
the Multidimensional Anger Inventory (n = 16) also had higher scores on each
subscale of the inventory than did those with fewer anger responses; given
the small sample size, this association was statistically significant only
for the overall score (P = .01).
COVARIATES
Information about body weight, height, smoking, alcohol consumption,
hypertension, hyperlipidemia, parental health history, diabetes mellitus,
and clinical depression was gathered at baseline and during follow-up from
annual questionnaires and medical records. Hypertension was defined as a blood
pressure of 160/105 mm Hg or greater on 1 annual questionnaire, 140/90 mm
Hg on at least 2 readings 1 week or more apart, or pharmacologic treatment
of hypertension. Body mass index was defined as weight in kilograms divided
by the square of height in meters. Starting with the class of 1949, nonfasting
serum cholesterol was measured during medical school.23
Premature parental CHD was defined as development of CHD before age 55 years
in a participant's father or before age 65 years in his mother.28
Number of cigarettes smoked per day was categorized as follows: 0, 1 to 10,
11 to 20, 21 to 39, and 40 or more. Alcohol consumption was categorized as
current, former, or none. Depression was defined as self-reported clinical
depression lasting more than 2 weeks and not related to grief.9
OUTCOME MEASURES
The main outcomes for this analysis were incidence of premature CVD,
defined as events before age 55 years,28 and
total CVD after graduation from medical school through December 31, 1995.
At the end of follow-up, 99.9% of the cohort was aged 55 years or older. Cardiovascular
disease was defined as follows: CHD, composed of myocardial infarction (MI),
sudden death, angina, chronic ischemic heart disease, and other coronary disease
that required coronary bypass surgery or percutaneous coronary interventions;
hypertensive heart disease; congestive heart failure; cerebrovascular disease;
atherosclerosis; aortic aneurysm; peripheral vascular disease; and arterial
embolization.
Diagnoses of CVD were assessed by annual questionnaires inquiring about
medical conditions in checklist format and by medical records submitted by
participants or their health care providers. Information on treatment was
assessed throughout follow-up. Diagnoses were assigned by a committee of 5
physicians after review of all available information.
STATISTICAL ANALYSIS
The primary independent variable was the highest level of anger, defined
as having all 3 self-reported reactions of anger to stress on the baseline
HNT survey. A lower level of anger was defined as reporting less than 3 anger
reactions. The relationship of the highest level of anger with covariates
was examined with t tests, analysis of variance,
and  2 tests. Relationships of the highest level of anger and
the number of reported anger reactions with subsequent incidence of premature
and total CVD outcomes were examined with Kaplan-Meier analysis and the log-rank
test to assess statistical significance. Age was the time variable used in
all survival analysis.
Cox proportional hazards analysis was used to estimate relative risk
(RR) and 95% confidence intervals (CIs) and to determine whether associations
with premature and total CVD were independent of covariates. Covariates included
serum cholesterol level, body mass index, alcohol use, and parental history
of premature CHD, as well as cigarette smoking, hypertension, diabetes, and
depression occurring during follow-up.9, 23
The effects of a change in cigarette-smoking status and the development of
hypertension, diabetes, and depression during follow-up were assessed by including
time-dependent covariates for these variables in Cox models. To account for
possible secular trends in anger level and incidence of CVD, Cox models were
stratified according to calendar time: 1948 through 1957 and 1958 through
1964. Time-dependent covariates were also used to test the proportionality
assumption. Relationships of each anger reaction alone and paired combinations
of the anger reactions with subsequent premature and total CVD incidence were
examined.
Because the small number of cases in the highest anger group limited
power, bivariate analysis was performed with serum cholesterol level, body
mass index, parental history of premature CHD, cigarette smoking, hypertension,
diabetes, depression, and alcohol use. Multivariate models were also constructed
including all variables. To ascertain whether any relationship of anger with
CVD was mediated through associations with depression and anxiety, measures
of these psychological states were derived from the HNT.25
These depression and anxiety constructs did not include any of the anger items
and were used in Cox models as continuous variables.
To examine potential physiologic mechanisms of anger, the association
of the HNT anger measure with vascular reactivity was examined with analysis
of variance and t tests. Vascular reactivity was
defined as the systolic blood pressure response to the cold pressor test administered
to 1028 men (97.4%) during the baseline examination in medical school.29 Alpha levels of less than .05 based on a 2-tailed
test were used to define statistical significance. All analyses were performed
with the SAS statistical package, version 6.12 (SAS Institute Inc, Cary, NC).
RESULTS
Characteristics of the cohort are presented in Table 1 by number of anger responses. Most participants were white,
smoked during medical school, drank alcohol, and had no parental history of
premature CHD by the end of follow-up. Levels of serum cholesterol, body mass
index, and mean blood pressures were similar across anger groups.
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Table 1. Characteristics of 1055 Men in Medical School by Number of
Anger Responses*
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Of the 1055 men who answered the HNT in medical school, 229 men reported
experiencing expressed or concealed anger; 169, gripe sessions; and 99, irritability.
Twenty-one men reported the highest level of anger (all 3 anger items) in
response to stress.
Median total follow-up for the cohort was 36 years (range, 4-48 years).
Their average age in 1995 (n = 921) was 64.5 years (range, 54-93 years). The
cumulative incidence of CVD was 34.5% at age 76 years (n = 205), with a median
age at onset of 56 years. Of the 205 men who developed CVD, 145 men had CHD
(94 with MI), and 59 men reported stroke; 128 men (62.4%) had medical records
confirming their diagnoses. The cumulative incidence of premature CVD was
7.9% (n = 77), with a median age at onset of 49 years. Of the 77 men with
premature CVD, 56 had CHD (34 with MI), and 13 reported premature stroke.
Figure 1 presents the Kaplan-Meier
incidence plot of CVD according to number of anger responses. Few men reported
all 3 anger responses, and only 6 CVD events occurred in this group. Although
the number of events was small, the incidence of CVD was significantly higher
for those with the highest level of anger compared with those with lower levels
of anger. The difference in CVD incidence between the groups decreased after
age 55 years. Inspection of the data suggests that the effect of anger on
cardiovascular risk is different in the early years than in the late years
of follow-up. Although the proportionality assumption was confirmed by statistical
analysis, power was limited.
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Cumulative incidences of cardiovascular disease (CVD) in 1055 men
according to the number of anger responses in medical school. Numbers below
the Kaplan-Meier plot are the numbers of men included in the analysis at each
time point according to number of anger responses. The P value is based on 3 anger responses (highest level of anger) compared
with less than 3 anger responses (lower levels of anger) for premature CVD.
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In univariate analysis, the highest level of anger was associated with
a greater incidence of subsequent premature CVD events, particularly MI (Table 2). The RR of premature MI was 5-fold
higher for those who reported the highest level of anger than for those who
reported lower levels. There was no statistically significant association
between the highest level of anger and premature stroke (RR, 4.3; 95% CI,
0.6-32.9), although the number of premature strokes was small (n = 13) and
CIs were correspondingly wide. When each anger reaction was examined separately,
the small number of events may have limited power. None of the risk estimates
with a single anger item or in pairwise combination were statistically significant.
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Table 2. Cumulative Incidence and Relative Risks of Premature and Total
Cardiovascular Disease, Associated With Highest Level of Anger Response to
Stress Compared With Lower Levels of Anger*
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In bivariate analysis with traditional CVD risk factors listed in Table 1, the highest level of anger remained
independently associated with increased risk of premature MI, CHD, and CVD,
although the 95% CI frequently included 1.0 for CHD (data not shown). In multivariate
analysis including all risk factors, despite concerns of limited power, anger
remained an independent predictor of premature MI, CHD, and CVD (Table 2).
Anger was related to the HNT measures of depression (P<.001) and anxiety (P = .006). In multivariate
analysis adjusting for HNT depression and anxiety measures, the highest level
of anger remained independently associated with risk of premature MI (RR,
3.9; 95% CI, 1.1-13.4). Results were similar for premature CVD and CHD.
When all cases of CVD, before and after age 55 years, were analyzed
as an outcome, the highest level of anger was associated with a slightly increased
risk of CVD that was not statistically significant (Table 2). When CVD events within the first 55 years of age were
censored, there was no association between the highest level of anger and
any CVD outcome, suggesting no relationship between anger at baseline and
CVD occurring at older ages.
A high level of anger demonstrated a trend toward greater vascular reactivity
as assessed during medical school. Men with all 3 anger reactions (n = 21)
had a slightly greater increase in systolic blood pressure in response to
the cold pressor test (15.2 ± 8.5 mm Hg) than those with fewer anger
reactions (n = 1007; 12.1 ± 8.4 mm Hg; P =
.10). Men with 2 or fewer anger responses had similar mean changes in systolic
blood pressure (no anger responses, 12.3 ± 8.4 mm Hg; 1 anger response,
12.0 ± 8.0 mm Hg; 2 anger responses, 11.5 ± 9.9 mm Hg; P = .68).
COMMENT
The present study isolates the powerful effect of a high level of anger
in young men on subsequent incidence of premature CVD, particularly MI, during
48 years of follow-up. These increased risks were present only for premature
CVD events, but similar trends were seen for CVD during all of the follow-up
period. The relationship between the highest level of anger and incident CVD
was specific, as 1 or 2 anger responses were not associated with increased
risk of subsequent premature CVD. Moreover, no specific anger reaction was
more or less predictive than another. Adjustment for other CVD risk factors
did not substantially change the RR of premature CVD associated with anger.
Although the number of premature events was small in this cohort, the relationship
of a high level of anger with premature disease was statistically significant.
We did not have the power to differentiate threshold effect vs a dose-response
relationship.
Previous prospective studies, most conducted in midlife with a follow-up
of less than 10 years, have shown a relationship between anger or hostility
and increased risk of CVD.11-21
A recent analysis in the Atherosclerosis Risk in Communities Study sample
demonstrated a dose-response relationship between anger and CHD.19
Similar to the current study, the increased risk of CHD was statistically
significant only in individuals with high trait anger, particularly those
who were normotensive. The longest study, with 27 years of follow-up, observed
that higher scores on the abbreviated Cook-Medley Hostility Scale in 50-year-old
men and women predicted subsequent acute MI.15
Only 2 previous prospective studies have been carried out in young persons.
One analysis of 255 medical students found hostility predictive of CHD, but
only hypertension was available as a covariate.20
Another study found no relationship but did not differentiate early from late
events.21
Although the exact mechanism by which anger may cause premature CVD
remains unclear, anger may have a role in underlying atherogenesis as well
as triggering clinical events. Angry people have increased platelet reactivity
and hyperaggregability.30 Anger also increases
cardiovascular reactivity as manifest by increased catecholamine levels, heart
rates, and blood pressure.31-32
High levels of anger during anger recall have produced coronary vasoconstriction
of narrowed arteries, but not of nonnarrowed arteries.33
In patients with stable coronary artery disease, anger recall reduced left
ventricular ejection fraction and cardiac output, and increased diastolic
blood pressure and peripheral vascular resistance, more than exercise or other
psychological stressors.34-36
In our cohort, vascular reactivity was not associated with CVD.29
However, men with the highest level of anger tended to have greater vascular
reactivity than men with lower levels. This association suggests that the
group with highest anger differs physiologically from those with lower anger
levels. Additional physiological responses should be studied to determine
mediators of the anger-CVD association.
One explanation for our findings may be that those who experienced a
coronary event at a young age already had premature coronary atherosclerosis
that was further exacerbated by a high level of anger. Another possibility
is that anger assessed in young adulthood may not predict CVD events after
age 55 years because other CVD risk factors become more important later in
life or the level of anger changes over time. Additional follow-up in this
cohort to ascertain CVD events after 1992, when anger was assessed for a second
time, will aid in sorting out these competing hypotheses.
Potential limitations of this study should be discussed. Because the
number of men with the highest level of anger was small, misclassification
of 1 person can make a large difference. Moreover, our results are strictly
generalizable to white men of high socioeconomic status. Nonetheless, the
RR estimates are likely generalizable because potential biases, such as socioeconomic
factors, would tend to affect those with and those without the highest level
of anger to a similar degree. Because this analysis included only men, however,
these results cannot be applied to women. As in most observational studies,
anger responses were based on subjective assessment by respondents and not
on observation during an interview. The correlation of the anger construct
with other anger measures later in life and similar structure in factor analysis
in assessments separated by decades support its construct validity. Furthermore,
the association of anger with incident CVD was not explained by its relationship
with depression and anxiety.
In this study, the highest level of anger assessed with a brief self-administered
questionnaire indicated an elevated risk for premature MI and other premature
CVD events. Community studies in older populations have observed that secondary
prevention efforts to reduce stress and anger may lead to decreased incidence
of recurrent ischemic events.11, 37-38
Whether knowledge about anger can be translated into effective primary prevention
strategies in younger populations needs to be determined.
AUTHOR INFORMATION
Accepted for publication August 29, 2001.
This study was supported by grants AG01760 and DK02856 from the National
Institutes of Health, Bethesda, Md, and by the Four Schools Physician Scientist
Program in Internal Medicine, sponsored by the Lucille P. Markey Foundation
Charitable Trust, Palo Alto, Calif.
A preliminary abstract was presented at the 67th Scientific Sessions
of the American Heart Association, Dallas, Tex, November 16, 1994.
We thank the members of the Precursors Study for their continued participation
in this ongoing prospective study.
Corresponding author and reprints: Patricia P. Chang, MD, MHS, Johns
Hopkins Precursors Study, 2024 E Monument St, Suite 2-200, Baltimore, MD 21205-2223
(e-mail: pchang{at}jhmi.edu).
From the Departments of Medicine (Drs Chang, Ford, Wang, and Klag and
Ms Meoni), Epidemiology (Drs Chang, Ford, and Klag), Health Policy and Management
(Drs Ford and Klag), and Biostatistics (Ms Meoni), The Johns Hopkins University
School of Medicine and School of Hygiene and Public Health, Baltimore, Md.
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