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Journal of Consulting and Clinical Psychology
2002, Vol. 70, No. 3, 548 –568
Copyright 2002 by the American Psychological Association, Inc.
0022-006X/02/$5.00 DOI: 10.1037//0022-006X.70.3.548
Psychosocial Influences on the Development and Course of Coronary Heart
Disease: Current Status and Implications for Research and Practice
Timothy W. Smith and John M. Ruiz
University of Utah
Psychosocial characteristics predict the development and course of coronary heart disease (CHD). In this
review, the authors discussed human and animal research on psychophysiological mechanisms influencing coronary artery disease and its progression to CHD. They then reviewed literature on personality and
characteristics of the social environment as risk factors for CHD. Hostility confers increased risk, and a
group of risk factors involving depression and anxiety may be especially important following myocardial
infarction. Social isolation, interpersonal conflict, and job stress confer increased risk. Psychosocial
interventions may have beneficial effects on CHD morbidity and mortality, although inconsistent results
and a variety of methodological limitations preclude firm conclusions. Finally, they discussed implications for clinical care and the agenda for future research.
Like the article on CHD in the previous special issue on behavioral medicine in this journal (Thoresen & Powell, 1992), we
focused primarily on the second major topic—psychosocial influences on the development and course of CHD. We also reviewed
one aspect of the third topic—interventions targeting psychosocial
risk factors and their underlying psychophysiological mechanisms.
Perhaps the most important implication of research on psychosocial risk factors for coronary disease is that interventions targeting
these factors could reduce cardiac morbidity and mortality. This is
not to say that behavioral approaches to prevention of CHD (e.g.,
smoking cessation) and management of other psychosocial aspects
of established CHD (i.e., adherence to medical regimens) are less
important. They are essential in a comprehensive approach (Smith
& Ruiz, in press), but simply beyond our present scope.
Research on psychosocial influences on CHD and related interventions has expanded dramatically over the past decade. The
landscape is no longer dominated by the Type A behavior pattern,
though research evolving from this risk factor continues. Research
on the psychobiologic mechanisms linking psychosocial risk factors to the course of CHD has grown in sophistication and is tied
more closely to the complex pathophysiology of coronary artery
disease (CAD) and CHD. Finally, evidence regarding the efficacy
of adjunctive psychosocial interventions has grown substantially,
in its technical sophistication, in the number and scale of the trials,
and in the array of interventions it addresses. In this update, we
review these topics and discuss emerging issues in research and
practice. First, however, we review the pathophysiology of CAD
and CHD, with a specific emphasis on the potential role of stress
and related emotions. This research provides a firm scientific
foundation for the role of psychological and social influences on
the development and course of CHD and for related intervention
strategies.
Coronary heart disease (CHD) is the leading cause of death in the
United States; each year about 450,000 people die from CHD,
and 1,000,000 experience an initial or recurrent coronary event
(American Heart Association, 2001). Among healthy 40-year olds,
between 40% and 50% of men and between 25% and 35% of women
will later develop CHD (Lloyd-Jones, Larson, Beiser, & Levy, 1999).
Over $100 billion is spent on CHD each year in the United States in
direct medical costs, disability payments, and lost productivity (American Heart Association, 2001). This disease involves the three major
topics composing behavioral medicine and health psychology, making it a central focus throughout their 30-year history. In the first (i.e.,
health behavior and prevention), modifiable behavioral risk factors
(e.g., smoking, activity level, diet) are important risk factors for the
development of CHD (Stamler et al., 1999; Wannamethee, Shaper,
Walker, & Ebrahim, 1998), and behavior change is an essential
component of prevention. In the second topic (i.e., stress and disease
or psychosomatics), other psychological and social factors have more
direct effects on the development and course of CHD through the
intervening psychobiological effects of stress and negative emotions.
In the third (i.e., psychosocial aspects of medical illness and care),
established CHD has extensive emotional and social impacts on
patients and their families, behavior is a key element of standard care
(e.g., medication adherence, dietary change, exercise), and psychosocial interventions are useful additions to traditional medical and
surgical treatment.
Editor’s Note. Philip C. Kendall served as the action editor for this
article.—TWS
Timothy W. Smith and John M. Ruiz, Department of Psychology,
University of Utah.
John M. Ruiz is now in the Department of Psychiatry, University of
Pittsburgh School of Medicine.
Preparation of this article was supported by National Institutes of Health
Grant 1 R01 AG18903-01.
Correspondence concerning this article should be addressed to Timothy
W. Smith, Department of Psychology, University of Utah, 390 South 1530
East, Room 502, Salt Lake City, Utah 84112. E-mail: tim.smith@
psych.utah.edu
Mechanisms Linking Psychosocial Characteristics and
Coronary Disease
CHD is composed of several manifestations of one underlying
condition—CAD. Initially, lipids and related cells (e.g., macrophages, foam cells) accumulate in microscopic amounts in artery
walls. These deposits grow into visible fatty streaks as early as
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SPECIAL ISSUE: CORONARY HEART DISEASE
middle childhood and increase in prevalence with age (Strong et
al., 1999; Tuzcu et al., 2001). Components of the inflammatory
and reparative response to injury (e.g., monocytes, smooth muscle
cell proliferation) foster the deposit of lipoprotiens into cellular
structures within artery walls (Ross, 1999). Later, extracellular
accumulation of lipid deposits causes a thickening of the wall,
extending outward. Eventually, these lesions include fibrous tissues and calcification and encroach into the artery opening (i.e.,
lumen) in a progressive manner (Stary et al., 1995). Advanced
lesions can occur in late adolescence and early adulthood and
become increasingly common and extensive with age (McGill et
al., 2000). As lesions intrude into the lumen, blood flow is impeded and oxygen supply reduced in the area of myocardium
supplied by the vessel.
Clinical manifestations of CHD appear decades after the initial
stages and asymptomatic progression of CAD. Myocardial ischemia occurs when oxygen demand exceeds supply. Many episodes
of ischemia are without symptoms or “silent,” but ischemia during
physical exertion or, in some instances, emotional stress can produce chest pain (i.e., angina pectoris). Structural narrowing of the
lumen at lesion sites can be exacerbated temporarily by contraction
of smooth muscle within the artery wall. In advanced lesions, the
calcified and fibrous cap may rupture or fragment. Exposed tissues
promote clotting (i.e., thrombus), further impeding blood flow.
Portions of thrombi may be dislodged (i.e., emboli), often blocking
narrower artery segments (Muller, Abela, Nesto, & Tofler, 1994).
Thrombi and emboli can cause near or complete blockage of blood
flow resulting in severe ischemia. This causes rapidly worsening
chest pain (i.e., unstable angina) or death of heart muscle (myocardial infarction, MI) (Stary et al., 1995). Ischemia also renders
the myocardium electrically unstable, promoting disturbances in
heart rhythm (i.e., arrhythmia). In the most severe (i.e., ventricular
fibrillation), myocardial contractions become chaotic, and cessation of circulation may cause sudden cardiac death (SCD).
Statistical associations between psychosocial risk factors and
CHD endpoints (e.g., MI, SCD) could reflect an effect on initial
stages of CAD, pace of progression, precipitation of manifestations of CHD (i.e., triggers) among individuals with advanced or
unstable CAD lesions, or some combination (Cohen, Kaplan, &
Manuck, 1994). As we discuss later, the disease stage affected by
psychosocial risk factors has implications for research and practice. As for specific mechanisms through which psychosocial
factors affect the development of CAD and manifestations of
CHD, a growing body of research suggests that stress and negative
emotions—the primary psychological pathway hypothesized in
current models—alter several physiological processes relevant to
this complex pathophysiology (see Kop, 1999; Rozanski, Blumenthal, & Kaplan, 1999, for reviews). Of course, psychosocial risk
factors (e.g., hostility, depression, social isolation) might also
contribute to CAD and CHD through behavioral pathways (Smith
& Gallo, 2001), such as health habits (e.g., smoking, inactivity)
and behavioral components of standard care (e.g., adherence to
medication regimens, diet restrictions).
Effects of Psychophysiological Reactivity on CAD
Cardiovascular reactivity (CVR) has been extensively studied as
a mechanism linking psychosocial risk factors and CAD (Manuck,
1994). Briefly, more frequent, pronounced, and prolonged in-
549
creases in blood pressure and heart rate, as well as related cardiovascular changes (e.g., increased sympathetic stimulation of the
myocardium, reduced parasympathetic dampening, increased cardiac output and peripheral resistance), are hypothesized to initiate
and hasten the development of CAD. There are two distinct hypotheses regarding CVR (Smith & Gerin, 1998). First, it is seen as
an individual difference variable that marks or itself confers risk.
Second, CVR is seen as a mediating mechanism through which
psychosocial risk factors (e.g., social isolation, trait hostility) affect CAD and CHD.
Findings from several types of studies suggest that CVR promotes development of CAD. The magnitude of CVR to psychological stressors is associated with severity and progression of
carotid artery atherosclerosis, assessed with ultrasound (Barnett,
Spence, Manuck, & Jennings, 1997; Kamarck et al., 1997; Matthews, Owens, Kuller, Sutton-Tyrrell, Lassila, & Wolfson, 1998).
Further, individual differences in CVR potentiate the effects of
other psychosocial risk factors (e.g., low socioeconomic status;
SES) on carotid atherosclerosis (Lynch, Everson, Kaplan, Salonen,
& Salonen, 1998). Carotid atherosclerosis contributes to stroke but
is also associated with the presence and severity of CAD. Prevailing models suggest that stress-induced increases in heart rate and
blood pressure promote damage to the endothelium, making it
more susceptible to inflammation and lipid deposition (Fuster,
Badimon, Badimon, & Chesebro, 1992; Manuck, 1994). In a
recent study of healthy adults, Sherwood, Johnson, Blumenthal,
and Hinderliter (1999) found that an underlying determinant of
CVR (i.e., increased peripheral resistance) was associated with
endothelial dysfunction in healthy young adults, an early indication
of atherosclerosis. Hence, CVR may contribute to earlier stages of
initiation and progression of CAD. Alternatively, this association
could reflect the fact that CVR and early, subclinical CAD reflect a
common etiology (e.g., autonomic or neuroendocrine responsiveness)
that marks or confers vulnerability to CAD and CHD.
Animal research provides converging evidence regarding CVR
and CAD, as well as other psychophysiological mechanisms. In
nonhuman primates, the magnitude of stress-induced increases in
heart rate is associated with the severity of coronary atherosclerosis (Manuck, Kaplan, Adams, & Clarkson, 1989). In this model,
pharmacological blockade of sympathetically mediated CVR eliminates the effects of chronic stress on initial endothelial injury and
advanced lesions (J. R. Kaplan, Manuck, Adams, Weingand, &
Clarkson, 1987; Skantze et al., 1998). These findings constitute
strong evidence that physiological stress responses mediate the
effect of psychosocial stress on CAD. Stress-induced changes in
circulating concentrations of cortisol, other neuroendocrine factors, and lipids are also associated with atherosclerosis in human
and animal models (for a review, see Kop, 1999).
Psychophysiological Triggers of CHD
Cardiologic assessments can be used to test the effects of stress
on later manifestations of CHD (Rozanski, 1998). In both laboratory and ambulatory paradigms, these techniques provide evidence
that stress can evoke myocardial ischemia and that such changes
predict important clinical outcomes (Kop, Gottdiener, & Krantz,
2001; Rozanski et al., 1999). Parallel research in humans and
animals has elucidated mechanisms underlying these acute effects.
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SMITH AND RUIZ
In an early study using positron emission tomography, Deanfield et al. (1984) found that a stressful mental arithmetic task
decreased myocardial perfusion in 75% of CHD patients. Rozanski
et al. (1988) used radionuclide ventriculography to demonstrate
that a stressful speech task produced transient defects in ventricular wall motion, an indicator of ischemia, and this result was
recently replicated by Stone et al. (1999). Related diagnostic
techniques and stressors have been used to demonstrate that mental
stress evokes ischemia (Burg, Jain, Soufer, Kerns, & Zaret, 1993;
Goldberg et al., 1996; Gottdiener et al., 1994; Legault, Langer,
Armstrong, & Freeman, 1995), including anger-arousing events
(Ironson et al., 1992). Several studies using ambulatory electrocardiogram recording (i.e., Holter monitoring) demonstrated that
stress and negative emotions during daily activities are associated
with ischemia (Barry et al., 1988; Gabbay et al., 1996; Gullette et
al., 1997; Krantz et al., 1996), including anger (Gabbay et al.,
1996), tension, and sadness (Gullette et al., 1997). It is important
to note that many of the studies on mental stress and ischemia were
based on relatively small and select samples of patients (e.g., those
with exercise-induced ischemia). Hence, although there are many
positive findings, the generalizability of this association to a
broader range of CHD patients requires additional research.
As discussed above, ischemia results when myocardial oxygen
demand outstrips supply. Stress and negative emotions increase
heart rate and contractile force in both healthy and CHD populations (Brownley, Hurwitz, & Schneiderman, 2000; Goldberg et al.,
1996), thereby increasing oxygen demand. CHD patients with
greater CVR to laboratory mental stressors are more likely to
display ischemia during exercise testing (Kral et al., 1997), laboratory mental stressors (Goldberg et al., 1996; Krantz et al., 1991),
and ambulatory monitoring (Blumenthal, Jiang, et al., 1995). Of
interest, CVR to mental stress has also been found to predict
recurrent events in post-MI patients (Manuck, Olsson, Hjemdahl,
& Renqvist, 1992). However, ischemia occurs in response to
mental stressors at lower heart rates than in response to physical
stressors (Kop et al., 2001). If heart rate provides an index of
oxygen demand, then effects of mental stress on ischemia occur
during relatively low demand. This suggests that mental stress may
also reduce cardiac oxygen supply.
Both human and animal investigations have demonstrated
mechanisms involving reduced supply. In these studies, CAD and
psychological stress combine to reduce blood flow, primarily
through coronary artery spasm or constriction due to endothelial
dysfunction. For example, in patients undergoing coronary angiography, Yeung et al. (1991) found that mental stress decreased the
diameter of coronary arteries. This decrease did not occur in
nondiseased sections, was significant at sites of mild lesions, and
was pronounced at more severe lesions. Other studies have replicated this effect (Boltwood, Taylor, Burke, Grogin, & Giacomini,
1993; Lacy et al., 1995). Ischemia induced by mental stress in
patients with CAD might also be due to failure of coronary vessels
to dilate in response to stress (Dakak, Quyyumi, Eisenhofer, Goldstein, & Cannon, 1995). Dilation in response to mental stress does
occur in persons without CAD, reflecting an appropriate reaction
to increased myocardial oxygen demand. In a canine model, induction of an angerlike state (i.e., access to food threatened by a
second dog) evoked a large decrease in coronary artery blood flow
in animals with a partially occluded coronary artery (Verrier,
Hagestad, & Lown, 1987) and promoted electrical instability of the
myocardium, a condition that increases susceptibility to arrhythmia (Kovach, Nearing, & Verrier, 2001).
Stress also affects a variety of factors related to the readiness
with which blood coagulates and clots (Von Kanel, Mills,
Fainman, & Dimsdale, 2001), perhaps promoting thrombolytic
events. Further, acute stress increases the viscosity of blood
through decreases in plasma volume (Allen & Patterson, 1995).
Increased viscosity, in turn, is associated with greater risk of MI,
perhaps through increased coagulation or the oxygen demands of
circulating more viscous blood (Lowe, Lee, Rumley, Price, &
Fowkes, 1997). Stress can also increase the susceptibility of patients with advanced CAD to the development of arrhythmias
(Verrier & Lown, 1984).
Regardless of its origins in oxygen demand and supply, ischemia induced during mental stress is potentially quite important. In
recent studies, patients who displayed ischemia during laboratory
mental stress testing were at increased risk of recurrent coronary
events and death (e.g., MI, SCD, bypass graft surgery, or angioplasty; Jiang et al., 1996; Krantz et al., 1999; Sheps et al., 2002).
However, some of these studies have involved relatively small and
select samples. Hence, the prognostic importance of mental-stressinduced ischemia should be examined in additional research.
These effects of acute stress on ischemia among persons with
advanced CAD may contribute to the noticeable increase in acute
coronary events following dramatic stressors (e.g., earthquakes,
missile attacks; Dobson, Alexander, Malcolm, Steele, & Miles,
1991; Meisel et al., 1991).
Conclusions Regarding Effects of Stress on CAD
and CHD
Pathways linking psychological stress and negative emotions
with CHD are summarized in Figure 1. From even this brief
review, several conclusions are warranted. First, there are several
plausible mechanisms linking stress and negative emotions to the
initiation and progression of CAD and to the subsequent emergence and course of CHD. Second, associations between psychosocial risk factors and CHD endpoints (i.e., MI, SCD) examined in
epidemiological studies of initially healthy populations could reflect an effect at one or more places during its decades-long
development. That is, such associations could indicate that these
characteristics initiate or hasten the progression of CAD or precipitate manifestations of CHD after the development of severe
CAD. Of course, risk factors could have both types of effects.
Finally, in studies of the incidence and course of CHD, effects of
risk factors could reflect one or more specific psychophysiological
mechanisms. Hence, the current literature on mechanisms represents a maturing scientific base, but it also poses important questions for future research.
Two of these issues are likely to receive increasing attention
over the next decade. First, traditional models of these psychosomatic effects emphasize the sympathetic branch of the autonomic
nervous system. However, more recent research has implicated
parasympathetic mechanisms as well. Higher levels of parasympathetically mediated heart rate variability (vagal tone, respiratory
sinus arrhythmia, etc.) confer reduced risk of CHD morbidity and
mortality (Bigger et al., 1992). As we discuss later in the article,
these parasympathetic mechanisms have been linked to several
psychosocial risk factors. Second, an intriguing body of research
SPECIAL ISSUE: CORONARY HEART DISEASE
551
Figure 1. Psychophysiological influences on coronary artery disease and coronary heart disease. From
“Chronic and Acute Psychological Risk Factors for Clinical Manifestations of Coronary Artery Disease,” by
W. J. Kop, 1999, Psychosomatic Medicine, 61, p. 477. Copyright 1999 by the American Psychosomatic Society.
Adapted with permission. HR ⫽ heart rate; BP ⫽ blood pressure; Sympatho/vagal ⫽ sympathetic/vagal
imbalance; SES ⫽ socioeconomic status.
has indicated that infectious and inflammatory mechanisms contribute to CAD and the course of CHD (Anderson et al., 1998;
Mueller et al., 2002; Muhlestein et al., 1999; Zhu et al., 2001; for
reviews, see Becker, de Boer, & van der Wal, 2001; Libby, Ridker,
& Maseri, 2002). This suggests a point of integration of research
on psychosocial mechanisms in CHD with studies of psychosocial
influences on the immune system (Kiecolt-Glaser, McGuire, Robles, & Glaser, 2002; Kop & Cohen, 2001). That is, effects of stress
and negative emotion on immune responses and inflammation may
also contribute to the associations of psychological and social
characteristics with CAD and CHD.
Recent Research on Psychosocial Risk Factors
In prior decades, cross-sectional comparisons between CHD
groups and controls on personality traits, emotional disorders, and
aspects of the social environment were common, as were studies in
which psychosocial characteristics were correlated with the severity of CAD among patients referred for angiography. However,
differences between CHD and control groups in cross-sectional
studies may reflect psychosocial consequences of CHD rather than
causes (Cohen & Rodriguez, 1995). Further, selection into angiography samples and the inherent restriction in range of predictors
and outcomes may produce invalid estimates of associations between psychosocial characteristics and CAD (T. Q. Miller, Turner,
Tindale, Posavac, & Dugoni, 1991). Studies of psychosocial risk
factors increasingly rely on more definitive methods. Wellcontrolled, prospective studies of initially healthy populations or
groups with carefully documented CHD are now much more
common. Further, well-validated assessments of psychosocial predictors and reliable classification of coronary outcomes are more
routine, as are appropriate statistical controls for possible confounds. Hence, this literature has grown in quality as well as size.
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SMITH AND RUIZ
Hostility as the Toxic Component of the Type A Pattern
Historically, the Type A coronary-prone behavior pattern has
been the best known psychosocial risk factor. Despite quantitative
reviews indicating that the Type A pattern (as defined by behavioral assessment) is a significant risk factor for CHD in initially
healthy populations (Matthews, 1988; T. Q. Miller et al., 1991),
inconsistencies in research findings led investigators to examine
individual components of the multifaceted pattern. This research
has identified individual differences in hostility as an important
predictor of CHD, as well as all cause mortality (T. Q. Miller,
Smith, Turner, Guijarro, & Hallet, 1996). As typically used in this
research, the term hostility itself refers to a multidimensional
construct (Smith, 1994). The emotional component involves anger
but also includes contempt and scorn. The behavioral component
refers to verbal and physical aggression, which share an intent to
inflict harm. Finally, the term hostility most accurately describes
cognitive factors, such as cynicism, mistrust, and the tendency to
interpret others’ actions as reflecting aggressive intent.
A quantitative review of studies published before 1995 found
that hostility predicted CHD, though the association was stronger
for behavioral ratings of hostility as opposed to self-reports (T. Q.
Miller et al., 1996). Subsequent studies have indicated that selfreports of trait hostility and anger predict new coronary events
among previously healthy people (Chang, Ford, Meoni, Wang, &
Klag, 2002; Everson et al., 1997; Kawachi, Sparrow, Spiro, Vokonas, & Weiss, 1996; J. E. Williams et al., 2000). Further, selfreports of hostility have been associated with the severity and
progression of atherosclerosis (Iribarren et al., 2000; Julkunen,
Salonen, Kaplan, Chesney, & Salonen, 1994; Matthews, Owens,
Kuller, Sutton-Tyrrell, & Jansen-McWilliams, 1998; Whiteman,
Dreary, & Fowkes, 2000), although there have been negative
findings (O’Malley, Jones, Feuerstein, & Taylor, 2000). One study
found that the tendency to express anger outwardly predicted the
progression of coronary atherosclerosis as measured by repeated
angiography, but cynical hostility did not (Angerer et al., 2000).
Finally, hostility also predicts more rapid restenosis of coronary
arteries following angioplasty (Goodman, Quigley, Moran, Meilman, & Sherman, 1996; Mendes De Leon, Kop, de Swart, Bar, &
Appels, 1996). These studies confirmed that hostility is a CHD risk
factor and suggest that it may contribute to the development and
course of CAD. However, it is important to note that in prospective
studies of patients with established CHD, individual differences in
anger and hostility do not appear to be robust predictors of recurrent cardiac events or survival (Hemingway & Marmot, 1999).
However, studies of ischemia and other outcomes provide evidence that anger and hostility can contribute to coronary events in
persons with CAD. For example, in samples with documented
CHD, hostile persons are more susceptible to ischemia (Burg et al.,
1993; Helmers et al., 1993), and preliminary evidence suggests
that they may be more susceptible to constriction of the coronary
arteries during mental stress (Boltwood et al., 1993). As described
above, in the context of significant CAD the arousal of anger can
evoke ischemia (Gabbay et al., 1996; Ironson et al., 1992). Finally,
in two retrospective but well-controlled studies, episodes of anger
conferred a twofold increase in the likelihood of acute MI during
the following 1–2 hr (Mittleman et al., 1995; Möller et al., 1999).
This risk was greater among persons who did not routinely take
aspirin or beta-blocking medication, suggesting that thrombolytic
or sympathetically mediated mechanisms may be involved in the
effects of anger arousal on acute MI. Hence, although the prospective evidence suggests that trait anger and hostility are more
consistent predictors of initial CHD than of its course, clinical
studies do suggest that they could contribute to acute events. The
more consistent association of hostility with CHD incidence and
mortality than with the course of established disease could reflect
a selection process; hostile persons who survive initial events to be
included in studies of CHD course may be at lower risk or more
resilient for other reasons and may therefore be less likely to suffer
recurrent or fatal disease (R. B. Williams, 2000).
A substantial body of research supports the prevailing view that
psychophysiological correlates of stress and negative emotion
compose the mechanism linking hostility and CHD (R. B. Williams, Barefoot, & Shekelle, 1985). Hostility is associated with
heightened cardiovascular and neuroendocrine reactivity to stressful social situations in the laboratory involving strangers (Christensen & Smith, 1993; S. B. Miller et al., 1998; Powch & Houston,
1996; Suarez, Kuhn, Schanberg, Williams, & Zimmermann, 1998)
and family members (Smith & Brown, 1991; Smith & Gallo,
1999), as well as during daily activities, as assessed by ambulatory
assessments of blood pressure and cortisol excretion (Benotsch,
Christensen, & McKelvey, 1997; Jamner, Shapiro, Goldstein, &
Hug, 1991; Linden, Chambers, Maurice, & Lenz, 1993; Polk,
Kamarck, & Shiffman, 2002; Pope & Smith, 1991). When recalling previous anger-arousing events, hostile persons display larger
and more prolonged increases in blood pressure (Fredrickson et al.,
2000). Also, unlike their more agreeable counterparts, hostile
persons do not respond to social support with reduced CVR to
stressors (Lepore, 1995; Smith, Uno, Uchino, & Ruiz, 2000). In
addition to greater psychophysiological response to stressors, hostility is also associated with lower levels of social support and
greater exposure to stress at home and work (T. Q. Miller, Marksides, Chiriboga, & Ray, 1995; Newton & Kiecolt-Glaser, 1995;
Smith, Pope, Sanders, Allred, & O’Keefe, 1988). This greater
psychosocial vulnerability (Smith, 1994), in turn, may reflect a
transactional process in which hostile persons undermine sources
of support and foster conflicts through their mistrusting thoughts
and antagonistic actions (Smith, 1995). Unhealthy lifestyles could
also contribute to the CHD risk associated with hostility. However,
in most studies, but not all (Everson et al., 1997), statistical
controls for health behaviors (e.g., smoking, inactivity) do not
eliminate the association between hostility and subsequent CHD.
Dominance as a Potential Coronary-Prone Trait
In their prior review in this journal, Thoresen and Powell (1992)
questioned the emerging view that hostility was the only pathogenic component of the Type A pattern. Subsequent studies suggested they may have been correct. Individual differences in social
dominance may be a second risk factor within that constellation. In
analyses of the original prospective study of Type A (Western
Collaborative Group Study; Rosenman et al., 1975), Houston and
his colleagues (Houston, Chesney, Black, Cates, & Hecker, 1992;
Houston, Babyak, Chesney, Black, & Ragland, 1997) found that
behavioral ratings of hostility and social dominance were independent predictors of CHD and mortality. Social dominance was the
label given to a set of controlling behaviors, including the tendency
to cut off and talk over the interviewer. A cross-sectional study of
SPECIAL ISSUE: CORONARY HEART DISEASE
patients referred for thalium exercise stress testing found that
behavioral ratings of hostility and dominance were independently
related to CHD (Siegman, Townsend, Civelek, & Blumenthal,
2000). In prospective studies, self-report measures of social dominance predicted the development of CHD (Siegman, Kubzansky,
et al., 2000; Whiteman, Deary, Lee, & Fowkes, 1997).
The nonhuman-primate model described above provides an intriguing parallel to this research (J. R. Kaplan & Manuck, 1998).
The chronic stress of repeated social reorganization (i.e., housing
in unstable vs. stable social groups) produced more severe CAD
among male macaques, but only among those in the top half of
behaviorally assessed dominance hierarchies. Administration of
beta-adrenergic blockade of sympathetic input to the heart eliminates the susceptibility of dominant animals to the atherogenic
effects of stress. Hence, physiological effects of recurring efforts
to assert social dominance may promote the initiation and progression of CAD (J. R. Kaplan et al., 1987; Skantze et al., 1998).1 In
humans, efforts to assert social influence or interpersonal control
evoke heightened CVR (Smith, Nealey, Kircher, & Limon, 1997;
Smith, Ruiz, & Uchino, 2000), and persons scoring high on personality measures of dominance display greater CVR during social
interaction (Newton, Bane, Flores, & Greenfield, 1999). Although
this literature is small, the available epidemiological, animal, and
psychophysiological studies suggest that dominance may confer
risk for CHD.
Depression, Anxiety, and Negative Affectivity
Negative emotions other than anger have been widely studied
over the past decade, and the findings resolve prior debates
(Booth-Kewley & Friedman, 1987; Matthews, 1988; Stone &
Costa, 1990). In a meta-analysis, Booth-Kewley and Friedman
(1987) concluded that symptoms of depression and anxiety predict
CHD. This conclusion was criticized (Matthews, 1988; Stone &
Costa, 1990) as based in part on “soft” or less definitive CHD
endpoints (e.g., chest pain). Individual differences in the tendency
to experience negative emotions (i.e., neuroticism or negative
affectivity) are associated with somatic complaints in the absence
of actual disease, including chest pain in persons with normal
coronary arteries (Costa & McCrae, 1987; Watson & Pennebaker,
1989). Hence, the findings of Booth-Kewley and Friedman (1987)
could have been biased by an association between individual
differences in negative affect and symptom reporting similar to—
but not actually reflecting—CHD.
However, over the past decade, a number of methodologically
sound studies indicated that symptoms of depression and anxiety,
related emotional disorders, individual differences in the tendency
to experience negative affect, and related personality traits indeed
confer increased risk of MI, SCD, and other “hard” indicators of
CHD. Studies of initially healthy populations have shown that
symptoms of depression and anxiety and reports of hopelessness
predict future coronary events (i.e., MI, coronary death), even with
statistical controls for health behavior (e.g., smoking) and other
potential confounding factors (Anda et al., 1993; Ariyo et al.,
2000; Aromaa et al., 1994; Barefoot & Schroll, 1996; Eaker,
Pinsky, & Castelli, 1992; Everson et al., 1996; Everson, Roberts,
Goldberg, & Kaplan, 1998; Ford et al., 1998; Jonas & Mussolino,
2000; Kawachi, Colditz, Ascherio, Rimm, & Giovannucci, 1994;
Kubzansky et al., 1997; Penninx et al., 2001; Pratt et al., 1996).
553
Although there have also been negative findings (WassertheilSmoller et al., 1996).2 Among patients with established CHD,
depression, anxiety, pessimism, and related characteristics have
even stronger associations with recurrent coronary events (e.g.,
MI, cardiac procedures) and reduced survival (Ahern et al., 1990;
Allison et al., 1995; Barefoot et al., 1996, 2000; Carney, Rich,
Freedland, & Sanai, 1988; Denollet & Brutsaert, 1998; Follick et
al., 1988; Frasure-Smith, Lespérance, Juneau, Talajic, & Bourassa,
1999; Frasure-Smith, Lespérance, & Talajic, 1995; Irvine et al.,
1999; Lespérance et al., 2002; Pennix et al., 2001; Scheier et al.,
1999), although here too there are negative findings (Lane, Carroll,
Ring, Beevers, & Lip, 2001; Mayou et al., 2000). A characteristic
labeled vital exhaustion— consisting of low energy, irritability,
and demoralization— has also been linked to poor prognosis in
CHD patients (Kop, Appels, Mendes de Leon, De Swart, & Bar,
1994; Mendes de Leon et al., 1996). Further, the effects of depression and other indications of distress are significant even when
controlling for the possible confounding effects of initial illness
severity.
Clinical psychologists would be understandably concerned by
pooling measures of depressive symptoms, anxiety symptoms,
related personality characteristics, and diagnosable anxiety and
affective disorders, because diagnosis and treatment are facilitated
in their differentiation. However, questions about a graded–
continuous versus qualitative– discontinuous distinction between
depressive symptoms and depressive disorders has been the source
of considerable controversy (e.g., Coyne, 1994; Flett, Vredenburg,
& Krames, 1997), with recent empirical support for both views
(Ruscio & Ruscio, 2000; Santor & Coyne, 2001). Further, diagnosable disorders, subclinical symptoms, and personality traits
involving depression and anxiety are closely related (Clark,
Watson, & Mineka, 1994; Watson, Clark, & Harkness, 1994), and
individual differences in negative affectivity or neuroticism predict
future emotional disorders (Zonderman, Herbst, Schmidt, Costa, &
McCrae, 1993). Future research may identify important differences among these predictors in the levels of CHD risk they confer
(e.g., Herrmann, Brand-Driehorst, Buss, & Ruger, 2000) or their
underlying mechanisms, but presently these closely correlated
emotional characteristics seem to have similar and perhaps overlapping effects.
Autonomic processes have been identified as possible psychophysiological mechanisms linking this group of risk factors and
CHD. For example, both anxiety and depression are associated
with reduced heart rate variability—which can reflect either
heightened sympathetic activity or decreased parasympathetic activity (or both)—and more specific indicators of vagal tone or
parasympathetic responsivity (Carney et al., 1995, 2001; Hughes
& Stoney, 2000; Krittayaphong et al., 1997; Sheffield et al., 1998;
Stein et al., 2000; Watkins, Grossman, Krishnan, & Sherwood,
1998). Other studies have found that depressive symptoms are
1
It is important to note that among females in this model, subordinate
rather than dominant social status confers risk. Subordinate females engage
in less sexual intercourse. This results in lower levels of estrogen activity
in this species, which may account for the association between social status
and CAD (J. R. Kaplan et al., 1996).
2
Wassertheil-Smoller et al. (1996) did find that increasing levels of
distress over time predicted CHD, although initial levels did not.
554
SMITH AND RUIZ
associated with sympathetically mediated cardiovascular and neuroendocrine reactivity (Light, Kothandapani, & Allen, 1998).
Depression and individual differences in negative affect are also
associated with increased exposure to stressful social circumstances (Bolger & Schilling, 1991; Bolger & Zuckerman, 1995;
Coyne, Thompson, & Palmer, 2002; Daley & Hammen, 2002;
Daley et al., 1997; Davila, Bradbury, Cohan, & Tochluk, 1997;
Fincham, Beach, Harold, & Osborne, 1997; Harkness & Luther,
2001; S. L. Johnson & Jacob, 1997). Through a variety of cognitive and interpersonal processes, emotionally distressed individuals may experience more environmental stress, as well as respond
to it with greater psychophysiological reactivity and/or reduced
parasympathetic dampening of stress responses. However, the
extent to which these mechanisms account for the effects of this
group of risk factors on CHD requires further investigation.
Also, depression and other chronic negative affects are associated with suppressed immune function (Herbert & Cohen, 1993;
Irwin, 2001), and in one recent study of patients with CAD,
depressive symptoms were associated with immunologic markers
of chronic infection and inflammation (Appels, Bar, Bruggeman,
& De Baets, 2000). Hence, effects of depression in particular—and
psychosocial risk factors generally— on immunologic mechanisms
warrant further research (Kop & Cohen, 2001). Finally, other
psychophysiological (e.g., coagulation) or behavioral (e.g., medical adherence, lifestyle) mechanisms may also contribute to the
association of negative affect with CHD (DiMatteo, Lepper, &
Croghan, 2000; Von Kanel et al., 2001).
Social Isolation and Conflict
Decades of research has indicated that social isolation and low
levels of perceived social support confer increased risk of CHD
(for reviews, see Berkman, 1995; Hazuda, 1994; Orth-Gomer,
1994). Recent studies of CHD morbidity and mortality have confirmed this association in initially healthy populations (e.g., G. A.
Kaplan et al., 1994; Orth-Gomer, Rosengren, & Wilhelmsen,
1993; Pennix et al., 1997; Seeman et al., 1993; Vogt, Mullooly,
Ernst, Pope, & Hollis, 1992). Social isolation is particularly unhealthy in patients with preexisting CHD (Angerer et al., 2000;
Berkman, Leo-Summers, & Horwitz, 1992; Case, Moss, Case,
McDermott, & Eberly, 1992; Gorkin et al., 1993; Horsten et al.,
2000; Krumholz et al., 1998; Welin, Lappas, & Wilhelmsen, 2000;
R. B. Williams et al., 1992; Woloshin et al., 1997), although
different indicators of support and isolation sometimes produce
inconsistent effects (Irvine et al., 1999). In one recent study, in
which low social support did not predict post-MI prognosis, high
support reduced the negative effects of depression on survival
(Frasure-Smith, Lespérance, Gravel, Masson, Juneau, Talajic, &
Bourassa., 2000). In nonhuman-primate models, social isolation
(i.e., solitary vs. stable group housing) promotes CAD (Shively,
Clarkson, & Kaplan, 1989).
Many indicators of social support and isolation have been used
in epidemiological studies, ranging from quantitative measures of
network characteristics and activities (e.g., membership in organizations, marital status) to more subjective measures of network
quality (e.g., perceived adequacy or satisfaction with support). For
both types of measures, it is generally assumed that they reflect
actual network characteristics and social experiences. However,
recent theory and research has challenged this assumption, sug-
gesting that such measures reflect the individual’s general sense of
acceptance, the accessibility of internal representations of social
ties, and other personality processes to an equal or even greater
extent than actual interpersonal events (Lakey & Drew, 1997;
G. R. Pierce, Lakey, Sarason, Sarason, & Joseph, 1997). For
example, individuals with low levels of social support tend to
appraise potentially supportive behavior as less supportive than do
individuals with high support (T. Pierce, Baldwin, & Lydon,
1997). Hence, although epidemiological studies have clearly indicated that something tapped by measures of social isolation and
support predicts the development and course of CHD, recent
research has raised questions about the precise nature of this
predictive factor. This ambiguity could complicate the design of
risk-reducing interventions, despite the clear evidence of a predictive association.
Studies of stress and adaptation increasingly have recognized
that social strain and isolation are distinct concepts with potentially
independent effects (Coyne & Bolger, 1990; Rook, 1990; Uchino,
Holt-Lunstad, Uno, & Flinders, 2001). Recent studies of patients
with cardiovascular disease have suggested that conflict in personal relationships predicts poor outcomes. Orth-Gomer et al.
(2000) found that women with CHD who reported high levels of
marital conflict were nearly three times as likely to experience a
recurrent coronary event as married but nondistressed women.
Coyne et al. (2001) reported a similar association between marital
conflict and death in a sample of patients with congestive heart
failure, most of whom had experienced a prior MI. In a large
sample of initially healthy but high-risk men, Matthews and Gump
(2002) found that increasing levels of marital stress were associated with increased risk of death from CHD. Nonhuman-primate
models suggest that chronic social stress involving conflict can
promote atherosclerosis (J. R. Kaplan et al., 1983; J. K. Williams
et al., 1993), and this effect has recently been replicated in a rabbit
model of atherosclerosis (McCabe et al., 2002). However, compared with the literature on isolation, there has been limited research on this potentially important risk factor.
Psychophysiological studies have indicated that social support
and conflict are associated with plausible mechanisms. Individual
differences in perceived support and the experimental manipulation of support are generally associated with reduced cardiovascular and neuroendocrine reactivity to stressors (Kamarck, Peterman, & Raynor, 1998; Lepore, 1998; Thorsteinsson & James,
2000; Uchino, Cacioppo, & Kiecolt-Glaser, 1996). For example,
the presence of a friend attenuates CVR in response to stressful
laboratory tasks (Christenfeld et al., 1997). Consistent with the
view that beneficial effects of social support do not require actual
supportive transactions, mental activation of supportive network
ties also attenuates CVR to stressors (Smith, Ruiz, & Uchino,
2001). Further, positive social ties may lower risk of CAD and
CHD not only through direct dampening of CVR and other
components of the stress response but also through separate
physiological mechanisms (e.g., release of oxytocin) involved in
attachment and affiliation (Knox & Uvnas-Moberg, 1998; UnvasMoberg, 1997). Finally, conflictual interactions produce heightened cardiovascular and neuroendocrine responses in laboratory
(for a review, see Kiecolt-Glaser & Newton, 2001) and ambulatory
studies (e.g., Holt-Lunstad, Uchino, & Smith, 2000).
SPECIAL ISSUE: CORONARY HEART DISEASE
Job Stress
Two models of job stress have been examined as CHD risk
factors. The job strain model posits that jobs high in demand
(mental and physical effort, etc.) but low in control increase risk
(Karasek, 1979; Theorell & Karasek, 1996). The second model
suggests that an asymmetry of effort relative to rewards confers
risk (Siegrist, 1996). Prospective studies have found that job strain
is associated with increased risk of CHD morbidity and mortality
(Bosma, Peter, Siegrist, & Marmot, 1998; Hall, Johnson, & Tsou,
1993; Theorell et al., 1998), although low job control (e.g., decisional latitude) may have more impact than job demands or the
combination of these characteristics (Bosma et al., 1998; Hammar,
Alfredsson, & Johnson, 1998; J. V. Johnson, Stewart, Hall, Fredlund, & Theorell, 1996; Marmot, Bosma, Hemingway, Brunner, &
Stansfeld, 1997; Wamala, Mittleman, Horsten, SchenckGustafsson, & Orth-Gomér, 2000). Further, some negative results
have been reported (Hlatky et al., 1995). The effort–reward model
has been the focus of less research, although this imbalance has
been found to predict the progression of atherosclerosis and new
coronary events (Lynch, Krause, Kaplan, Salonen, & Salonen,
1997; Peter, 1995; Siegrist, Peter, Junge, Cremer, & Seidel, 1990).
Effort–reward imbalance is also associated with increased risk of
CHD even when variance associated with job strain is controlled
(Bosma et al., 1998). A recent review concluded that both types of
job stress confer increased risk of future CHD, independent of any
associations between job stress and negative health behaviors
(Peter & Siegrist, 2000). Further, Matthews and Gump (2002)
recently found that the number of self-reported work stressors was
associated with increased risk of death from CHD.
Studies of mechanisms potentially underlying these effects generally indicated that job stress is associated with CVR and other
stress responses. For example, persons with high levels of job
strain display higher levels of workday blood pressure, as assessed
through ambulatory monitoring (Schnall et al., 1990; Schnall,
Schwartz, Landsbergis, Warren, & Pickering, 1998). However,
other studies have not replicated this effect (Matthews et al., 2000)
or found inconsistent effects for men and women (Blumenthal,
Thyrum, & Siegel, 1995; Light, Turner, & Hinderliter, 1992).
Hence, the mechanisms underlying the effects of job stress on
CHD are not yet clearly established.
Conclusions Regarding Risk Factors
Over the past 10 years, evidence has expanded indicating that
psychosocial characteristics predict the development and course of
CHD. Support for the effects of anger and hostility continues to
mount, as does evidence of the association of these personality
characteristics with mechanisms that potentially influence CAD
and CHD. However, prospective studies of initially healthy persons have produced some negative findings. Further, there is little
evidence that individual differences in anger and hostility are
consistent risk factors among patients with established disease,
even though some studies of persons with CAD find that episodes
of anger can trigger ischemia and coronary events. The evolution
of research on the Type A pattern has produced preliminary
evidence of another possible coronary-prone characteristic—social
dominance. Here too, human and animal studies have identified
associations between this stable social behavior and plausible
pathophysiological mechanisms.
555
Although there are some inconsistencies, individual differences
in negative affect and related disorders and traits confer increased
risk of initial development of CHD in initially healthy populations
and increased risk of recurrent events and reduced survival among
patients with preexisting CHD. The effect of depression on prognosis following MI currently appears to be a particularly important
risk factor, underscoring the importance of routine assessments of
its potentially unique presentation in cardiac populations (Lespérance & Frasure-Smith, 2000). The mechanisms underlying these
effects may involve parasympathetic components of autonomic
functioning, sympathetic reactivity, altered homeostasis, and
heightened exposure to stressors. Social isolation and low perceived support are clearly associated with increased risk of CHD
and reduced survival, and considerable evidence suggests that their
impact on stress reactivity is a plausible mechanism. However,
recent models of the nature of social support and isolation and the
meaning of related measures raise important questions about the
specific psychosocial characteristic that confers risk. Social conflict may prove to be an independent interpersonal influence on
CHD. Finally, job stress predicts CHD, although the specific work
characteristics and underlying mechanisms responsible for these
effects remain to be clarified.
With some notable exceptions (e.g., Iribarren et al., 2000; Lynch
et al., 1997; Matthews, Owens, Kuller, Sutton-Tyrrell, & JansenMcWilliams, 1998), most studies have examined indications of
CHD that reflect late stages of the disease (e.g., MI, CHD, death).
Although these outcomes are obviously important, this approach
obscures the point(s) in the natural history of the disease where
risk factors exert their effects. Noninvasive measures of the severity and progression of atherosclerosis (e.g., carotid artery ultrasound; computed tomography scans of coronary artery calcium
deposits) in representative samples of initially asymptomatic
adults can clarify the impact of psychosocial risk factors on earlier
stages of disease, as can the use of still earlier indications of
arterial changes (e.g., endothelial dysfunction) in adolescents and
young adults. Cardiac imaging and other diagnostic procedures can
determine the role of psychosocial risk factors in later stages of
disease (Rozanski, 1998). Findings from these types of research
would not only answer basic questions about the timing of psychosocial effects but also help to refine psychosocial interventions.
Further, assessments of subclinical indications of atherosclerosis
and ischemia provide alternatives to the less frequent occurrence
of clinical events. This permits studies of clinically relevant outcomes without the sample sizes and long follow-up periods necessitated by a focus on clinical events.
Most psychosocial risk factors are clearly related to plausible
psychophysiological mechanisms. However, these associations are
best seen as consistent with— but not providing direct evidence
of—their hypothesized mediational role in the psychosomatic process. Animal models provide important evidence in this regard, but
future human studies must incorporate measures of risk factors,
psychophysiological mechanisms, and CAD or CHD outcomes for
more definitive tests of mediational hypotheses. This is an ambitious research strategy that may be difficult to implement in large
epidemiological studies, but analyses of this type are needed to
evaluate the mediational models currently guiding the field.
A major challenge in the coming decade will be to develop
useful approaches for studying conceptually distinct but often
highly correlated risk factors. These risk factors are typically
SMITH AND RUIZ
556
studied separately, despite their intercorrelation. When multiple
psychosocial characteristics are studied, usually their independent
statistical effects are tested in multivariate analyses or, in rare
occasions, interactive effects (i.e., moderation) are tested. Future
research should determine if the overlapping aspect of correlated
risk factors (e.g., social conflict, anger, and depression) is the most
robust predictor of initial and/or recurrent events to examine
possible core dimensions of psychosocial risk. Alternatively, correlations among risk factors may indicate distinct processes
through which characteristics of individuals and their social contexts jointly influence the development of CAD and CHD. For
example, hostile persons experience increased exposure to stressful interpersonal events as well as low levels of social support
(Smith, 1995), and similar patterns have been found in persons
with depression (Joiner & Coyne, 1999). Hence, rather than a core
dimension of psychosocial risk, these aggregations of risk factors
could reflect transactional processes in which people both influence and are influenced by their social networks in such a way as
to increase or reduce cardiovascular risk. The interpersonal and
cognitive–social traditions in personality psychology (Kiesler,
1996; Mischel & Shoda, 1999) provide concepts and methods for
studying connections between the personality traits and social
contexts that predict CHD. Further, they can be adapted to research
on both risk factors (Gallo & Smith, 1999) and underlying mechanisms (Smith, Gallo, & Ruiz, in press). Such approaches to
correlated risk factors could help construct a more accurate “psychosocial epidemiology of everyday life”3 and a social psychophysiology of the underlying mechanisms.
Psychosocial Interventions for CHD
At the time of the review by Thoresen and Powell (1992), the
Recurrent Coronary Prevention Project (Friedman et al., 1986)
represented the most compelling evidence that psychosocial risk
factors for CHD could be modified through psychological interventions, with beneficial effects on medical outcomes. Patients
randomized to a control condition received counseling about appropriate lifestyle changes following MI, whereas patients randomized to the active intervention received group therapy consisting of relaxation training, self-monitoring of stress and Type A
behavior, cognitive restructuring, and other cognitive– behavioral
techniques. The intervention reduced nonfatal recurrent cardiac
events by 44% (Friedman et al., 1986). Among patients with less
severe initial disease, the intervention also significantly reduced
cardiac deaths (Powell & Thoresen, 1988). Internal analyses suggested that larger reductions in Type A behavior were related to
reduced risk of recurrent events. In a second influential study from
that period, Frasure-Smith and Prince (1985) found that an intervention in which nurses monitored stress levels of post-MI patients
and provided supportive counseling when needed (i.e., the Ischemic Heart Disease Life Stress Monitoring Program, IHDLSM)
produced a significant reduction in cardiac deaths, relative to
randomized controls. At the time of the previous special issue,
these studies and a number of smaller controlled trials suggested
that such interventions were useful additions to CHD care (Thoresen & Powell, 1992).
Recent Studies
Intervention trials designed to modify psychosocial risk factors
among CHD patients have produced mixed results over the past
decade. It is important to distinguish between interventions where
stress reduction, modification of coronary-prone behavior, or related risk factors are the primary focus and those focusing on
modification of traditional behavioral risks (e.g., smoking, exercise, diet; Blumenthal & Emery, 1988). As we discuss later in the
article, the latter type of intervention has been found to have
beneficial effects, some of which include reductions in stress and
related psychological risk factors. However, specific comparisons
of stress management and similar interventions with appropriate
control conditions permit clear evaluations of the effects of psychosocial risk interventions.
In a large and well-controlled replication of the IHDLSM intervention, Frasure-Smith et al. (1997) did not find significant intervention effects. A second large and well-controlled trial of stress
management for post-MI patients also found no effects on cardiac
recurrences (Jones & West, 1996). However, Blumenthal et al.
(1997) did find that a stress management intervention reduced
clinical cardiac events. The intervention also reduced the amount
of ischemia evident during ambulatory (i.e., Holter) monitoring,
particularly among patients with high initial levels of daily ischemia. It is important to note, however, that although controls were
well matched to intervention participants on important medical and
demographic risk factors, the study relied on a nonrandomized
no-treatment comparison group.
Of the behavioral interventions in CHD, a multicomponent
program developed by Ornish et al. (1990) has received the most
attention. Stress management through meditation and other techniques is combined with aerobic exercise, a very-low-fat diet, and
group support. In recent tests, the approach produced clear reductions in recurrent events, CAD severity, and evidence of improved
coronary circulation compared with standard care (Gould et al.,
1995; Ornish et al., 1998). However, it is not clear which feature
of the multicomponent intervention is most responsible for its
effects, and the extent of behavior change required has raised
concerns about its usefulness in general patient populations (Billings, 2000). In a small study, Gidron, Davidson, and Bata (1999)
found that a cognitive– behavioral intervention specifically targeted at modifying hostility was effective in reducing hostility and
blood pressure in CHD patients. Preliminary results also indicate
that treated patients in this trial experienced fewer and briefer
rehospitalizations, with significantly lower associated medical
costs (Davidson, 2000). In a study of high-risk persons before the
onset of CHD, Castillo-Richmond et al. (2000) randomized hypertensive African American participants to receive a stress management intervention or usual care. Relative to control participants,
those receiving the intervention were found to have a reduction in
carotid atherosclerosis.
Findings From Quantitative Reviews
This diverse literature has been evaluated in several quantitative
reviews (e.g., Linden, Stossel, & Maurice, 1996). The most recent
3
We are indebted to George A. Kaplan for this descriptive phrase.
SPECIAL ISSUE: CORONARY HEART DISEASE
and complete of these (Dusseldorp, van Elderen, Maes, Meulman,
& Kraaij, 1999) found evidence of beneficial effects and provided
a potential explanation for inconsistent findings. Health education
(e.g., targeted toward behavioral risk reduction) and stress management had equivalent significant effects on cardiac recurrences,
producing on average a 34% reduction in cardiac mortality and a
29% reduction in recurrent MI. However, small sample sizes in
many of the treatment studies, limitations in randomization and the
documentation of clinical events, and other methodological issues
may have resulted in inflated estimates of treatment effects.
Of importance, Dusseldorp et al. (1999) found that intervention
effects were moderated by effects on intermediate targets, such as
change in behavioral risk factors, reductions in blood pressure, and
reductions in emotional distress. Overall treatment effects on cardiac outcomes were significantly greater in studies where positive
results were found for proximal intervention targets— especially
proximal psychological outcomes. Also of interest, the large recent
studies that failed to replicate beneficial effects of psychosocial
interventions (i.e., Frasure-Smith et al., 1997; Jones & West,
1996)—included in the analyses of Dusseldorp and colleagues
(1999)— did not find significant treatment effects on emotional
distress. In contrast, the positive findings for cardiac events and
ambulatory ischemia reported by Blumenthal et al. (1997)—not
included in this meta-analysis—were accompanied by significant
reductions in reported stress and hostility. Also consistent with the
potential importance of intervention effects on emotional outcomes, in a nonrandomized trial Denollet and Brutsaert (2001)
found that participation in a multicomponent cardiac rehabilitation
program (i.e., exercise, stress management, individual counseling)
as opposed to standard medical care was associated with less
negative affect over the 3-month intervention period and improved
survival over the subsequent 9 years.
Conclusions Regarding Intervention Research
The results of the quantitative review discussed previously
suggest that interventions intended to prevent recurrent cardiac
events through the reduction of stress and modification of related
psychosocial risk factors are clearly promising, and there is considerable evidence in support of their efficacy (Kendall, FlannerySchroeder, & Ford, 1999). Were it not for the heterogenous treatments evaluated, the intervention literature would seem to satisfy
recently proposed criteria for empirically supported psychological
therapies (i.e., internally valid evidence of treatment effects;
Chambless & Hollon, 1998). This research has included variations
in treating personnel, modes of delivery, and settings, though
perhaps not in a sufficiently systematic or extensive manner as to
support firm conclusions about effectiveness (i.e., external validity
or generalizability to typical clinical settings; Kendall et al., 1999).
The clinical significance (Kendall, 1999) of these intervention
effects (e.g., reductions in cardiac mortality of 30%) seems obvious, but comparisons with other standard interventions provide
further evidence. For example, widely utilized medical treatments
(e.g., beta-adrenergic blocking medications, anticoagulants) reduce mortality on average by 20% (Lau et al., 1992). In a quantitative comparison across types of studies, Ketterer (1993) concluded that psychosocial interventions produced reductions in
mortality at least as large as those observed for medical and
surgical interventions. It is important to note that evidence of the
557
efficacy of medical therapies has generally come from larger and
better controlled trials and that this comparison is somewhat dated.
The specific medical therapies and protocols continue to be refined. Nonetheless, this literature indicates that interventions intended to reduce psychosocial risk in established CHD may improve medical outcomes.
However, a careful examination of the relevant studies suggests
that these conclusions are quite tentative, and many questions
remain for future research. Of most importance, many of the
available studies were small and/or contained methodological limitations (i.e., nonrandomized designs). Hence, large, wellcontrolled replications are needed. Many of the psychosocial intervention studies included in recent reviews are 10 and even 20
years old. The medical management of CHD has changed significantly during this period, raising two important concerns. First, it
is not clear that results of older psychosocial treatment studies
generalize to the context of current cardiologic care that involves
treatments (e.g., greater use of beta-blockers, aspirin and anticoagulants, lipid lowering agents) that impact several of the pathways through which psychosocial risk factors may affect the
pathophysiology of CHD. Second, the changes in standard care
have resulted in improved prognosis for CHD, and the reduced
variance in morbidity and mortality may make it more difficult to
detect the incremental beneficial effects of psychosocial
treatments.
At a minimum, the improved prognosis for CHD resulting from
refinements in routine care increases the sample size requirements
for trials intended to evaluate the effects of psychosocial interventions on cardiac recurrences and mortality. Blumenthal et al.
(1997) recently illustrated the intermediate strategy of using ambulatory ischemia as an outcome variable. Ambulatory ischemia is
a robust predictor of subsequent cardiac events (Kop et al., 2001).
Further, ambulatory ischemia is much more common than recurrent events and therefore can provide a sensitive, clinically relevant index of intervention outcomes. Smaller studies that demonstrate positive results on this measure could then be replicated in
larger trials with adequate power and longer follow-ups required to
detect effects on morbidity and mortality.
The focus on cardiac recurrences and mortality may actually
underestimate intervention effects. Psychosocial interventions also
improve emotional adjustment and functional status or activity
levels (e.g., Johnston, Foulkes, Johnston, Pollard, & Gudmundsdottir, 1999; Trzcieniecka-Green & Steptoe, 1996). These are
important consequences of CHD (Swenson & Clinch, 2000) and
integral components of comprehensive evaluations of health care
interventions (R. M. Kaplan, 1994). The use of standardized outcome units, such as quality of life adjusted years (QALYs; R. M.
Kaplan, 1994), in future studies of psychosocial risk reduction
would not only capture these additional benefits but also facilitate
comparisons with a variety of other treatments including standard
medical therapies (Kaplan & Groessl, 2002). It may be that stress
management and related interventions produce improvements in
QALYs that match or exceed some medical or surgical approaches
and do so at less cost. Further, emotional distress is associated with
significant health care expenditures in CHD patients, primarily
because of greater rates of rehospitalization and related procedures
(Allison et al., 1995; Frasure-Smith, Lespérance, Gravel, Masson,
Juneau, & Talajic, 2000). Hence, effective treatments could reduce these costs (e.g., Davidson, 2000). Cost-utility and cost-
558
SMITH AND RUIZ
effectiveness analyses in future intervention studies have obvious
importance in the current climate of health care financing and
related policy debates.
In studies with null results for cardiac outcomes (Frasure-Smith
et al., 1997; Jones & West, 1996), it is not clear whether the failure
to find significant reductions in psychosocial risk factors reflects
ineffective interventions provided to appropriate patients or use of
otherwise-effective treatments with patients who did not need
them (Linden, 2000). For example, in Jones and West’s (1996)
study, stress management was provided to an unselected sample of
consecutive patients, who reported generally low levels of psychological distress. Future research should examine the efficacy
of these interventions in patients selected for higher levels of
psychosocial risk and, perhaps, examine interventions targeted
to patients’ predominant problem (i.e., general stress, anger,
depression).
Despite mounting evidence of their status as risk factors, only
recently have social isolation and depression been specific targets
in controlled intervention trials. They were addressed in a recently
completed, multicenter trial—Enhancing Recovery in Coronary
Heart Disease (ENRICHD; ENRICHD Investigators, 2000). Approximately 3,000 acute-MI patients who met criteria for depression or social isolation (or both) were randomized to either standard care or a psychosocial intervention on the basis of cognitive
therapy techniques. Depressed patients received cognitive therapy
for depression, and isolated patients received treatment to increase
support using similar techniques. Preliminary evidence suggested
that the psychosocial intervention reduced depression and improved social functioning, but it had no overall effect on cardiac
events (recurrent MI or death; National Heart, Lung, and Blood
Institute, 2001).4 However, the potential importance of effective
treatments for depression in CHD is evident in its multiple effects.
Depression is itself a major threat to quality of life, predicts poor
medical outcome, and can undermine adherence to other components of care (DiMatteo et al., 2000; Ziegelstein et al., 2000).
In addition to evaluating the usefulness of adjunctive treatments,
intervention studies also provide opportunities to test the relatively
well-developed mediational models of psychosocial risk. Intervening psychophysiological or transactional–stress exposure mechanisms could be assessed in intervention studies and used in formal
mediational analyses. Such studies are valuable in theory testing
and could also suggest directions for refining interventions.
General Conclusions, Implications, and Future Directions
Over the past decade, evidence regarding the role of psychosocial risk factors in the development of CHD has grown considerably. Pathways through which stress and negative emotions influence the development of CAD and CHD have been identified in an
extensive body of human and animal research. Epidemiological
studies have demonstrated generally consistent and substantial
prospective effects of hostility, depression, related individual differences in negative affect, and social isolation on CHD. Smaller
but potentially important literatures suggest similar roles for job
stress, social dominance, and social conflict. In each case, these
risk factors are associated with psychophysiological mechanisms
through which stress and emotions could influence CAD and
CHD. Finally, a small and methodologically varied literature suggests that psychosocial interventions may improve CHD progno-
sis. In each topic, as we have outlined previously, there are also
important limitations of this research and many equally important
issues for future investigations.
Implications for Patient Care
Although acceptance of the potential role psychosocial factors
in the development and management of CHD is growing among
medical professionals (Rozanski et al., 1999), it has not become a
standard component of care for most patients. Additional evidence
of the reliability and predictive utility of psychosocial and psychophysiological assessments in clinical cardiologic settings would
likely prompt further progress in this regard. Of even more importance, additional supportive evidence of effective interventions
from large and well-controlled randomized trials is needed to
guide current care, as are criteria for the identification of patients
likely to benefit from specific psychosocial interventions.
Given the incidence and typical course of CHD and the supportive evidence regarding psychosocial factors available to date,
many health care professionals understandably believe they cannot
wait for these remaining issues to be resolved definitively before
implementing these variables in risk stratification and intervention
strategies. Although more detailed discussions are available elsewhere (Allan & Scheidt, 1996; Bellg, 1998; Smith & Ruiz, in
press), we can draw some implications from the research over the
past decade for current clinical practice. Psychosocial risk factors
certainly should be included in the evaluation of CHD patients, and
following such assessments, adjunctive psychosocial interventions
should be considered. The efficacy findings generally support their
use. However, an excessive set of behavior change requirements
would likely discourage or overwhelm patients. Hence, interventions should be prioritized and approaches with multiple benefits
given particular consideration.
For example, smoking cessation among CHD patients is associated with a 40% or larger reduction in mortality (Wilson, Gibson,
Willan, & Cook, 2000), and its cost effectiveness compares favorably with standard medical treatments (e.g., thrombolytic therapy,
cholesterol lowering medication) and behavioral approaches to
rehabilitation (e.g., exercise; Ades, Pashkow, & Nestor, 1997).
Hence, these interventions should be a priority among smokers
with CHD. Exercise interventions reduce cardiac recurrences and
death, and they also compare favorably to medical approaches in
cost-effectiveness analyses (Ades et al., 1997). Further, exercise
interventions can reduce hypertension (Blumenthal et al., 2000;
2002) and depressive symptoms (Babyak et al., 2000; Blumenthal
et al., 1999) and have been found to increase heart rate variability
among CHD patients (Stahle, Nordlander, & Bergfeldt, 1999).
Hence, unless medically contraindicated, the broad psychological
and physiological benefits of exercise (Dubbert, 2002; Salmon,
4
It is important to note that this pattern of outcomes is inconsistent with
the meta-analytic finding of Dusseldorp et al. (1999) in which interventions
that improved psychosocial functioning were more likely to have beneficial
effects of morbidity and mortality. However, additional—albeit preliminary—analyses from the ENRICHD trial indicate that the psychosocial
intervention significantly reduced recurrent CHD events among White men
(Schniederman, 2002). Hence, it may be that the treatment was effective
for subgroups of patients.
SPECIAL ISSUE: CORONARY HEART DISEASE
2001) make this a reasonable selection as a central element of
intervention plans.
If depression or hostility are selected for more direct interventions, there are several empirically supported interventions (Beck
& Fernandez, 1998; Deffenbacher, Dahlen, Lynch, Morris, &
Gowensmith, 2000; DeRubeis & Crits-Christoph, 1998). Certainly
most psychosocial treatments contain an element of social support,
but more focused interventions for social isolation or low support
have not undergone a similar degree of controlled evaluation
(Cutrona & Cole, 2000; Helgeson & Gottlieb, 2000). In the context
of close relationships, several interventions are available for conflict (Baucom, Shoham, Mueser, Daiuto, & Stickle, 1998; Christensen & Heavey, 1999), but there is only limited evidence of their
usefulness in treating cardiovascular disease (Ewart, Taylor, Kraemer, & Agras, 1984). It is important to note that many stress
management approaches used with CHD patients have broad applicability to these psychosocial risk factors (e.g., Blumenthal et
al., 1997). Finally, some evidence suggests that specific pharmacologic approaches may be safe and effective in reducing symptoms of depression and hostility (Lespérance & Frasure-Smith,
2000; Strik et al., 2000), and correlational evidence suggests that
they may be associated with reduced coronary risk (Sauer, Berlin,
& Kimmel, 2001). However, until ongoing randomized trials are
completed (Shapiro et al., 1999), their impact on CHD recurrence
and mortality is not clearly established.
Implications for Prevention
Decades of research on behavioral risk factors has shaped agendas for CHD prevention. Smoking cessation, reductions in dietary
fat and excess weight, and increases in physical activity among the
sedentary are important public health goals and the focus of
evolving behavior change technologies. Further, the prevention of
smoking, high-fat diets and obesity, and inactivity before these
risks are established relatively early in life are potentially even
more useful strategies. Preventing costly disease through behavior
change in childhood and adolescence has an obvious appeal,
especially given that early indications of CAD appear in these age
groups.
In light of these increasingly accepted preventive approaches to
the public health challenges posed by CHD, the literature on
psychosocial risks and related interventions suggests additional
avenues for research and application. There is limited evidence
regarding the developmental origins of specific psychosocial risk
factors as measured in studies of adults. However, there is a vast
literature on related concepts in emotional and social development
(Caspi, 1998; Coie & Dodge, 1998; Rubin, Bukowski, & Parker,
1998). This field has guided the development of effective interventions for other prevention goals (e.g., reducing emotional distress and aggressiveness, increasing social and emotional competence) in children and adolescents (e.g., Blechman, 1996;
Greenberg, Kusche, Cook, & Quamma, 1995; Tolan, Guerra, &
Kendall, 1995), and they could be adapted to examine their effects
on early indications of psychosocial risk for CHD and early
indications of cardiovascular disease (e.g., blood pressure, endothelial dysfunction) among vulnerable children and adolescents.
Certainly, the traditional psychosocial research agenda in CHD is
rather full. Yet, the benefits of past and future studies might not be
limited to treatments for established CHD or risk reduction pro-
559
grams for physically healthy but hostile, depressed, or socially
isolated adults approaching the age of onset for CHD. Rather,
partnerships with developmental and prevention scientists could
identify new directions and applications for psychosocial research
on CHD to younger populations (R. B. Williams, 1998).
Emerging Issues
Future studies of psychosocial influences on CHD should attend
to the generalizability of results across sociodemographic characteristics, particularly gender, ethnicity, and SES. These characteristics are themselves related to CHD risk, perhaps in part through
mechanisms involving the psychosocial risk factors reviewed here.
Further, these sociodemographic variables may moderate effects of
risk factors on mechanisms or CHD outcomes, as well as the
effectiveness of interventions. For example, whether defined as a
characteristic of individuals (e.g., income, occupational status;
Gonzalez, Rodriguez, & Calero, 1998) or the neighborhoods where
they live (Yen & Kaplan, 1999), low SES confers increased risk of
CHD morbidity and mortality. Further, at least some of this risk is
attributable to psychosocial risk factors (Lynch, Kaplan, Cohen,
Tuomilehto, & Salonen, 1996). Some ethnic minorities are at
increased risk, and again, this effect may be attributable at least in
part to psychosocial factors such as discrimination and stressful
living circumstances (Anderson & Armstead, 1995; D. R. Williams & Collins, 1995). In both human and animal models, there
are gender differences in the association between psychosocial risk
factors and CHD, as well as in the likely underlying mechanisms
(J. R. Kaplan et al., 1996; Kiecolt-Glaser & Newton, 2001).
Ultimately, interventions should be evaluated in specific underrepresented sociodemographic groups (cf. Castillo-Richmond et al.,
2000) to determine their generalizability.
Developments in medical science will also shape the psychosocial research agenda in CHD. Advances in noninvasive assessment methods have permitted more informative tests of the influence of psychosocial factors on asymptomatic atherosclerosis.
Other noninvasive procedures have provided clear evidence that
psychological stress and related variables can evoke myocardial
ischemia (Rozanski, 1998). These same procedures have been used
to evaluate the outcomes of psychosocial interventions (Blumenthal et al., 1997; Castillo-Richmond et al., 2000; Gould et al.,
1995). Continuing refinements of cardiologic assessments and
related procedures will encourage even more compelling tests of
psychosomatic hypotheses and more sensitive and persuasive evidence of intervention effects. As in all areas of biomedical science, developments in the genetics of CAD and CHD will pose
new questions for psychosocial research. Genes implicated in
atherosclerotic processes (e.g., Anderson et al., 2000) or in psychophysiological individual differences (R. B. Williams et al.,
2001) could identify higher and lower risk groups, and this genetic
status could moderate the effects of psychosocial risk factors
or identify groups most likely to benefit from psychosocial
intervention.
Finally, future research will addresses new versions of classic
psychological questions. The interplay of early experience and
biology in social and emotional development will inform CHD
prevention research and, perhaps, suggest additional psychosomatic mechanisms (Caldji, Diorio, & Meaney, 2000; Repetti,
Taylor, & Seeman, 2002). Matching subgroups of CHD patients or
SMITH AND RUIZ
560
persons at risk to different psychosocial interventions could improve their efficacy. Last, the study of psychosocial aspects of this
costly and prevalent disease will continue to reflect the cutting
edge of research on connections between mind and body.
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Received August 15, 2001
Revision received November 27, 2001
Accepted November 28, 2001 䡲