OCTOBER 2011 DELHI PSYCHIATRY JOURNAL Vol. 14 No.

Original Article

A Descriptive Study to Assess the

Psychiatric Morbidity among Patients with
Coronary Artery Disease
Sandeep Chopra, Arvind Sharma, Prashant Paul Verghese, Chris Baby P
Department of Psychiatry, Christian Medical College & Hospital, Ludhiana

ABSTRACT
Background: Symptoms of depression and anxiety are known to be associated with
cardiac events. Anxiety is an independent predictor of both cardiac events and increased
health care consumption and accounts for the relationship between depressive symptoms
and prognosis. Psychological Symptoms need to be considered in the risk stratification and
treatment of coronary artery disease (CAD) patients. Materials and Method: A non
experimental research design was utilized to assess the psychiatric morbidity in a sample
of 60 patients with CAD, attending the outpatient clinic of the Department of Cardiology
of a tertiary hospital in Punjab. Symptom checklist -80 was used to assess the psychological
deficits. Analysis and interpretation of the data was done using descriptive and inferential
statistics. Results: Out of 60 patients, 39.9% of patients had symptoms of moderate
depression and 7.70% had severe depressive symptoms. 12.5 % patients had severe anxiety
and 39.41% had moderate anxiety symptoms. Anger hostility in both moderate and severe
range was observed in 10.14 % of the subjects. Moderately severe depression and anxiety
was higher in males as compared to females and the difference was statistically significant.
(p=0.024 & p=0.0424). Females had significantly higher anger hostility than males
(p=0.0176). Mean score on additional symptoms was 2.71± 4.14 and 5.21± 4.52 among
male and female patients respectively. On an average, depression and anger hostility
were significantly more in patients with co morbid medical illnesses (p=0.0066), recent
invasive procedure undertaken (p=0.03) and who were living alone (p=0.039).
Conclusions: Our study concludes that CAD can lead to various psychiatric disorders,
which further can complicate the course and outcome of the primary disease itself.
Moreover the cost of treatment of CAD and its complication can further worsen the
psychiatric disorder. Psychiatric disorders also lead to poor compliance and follow up in
CAD patients.
Key words: Psychiatric morbidity, CAD, symptom check list (SCL)-80

Introduction aggregation.6 It is unclear whether treatment of

Negative emotions, such as depression and depression may lead to a decrease in post-MI
anxiety, have been related to coronary artery disease mortality.7-11 Negative emotions may also have an
(CAD)1-3 and a poor prognosis after myocardial adverse effect on other “softer” end points such as
infarction (MI). 4 Possible mechanisms linking angina, quality of life, and incomplete recovery.12
negative emotions to the post-MI period include The effect of depression on angina and re-
increased vulnerability to arrhythmias as a result of hospitalization is even more strongly established
increased sympathetic tone5 and increased platelet than its effect on mortality.13
Depression is frequently studied and
Delhi Psychiatry Journal 2011; 14:(2) © Delhi Psychiatric Society 237
DELHI PSYCHIATRY JOURNAL Vol. 14 No.2
considered as a pathogenic factor in post-MI
patients 8 . Minor depression and depressive
symptoms also have a negative effect on prognosis
in cardiac patients9. The increased risk of cardiac
events may extend to patients with symptoms of
negative affect other than depression10,11. Depre-
ssion has been identified as a risk factor for the
development of cardiovascular disease and for
recurrent cardiac events and mortality among those
with established coronary artery disease (CAD).14,15
Depression is commonly present in patients
with CAD and is independently associated with
increased cardiovascular morbidity and mortality.
Screening tests for depressive symptoms should be
applied to identify patients who may require further
assessment and treatment. This multispecialty
consensus document reviews the evidence linking
depression with CAD and provides recommen-
dations for healthcare providers for the assessment,
referral, and treatment of depression.16
Recognition and treatment of major depression
is crucial, especially for patients after MI. Not only
do depressed patients experience great difficulties
in problem solving and coping with challenges, but
depression adversely affects compliance with
medical therapy and rehabilitation and increases
medical comorbidity. Minor depressive disorder is
also associated with significant functional
impairment and substantial increases in health care
utilization.17,18
There is a growing body of research on
psychosocial factors in patients who have
undergone heart transplantation (HTx).19 Findings
indicate high prevalence rates for moderate and
severe levels of depression in the waiting period20,
in the first year after successful HTx21, and on long-
term follow-up22,23. Earlier studies have reported
that coping styles and social support may be
significant predictors of morbidity and mortality in
patients awaiting HTx24,25 and also after successful
HTx.26-28
Among CAD patients the rates of depression
range from 7%–40%. In this population, depression
is associated with poorer medical outcomes and
quality of life, medication non adherence and is a
consistent predictor of mortality post MI. Patients
who have suffered MI are also at risk for
experiencing symptoms of Post Traumatic Stress
Disorder. In the first year after MI, as many as 8%–
238 Delhi Psychiatry Journal 2011; 14:(2) © Delhi Psychiatric Society
OCTOBER 2011
25% of patients develop this disorder, which is also
associated with poorer medical outcomes.
Material and Methods
For the present study, a non experimental
research design was utilized to assess the psychiatric
morbidity among CAD patients. The study included
60 subjects randomly selected from the CAD
patients attending the outpatient clinic of the
Department of Cardiology. Selection of field was
done because of reasons such as familiarity with
the setting, availability of subjects, administrative
approval, and economy of time, money, energy and
willingness of study subjects to participate in the
study. CAD included conditions like stable angina,
unstable angina and post MI.
Informed consent was taken. Purposive
sampling technique was used to collect the data. A
detailed medical and psychiatric history was taken
and cardiovascular examination done for each
patient. Sociodemographic profile was recorded.
History of any invasive cardiac procedure in the
past like coronary artery bypass graft (CABG),
percutaneous transluminal coronary angioplasty
(PTCA) and coronary angiography was taken. The
independent variables included age, gender, marital
status, duration of illness, number of admissions in
last one year, and the monthly expenditure on
medicine was also recorded.
A Symptom Checklist-80 (SCL-80) was used
to assess the psychological deficit. Standard scoring
patterns were used to assess the outcome. SCL -80
score were later subjected to ICD-10 criterion to
evaluate the clinical psychiatric diagnosis. Analysis
and interpretation of data was done by using
descriptive and inferential statistics as mean, mean
percentage, S.D, T-test, Mann Whitney and Chi
square test.
Results
The study included 60 patients, 41 males and
19 females. 30 patients had clinical diagnosis of
unstable angina, 34 were post MI and 4 had stable
angina. 25% of patient had average an duration of
CAD of 3 years and 28.33% of 10 years. More than
two admissions were noted in 46% subjects while
50.70% of patient had two admissions in last one
year due to decompensation in cardiac status. 55%
of the patients had undergone at least one invasive
OCTOBER 2011 DELHI PSYCHIATRY JOURNAL Vol. 14 No.2

intervention because of CAD. 55% of patients had

monthly income of more than Rs 20,000, while only
10% had earning of less than Rs 5,000 per month.
66.67% of the patients were spending up to Rs 2,000
per month for CAD medication.
Multiple comorbid medical illnesses like
diabetes mellitus and hypertension were seen in
37% patients. None had premorbid psychiatric
illness.
Symptoms of moderate depression was seen in

Socio-Demographic Profile
Male Total % Female Total %
Marital Status
Married 36 41 87.80488 16 19 84.21053
Unmarried 0 41 0 19 0
Widower 5 41 12.19512 3 19 15.78947
Av. Amount Spent on Med per Month
< 1000 3 41 7.317073 1 19 5.263158 5.263158
1000 - 2000 26 41 63.41463 14 19 73.68421 73.68421
> 2000 12 41 29.26829 4 19 21.05263 21.05263
Av. Income per month
< 5000 3 41 7.317073 3 19 15.78947
5 - 10,000 4 41 9.756098 2 19 10.52632
10-15,000 2 41 4.878049 5 19 26.31579
15-20,000 3 41 7.317073 4 19 21.05263
> 20,000 29 41 70.73171 4 19 21.05263
Clinical Diagnosis
Stable Angina 2 41 4.878049 2 19 10.52632
Unstable Angina 15 41 36.58537 5 19 26.31579
Post MI 24 41 58.53659 12 19 63.15789
Duration of Illness 10 41 24.39024 2 19 10.52632
< 1 year 10 41 24.39024 5 19 26.31579
1-3 yrs 6 41 14.63415 4 19 21.05263
4-6 yrs 6 41 14.63415 0 19 0
7-9 yrs 9 41 21.95122 8 19 42.10526
> 10 yrs 10 41 24.39024 2 19 10.52632
No. of adm in last year
Nil 7 41 17.07317 2 19 10.52632
One 20 41 48.78049 5 19 26.31579
Two 10 41 24.39024 5 19 26.31579
Multiple 4 41 9.756098 7 19 36.84211
Delhi Psychiatry Journal 2011; 14:(2) © Delhi Psychiatric Society 239
DELHI PSYCHIATRY JOURNAL Vol. 14 No.2
39.9% subjects whereas 7.70% had severe
depressive symptoms. 12.5% patients had severe
anxiety and 39.41% had moderate anxiety
symptoms. Anger hostility in both moderate and
severe range was observed in 10.14 % subjects.
Moderately severe depression and anxiety was
higher in males as compared to females and the
difference was statistically significant. (p = 0.024
and p = 0.0424). Females had significantly higher
anger hostility than males (p = 0.0176). Mean score
on additional symptoms was 2.71 ± 4.14 and 5.21
± 4.52 among male and female patients respectively.
On an average, depression and anger hostility were
significantly more in patients with comorbid
medical illnesses (p = 0.0066), recent invasive
procedure undertaken (p = 0.03) and who were
living alone (p = 0.039). On other subscale of SCL-
80, no major abnormality was found.
Discussion
There is a well established relationship between
anxiety, depression and CAD30, which may be due
in part to the poor risk factor profiles, including
diet, smoking and exercise. Previous studies have
shown that cardiac rehabilitation improves
symptoms of anxiety and depression in patients with
CAD31,32. The prevalence of depression in CAD
patients ranges from 16% to 25% and from 10% to
29% for anxiety disorders. Anxiety and depression
can affect heart rhythms and blood pressure, elevate
insulin and cholesterol levels and increase the
incidence of smoking, with highly anxious patients
at 3-6 times greater risk of MI and sudden death.33
A comprehensive study, the National
Comorbidity Study, reported lifetime prevalence
rates of major depression and dysthymia of 13%
and 5%, respectively34. Point prevalence rates of
major depression in primary care outpatients range
from 2% to 16% and from 9% to 20% for all
depressive disorders35,36 and are even higher in
medical inpatients; 8% for major depression and
15% to 36% for all depressive disorders.37,38
Frasure-Smith and colleagues38,39 found depre-
ssion to be a significant predictor of mortality (p -
0.001) in 222 patients 6 months after MI. Depre-
ssion remained a significant predictor of mortality
(p – 0.01), even after multivariate statistical
methodology was used to factor out the effects of
left ventricular dysfunction and previous MI.
240 Delhi Psychiatry Journal 2011; 14:(2) © Delhi Psychiatric Society
OCTOBER 2011
Weiss and Marmar found that on multiple
logistic regression analysis depression was
significantly related to 18- month cardiac mortality,
even after controlling for other significant
multivariate predictors of mortality (previous MI,
Killip class, frequency of premature ventricular
contractions [PVCs]) (p = .003).41
The IES is a 15-item self-report questionnaire
consisting of two subscales measuring experiences
of avoidance and intrusion related to the traumatic
event. Good reliability and validity have been
reported in multiple studies. A high score on the
IES was shown to be associated with increased risk
for non adherence to medical recommendations,
cardiovascular admissions, and a higher cardio-
vascular risk profile in patients with cardiovascular
illnesses40, 41.
In our study 39.9% of patients had symptoms
of moderate depression and 7.70% had severe
depressive symptoms. 12.5 % patients had severe
anxiety and 39.41% had moderate anxiety
symptoms. As compared to females, males had more
moderately severe depression (p=0.024) and anxiety
(p = 0.0424).
Depression as a Risk Factor for Ischemic Heart
Disease. The notion that having a psychiatric illness
such as major depression increases one’s risk for
developing ischemic heart disease remains
controversial and has been often intuitively
“explained” by the hypothesis that persons with
psychiatric disorders generally have other risk
factors for the development of CAD. Studies with
the most rigorous methods that are prospective in
design, have used structured clinical interviews or
diagnostic instruments, have included other risk
factors for CAD in their analysis (such as
hypertension, hypercholesterolemia, nicotine and
other substance abuse, and physical inactivity), and
controlled for demographic factors (such as age,
sex, and socioeconomic status). Nearly all the recent
studies document increased cardiovascular
morbidity and mortality in patients with depressive
symptoms or major depression, thereby implicating
depression as an independent risk factor in the
pathophysiological progression of CAD, rather than
merely a secondary emotional response to the
illness. Such large epidemiologic studies may use
self report instruments, rather than clinical
interviews, to evaluate the importance of psycholo-
OCTOBER 2011
gical factors in predicting CAD. Assessments of this
type are typically added to large, multiple risk factor
studies in which population-based samples are
followed up prospectively. The advantage of using
“dimensional” measures of depression (rather than
a categorical diagnosis of major depression) is the
increased statistical power to detect smaller
“effects.” However, such epidemiologic data are not
equivalent to clinical data42.
Pathophysiological Mechanisms of depression
Considerable evidence indicates that depre-
ssion has both behavioral and direct pathophysio-
logical effects. With respect to behavioral
mechanisms, depression is associated with both
unhealthy lifestyle behaviors, such as smoking, and
poor patient compliance. Direct pathophysiological
effects of depression involve at least 3 mechanisms.
First, depression is accompanied by hypercorti-
solemia. Associated findings include attenuation of
the adrenocorticotropin hormone response to
corticotropin-releasing factor administration,
nonsuppression of cortisol secretion after
dexamethosone administration, and elevated
corticotropin-releasing factor concentrations in the
cerebrospinal fluid of depressed patients.
Second, depressed individuals may develop
significant impairments in platelet function,
including enhanced platelet reactivity and release
of platelet products such as platelet factor 4 and ß-
thromboglobulin. The combination of hypercorti-
solemia and enhanced platelet function establishes
the theoretical basis for explaining the
proatherogenic effects of depression. In addition,
reduced heartrate variability and impaired vagal
control have been reported among depressed
patients. These findings suggest that depressed
patients may also be subject to enhanced
arrhythmogenic potential42.
Pathophysiological Mechanism of anxiety
The association between anxiety and sudden
death, but not MI, suggests that ventricular
arrhythmias may be the mechanism for cardiac
death among individuals with anxiety disorders. In
support of this hypothesis, it has been observed that
individuals with anxiety disorders have reduced
heart rate variability. Hence, there may be a
pathological alteration in cardiac autonomic tone.
Delhi Psychiatry Journal 2011; 14:(2) © Delhi Psychiatric Society
DELHI PSYCHIATRY JOURNAL Vol. 14 No.2
This alteration could involve either increased
sympathetic stimulation, which has been linked to
the occurrence of arrhythmias and sudden death, or
impaired vagal control, which has also been linked
to increased cardiac mortality. With respect to the
latter possibility, reduced vagal control has been
linked to impaired, vagally mediated baroreflex
control of the heart. Such impairment appears to be
a particularly important risk factor for sudden
death. Along these lines, a recent study reported
reduced baroreflex cardiac control in patients
with anxiety, but prospective work is needed to
determine whether this is a common operative
mechanism for sudden deaths among patients with
anxiety syndromes. Individuals with anxiety
disorders are prone to unhealthier lifestyle
behaviors; however, the lack of correlation between
anxiety syndromes and myocardial infarction (a sign
of underlying atherosclerosis) suggests that, at least
among initially healthy individuals, this behavioral
association is not a significant pathogenic
mechanism. It is conceivable, nonetheless, that this
behavioral association could be of importance
among CAD patients manifesting anxiety42.
Brydon et al, found participants with higher
hostility scores had heightened systolic and diastolic
blood pressure (BP) reactivity to tasks (both P <
.05), as well as a more sustained increase in systolic
BP at 2 h post-task (P = .024), independent of age,
BMI, smoking status, medication, and baseline BP.
Hostility was also associated with elevated plasma
interleukin-6 (IL-6) levels at 75 min (P = .023) and
2 h (P = .016) post stress and was negatively
correlated with salivary cortisol at 75 min (P =
.034). Hostility was measured using a 39-item
abbreviated version of the Cook Medley Hostility
Scale (CMHS)43.
In our study anger hostility was observed in
10.14 % in both moderate and severe range. Females
had significantly higher anger hostility as compared
to males (p = 0.0176). ). Mean score on additional
symptoms was 2.71 ± 4.14 and 5.21 ± 4.52 among
male and female patients respectively. On an
average, depression and anger hostility were
significantly more in patients with comorbid
medical illnesses (p = 0.0066), recent invasive
procedure undertaken (p = 0.03) and those who
were living alone (p = 0.039). On other subscale
of SCL-80, no major abnormality was found.
241
DELHI PSYCHIATRY JOURNAL Vol. 14 No.2
Pathophysiological mechanism of anger hostility
Hostility may affect atherogenic activity by
behavioral mechanisms. Hostility is associated with
a higher concentration of unhealthy lifestyle
behaviors, including smoking, poor diet, obesity,
and alcoholism. Hostile individuals are also more
likely to manifest other psychosocial factors
associated with CAD, such as social isolation. An
accumulating body of evidence also suggests
multiple pathophysiological mechanisms by which
hostility may be linked to CAD. For example,
compared with nonhostile individuals, hostile
subjects manifest higher heart rate and blood
pressure responses to physiological stimuli, such
as mental tasks,as well as higher ambulatory blood
pressure levels during daily-life activity. Also,
evidence suggests that hostile individuals are more
likely to exhibit hypercortisolemia and high
levels of circulating catecholamines, as well as
diminished mononuclear leukocyte ß-adrenergic
receptor function. Preliminary data suggest that
hostile individuals may also manifest
diminished vagal modulation of heart function and
increased platelet reactivity42.
Like other psychosocial factors, social support
influences the extent to which individuals engage
in such high-risk behaviors as smoking, fatty diet
intake, and excessive alcohol consumption. In
addition, social factors may exert direct patho-
physiological effects, including hypercortisolemia.
Animal studies have reported an association
between social isolation and hypercortisolemia and
reversible increases in resting heart rates among
cynomolgus monkeys, depending on the presence
or absence of social separation. Similarly, human
studies have demonstrated an inverse relation-
ship between the quality of social relationships and
urinary levels of epinephrine and between the
degree of social support and resting heart rates.
Elevated resting heart rates may constitute a sign
of altered autonomic arousal. The presence of social
support may also attenuate blood pressure and
heart rate responses to stressful stimuli in humans. It
suggests that social factors promote atherogenesis
through activation of the autonomic nervous
system44.
Socioeconomic status was found to be
negatively associated with the psychological
outcomes and quality of life among cardiac patients.
242 Delhi Psychiatry Journal 2011; 14:(2) © Delhi Psychiatric Society
OCTOBER 2011
Socioeconomic inequalities should be taken into
account when designing suitably-adapted
interventions focusing on psychosocial factors
among cardiac patients.
A structured interview was conducted with 362
patients (32 % women, mean age 56 ± 7.3 years)
referred for coronary angiography with GHQ-28
was used to measure psychological well-being, the
SF-36 for perceived mental health status. Income
and education indicated socioeconomic position.
Logistic regressions were employed, adjusted for
age, gender, functional status and severity of
disease. Patients with low income or education had
a higher probability of having poor psychological
well-being compared to participants with high
income or education (OR 5.5,CI 2.32-12.80; OR
3.1,CI 1.52-6.37 resp.), and were also more likely
to have worse mental health status (OR2.9,CI 1.02-
8.51;OR 4.8,CI1.36-16.99 resp.), and low quality
of life (OR 2.9,CI 1.02-8.51;OR 4.8,CI 1.36-16.99
resp.)45.
In our study 46% of the total patients had more
than two admissions in last one year whereas
50.70% of the patients had two admissions in last
one year. 55% of the patients underwent at least
one invasive intervention because of CAD. 55% of
patients had monthly income of more than Rs
20,000, while only 10% had earning of less than
Rs 5000 per month. 66.67% of the patients were
spending up to Rs 2000 per month for CAD
medication.
Future Directions
The principal unanswered questions in this
field remain primarily prognostic, etiologic, and
treatment related: By what mechanisms do
dysphoria and other depressive symptoms affect the
cardiovascular and thrombotic systems — and will
treatment of depression prevent or reduce CVD?
Because sociodemographic and medical variables
do not reliably identify post-MI patients who are
depressed while hospitalized nor predict those who
will become depressed soon after hospital
discharge, identification of certain so-called
biologic markers associated with depression (such
as HPA axis or sympathoadrenal system
hyperactivity) might accurately identify those CAD
patients with prodromal or subsyndromal
depressive symptoms vulnerable to complications
OCTOBER 2011
or even early death after MI. Future studies should
focus on women to assess gender-specific
psychosocial and physiologic measures. Which
treatment modalities (psychotherapeutic vs
psychopharmacologic or a combination) will be
most effective in patients with recurrent or more
severe depression remains to be determined.
Treatment studies may also assess the relationship
between depression and subsequent compliance
with medication and risk factor modification for
CVD. Illumination of the interplay between central
nervous system, platelet, and cardiovascular
processes, particularly in those patients with CVD
and major depression, will undoubtedly lead to the
development of new treatment modalities that will
not only improve these patients’ quality of life but
potentially decrease their morbidity and improve
long-term survival rates.
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