The epidemiology pathophysiology, and management of psychosocial risk factors in cardiac practice: The emerging field of behavioral cardiology

Article (PDF Available)inJournal of the American College of Cardiology 45(5):637-51 · April 2005with76 Reads
DOI: 10.1016/j.jacc.2004.12.005 · Source: PubMed
Observational studies indicate that psychologic factors strongly influence the course of coronary artery disease (CAD). In this review, we examine new epidemiologic evidence for the association between psychosocial risk factors and CAD, identify pathologic mechanisms that may be responsible for this association, and describe a paradigm for studying positive psychologic factors that may act as a buffer. Because psychosocial risk factors are highly prevalent and are associated with unhealthy lifestyles, we describe the potential role of cardiologists in managing such factors. Management approaches include routinely screening for psychosocial risk factors, referring patients with severe psychologic distress to behavioral specialists, and directly treating patients with milder forms of psychologic distress with brief targeted interventions. A number of behavioral interventions have been evaluated for their ability to reduce adverse cardiac events among patients presenting with psychosocial risk factors. Although the efficacy of stand-alone psychosocial interventions remains unclear, both exercise and multifactorial cardiac rehabilitation with psychosocial interventions have demonstrated a reduction in cardiac events. Furthermore, recent data suggest that psychopharmacologic interventions may also be effective. Despite these promising findings, clinical practice guidelines for managing psychosocial risk factors in cardiac practice are lacking. Thus, we review new approaches to improve the delivery of behavioral services and patient adherence to behavioral recommendations. These efforts are part of an emerging field of behavioral cardiology, which is based on the understanding that psychosocial and behavioral risk factors for CAD are not only highly interrelated, but also require a sophisticated health care delivery system to optimize their effectiveness.
The Epidemiology,
Pathophysiology, and Management
of Psychosocial Risk Factors in Cardiac Practice
The Emerging Field of Behavioral Cardiology
Alan Rozanski, MD, FACC,* James A. Blumenthal, PHD,† Karina W. Davidson, PHD,‡
Patrice G. Saab, P
HD,§ Laura Kubzansky, PHD
New York, New York; Durham, North Carolina; Coral Gables, Florida; and Boston, Massachusetts
Observational studies indicate that psychologic factors strongly influence the course of
coronary artery disease (CAD). In this review, we examine new epidemiologic evidence for
the association between psychosocial risk factors and CAD, identify pathologic mechanisms
that may be responsible for this association, and describe a paradigm for studying positive
psychologic factors that may act as a buffer. Because psychosocial risk factors are highly
prevalent and are associated with unhealthy lifestyles, we describe the potential role of
cardiologists in managing such factors. Management approaches include routinely screening
for psychosocial risk factors, referring patients with severe psychologic distress to behavioral
specialists, and directly treating patients with milder forms of psychologic distress with brief
targeted interventions. A number of behavioral interventions have been evaluated for their
ability to reduce adverse cardiac events among patients presenting with psychosocial risk
factors. Although the efficacy of stand-alone psychosocial interventions remains unclear, both
exercise and multifactorial cardiac rehabilitation with psychosocial interventions have dem-
onstrated a reduction in cardiac events. Furthermore, recent data suggest that psychophar-
macologic interventions may also be effective. Despite these promising findings, clinical
practice guidelines for managing psychosocial risk factors in cardiac practice are lacking.
Thus, we review new approaches to improve the delivery of behavioral services and patient
adherence to behavioral recommendations. These efforts are part of an emerging field of
behavioral cardiology, which is based on the understanding that psychosocial and behavioral
risk factors for CAD are not only highly interrelated, but also require a sophisticated health
care delivery system to optimize their effectiveness. (J Am Coll Cardiol 2005;45:637–51)
© 2005 by the American College of Cardiology Foundation
Various lifestyle behaviors promote the development and
clinical manifestations of coronary artery disease (CAD),
including an unhealthy diet, physical inactivity, and smok-
ing. Emotional factors and the experience of chronic stress
also promote atherosclerosis and cardiac events, as previ-
ously reviewed (1). However, although cardiologists are
accustomed to managing lifestyle behaviors such as overeat-
ing and physical inactivity, they are less likely to assess and
treat psychosocial risk factors, perhaps because of their
limited familiarity with effective strategies and recommen-
dations. A potential dilemma is that, on the one hand, it is
not the function of cardiologists to serve as mental health
professionals; on the other hand, the strong and robust
relationship between psychosocial risk factors and CAD
suggests that cardiologists need to be proactive in addressing
this important aspect of patient care. What then should the
cardiologist’s role be? Herein, we address the question of the
role of the cardiologist by exploring various ways for
effective clinical involvement. We also provide an update on
the epidemiologic and pathophysiologic evidence linking
psychosocial factors and the progression of CAD, empha-
sizing recent select studies rather than providing a compre-
hensive review, and suggesting areas for future research.
Thus, this review is designed to provide an integrated
understanding of how psychosocial risk factors influence the
current and future practice of cardiology.
Psychosocial factors that promote atherosclerosis and ad-
verse cardiac events can be divided into two general cate-
gories: emotional factors and chronic stressors. Emotional
factors include affective disorders such as major depression
and anxiety disorders as well as hostility and anger. Chronic
stressors include factors such as low social support, low
socioeconomic status, work stress, marital stress, and care-
giver strain.
From the *Division of Cardiology, St Luke’s-Roosevelt Hospital Center, and the
Department of Medicine, Columbia University College of Physicians and Surgeons,
New York, New York; †Department of Psychiatry and Behavioral Sciences, Duke
University Medical Center, Durham, North Carolina; ‡Division of General Medi-
cine, Columbia College of Physicians and Surgeons, and Cardiovascular Institute,
Mount Sinai School of Medicine, New York, New York; §Department of Psychol-
ogy, University of Miami, Coral Gables, Florida; and the Department of Society,
Human Development and Health, Harvard School of Public Health, Boston,
Manuscript received September 29, 2004, accepted October 6, 2004.
Journal of the American College of Cardiology Vol. 45, No. 5, 2005
© 2005 by the American College of Cardiology Foundation ISSN 0735-1097/05/$30.00
Published by Elsevier Inc. doi:10.1016/j.jacc.2004.12.005
Emotional factors. Among emotional factors, depression
has been most studied in recent years. Depressive disorders
vary from mild (subclinical) depressive symptoms to classic
major depression. According to the Diagnostic and Statistical
Manual of Mental Disorders-4th edition, depression is char-
acterized by severely depressed mood and/or anhedonia
(inability to take pleasure in life) that lasts for two weeks or
more and is accompanied by significant functional impair-
ment and somatic complaints. Research in this area has
evaluated the effects of depression in both initially healthy
individuals and in patients with known CAD. Depression
plays a role in promoting CAD events in both cohorts (1).
Most epidemiologic studies have primarily assessed depres-
sive symptoms rather than major depression. Data indicate
the presence of a strong consistent gradient between the
level of depressive symptoms and the likelihood of adverse
cardiac events, beginning at relatively low levels of depres-
sive symptoms (2)(Fig. 1). Such data suggest that the
pathophysiologic effects of depression may be triggered by
even mild subclinical symptoms.
Major depression has been studied less commonly, partly
because its identification requires a formal interview per-
formed by trained professionals. However, consistent with
the evidence derived from assessing symptom measures,
major depression has also been found to be associated with
a highly significant increase in adverse cardiac events, over
and above that observed for the presence of depressive
symptoms alone (3).
Epidemiologic studies have also considered two other
emotional factors relative to prognosis: anxiety and anger/
hostility. Those that have examined the risk of cardiovas-
cular outcomes associated with anxiety disorders are limited.
Three large studies have shown a significant relationship
between phobias and sudden cardiac death (1), but data
linking other forms of anxiety to CAD are relatively scant or
conflicting and more work is needed. Although hostility and
chronic anger have been linked to cardiovascular outcomes
in a number of studies, results have been generally mixed.
Several factors may contribute to inconsistent findings in
this area. Measures used to assess anger and hostility have
varied widely, making it difficult to compare results. A
recent study suggests that there is some self-denial and lack
of self-awareness associated with self-reported hostility (4).
This may be overcome by using a structured interview
approach (4), but the approach has not been widely tested.
Interestingly, a number of recent studies have demonstrated
a relationship between hostility or anger and measurements
of subclinical atherosclerosis (5– 8) and also have linked
hostility to progression of atherosclerosis during serial cor-
onary angiography (9). Such findings suggest that hostility
and chronic anger merit further study as potential psycho-
social risk factors.
Chronic stressors. A variety of adverse life circumstances
that promote chronic stress have been evaluated for their
relationship to adverse cardiac outcomes. For instance,
whereas the presence of high levels of social support is
known to promote psychologic and physical well being, a
consistent literature indicates that low levels of social sup-
port are health damaging. Although historically there has
been little integration of differing theories of social support,
there is increasing agreement that social support can be
divided into two broad categories: social networks, which
describe the size, structure, and frequency of contact with
the network of people surrounding an individual; and
functional support, which may be further divided into
received social support, which highlights the type and
amount of resources provided by the social network, and
perceived social support, which focuses on the subjective
satisfaction with available support or the perception that
support would be available if needed. Received and per-
ceived social support are often further delineated by type,
including instrumental (e.g., help getting tangible tasks
done), financial (economic support), informational (provid-
ing needed information), appraisal (help evaluating a situ-
ation), and emotional support (e.g., providing emotional
support, feelings of being loved). The term “tangible sup-
port” also is used to describe types of support that are readily
seen or quantified, such as instrumental or financial support.
Both inadequate structural and functional support have been
consistently linked to the occurrence of cardiac death and
all-cause mortality in many studies (1). For example, low
structural support has been associated with increased mor-
Abbreviations and Acronyms
CAD coronary artery disease
HPA hypothalamic-pituitary-adrenocorticol
MI myocardial infarction
SES socioeconomic status
SSRI selective serotonin reuptake inhibitor
PET positron emission tomography
Figure 1. Post-myocardial infarction (MI) patients were recruited and
assigned to one of four categories based on the Beck Depression Inventory
(BDI), ranging from no depressive symptoms (BDI 5) to moderate to
severe depressive symptoms (BDI 19). During the five-year follow-up
period, a gradient relationship was observed between the magnitude of
depressive symptoms and the frequency of deaths, with increased events
occurring even in patients with mild depressive symptoms (BDI 5 to 9) (2).
638 Rozanski
et al.
JACC Vol. 45, No. 5, 2005
Psychosocial Factors and CAD
March 1, 2005:637–51
tality within cardiac populations, including such factors as
living alone (10), lacking a confidant (11), and suffering
from social isolation (12). Furthermore, low emotional
support (13), lack of available support (14), and low per-
ceived social support (15) also have been associated with
increased mortality, and preliminary evidence suggests that
functional support may be more important than structured
support in cardiac populations (16). As with depression, a
strong and consistent inverse gradient consistently charac-
terizes the relationship between the magnitude of social
support and adverse clinical outcomes among both initially
healthy subjects and those with known CAD (1).
Socioeconomic status (SES), generally characterized as a
composite of factors such as occupational status, economic
resources, education, and social status, has also attracted
attention because longitudinal studies indicate a strong
inverse gradient between SES level and adverse cardiac
events. Low SES is characteristically accompanied by poorer
health habits and higher frequencies of coronary risk factors,
which account for half or less of the SES-CAD gradient
(17). More financial hardship, poorer housing conditions,
and increased levels of chronic stress also characterize low
SES, as does poorer and more physically repetitious working
conditions and less job security and job latitude (17). Thus,
low SES can be viewed as a composite chronic psychologic
stressor (18), a perspective that is supported by pathophys-
iologic evidence. Hypothalamic-pituitary-adrenal (HPA)
dysfunction frequently accompanies chronic stress, and in-
creased dysfunction is observed as SES levels decline. For
example, this relationship has been documented by an
inverse relationship between SES levels and measurements
of cortisol variability (more variability being healthy) and
measurements of central obesity (19).
Work stress is another form of chronic stress that has
been increasingly studied for its potential adverse cardiovas-
cular effects. Various aspects of work stress have been
studied, but two leading epidemiologic models have re-
ceived the most attention (Fig. 2). One model is the “job
strain” model developed by Karasek et al. (20), in which
individuals are evaluated according to two factors: “job
demand” and “job latitude.” Individuals with high job
demand but low job latitude are categorized as being under
“job strain,” performing excessive routine work with a lack
of creative outlets or a sense of rigid confinement. The other
model is the effort-reward imbalance model developed by
Siegrist et al. (21), but extensively evaluated so far only in
Europe. In this model, job “effort” is compared with job
“reward,” with effort measured in terms of either extrinsic
demands (e.g., having a demanding employer) or one’s
intrinsic pattern of responding to work demands, and
rewards measured in terms of financial incentive, self-
esteem, career opportunity, or security. Three lines of
evidence link work stress to adverse clinical outcomes. First,
an increasing epidemiologic literature indicates that job
strain and effort-reward imbalance (22–25), as well as other
work parameters (26 –28), are associated with an increased
frequency of adverse clinical outcomes. Both the job strain
and effort-reward imbalance model appear comparable for
their ability to predict adverse events (25). Second, work
parameters, such as low job control, account for a substantial
portion of the inverse gradient noted between SES status
and cardiovascular disease (17). Third, several recent studies
have also linked work stress to measures of subclinical
atherosclerosis (29–31), with findings varying between gen-
ders and/or among ethnic groups (30,31). Because most
epidemiologic studies that showed an association between
work stress and adverse clinical outcomes have focused
primarily on white men, prospective studies in women and
other ethnic groups are needed.
Marital stress also represents a chronic stressor with
apparent pathophysiologic effects (27,32,33). For instance,
Orth-Gomer et al. (32) reported that following myocardial
infarction (MI), women with concomitant marital stress had
a higher frequency of recurrent cardiac events during a
five-year follow-up compared to those with less marital
stress. These data are supported by a recent study that found
a higher prevalence of subclinical atherosclerosis, and accel-
erated progression over time, among healthy women report-
ing marital dissatisfaction (Fig. 3)(34), supporting the
assertion that marital stress is atherogenic.
Caregiving strain is an increasingly prevalent stressor that
has recently been studied for potential cardiovascular se-
quelae (35,36). In the Nurses’ Health Study, caregiving for
an ill or disabled spouse was associated with a nearly twofold
adjusted risk ratio for experiencing an adverse cardiac event
during a four-year follow-up period (35). However, this
report did not stratify patients based on the emotional
appraisal of their caregiving experience. Because other
research indicates that highly meaningful and altruistic
experiences can be of psychologic benefit (37), it is possible
that the effects of caregiving are dependent on the meaning
Figure 2. Two leading conceptual models of work stress. In the job strain
model (left), the amount of job demand and decision latitude determines
the degree of job strain. High demand but low decision latitude charac-
terizes job strain. In the effort-reward imbalance model (right), increased
job effort may result from either extrinsic demands or personal overcom-
mitment, and “reward” may occur in the form of money, recognition,
prestige, security, or career opportunities. High effort with low reward
characterizes job imbalance.
JACC Vol. 45, No. 5, 2005
et al.
March 1, 2005:637–51
Psychosocial Factors and CAD
attached to such activities. In support, another study ob-
served that when caregivers were divided into those with
and without a sense of emotional strain during caregiving,
only those reporting strain had an increased death rate
during follow-up (36).
Clustering of psychosocial risk factors. Although we have
discussed emotional factors and chronic stressors as separate
entities, they frequently cluster. For example, individuals
who experience job strain tend to have higher rates of
depression compared to those who do not report strain (38).
The strong overlap between chronic stress and emotional
factors suggests that any life situation that has the capacity
to evoke chronic negative emotional responses may promote
heart disease. For instance, a recent study found that
childhood maltreatment (39) was associated with a signifi-
cant increase in both depression and cardiovascular disease
among adult women. Similarly, exposures ranging from the
death of a child to adverse wartime experiences may poten-
tially affect the risk of CAD development and should be
candidates for study.
Comparison of psychosocial risk factors with traditional
CAD risk factors. The characterization of psychosocial
risk factors as “major” CAD risk factors has been debated.
However, more consistent and reproducible outcome stud-
ies confirm that psychosocial risk factors such as depression,
poor social support, and low SES represent potent CAD
risk factors. Furthermore, many reported studies now link
psychosocial risk factors to the presence of subclinical
atherosclerosis or its progression, as measured by carotid
ultrasonography (5–8,29–31,34,40,41). Meta-analyses of
psychosocial studies have been limited by the use of varying
measures and inconsistent methods for calculating risk
ratios. However, a recent meta-analysis of outcomes asso-
ciated with depressive symptoms indicates a relative risk
that is comparable to those noted for traditional CAD risk
factors reported from the Framingham study (Fig. 4)(3,42).
This observation is supported by the recently reported
INTERHEART case-control study, which uniquely as-
sessed eight coronary risk factors and a composite index of
psychosocial factors within a single standardized interna-
tional population of 12,461 acute post-MI patients and
14,637 matched controls gathered from 52 countries (43).
The psychologic index was necessarily limited by the study’s
design to either brief or even single-item assessments of
depression, locus of control, perceived stress at home or
Figure 3. Postmenopausal females (n 390) were divided into those in satisfying marriages (left of each panel), unmarried (middle of each panel),
and in low-satisfying marriages (right of each panel). After 11 years of follow-up, the women in satisfied marriages had the lowest and the women
in unsatisfying marriages had the highest percentage of significant plaque (left panel). Serial carotid ultrasonography was performed after three years
in a subgroup of this patient population (n 206) and revealed that women in low-satisfying marriages also had the greatest progression of plaque
during follow-up (right panel). Reprinted with permission from Gallo et al. Psychosom Med 2003;65:952– 62 (34). *Groups differ significantly at
p 0.05.
Figure 4. The risk ratios for traditional risk factors reported for men in the
Framingham study (28). The risk ratios for depressive symptoms and
clinical depression are from a recent meta-analysis by Rugulies et al. (3).
The risk ratios for traditional risk factors are for death due to cardiac
disease, myocardial infarction, coronary artery insufficiency, and develop-
ment of angina. For depressive symptoms and clinical depression, the risk
ratios are for death due to cardiac disease and myocardial infarction. CI
confidence interval; HT hypertension; LDL low-density lipoprotein;
HDL high-density lipoprotein.
640 Rozanski
et al.
JACC Vol. 45, No. 5, 2005
Psychosocial Factors and CAD
March 1, 2005:637–51
work, moderate to severe financial stress, and experience of
adverse life events. Nevertheless, the odds ratios and
population-attributable risk for acute MI by this limited
subjective measure of psychosocial stress was substantial,
comparable to those noted for other major CAD risk factors
(Fig. 5). In addition, this psychosocial index remained a
robust predictor of MI independent of geographic or ethnic
context (26).
Moreover, for a variety of reasons, the risk associated with
psychosocial factors may actually be greater than such
statistical evidence suggests. First, behavioral and metabolic
risk factors tend to aggregate disproportionately among
individuals with psychosocial stress (1). However, this
potentially powerful effect is reduced because of the statis-
tical convention to adjust psychosocial risk ratios for behav-
ioral and metabolic risk factors. Second, because measures
of psychosocial stress may be imprecise, they may underes-
timate the relationship between psychosocial stress and
CAD outcomes. For example, although depressive disorders
are generally episodic, the scales used to measure self-
reported depressive symptoms assess only the presence of
relatively current depressive symptoms. Thus, it is not
surprising to find that the chronicity and level of depressive
symptoms are together more strongly associated with mea-
sures of atherosclerosis compared with symptom levels alone
(40). Third, psychosocial risk factors tend to aggregate.
Such clustering is associated with an increased likelihood of
cardiac events (1) and more subclinical atherosclerosis (8,9).
Future epidemiologic directions. In contrast to the data
linking negative emotional states and chronic stress to
CAD, the potential protective effect of positive psychologic
factors has not been extensively investigated. Building on
work in other areas, we suggest that one potential direction
for clinical investigations in this neglected area could be to
explore the notion of flexibility as it relates to mental health
(44). In the physical domain, the ability to demonstrate
variability in response to stressors may be associated with
better clinical outcomes (45). Similarly, having the capacity
to respond to situations in a variety of different ways (i.e., to
flexibly adapt one’s emotional and coping responses to any
given situation) may be associated with better mental health.
We consider three psychologic components that may be
central to developing emotional and coping flexibility (Fig.
6). One key component is “vitality,” which refers to the
presence of energy and enthusiasm and a sense of aliveness
(46). It is characterized by two positive emotions, joy and
interest, and is fueled by both a sense of purpose and a sense
of self-worth. Vitality may be considered both restorative
and regenerative and, as such, connotes a sense of freshness
and positive excitement. Conversely, when someone lacks
vitality, the likelihood of becoming excited and investing
energy toward goals and in interactions with others is
Figure 5. Risk of acute myocardial infarction for men and women for each of nine coronary artery disease (CAD) risk factors evaluated in the international
INTERHEART case-control study. Results are adjusted for age, gender, and geographic location. The prevalence of each CAD risk factor is presented
for controls and cases in the third and fourth columns; prevalence rates are not calculated for the psychosocial (PS) index as it is derived from a statistical
model. Reprinted with permission from Yusuf et al. Lancet 2004;364:937–52 (43). Abd abdominal; CI confidence interval; Curr current; OR
odds ratio; PAR population-attributable risk; Smok smoking; Veg vegetables.
JACC Vol. 45, No. 5, 2005
et al.
March 1, 2005:637–51
Psychosocial Factors and CAD
diminished. The availability of this energy promotes two
key adaptive responses (which may in turn promote vitality):
development of various positive response mechanisms (such
as patience, discipline, and maintaining friendships) and
emotional competence, or the ability to regulate emotions
across a range of situations (47). An important aspect of
emotional competence is the ability to either enhance or
suppress emotional expression, a trait that may be termed
“emotional flexibility,” as discussed by Bonanno et al. (48)
and others.
From this perspective, depression and various exhaustive
states can be viewed as a long-term deficit in vitality and an
escalating inability to be flexible and responsive to life and
daily challenges. Anxiety and anger can also be viewed as
emotionally inflexible responses, with the constant negative
emotions dissipating energy and taxing positive coping
mechanisms. Job strain is also an excellent example of a
situation that can drain energy and vitality. For example, a
recent study has demonstrated that chronic job strain can
lead to exhaustion and an inability to unwind after work
(28). Such sequelae can increase the risk for adverse cardiac
events (49). By contrast, professional, marital, interpersonal,
and avocational activities that require effort but that also
promote joy and interest serve to preserve vitality and
Early emotional theorists suggested that positive emo-
tions such as joy might provide recuperative power. Support
for this concept is provided by recent data showing that
positive psychologic factors can dampen physiologic reac-
tivity to negative emotional stimuli (50). Similarly, individ-
uals who score high on the trait of forgiveness (51)orwho
are provided with social support (52) demonstrate lower
heart rate and blood pressure elevations during laboratory
mental stress. Other data indicate that positive emotions can
enhance immune function (53). Evaluation of the impact of
positive psychologic factors upon clinical outcomes is also
limited and recent. In the largest study to date, Kubzansky
et al. (54) conducted a 10-year follow-up study of 1,306
men from the Normative Aging Study, who were assessed
for optimistic versus pessimistic “explanatory style” (i.e.,
how one explains the causes of bad events). Stratification of
individuals according to optimistic, neutral, and pessimistic
explanatory styles revealed a gradient relationship between
levels of optimism and cardiac outcomes, with optimism
halving the risk for cardiac events. A separate measure of
dispositional optimism has been linked to more favorable
outcomes following bypass surgery (55). A strong relation-
ship has also been noted between positive emotions and
longevity in the long-term follow-up of nuns whose diaries
in early adult life were assessed for positive emotional
content (56). Such findings suggest the value of further
exploring positive psychologic factors that may promote
health or protect against disease.
Emotional disturbance and chronic stress can have a pro-
found impact on the central nervous system, including
increased output from the sympathetic nervous system and
the HPA axis. Chronic stimulation from these central
outputs can induce a wide variety of pathophysiologic
responses, as displayed in Figure 7. Depression has been
particularly studied in this regard. Chronic stimulation of
the HPA axis by depression frequently results in hypercor-
tisolemia, blunted HPA activity, and diminished feedback
control, as evidenced by nonsuppression of cortisol secretion
Figure 6. The mental health paradigm in which individuals who have a
strong sense of purpose coupled with a sense of self-worth derive benefit in
terms of a greater sense of vitality. The positive emotion associated with
vitality provides energy needed to develop and maintain greater emotional
competence and positive response mechanisms. In turn, the presence of
emotional competence and positive response mechanisms provide a stabi-
lizing force for maintaining a sense of vitality.
Figure 7. Pathophysiologic mechanisms by which chronic stress and
affective disorders, such as depression, appear to promote atherosclerosis.
These stressors activate the hypothalamic-pituitary-adrenal (HPA) axis
and the sympathetic nervous system (SNS) and affect behaviors. Multiple
adverse peripheral effects can ensue from this neuroendocrine, sympathetic,
and behavioral activation, as shown. The neuroendocrine and neuroplastic
changes emanating from these stressors can also induce a state of
heightened physiologic responsivity to acute stress which may interact with
chronic stressors to cause more adverse effects. ANS autonomic nervous
system; Endo. endothelial.
642 Rozanski
et al.
JACC Vol. 45, No. 5, 2005
Psychosocial Factors and CAD
March 1, 2005:637–51
following dexamethasone suppression. When present, hy-
percortisolemia is associated with suppression of growth and
sex hormones. Heightened stimulation of the sympathetic
nervous system is also common in depression and is asso-
ciated with higher concentrations of circulating plasma
norepinephrine and an increase in total body sympathetic
activity (57). As a consequence, depressed patients com-
monly manifest higher resting heart rates than healthy
controls and exhibit autonomic nervous system dysfunction,
including diminished heart rate variability, baroreflex dys-
function, and increased QT variability (57).
Hypercortisolemia, in association with blunted growth
and sex hormones, promotes central obesity (58), which
may occur despite overall weight loss, and an increase in
peripheral and portal fatty acids. These metabolic changes
also contribute to more insulin resistance and diabetes
among depressed subjects, and a higher frequency of dia-
betic complications (59). Depressed patients manifest sub-
stantial platelet abnormalities, including increased concen-
trations of beta-thromboglobulin and platelet factor 4 and
increased concentration of functional glycoprotein IIb/IIIa
receptors. In addition, there is evidence that depression is
associated with a hyperactive 5-hydroxytryptamine (5-HT)
receptor signal transduction system and, re
latedly, increased responsiveness of platelets to serotonin
(60). Other recent studies indicate that depression is asso-
ciated with increases in C-reactive protein, interleukin-6,
tumor necrosis factor, and other inflammatory proteins (61).
The potential mechanism for this association may be com-
plex, involving not only stimulation of the HPA axis and the
sympathetic nervous system but also potential synergy in-
duced by peripheral effects, such as hyperglycemia (62).
More recent data indicate that depression is associated with
a heightened incidence of endothelial dysfunction among
various cohorts, including young and otherwise healthy
depressed patients (63). Finally, depression is also associated
with decreased bone mineralization, which is the result of
increased cortisol and decreased concentrations of growth
and sex hormone concentrations, and probable interaction
with local inflammatory proteins. Thus, depression is capa-
ble of inducing virtually the full spectrum of pathophysio-
logic effects noted in Figure 6.
Future research directions. Because other psychosocial
risk factors have not yet been investigated as extensively as
depression, the full spectrum of their pathophysiologic
effects requires further study. In addition, we highlight three
areas where clinical observations provide new research
directions. First, the observation that cardiac event rates
increase when psychosocial risk factors cluster has focused
interest on explanatory mechanisms. Whether this increase
is due to greater overall stress or the synergistic effects of
stressors that evoke different pathophysiologies needs to be
determined. The latter possibility is supported by recent
data indicating distinct pathophysiologic differences accord-
ing to the exposure of Watanabe Heritable Hyperlipidemic
rabbits to two different chronic stressors: an unstable social
environment versus social isolation. Both forms of stress
produced more atherosclerosis compared to a control group,
but the groups exposed to different forms of stress exhibited
different metabolic consequences and patterns of accrued
atherosclerosis (64).
Second, various data suggest links between chronic psy-
chologic distress and certain adverse behaviors, such as
overeating (65,66). New technologies that study brain
function suggest that such links may be centrally mediated.
Immunohistochemistry has been used to identify an ana-
tomic chronic stress response network, localized to several
specific brain centers, in a rat model of chronic stress (67).
Whereas glucocorticoids help end acute stress responses by
exerting negative feedback upon the HPA axis, glucocorti-
coids occupy central glucocorticoid receptors during chronic
stress, with resultant activation of the chronic stress re-
sponse network, including continued glucocorticoid produc-
tion, in these experimental animals (66,67). This combina-
tion of chronic stress and high glucocorticoid levels appears
to stimulate a preferential desire to ingest sweet and fatty
foods (66). Further study indicates that glucocorticoids
affect dopaminergic transmission in areas of the brain
associated with motivation and reward (68). Positron emis-
sion tomography (PET) has been used to identify the
presence of diminished dopamine D
binding potential
within midbrain systems under conditions of chronic stress
in the cynomolgus monkey (69). In humans, PET studies
have revealed that this area is involved specifically in food
motivation (70), and that, like stressed monkeys, obese
individuals also have decreased D
receptor function in this
same reward area of the brain, varying inversely with body
mass index (71).
Third, data suggest that enhanced physiologic reactivity
to acute stress is clinically important, linked to subclinical
atherosclerosis (72,73) and interacting with known psycho-
social risk factors to produce greater degrees of subclinical
atherosclerosis (41). Clinical observations suggest that
chronic stress, per se, may be an important cause for such
enhanced physiologic reactivity (as exemplified in Fig. 7).
For instance, depressed (57), hostile (74), and low-SES
subjects (19) all manifest exaggerated physiologic responses
to acute stressors. These observations are complemented by
experimental animal studies that indicate that repeated
exposure to a chronic stressor results in increased adrenal
and pressor responses to acute novel stressors (66,75). Other
animal research indicates that the mimicking of chronic
stress by experimentally elevating glucocorticoids within the
brain produces enhanced adrenocorticotropic hormone re-
sponses (76) and increases in both baseline arterial blood
pressure (77) and blood pressure and heart rate responses to
an acute novel stressor (78). Research that further eluci-
dates the neurophysiology of the chronic stress circuitry,
and the mechanisms of neuroplasticity that produce
long-term stress-induced changes in the control of phys-
iologic functions, could pave the way for understanding
JACC Vol. 45, No. 5, 2005
et al.
March 1, 2005:637–51
Psychosocial Factors and CAD
and mitigating the adverse effects of chronic stress in
cardiovascular disease.
As illustrated in Figure 8, there are important reasons that
cardiologists should be interested and skilled in recognizing
and managing psychosocial risk factors in practice. We have
already discussed two compelling reasons: psychosocial risk
factors are strongly linked to the development of adverse
cardiac events and cluster with adverse behaviors that
promote CAD. We now discuss four additional factors that
link psychosocial risk factors to cardiac practice.
First, psychosocial risk factors are highly prevalent within
cardiac populations. For instance, the National Comorbid-
ity Survey (79) assessed the frequency of serious psychiatric
illness and found that the 12-month and lifetime prevalence
rates of certain depressive and anxiety disorders, as well as
serious substance abuse, were remarkably high, with 48%
reporting at least one of these disorders in their lifetime. To
compare these prevalence rates with those noted in general
medical and CAD populations, it is also useful to examine
point prevalence rates, the percentage of persons with
psychiatric disorders at a specific point in time. For example,
the prevalence rate of major depression disorder in the
National Comorbidity Survey was approximately 5%, com-
pared with a prevalence of 15% or greater in populations
with CAD (1). In addition, at least another 15% to 20% of
patients with cardiac disease exhibit depressive symptoms
that do not necessarily meet criteria for major depressive
disorder (1). Similarly, anxiety disorders, such as phobic
anxiety or panic disorder, are relatively common among
patients with CAD. As a consequence, cardiologists are
likely to encounter a significant number of psychologically
distressed patients in clinical practice.
Second, psychologic distress commonly presents as symp-
toms of cardiac disease in clinical practice. Notably, whereas
certain psychosocial risk factors such as depression and
anxiety can present with either psychologic and/or somatic
manifestations, it is those with primarily somatic symptoms,
such as chest pain or palpitations, who seek medical evalu-
ation preferentially, thus exacerbating this tendency. In fact,
estimates indicate that more than three-fourths of patients
with major depression or panic disorder seen in primary care
settings present with somatic complaints only (80,81).
Because chest pain and palpitations are common somatic
complaints, a high proportion of patients presenting with
such symptoms in medical settings have psychologic distress
in the absence of objective evidence of organic heart disease.
For instance, whereas panic disorder occurs in 4% of the
general population (79), it occurs in more than 15% to 20%
of patients presenting with chest pain complaints in emer-
gency departments, reflecting the high rate of medical care
use by these patients (82). Physician awareness of these
relationships is important, because psychologic distress is
frequently underdiagnosed in medical evaluations of cardiac
symptoms. For example, in a prospective evaluation of 441
patients presenting to a cardiac care emergency department
with chest pain and evaluated blindly for psychiatric diag-
nosis, approximately 25% had panic disorder, but in 98% of
the patients with panic disorder, the diagnosis was missed
by the cardiologists in the cardiac care emergency depart-
ment (83).
Third, psychosocial risk factors can adversely affect treat-
ment adherence. For instance, a meta-analysis has demon-
strated that patients with depression were three times more
likely to be nonadherent with treatment recommendations
(84). Similarly, a recent meta-analysis of 122 social support
studies (85) has revealed that patient adherence is strongly
influenced by the magnitude of adequate functional or
structural social support. However, although it seems intu-
itively reasonable, it has not yet been conclusively demon-
strated that alleviation of psychologic distress improves
treatment adherence.
Fourth, acute psychologic stress shapes the course of
cardiac disease in both positive and negative fashion. On the
one hand, acute emotional stress represents an important
trigger for exacerbating pathophysiologic processes, ranging
from the induction of endothelial dysfunction to the pre-
cipitation of myocardial ischemia. The latter occurs during
laboratory mental stress in approximately 50% of patients
with exercise-induced ischemia (1). On the other hand,
patients’ experience of acute cardiac events and premonitory
symptoms, such as angina pectoris, is itself a form of acute
psychologic stress that can sometimes transform patients’
lives by signaling a need for personal reflection, inducing a
reevaluation of values and/or shifting the perspective of time
from “years since birth” to “years remaining” (86). Such
events may cause patients to be more receptive to adopting
new attitudes and be more successful in altering unhealthy
behaviors, as indicated by various studies. Because cardiol-
ogists commonly treat patients who experience acute life-
threatening events and who may be more receptive to
Figure 8. Six reasons that promote interest in the evaluation and manage-
ment of psychosocial stress in cardiac practice.
644 Rozanski
et al.
JACC Vol. 45, No. 5, 2005
Psychosocial Factors and CAD
March 1, 2005:637–51
physician advice, cardiologists may be ideally positioned to
initiate these interventions.
Given that psychologic distress is often first detected in
clinical health care settings, the cardiologist can play a
critical role in the identification and management of psy-
chosocial risk factors. This role can be divided into three
broad categories: screening for psychosocial risk factors,
referring of appropriate patients to behavioral health care
providers, and managing milder forms of psychologic dis-
tress in the context of clinical practice.
Screening for psychosocial risk factors. Cardiologists can
increase the detection of psychosocial risk factors by sys-
tematically screening for them. Querying patients about
psychosocial risk factors conveys the message that these
factors are important and relevant to providing optimal care.
Screening can be accomplished by structured interviews
and/or by validated questionnaires. Although questionnaire
measures are easily administered and objectively scored,
interviews allow greater flexibility and offer richer clinical
information than that provided by written inventories.
Because cardiologists are accustomed to obtaining medical
histories through a brief review of systems, additional
questions about psychosocial risk factors could easily be
incorporated into such assessment. These questions should
cover three kinds of experiences that may help to identify
psychologic distress: 1) emotional factors, such as depres-
sion, anxiety, and anger; 2) chronic stressors, such as work
strain and home stress; and 3) somatic complaints that may
be stress-related, such as fatigue and disrupted sleep. Some
questions for screening patients’ psychosocial status are
suggested in Table 1.
The identification of emotional distress can often be
challenging in the medical setting. Hallmarks of disorders
such as depression (e.g., changes in appetite and/or signif-
icant changes in weight) and panic disorder (e.g., palpita-
tions, and/or shortness of breath) can indicate either a
cardiac or psychiatric condition. Inaccuracy in determining
the cause of such symptoms can result in misdiagnosis and
mistreatment. Moreover, because physicians’ time is often
limited, psychosocial problems need to be assessed relatively
quickly and efficiently. However, research suggests that such
skills can be learned and effectively implemented. Finally,
following acute events or surgical interventions, cardiac
patients may feel especially vulnerable and helpless. During
such times, inquiries about mental health and psychosocial
functioning can be perceived as highly threatening, and may
elicit defensiveness, resentment, and denial. The cardiolo-
gist can help preempt this response by openly addressing the
patient’s concerns and establishing rapport.
Referring patients to behavioral health care providers.
The benefits of screening for psychosocial risk factors will be
realized only if proper identification leads to appropriate
intervention and follow-up. Patients with apparently signif-
icant psychologic distress or behavioral maladjustment
should be referred to appropriate specialists for counseling
and/or psychiatric treatment (87). Thus, part of the cardi-
ologist’s role in managing psychologic distress may be the
development of a referral network of specialists. However,
close follow-up of patients even after referral is highly
advisable because early dropout from both pharmacotherapy
and psychotherapy is common (87).
Managing psychologic distress in clinical practice. Sub-
clinical presentations of psychologic distress, such as minor
depression, work stress, inability to relax, and difficulty
sleeping, may be appropriately handled in routine cardiac
practice. Tools that are readily available to cardiologists for
direct management of psychosocial risk factors are practical
behavioral interventions, as outlined in Table 2. Cardiolo-
gists are familiar with some of these interventions, such as
exercise and nutritional counseling, but physicians may
underestimate the potential effectiveness of such counseling
techniques (88) and the other tools listed in Table 2.
As for the treatment of obesity, poor nutritional habits,
smoking, and sedentary lifestyles, patient non-adherence
can complicate physician attempts to modify psychosocial
risk factors. Helping patients to initiate behavior change is
challenging, requiring mastery of techniques and approaches
derived from psychology and the behavioral and social
sciences, and recommendations stemming from the Amer-
ican Heart Association’s Expert Panel on Compliance (89).
Representative techniques that cardiologists can use to
promote patient adherence are summarized in Table 3. For
example, the use of “micro goals” for poorly adherent
patients, such as those who may claim to not have the time,
willingness, or belief that they can exercise, can be applied.
In such patients, initiating a modest exercise program
requiring only 5 to 10 min of walking per day may be useful,
increasing exercise at a measured pace. All new behaviors
represent transitional intentional practices that initially re-
quire more intense physician monitoring and personal
feedback before becoming more automatic and habitual.
Because no single approach is effective for all patients,
mastery of multiple approaches and diverse strategies may
improve behavioral adherence rates typically reported in
clinical practice.
Although mastery of techniques to promote adherence
may be highly desirable, these add to the time, diligence,
Table 1. Suggested Open-Ended Questions to Screen for
Psychosocial Risk Factors
1. How would you describe your energy level?
2. How have you been sleeping?
3. How has your mood been recently?
4. What kind of pressure have you been under at work or at home?
5. What do you do to unwind after work or at the end of the day? Do
you have difficulty unwinding?
6. Who do you turn to for support?
7. Are there any personal issues that we have not covered that you
would like to share with me?
JACC Vol. 45, No. 5, 2005
et al.
March 1, 2005:637–51
Psychosocial Factors and CAD
training, and complexity required to manage multiple risk
factors in cardiac practice. As a consequence, cardiologists
may rely on a nurse or other qualified office personnel, an
organized community or hospital program, and/or comple-
mentary instructional material to assist them in managing
psychosocial risk factors, particularly for the more intense
interventions noted in Table 3.
Results of behavior and psychopharmacologic interven-
tion trials. A variety of behavioral and psychosocial inter-
ventions have been implemented in cardiac patients, includ-
ing exercise training, psychosocial interventions as part of
multifactorial risk factor modification, organized psychoso-
cial interventions designed to reduce psychosocial risk fac-
tors, and psychopharmacotherapy. The results of cardiac
outcome studies involving these approaches are reviewed
Exercise is commonly recommended by cardiologists to
promote both primary and secondary CAD prevention, but
evidence suggests that exercise may also modify psychosocial
risk factors, including depression. For instance, cross-
sectional studies of both medical populations and healthy
cohorts have consistently demonstrated lower depression
scores among those who are most active. The ability of
exercise to reduce depression also has been demonstrated in
randomized controlled trials, although many of these studies
have had methodologic limitations (90). More recently, a
randomized controlled comparison between antidepressant
medication versus exercise was performed in a group of 156
men and women with depression (91). After 16 weeks,
exercise was just as effective as sertraline hydrochloride in
reducing depressive symptoms. Follow-up of these patients
after six months revealed a low rate of relapse in the exercise
group (92). Although the study may have had some meth-
odologic limitations, these intriguing data suggest the need
for additional prospective trials.
The utility of organized psychosocial interventions has
been most commonly assessed by evaluating their incremen-
tal impact upon prognosis among patients referred to formal
cardiac rehabilitation programs. For instance, Linden et al.
(93) performed a meta-analysis of 23 randomized controlled
Table 2. Behavioral and Medical Interventions for Psychosocial Risk Factors
Type of Intervention Targeted Condition
Intensity of Intervention
Less Intense* More Intense
Exercise training Psychologic distress Exercise prescription plus general guidelines Supervised exercise
Nutritional counseling Management of stress
by overeating
Provide nutritional advice Supervised dietary instruction,
weight management, and
behavior modification
Relaxation training General stress and stress
caused by specific
Advise patient to initiate relaxation training;
provide audiotapes, videotapes, or
instructional scripts
Teach muscle relaxation, imagery,
autogenic training,
diaphragmatic breathing, or
Stress management General stress and stress
caused by specific
Recommend vacations, hobbies, yoga,
relaxing music, pets, or pleasurable
Teach behavioral strategies (e.g.,
problem-solving, self-
monitoring, appropriate goal-
setting, relapse-prevention
Social support Poor structural or
functional support
Provide specific social suggestions (e.g., join
walking groups or engage in socially
altruistic activities)
Use staff as a support base, enroll
patient in support group, or
facilitate family involvement
Health information Specific stress situations
(e.g., at work or
home) or low health
Provide situation-specific information in
form of book, articles, pamphlet,
audiotapes, videotapes, or Web sites
Discuss and answer patient
questions regarding materials
related to health and treatment
*Most amenable to direct cardiologist management.
Table 3. Steps to Promote Effective Adherence to Behavioral
1. Use clear and effective communication, including making
recommendations that are as specific and simple as possible.
2. Schedule follow-up visits to check adherence, especially during the
early practice phase, as opposed to the later, more ingrained habit
3. Provide a motivating rationale for the patient’s treatment regimen,
with consideration of explanations that befit the patient’s health
4. Follow oral suggestions with written ones to reinforce the
cardiologist’s message and aid memory and concentration.
5. Begin with “micro” goals for patients who are resistant to behavior
change or who have fewer available personal resources.
6. Help patients establish realistic goals and expectations.
7. Involve patients in tailoring behavioral suggestions rather than
dictating change.
8. Suggest activities that are commensurate with patients’ abilities and
that provide positive feedback (factors that tend to promote a sense
of pleasure).
9. Openly and candidly explore potential patient barriers to adherence
(such as lack of personal motivation, time, family support, facilities,
or knowledge; fears; job, home or other pressures; and cultural
issues) and assist patients with problem-solving and developing
strategies (e.g., self-monitoring approaches, written agreements, and
relapse prevention) at the time of recommendations.
10. Refer patients with poor structural or functional social support to
programs or activities that will enhance adherence by providing
social support.
646 Rozanski
et al.
JACC Vol. 45, No. 5, 2005
Psychosocial Factors and CAD
March 1, 2005:637–51
trials that evaluated the impact associated with adding
psychosocial interventions to standard cardiac rehabilitation
regimens. During the first two years of follow-up, lack of
psychosocial intervention was associated with greater rates
for mortality and recurrent infarction. In a separate meta-
analysis of psychosocial interventions and cardiac rehabili-
tation, Dusseldorp et al. (94) observed differential effects
depending on the efficacy of the psychosocial intervention.
When psychologic distress was reduced, the odds ratio for
mortality and recurrent MI also was reduced, but when no
reduction in psychologic stress occurred, mortality was
higher in intervention than in control rehabilitation pa-
tients. Along these lines, recent data suggest that the failure
to respond to psychosocial interventions may identify a
subgroup of patients who are particularly susceptible to
adverse clinical events (95).
The utility of stand-alone psychosocial interventions has
also been evaluated in five large-scale behavioral interven-
tion trials in cardiac patients, with mixed results. The
Recurrent Coronary Prevention Project Study was a group
therapy behavior modification program that succeeded in
decreasing both Type A behavior and negative affect and
also reduced the rates of cardiovascular mortality and
nonfatal MI (96). The Ischemic Heart Disease study was a
second successful intervention trial, using a unique home-
based stress-reduction program to reduce cardiac events
(97). Two other large trials did not reduce subsequent
cardiac events in the treatment groups, but neither inter-
vention successfully reduced psychosocial distress (98,99).
In fact, one of these trials was a follow-up of the approach
used in the Ischemic Heart Disease trial, and secondary
analysis of the data from this trial revealed that the results
could be attributed to inadequate psychologic intervention
in the experimental group (100). Indeed, cardiac mortality
was significantly reduced at one year among the subgroup of
experimental treatment patients who experienced an early
reduction in psychologic distress. The Enhancing Recovery
in Coronary Heart Disease Patients (ENRICHD) study
was the fifth and largest stand-alone psychosocial interven-
tion trial to date. It evaluated the effect of psychologic
treatment on the composite end point of all-cause mortality
and nonfatal MI in post-MI patients who were either
depressed and/or who reported low perceived social support
(101). Patients were randomized within four weeks of the
index MI, and treatment consisted of individual cognitive
therapy and, when possible, group therapy supplemented by
the use of a selective serotonin reuptake inhibitor (SSRI) for
severe or unremitting depression. Primary analyses found no
treatment differences in event-free survival (101). However,
analyses suggested only a modest difference in psychosocial
functioning between the treatment and control groups.
Psychosocial functioning was better than anticipated in the
control group, perhaps due to aggressive treatment as part of
routine medical care, including participation in cardiac
rehabilitation and psychologic therapies, thereby reducing
treatment group differences.
The paucity of stand-alone behavioral intervention trials
is partly due to the large sample sizes, long follow-up, and
high costs required of such trials. One way to reduce this
problem would be to use a three-stage approach for devel-
oping future interventions (Fig. 9) based on initial evalua-
tions of surrogate end points, such as measures of subclinical
atherosclerosis, myocardial ischemia, or flow-mediated di-
lation in smaller samples. Although there are limitations to
the use of surrogate end points, they can be effective for
developing new and innovative interventions for CAD
before launching large multicenter randomized trials.
The impact of psychopharmacologic therapies upon car-
diac outcomes represents an area of new interest. An initial
trial in this arena, the Sertraline Antidepressant Heart
Attack Randomized Trial (SADHART), demonstrated
that an SSRI (sertraline) could be safely prescribed for the
treatment of clinical depression in patients with known
CAD (102). However, this trial was not powered to evaluate
the influence of sertraline use on adverse cardiac events, as
it was a safety study. Cohen et al. (103) assessed antide-
pressant use in a large group of union health plan members
divided into those who were taking antidepressants and
those who were not. Participants using tricyclic antidepres-
sants had a more than a twofold increased risk of subsequent
MI, but there was no increase in adverse cardiac events
among the patients taking SSRIs. A recent case-control
study suggests that the protective effect of SSRIs may be
related to their degree of serotonin transporter affinity (104).
If confirmed, these findings suggest that SSRIs with high
serotonin transporter affinity may be the preferred pharma-
cologic means for treating depression in CAD patients
because of a biologic antiplatelet effect. A biologic protective
Figure 9. Proposed three-stage approach for developing behavioral inter-
vention trials. Stage 1 consists of a single-center evaluation of a specific
behavioral intervention. If successful, this intervention would be repeated at
multiple centers to assess the reproducibility of findings (stage 2). In both
stages, intermediate end points, such as change in carotid intimal wall
thickening or plaque size during carotid ultrasonography, would be used to
minimize necessary sample size and follow-up time. If reproducible results
are obtained during stage 2, a multicenter intervention trial would be
performed in stage 3, during which subjects would be observed for the
occurrence of hard cardiac events. IMT intima medial thickness.
JACC Vol. 45, No. 5, 2005
et al.
March 1, 2005:637–51
Psychosocial Factors and CAD
effect for depressed patients also may be introduced by the
use of statin therapy, as suggested by preliminary data
indicating that statin therapy lowers the high levels of
C-reactive protein associated with depression (105).
Future directions in behavioral interventions. Although
clinical practice guidelines advocate psychosocial interven-
tions in the context of cardiac rehabilitation programs, there
are no existing recommendations to guide the delivery of
psychosocial interventions in cardiac practice. Cardiac reha-
bilitation programs are widely recognized as effective in
providing multifactorial multidisciplinary treatment for car-
diac patients (106), but these programs are geographically
limited and third-party reimbursement policies may limit
patient participation. Overall, only 10% to 20% of eligible
cardiac patients are referred to cardiac rehabilitation pro-
grams (106). Thus, these programs represent an incomplete
delivery system for behavioral health care in cardiac practice.
Moreover, because of time constraints and lack of formal
training in behavioral techniques, many cardiologists may
find it difficult to provide psychosocial interventions to their
patients. In addition, even though cardiologists commonly
manage behavioral risk factors, such as physical inactivity,
poor diets, and smoking, lack of patient adherence to their
behavioral recommendations remains an important problem
(89) for which there is no easy solution. For all these
reasons, development of effective models for the provision of
psychologic and behavior services for cardiologists is
Accordingly, programs of various complexities have been
examined for their ability to improve physician management
of behavioral risk factors. These programs include providing
brief targeted physician training, monitoring patients by
telephone follow-ups, using nurse managers in cardiology
practice, and involving patients’ primary care physicians in
collaboration with mental health professionals such as psy-
chologists and psychiatrists. This latter approach has shown
promise for optimizing primary care physician management
of serious psychologic illnesses such as depression (107) and
panic disorder (108). Although critical assessment of these
approaches is beyond the scope of our review, a conceptual
approach for organizing behavioral health care interventions
for cardiac patients, based on the collective experience
garnered from these approaches, is shown in Figure 10.In
this approach, guidelines would be developed for stepped
collaborative care interventions, based on the complexity of
patients’ psychosocial and behavioral problems and their
ability to adhere to behavioral recommendations.
The difficulty in maintaining long-term behavioral
change among cardiac patients, coupled with the growing
epidemic in obesity and type 2 diabetes, makes it imperative
to develop more effective adherence strategies. Bellg (109)
suggests that standard efforts to optimize treatment adher-
ence most commonly view nonadherence as a form of
patient deficit that can be overcome by using external forms
of behavioral regulation, such as use of incentives or
structured provider support (Fig. 11). Such controlled be-
havior regulation may be very effective in eliciting short-
term behavioral change, but fostering patient autonomy is
critical to maintain long-term change (110). Conversely,
lack of internal motivation is a primary reason why patients
continue to engage in unhealthy shortsighted behaviors after
being informed about the long-term adverse consequences.
Approaches for fostering internal motivation are suggested
in Figure 11. An approach that incorporates many of these
principles is “motivational interviewing,” which is designed
to enhance patients’ intrinsic motivation to change un-
healthful behaviors by exploring and resolving ambivalence
Figure 10. Stepped collaborative care for cardiac patients depending on the
degree of psychological distress. Patients with mild psychologic distress
(step 1) would generally be treated by cardiologists without additional
collaborative intervention. The greater the degree of psychosocial distress,
the greater the need for collaborative intervention.
Figure 11. Approaches to promoting treatment adherence commonly
make use of techniques that involve external regulation, such as the use of
incentives or external network support. An alternative motivational para-
digm to such controlled behavior regulation focuses on attempts to
promote autonomy by fostering greater intrinsic motivation. Health
providers can foster this motivational process through a variety of steps,
including promoting patient ownership over recommended behavioral
changes (i.e., getting patients to voice their own reasons for initiating
change), helping patients to find a meaningful purpose for suggested
changes, formatting the specifics of behavior recommendations in a manner
most consistent with patients’ personal preferences, and recognizing what
coping mechanisms were best served by the old adverse behaviors (e.g.,
eating to decrease a sense of tension) and finding alternative solutions. At
the same time it is important to avoid ignoring a sense of conflict (which
can occur if behavioral recommendations are made without considering the
relationship of physician advice to patients’ internal values and preferences),
fostering a sense of coercion, or setting goals that are not readily achievable.
648 Rozanski
et al.
JACC Vol. 45, No. 5, 2005
Psychosocial Factors and CAD
March 1, 2005:637–51
to change (111). In this approach, the interviewer uses
empathy to help patients focus on discrepancies between
present behavior and long-term aspirations and values, and
avoids confrontation or playing an authoritarian role. This
approach has been applied to various behavior settings (99),
and is promising for treating cardiac patients. Other novel
strategies also may be used to create “teachable moments,”
for example, by showing patients personally relevant clinical
images of calcium deposits in their coronary arteries (112).
To date, this motivational approach has not yet been tested
in a sufficiently broad spectrum of patient populations.
Behavioral cardiology is an emerging field of clinical prac-
tice based on the recognition that adverse lifestyle behaviors,
emotional factors, and chronic life stress can all promote
atherosclerosis and adverse cardiac events. In recent years,
the pathophysiologic understanding of how psychosocial
risk factors contribute to atherosclerosis and adverse cardiac
events has broadened substantially. By contrast, the devel-
opment of effective therapeutic interventions both for mod-
ifying high-risk lifestyles and behaviors and for reducing
psychosocial risk factors for CAD patients remains a chal-
lenge. There have been few large-scale psychosocial inter-
vention trials, and the design of future trials is under debate.
Moreover, the lack of patient adherence to behavioral
interventions remains a significant problem. Nevertheless,
there is increasing evidence that interventions such as
exercise training, multifactorial secondary prevention efforts
that incorporate psychosocial interventions, and antidepres-
sant medication may be effective in treating psychologic
distress and improving outcomes among patients with
cardiac disease. Other preliminary evidence suggests that
stress management programs can improve surrogate markers
for CAD. Prospective investigations are needed to deter-
mine which patients may respond best to specific forms of
behavioral interventions and also define how cardiologists
can best collaborate with other health care providers and
health care delivery systems to reduce psychologic distress in
a cost-effective and practical manner. The field of behavioral
cardiology requires the development of such practical solu-
tions because the etiologic links among psychosocial risk
factors, behavioral risk factors, and atherosclerosis suggest
that cardiologists will consistently encounter many patients
with psychologic distress and unhealthy behaviors in clinical
We thank Elliot Brown, Tara Hannon, Elizabeth Mostof-
sky, Nina Rieckmann, Deborah A. Scheuer, and Kimberlee
Trudeau for their assistance and/or comments on prior
drafts. We also thank Mindy Weingarten for her secretarial
Reprint requests and correspondence: Dr. Alan Rozanski, Di-
vision of Cardiology, St. Luke’s-Roosevelt Hospital Center, 1111
Amsterdam Avenue, New York, New York 10025. E-mail:
1. Rozanski A, Blumenthal JA, Kaplan J. Impact of psychological
factors on the pathogenesis of cardiovascular disease and implications
for therapy. Circulation 1999;99:2192–217.
2. Lesperance F, Frasure-Smith N, Talajic M, Bourassa MG. Five-year
risk of cardiac mortality in relation to initial severity and one-year
changes in depression symptoms after myocardial infarction. Circu-
lation 2002;105:1049–53.
3. Rugulies R. Depression as a predictor for coronary heart disease. a
review and meta-analysis. Am J Prev Med 2002;23:51–61.
4. Matthews KA, Gump BB, Harris KF, Haney TL, Barefoot JC.
Hostile behaviors predict cardiovascular mortality among men en-
rolled in the Multiple Risk Factor Intervention Trial. Circulation
5. Matsumoto Y, Uyama O, Shimizu S, Michishita H, Mori R, Owada
T, Sugita M. Do anger and aggression affect carotid atherosclerosis?
Stroke 1993;24:983–6.
6. Julkunen J, Salonen R, Kaplan GA, Chesney MA, Salonen JT.
Hostility and the progression of carotid atherosclerosis. Psychosom
Med 1994;56:519–25.
7. Matthews KA, Owens JF, Kuller LH, Sutton-Tyrrell K, Jansen-
McWilliams L. Are hostility and anxiety associated with carotid
atherosclerosis in healthy postmenopausal women? Psychosom Med
8. Knox SS, Adelman A, Ellison RC, et al. Hostility, social support, and
carotid artery atherosclerosis in the National Heart, Lung, and Blood
Institute Family Heart Study. Am J Cardiol 2000;86:1086–9.
9. Angerer P, Siebert U, Kothny W, Muhlbauer D, Mudra H, von
Schacky C. Impact of social support, cynical hostility and anger
expression on progression of coronary atherosclerosis. J Am Coll
Cardiol 2000;36:1781–8.
10. Case RB, Moss AJ, Case N, et al. Living alone after myocardial
infarction. JAMA 1992;267:515–9.
11. Williams RB, Barefoot J, Califf R, et al. Prognostic importance of
social and economic resources among medically treated patients with
angiographically documented coronary artery disease. JAMA 1992;
12. Ruberman W, Weinblatt E, Goldberg J, et al. Psychosocial influences
on mortality after myocardial infarction. N Engl J Med 1984;311:
13. Berkman LF, Leo-Summers L, Howwitz RI. Emotional support and
survival after myocardial infarction: a prospective, population-based
study of the elderly. Ann Intern Med 1992;117:1003–9.
14. Gorkin L, Schron EB, Brooks MM, et al. Psychosocial predictors of
mortality in the cardiac Arrhythmia Suppression Trial-1 (CAST-1)
Am J Cardiol 1993;71:263–7.
15. Frasure-Smith N, Lesperance F, Gravel G, et al. Social support,
depression, and mortality during the first year after myocardial
infarction. Circulation 2000;101:1919–24.
16. Seeman TE, Syme L. Social networks and coronary artery disease: a
comparison of the structure and function of social relations as
predictors of disease. Psychosom Med 1987;49:341–54.
17. Marmot MG, Bosma H, Hemingway H, Brunner E, Stansfeld S.
Contribution of job control and other risk factors to social variations
in coronary heart disease incidence. Lancet 1997;350:235–9.
18. Baum A, Garofalo JP, Yali AM. Socioeconomic status and chronic
stress: does stress account for SES effects on health? In: Adler N,
Marmot M, McEwen BS, Steward J, editors. Socioeconomic Status
and Health in Industrial Nations: Social, Psychological, and Biolog-
ical Pathways, Annals of the New York Academy of Sciences. New
York, NY: New York Academy of Sciences, 1999;131–44.
19. Rosmond R, Bjorntorp P. Occupational status, cortisol secretory pattern,
and visceral obesity in middle-aged men. Obesity Res 2000;8:445–50.
20. Karasek R, Baker D, Marxer F, Ahlbom A, Theorell T. Job decision
latitude, job demands, and cardiovascular disease: a prospective study
of Swedish men. Am J Public Health 1981;71:694–705.
JACC Vol. 45, No. 5, 2005
et al.
March 1, 2005:637–51
Psychosocial Factors and CAD
21. Siegrist J. Adverse health effects of high-effort/low-reward condi-
tions. J Occup Health Psychol 1996;71:694 –705.
22. Johnson JV, Hall EM, Theorell T. Combined effects of job strain and
social isolation on cardiovascular disease morbidity and mortality in a
random sample of the Swedish male working population. Scand J
Work Environ Health 1989;15:271–9.
23. Kivimaki M, Leino-Arjas P, Luukkonen R, Riihimaki H, Vahtera J,
Kirjonen J. Work stress and risk of cardiovascular mortality: prospec-
tive cohort study of industrial employees (erratum appears in BMJ
2002;325:1386). BMJ 2002;325:857.
24. Johnson JV, Stewart W, Hall EM, Fredlund P, Theorell T. Long-
term psychosocial work environment and cardiovascular mortality
among Swedish men. Am J Public Health 1996;86:324–31.
25. Peter R, Siegrist J, Hallqvist J, Reuterwall C, Theorell T, Group
SS. Psychosocial work environment and myocardial infarction:
improving risk estimation by combining two complementary job
stress models in the SHEEP Study. J Epidemiol Community
Health 2002;56:294 –300.
26. Rosengren A, Hawkin S, Ounpuu S, et al. Association of psycho-
social risk factors with risk of acute myocardial infarction in 11,119
cases and 13,648 controls from 52 countries (the INTERHEART
study): case-control study. Lancet 2004;364:953– 62.
27. Matthews KA, Gump BB. Chronic work stress and marital dissolu-
tion increase risk of posttrial mortality in men from the Multiple Risk
Factor Intervention Trial. Arch Intern Med 2002;162:309–15.
28. Suadicani P, Hein HO, Gyntelberg F. Are social inequalities asso-
ciated with the risk of ischaemic heart disease a result of psychosocial
working conditions? Atherosclerosis 1993;101:165–75.
29. Lynch J, Krause N, Kaplan GA, Salonen R, Salonen JT. Workplace
demands, economic reward, and progression of carotid atherosclero-
sis. Circulation 1997;96:302–7.
30. Muntaner C, Nieto FJ, Cooper L, Meyer J, Szklo M, Tyroler HA.
Work organization and atherosclerosis: findings from the ARIC
study. Atherosclerosis Risk in Communities. Am J Prev Med
31. Nordstrom CK, Dwyer KM, Merz CN, Shircore A, Dwyer JH.
Work-related stress and early atherosclerosis. Epidemiology 2001;12:
32. Orth-Gomer K, Wamala SP, Horsten M, Schenck-Gustafsson K,
Schneiderman N, Mittleman MA. Marital stress worsens prognosis
in women with coronary heart disease: the Stockholm Female
Coronary Risk Study. JAMA 2000;284:3008 –14.
33. Coyne JC, Rohrbaugh MJ, Shoham V, Sonnega JS, Nicklas JM,
Cranford JA. Prognostic importance of marital quality for survival of
congestive heart failure. Am J Cardiol 2001;88:526–9.
34. Gallo LC, Troxel WM, Kuller LH, et al. Marital status, marital
quality, and atherosclerotic burden in postmenopausal women. Psy-
chosom Med 2003;65:952–62.
35. Lee S, Colditz GA, Berkman LF, Kawachi I. Caregiving and risk of
coronary heart disease in U.S. women: a prospective study. Am J Prev
Med 2003;24:113–9.
36. Schulz R, Beach SR. Caregiving as a risk factor for mortality: the
Caregiver Health Effects Study. JAMA 1999;282:2215–9.
37. Schwartz C, Meisenhelder JB, Ma Y, Reed G. Altruistic social
interest behaviors are associated with better mental health. Psycho-
som Med 2003;65:77885.
38. Mausner-Dorsch H, Eaton WW. Psychosocial work environment
and depression: epidemiologic assessment of the demand-control
model. Am J Public Health 2000;90:1765–70.
39. Batten S, Aslan M, Maciejewski PK, Mazure CM. Childhood
maltreatment as a risk factor for adult cardiovascular disease and
depression. J Clin Psychiatry 2004;65:249 –54.
40. Jones DJ, Bromberger JT, Sutton-Tyrrell K, Matthews KA. Lifetime
history of depression and carotid atherosclerosis in middle-aged
women. Arch Gen Psychiatry 2003;60:153– 60.
41. Everson SA, Lynch JW, Chesney MA, et al. Interaction of workplace
demands and cardiovascular reactivity in progression of carotid
atherosclerosis: population based study. BMJ 1997;314:553– 8.
42. Wilson PW, D’Agostino RB, Levy D, Belanger AM, Silbershatz H,
Kannel WB. Prediction of coronary heart disease using risk factor
categories. Circulation 1998;97:1837–47.
43. Yusuf S, Hawkin S, Ounpuu S, et al. Effect of potentially modifiable risk
factors associated with myocardial infarction in 52 countries (the IN-
TERHEART study): case-control study. Lancet 2004;364:937–52.
44. Rozanski A, Kubzansky LD. Psychological functioning and physical
health: a paradigm of flexibility. Psychosom Med 2005. In press.
45. Goldberger AL. Non-linear dynamics for clinicians: chaos theory,
fractals, and complexity at the bedside. Lancet 1996;347:1312–4.
46. Ryan RM, Frederick C. On energy, personality, and health: subjec-
tive vitality as a dynamic reflection of well-being. J Pers 1997;65:
529 65.
47. Gross JJ. Antecedent- and response-focused emotion regulation:
divergent consequences for experience, expression, and physiology. J
Pers Social Psychol 1998;74:224 –37.
48. Bonanno GA, Papa A, O’Neil K, Westphal M, Coifman K. The
importance of being flexible: the ability to enhance and suppress
emotional expression predicts long-term adjustment. Psychol Sci
49. Kant IJ, Bultmann U, Schroer KAP, Beurskems AJHM, Van
Amelsvoort LGPM, Swaen GMH. An epidemiological approach to
study fatigue in the working population: the Maastricht cohort study.
Occup Environ Med 2003;23;60:i32–9.
50. Fredrickson BL, Levenson RW. Positive emotions speed recovery
from the cardiovascular sequelae of negative emotions. Cogn Emo-
tion 1998;12:191–220.
51. Lawler KA, Younger JW, Piferi RL, et al. A change of heart:
cardiovascular correlates of forgiveness in response to interpersonal
conflict. J Behav Med 2003;26:373–93.
52. Gerin W, Pieper C, Levy R, Pickering TG. Social support in social
interaction: a moderator of cardiovascular reactivity. Psychosom Med
53. Cohen S, Doyle WJ, Turner RB, Alper CM, Skoner DP. Emotional
style and susceptibility to the common cold. Psychosom Med
54. Kubzansky LD, Sparrow D, Vokonas P, Kawachi I. Is the glass half
empty or half full? A prospective study of optimism and coronary
heart disease in the normative aging study. Psychosom Med 2001;
63:910 6.
55. Scheier MF, Matthews KA, Owens JF, et al. Optimism and
rehospitalization after coronary artery bypass graft surgery. Arch
Intern Med 1999;159:829–35.
56. Danner DD, Snowdon DA, Friesen WV. Positive emotions in early
life and longevity: findings from the nun study. J Pers Social Psychol
57. Carney RM, Freedland KE, Veith RC. Depression, the autonomic
nervous system, and coronary heart disease. Psychosom Med 2005. In
58. Weber-Hamann B, Hentschel F, Kniest A, et al. Hypercortisolemic
depression is associated with increased intra-abdominal fat. Psycho-
som Med 2002;64:274–7.
59. De Groot M, Anderson R, Freedland KE, Clouse RE, Lustman PJ.
Association of depression and diabetes complications: a meta-
analysis. Psychosom Med 2001;63:619 –30.
60. Schins A, Honig A, Crijns H, Baur L, Hamulyak K. Increased
coronary events in depressed cardiovascular patients: 5-HT
tor as missing link? Psychosom Med 2003;65:729–37.
61. Anisman H, Merali Z. Cytokines, stress, and depressive illness. Brain
Behav Immun 2002;16:513–24.
62. Esposito K, Nappo F, Marfella R, et al. Inflammatory cytokine
concentrations are acutely increased by hyperglycemia in humans:
role of oxidative stress. Circulation 2002;106:2067–72.
63. Rajagopalan S, Brook R, Rubenfire M, Pitt E, Young E, Pitt B.
Abnormal brachial artery flow-mediated vasodilation in young adults
with major depression (erratum appears in Am J Cardiol 2001;88:
722). Am J Cardiol 2001;88:196 8.
64. McCabe PM, Gonzales JA, Zaias J, et al. Social environment
influences the progression of atherosclerosis in the Watanabe herita-
ble hyperlipidemic rabbit. Circulation 2002;105:354 –9.
65. McElroy SL, Kotwal R, Malhotra S, Nelson EB, Keck PE Jr.,
Nemeroff CB. Are mood disorders and obesity related? A review for
the mental health professional. J Clin Psychiatry 2004;65:634–51.
66. Dallman MF, La Fluer S, Pecoraro NC, Gomez F, Houshyar H, Akana
SF. Minireview: glucorcorticoids—food intake, abdominal obesity, and
wealthy nations in 2004. Endocrinology 2004;145:2633– 8.
67. Bhatnagar S, Dallman M. Neuroanatomical basis for facilitation of
hypothalamic-pituitary-adrenal responses to a novel stressor after
chronic stress. Neuroscience 1998;84:1025–39.
650 Rozanski
et al.
JACC Vol. 45, No. 5, 2005
Psychosocial Factors and CAD
March 1, 2005:637–51
68. Lindley SE, Bengoechea TG, Schatzberg AF, Wong DL. Glucocor-
ticoid effects on mesotelencephalic dopamine neurotransmission.
Neuropsychopharmacology 1999;21:399 407.
69. Morgan D, Grant KA, Gage HD, et al. Social dominance in
monkeys: dopamine D
receptors and cocaine self-administration.
Nature Neurosci 2002;5:169–74.
70. Volkow ND, Wang GJ, Fowler JS, et al. “Nonhedonic” food
motivation in humans involves dopamine in the dorsal striatum and
methylphenidate amplifies this effect. Synapse 2002;44:175–80.
71. Wang GJ, Volkow ND, Logan J, et al. Brain dopamine and obesity.
Lancet 2001;357:354–7.
72. Kamarck TW, Everson SA, Kaplan GA, et al. Exaggerated blood
pressure responses during mental stress are associated with enhanced
carotid atherosclerosis in middle-aged Finnish men: findings from the
Kuopio Ischemic Heart Disease Study. Circulation 1997;96:3842–8.
73. Matthews KA, Owens JF, Kuller LH, Sutton-Tyrrell K, et al. Stress
induced pulse pressure change predicts women’s carotid atheroscle-
rosis. Stroke 1998;29:1525–30.
74. Suarez EC, Kuhn CM, Schanberg SM, Williams RB, Jr., Zimmer-
mann EA. Neuroendocrine, cardiovascular, and emotional responses
of hostile men: the role of interpersonal challenge. Psychosom Med
1998;60:78 88.
75. Grippo AJ, Moffitt JA, Johnson AK. Cardiovascular alterations and
autonomic imbalance in an experimental model of depression. Am J
Physiol 2002;282:R1333–41.
76. Laugero KD, Gomez F, Manalo S, Dallman M. Corticosterone
infused intracerebroventricularly inhibits energy storage and stimu-
lates the hypothalamo-pituitary axis in adrenalectomized rats drink-
ing sucrose. Endocrinology 2002;143:4552– 62.
77. Scheuer DA, Bechtold AG, Shank SS, Akana SF. Glucocorticoids
act in the dorsal hindbrain to increase arterial pressure. Am J Physiol
2004;286:H458 67.
78. Scheuer DA, Bechtold AG. Activation of dorsal hindbrain glucocor-
ticoid receptors enhances the arterial pressure response to acute stress
(abstr). FASEB J 2004;18:A675.
79. Kessler RC, McGonagle KA, Zhao S, et al. Lifetime and 12-month
prevalence of DSM-III-R psychiatric disorders in the United States:
results from the National Comorbidity Survey. Arch Gen Psych
80. Fleet RP, Dupuis G, Marchand A, Kaczorowski J, et al. Panic
disorder in coronary artery disease patients with noncardiac chest
pain. J Psychosom Res 1998;44:81–90.
81. Kirmayer LJ, Robbins JM, Dworkin M, Yaffe MJ. Somatization and
the recognition of depression and anxiety in primary care. Am J
Psychiatry 1993;150:734 41.
82. Katon WJ, Von Korff M, Lin E. Panic disorder: relationship to high
medical utilization. Am J Med 1992;92:Suppl 1A:7S–11S.
83. Fleet RP, Dupuis G, Marchand A, Burelle D, Arsenault A, Beitman
BD. Panic disorder in emergency department chest pain patients:
prevalence, comorbidity, suicidal ideation, and physician recognition.
Am J Med 1996;101:371– 80.
84. DiMatteo MR, Lepper HS, Croghan TW. Depression is a risk factor
for noncompliance with medical treatment. Meta-analysis of the
effects of anxiety and depression on patient adherence. Arch Intern
Med 2000;160:2101–7.
85. DiMatteo, MR. Social support and patient adherence to medical
treatment: a meta-analysis. Health Psychol 2004;23:207–18.
86. Neugarten BJ. Adult personality: towards a psychology of the life
cycle. In: Neugarten BL, editor. Middle Age and Aging. Chicago,
IL: University of Chicago Press, 1968.
87. Whooley MA, Simon GE. Managing depression in medical outpa-
tients. N Engl J Med 2000;343:1942–50.
88. Joos SK, Hickam DH. How health professionals influence health
behavior: patient provider interaction and health care outcomes. In:
Glanz K, Lewis FM, Rimer BK, editors. Health Behavior and Health
Education: Theory Research and Practice. San Fransisco, CA:
Jossey-Bass, 1990;216 41.
89. Miller NH, Hill M, Kottke T, Ockene IS. The multilevel compliance
challenge: recommendations for a call to action. A statement for
healthcare professionals. Circulation 1997;95:1085–90.
90. Lawlor DA, Hopker SW. The effectiveness of exercise as an
intervention in the management of depression: systematic review and
meta-regression analysis of randomised controlled trials. Br Med J
91. Blumenthal JA, Babyak MA, Moore KA, et al. Effects of exercise
training on older patients with major depression. Arch Intern Med
92. Babyak M, Blumenthal JA, Herman S, et al. Exercise treatment for
major depression: maintenance of therapeutic benefit at 10 months.
Psychosom Med 2000;62:633–8.
93. Linden W, Stossel C, Maurice J. Psychosocial interventions for
patients with coronary artery disease: a meta analysis. Arch Intern
Med 1996;156:745–52.
94. Dusseldorp E, van Elderen T, Maes S, Meulman J, Kraaij V. A
meta-analysis of psychoeducational programs for coronary heart
disease patients. Health Psychol 1999;18:506 –19.
95. Carney RM, Blumenthal JA, Freedland KE, et al. Depression and
late mortality after myocardial infarction in the Enhancing Recovery
in Coronary Heart Disease (ENRICHD) Study. Psychosom Med
96. Friedman M, Thoresen CE, Gill J, et al. Alteration of type A
behavior and its effect on cardiac recurrences in postmyocardial
infarction patients: summary results of the Recurrent Coronary
Prevention Project. Am Heart J 1986;112:653– 65.
97. Frasure-Smith N, Prince R. The ischemic heart disease life stress
monitoring program: impact on mortality. Psychosom Med 1985;47:
98. Jones DA, West RR. Psychological rehabilitation after myocardial
infarction: multicenter randomized control trial. Br Med J 1996;313:
99. Frasure-Smith N, Lesperance F, Prince RH, et al. Randomized trial
of home-based psychosocial nursing intervention for patients recov-
ering from myocardial infarction. Lancet 1997;350:473–9.
100. Cossette S, Frasure-Smith N, Lesperance F. Clinical implications of
a reduction in psychological distress on cardiac prognosis in patients
participating in a psychosocial intervention program. Psychosom
Med 2001;63:257–66.
101. The ENRICHD Investigators. Effects of treating depression and low
perceived social support on clinical events after a myocardial infarc-
tion: the Enhancing Recovery in Coronary Heart Disease Patients
(ENRICHD) randomized trial. JAMA 2003;289:3106 –16.
102. Glassman AH, O’Connor CM, Califf RM, et al. Setraline treatment
of major depression in patients with acute MI or unstable angina.
JAMA 2002;288:701–9.
103. Cohen HW, Gibson G, Alderman MH. Excess risk of myocardial
infarction in patients treated with antidepressant medications: asso-
ciation with use of tricyclic agents. Am J Med 2000;108:2–8.
104. Sauer WH, Berlin JA, Kimmel SE. Selective serotonin reuptake
inhibitors and myocardial infarction. Circulation 2001;104:1894 8.
105. Lesperance F, Frasure-Smith N, Theroux P, Irwin M. The associa-
tion between major depression and levels of soluble intercellular
adhesion molecule 1, interleukin-6, and C-reactive protein in patients
with recent acute coronary syndromes. Am J Psychiatry 2004;
106. Ades PA. Cardiac rehabilitation and secondary prevention of coro-
nary heart disease. N Engl J Med 2001;345:892–902.
107. Katon W, Von Korff M, Line E, Simon G, et al. Stepped collaborative
care for primary care patients with persistent symptoms of depression: a
randomized trial. Arch Gen Psychiatry 1999;56:119 –1115.
108. Katon WJ, Roy-Byrne P, Russo J, Cowley D. Cost-effectiveness and
cost offset of a collaborative care intervention for primary care patients
with panic disorder. Arch Gen Psychiatry 2002;59:1098–104.
109. Bellg AJ. Maintenance of health behavior change in preventative
cardiology: internalization and self-regulation of new behaviors.
Behav Modif 2003;27:103–31.
110. Williams GC, Rodin GC, Ryan RM, Grolnick WS, Deci EL.
Autonomous regulation and long-term medication adherence in
adult outpatients. Health Psychol 1998;17:269 –76.
111. Miller WR, Rollnick S. Motivational Interviewing: Preparing People
To Change Addictive Behavior. New York, NY: Guilford, 1991.
112. O’Malley PG, Feuerstein IM, Taylor AJ. Impact of electron beam
tomography, with and without case management, on motivation,
behavioral change, and cardiovascular risk profile. A randomized
controlled trial. JAMA 2003;289:2215–23.
JACC Vol. 45, No. 5, 2005
et al.
March 1, 2005:637–51
Psychosocial Factors and CAD
    • "Low income and education levels can cause disadvantaged individuals to live in chronically stressful environments , with financial insecurity, negative life events, and emotional and cognitive factors as contributing fac- tors [3, 4]. Previous hypotheses have stated that exposure to stress from low SES results in altered physiological responses, especially with regard to immune, neuroendocrine and cardiovascular functioning394041. Not all measures of altered physiological responses were measured in the current study. "
    [Show abstract] [Hide abstract] ABSTRACT: Background Lower socioeconomic status has been linked to long-term stress, which can manifest in individuals as physiological stress. The aim was to explore the relationship between low socioeconomic status and physiological stress in Aboriginal and Torres Strait Islander Australians. Methods Using data from the eGFR Study (a cross-sectional study of 634 Indigenous Australians in urban and remote areas of northern and central Australia), we examined associations between resting heart rate and demographic, socioeconomic, and biomedical factors. An elevated resting heart rate has been proposed as a measure of sustained stress activation and was used as a marker of physiological stress. Relationships were assessed between heart rate and the above variables using univariate and multiple regression analyses. Results We reported a mean resting heart rate of 74 beats/min in the cohort (mean age 45 years). On multiple regression analysis, higher heart rate was found to be independently associated with Aboriginal ethnicity, being a current smoker, having only primary level schooling, higher HbA1c and higher diastolic blood pressure (model R2 0.25). Conclusions Elevated resting heart rate was associated with lower socioeconomic status and poorer health profile in Aboriginal and Torres Strait Islander Australians. Higher resting heart rate may be an indicator of stress and disadvantage in this population at high risk of chronic diseases.
    Full-text · Article · Dec 2016
    • "These external variables were selected based on theoretical reasons cited in the literature that highlights the link between these factors and CVD. The clinical evolution and progression of established CVD are related to a range of psychosocial factors, such as anxiety and depression , which may partially explain the progression and recurrence of these diseases [71][72][73][74]. In addition to this focus on negative factors, other studies have underlined the role of psychological variables that may act as protective factors that buffer the effects of CVD and progression. "
    [Show abstract] [Hide abstract] ABSTRACT: Many studies have focused on Type A and Type D personality types in the context of cardiovascular diseases (CVDs), but nothing is known about how these personality types combine to create new profiles. The present study aimed to develop a typology of Type A and Type D personality in two groups of patients affected by and at risk for coronary disease. The study involved 711 patients: 51.6% with acute coronary syndrome, 48.4% with essential hypertension (mean age = 56.4 years; SD = 9.7 years; 70.7% men). Cluster analysis was applied. External variables, such as socio-demographic, psychological, lifestyle, and clinical parameters, were assessed. Six groups, each with its own unique combined personality profile scores, were identified: Type D, Type A-Negatively Affected, Not Type A-Negatively Affected, Socially Inhibited-Positively Affected, Not Socially Inhibited, and Not Type A-Not Type D. The Type A-Negatively Affected cluster and, to a lesser extent, the Type D cluster, displayed the worst profile: namely higher total cardiovascular risk index, physical inactivity, higher anxiety and depression, and lower self-esteem, optimism, and health status. Identifying combined personality profiles is important in clinical research and practice in cardiovascular diseases. Practical implications are discussed.
    Full-text · Article · Sep 2016
    • "Elevated glucocorticoid and catecholamine levels antagonize the effects of insulin and also increase blood glucose concentration independent of their effects on insulin (Björntorp, 1997). Thus chronic over-secretion of these stress mediators may therefore contribute to the development of insulin resistance, overweight, and obesity (Vanltallie, 2002; Ozcan et al., 2004; Rozanski et al., 2005). Although it has been shown that the expression of insulin receptors (INSR) and glucose transporter-4 (GLUT4) are disrupted in insulin resistant rodents (Pessin and Saltiel, 2000), these changes in rats exposed to restraint stress are scarcely available in literature. "
    [Show abstract] [Hide abstract] ABSTRACT: The study investigated the potential alteration in the level of insulin and adiponectin, as well as the expression of insulin receptors (INSR) and glucose transporter 4 GLUT-4 in chronic restraint stress rats. Sprague-Dawley rats were randomly divided into two groups: the control group and stress group in which the rats were exposed to one of the four different restraint stressors; 1 h, twice daily for a period of 7 days (S7D), 14 days (S14D) and 28 days (S28D). Glucose tolerance and insulin sensitivity were evaluated following the final stress exposure. ELISA were performed to assess the level of insulin and adiponectin as well as expression of INSR and GLUT4 protein in skeletal muscle. Plasma corticosterone level was also determined as a marker of stress exposure. Restraint stress for 7 days caused transient glucose intolerance, while S14D rats demonstrated increased glucose intolerance and insulin insensitivity. However, restraint stress for 28 days had no effect on glucose tolerance, but did cause an increase in glucose response to insulin challenge. The serum level of adiponectin was significantly (p< 0.05) lower compared with the control value while insulin remained unchanged except at in S28D rats that had a significant (p<0.05) increase. The expression of INSR and GLUT4 receptors were significantly (p< 0.05) decreased in the skeletal muscle of restraint stress exposed rats. There was a significant (p< 0.05) increase in the plasma corticosterone level of the stress rats compared with their control counterparts. Restraint stress caused glucose intolerance and insulin insensitivity in male Sprague-Dawley rats, which becomes accommodated with prolonged exposure and was likely related to the blunted insulin signalling in skeletal muscle.
    Full-text · Article · Aug 2016
Show more

Recommended publications

Discover more