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FRANCOIS LESPRANCE, MD
Objective: The natural course of elevated depressive symptoms or subthreshold depression in patients with an acute coronary
syndrome (ACS) is presented, as is the prognostic impact. Safe and effective psychological treatment options are desirable for
subthreshold depression in patients with ACS, should they prove tolerable, efficacious, and cost-effective to cardiologists and their
patients. To achieve this long-term goal, we propose focusing on 3 intermediate goals. First, we need to understand which symptoms
or patterns of symptoms (eg, fatigue, anhedonia, guilt feelings) are specifically predictive of ACS recurrence. Second, the
prevalence of known psychosocial vulnerabilities (proximal causes) of depressive disorders should be assessed in patients with
ACS, to understand better the etiology of these symptoms in these patients. Third, randomized controlled trials of vulnerabilityrelated, evidence-based psychological depression interventions in cardiac patients are needed. The ways in which psychological
proximal cause theories are relevant or irrelevantfor both the treatment of depressive symptoms in post-ACS patients and the
prevention of ACS recurrence are discussed. Key words: depression, acute coronary syndromes, psychosocial intervention.
CHD coronary heart disease; ACS acute coronary syndrome;
BDI Beck Depression Inventory.
INTRODUCTION
ven minor elevations in depressive symptoms (subthreshold depression, defined to include mood, somatic, and
interpersonal symptoms of depression, but not necessarily a
diagnosable depressive disorder) significantly increase the
risk of incidence of coronary heart disease (CHD) among
previously healthy participants or worsen the cardiac prognosis in patients with established CHD. The scientific evidence
is strongest for patients who have been hospitalized for an
acute coronary syndrome (ACS)that is, myocardial infarction or unstable angina (115).
Well-established theories of the psychosocial causes of
depression and their theory-related, evidence-based treatments
exist (16 20). However, these theories were formulated and
tested primarily on younger, psychiatric (depressive disordered), and treatment-seeking people rather than older, subthreshold depressed, post-ACS patients. Furthermore, as has
been previously found in psychiatric populations, there is
likely no single proximal depression cause that is inevitably or
necessarily present in post-ACS patients with depressive
symptoms. We suggest that the usefulness of various psychological depression treatments for post-ACS subthreshold depression will differ depending on the extent to which each of
these proximal causes presents in this specific population.
In this article, we outline current evidence for the natural
course of depressive symptoms after an ACS event and their
prognostic impact for ACS recurrence and cardiac death. We
then review 3 accepted depression etiologic theories (cognitive theory, behavioral theory, and interpersonal theory) that
all fulfill the following criteria: they have been tested for the
presence of their putative depression proximal cause in depressed patients, they have an associated evidence-based treatment protocol (2124), and they have been tested in elderly
patients of relevance for the majority of patients with ACS.
Each theory asserts that their proximal causes should apply
only to a subset of people with depression symptoms, because
depression itself is a heterogeneous disease (25). The applicability of the existing psychosocial depression theories and
their established treatment protocols to the population of ACS
patients is then discussed in light of the effects that such
treatments may have on preventing ACS recurrence and cardiac death, in addition to the effects on a general reduction in
depressive symptoms and related functional impairments (26).
Finally, alternative conceptualizations of subthreshold depressive symptoms in this patient population are discussed.
PROGNOSTIC VALUE OF DEPRESSIVE SYMPTOMS
FOR ACUTE CORONARY SYNDROME RECURRENCE
AND MORTALITY
Numerous studies have established that depression predicts
the incidence of CHD in previously healthy people. A recent
meta-analysis by Rugulies (15) reported that depression increases the risk of myocardial infarction or coronary death
(relative risk 1.64, 95% confidence interval 1.29 2.08,
p .001) and that the risk is not limited to patients with
clinical depression.
Similar findings have been reported in patients with established CHD. It appears that not only a psychiatric disorder
history but also the presence of mildly elevated depressive
symptoms, such as a Beck Depression Inventory (BDI) score
of 10 or higher, are associated with worse prognosis in patients recovering from ACS (9, 27). Indeed, there appears to
be a linear association between depressive symptoms at the
time of a myocardial infarction and the risk of subsequent
cardiac morbidity and mortality (6, 13). However, when accounting for naturalistic changes in the course of depressive
symptoms after the ACS event, the prognostic importance of
mild vs. severe depressive symptoms differs. A recent follow-up study by Lesperance et al. (14) reported the prognostic
importance of naturalistic improvement or deterioration of
depression symptoms over the period of 1 year postmyocardial infarction. In this study, improvements in depressive
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symptoms had only an independent positive impact on prognosis (5-year cardiac morbidity, and cardiac and noncardiac
mortality) in patients with initial BDI scores from 10 to 18
(mild depression symptoms). Among these patients, the
greater the improvement in depression symptoms, the better
the long-term prognosis. However, 1-year depression symptom improvement in those with higher initial depressive
symptoms (BDI 18) did not result in decreased 5-year cardiac
outcome risk. This finding provides preliminary evidence for
the potential cardiac benefit of reducing depressive symptoms
in a substantial proportion of patientsthose with subthreshold depression.
To conclude, even minor symptoms of depression at the
time of admission to the hospital predict post-ACS morbidity
and mortality. Furthermore, there is some suggestion that
previous history of major depressive episodes may further
enhance the strong prognostic impact of these symptoms (28).
Clearly, further studies should examine factors that potentially
moderate the impact of depression besides its severity at
baseline, such as the number, the timing and duration of
previous episodes, and previous depression treatment history.
Although an enticing prognostic prediction is available
from depression inventories, what is assessed by a depressive
symptom inventory in post-ACS patients is not entirely clear.
Some have argued that the symptoms endorsed by these
patients (fatigue, loss of concentration, sadness, pessimism)
may result from more severe cardiac illness that is not properly controlled for by assessing the number of diseased vessels
or other medical severity measures in published studies (29).
The meaning of depressive symptoms and depressive disorder
diagnosis post-ACS and possible treatments are presented
after reviewing the course of depressive symptoms in this
patient population.
NATURAL COURSE OF DEPRESSIVE SYMPTOMS
IN POST-ACUTE CORONARY SYNDROME
PATIENTS
The course of elevated depressive symptoms in postmyocardial infarction patients has been characterized by Schleifer
et al. (30). Of those admitted to the cardiology unit, 27% met
criteria for minor depression as assessed by the Schedule for
Affective Disorders and Schizophrenia (31), and an additional
18% met criteria for major depression when all were assessed
within 10 days of their event. Schleifer et al. (30) reassessed
their patients 3 to 4 months after admission. Seventy-seven
percent of those with major depression still met criteria for
this disorder, but only 35% of those with minor depression
continued to have elevated depressive symptoms.
Another study examined the natural course of depressive
symptoms in patients with CHD who had not experienced a
recent major cardiac event (32). At baseline, 17% of 200
patients met the DSM-IV criteria for major depression, and an
additional 17% met the DSM-IV criteria for minor depression.
Seventy-five percent of the depressed patients were followed
up over a period of 1 year. Of these, 42% of patients with
initial minor depression had progressed to major depression 1
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clusion of other treatment elements) was essential for successful depression relapse prevention.
Interpersonal psychotherapy focuses on the intuitively appealing concept that events in ones psychosocial environment
affect ones mood and vice versa. When major events occur,
mood worsens, and depression may result. Conversely, depressed mood compromises ones ability to handle ones social roles, generally leading to further negative events and
ongoing interpersonal distress (56). The crux of interpersonal
psychotherapy is to demonstrate empirically a link between
mood and interpersonal issues that appear temporally and
thematically related to the onset and maintenance of depression (19). Once a patient understands this link and identifies
the specific interpersonal area that is currently problematic,
the therapist and patient work together to alter the interpersonal environment so that the depression will lift (56). The
patient and therapist agree on 1 of the following 4 interpersonal problem areas that will be the focus of the depression
treatment: a) grief or complicated bereavement, b) role dispute
or ongoing disagreements with a significant person in the
patients life, c) a recent role transition that results in major
interpersonal role changes or alterations (eg, retirement, moving, being diagnosed with a major medical illness), and d)
interpersonal deficits (recurrent difficulties in social interactions, in their extreme form classified as personality disorders). Although depressed patients may fit into several or all
of the 4 interpersonal problem areas, the treatment demands
that 1 area (or occasionally 2) be chosen as the primary target
for intervention.
Presence of Interpersonal Problems in the Etiology of
Depression
Numerous studies have found interpersonal problems as
reflected in divorce, marital problems, and negative partner
and child interactions to be significantly more prevalent or
elevated in depressed people (57, 58). However, it is still
unclear whether interpersonal problems precede depressive
episodes rather than co-occur with or even result from depressive mood states. On a variety of interpersonal functioning
indicators, Hammen and Brennan (58) compared 83 women
with unipolar major depression or dysthymic disorder, 271
women who were not currently in a depressive episode but
who had past histories of either DSM-IV depression diagnosis,
and 458 never-depressed women. As expected, the currently
depressed women had the worst scores on all interpersonal
indicators. Compared with the never-depressed group, and
controlling for current subclinical depressive symptoms and
socioeconomic status, the past depression women reported a
more frequent use of coercive interpersonal tactics, more
interpersonal conflicts, less secure attachment representations
of relationships, and more dysfunctional personality traits.
Moreover, their close relationship functioning was found to be
more dysfunctional by interviewers, and the marital satisfaction of the womens spouses was worse. Although crosssectional, at least this 1 set of results suggests that impoverished relational skills and dysfunctional representations of
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cally demanding activities have to be restricted (eg, caregiving
for other family members), or partial or full work retirement is
recommended, the ACS event coincides with a major, irreversible role transition. Pre-existing, quiescent cognitive distortions may be reinforced or activated through the experience
of the uncontrollable, adverse, life-threatening event (eg, bad
things always happen to me, I will never be able to lead a
fulfilling life again). Because of the restrictions and demands
of lifestyle changes, patients may experience a decrease of
pleasant activities and increase of unpleasant activities (eg,
abstaining from smoking, drinking, adherence to aversive
medication and attendance at routine, but anxiety-provoking
medical checkups).
TREATING DEPRESSION IN PATIENTS WITH
ACUTE CORONARY SYNDROME: WHAT IS
REQUIRED?
For the application of existing psychosocial depression
treatments to post-ACS patients, a number of parameters on
which this population differs from psychiatric populations
studied by the major depression theories must be considered.
The original populations were generally self-identified; they
were usually without major medical comorbidity; they were
mostly young or middle-aged; they met full criteria for formal
psychiatric or depressive disorders; and finally and importantly, they sought and accepted psychological treatment. In
contrast, the majority of patients with ACS will not selfidentify as being depressed, they all have an acute medical
disease, many do not meet full criteria for a depressive disorder, and they may be unwilling to seek or accept depression
treatment. Moreover, most of these patients are older than 50
years, with a substantial proportion of these patients elderly or
very old.
These characteristics pose specific challenges for the implementation of psychosocial depression treatments. In patients with medical comorbidity, depressive symptoms are
typically underdiagnosed (67). This applies especially to subthreshold depression (68) and depressive symptoms in the
elderly population (69). Although depression is the most common mental health problem from which older adults suffer
(69), they underutilize mental health services, they are less
likely to self-identify as being depressed, and, once interested
in seeking treatment, they must overcome many practical
barriers to obtain mental health treatment (70). Even when
referred to a mental health professional, older patients are less
likely than younger patients to seek specialized mental health
care (71); this is probably in part because of the stigma
perceived by this patient population in seeking mental health
treatment (72).
As Coyne and Thompson (73) have pointed out, evidence
for successful treatment of depressive symptoms in populations of primary care patients is sparse and based on heterogeneous populations and interventions. Further, even when
treatments reduce depressive symptoms, improvements in
event-free survival rates are not necessarily achieved, as recent results of 1 medium-sized antidepressant and 1 large170
K. W. DAVIDSON et al.
those who will be more likely to remit spontaneously. Studying the point prevalence of the differing depression theory
proximal causes will allow us a window into the meaning of
these elevated depression symptoms in post-ACS patients.
Should depressogenic vulnerabilities be highly prevalent and
predictive of nonremission and ACS recurrence, the selection
of evidence-based depression treatments most likely to treat
depressive symptoms successfullyand possibly prevent
ACS recurrencein these patients becomes clear. Alternatively, should the commonly studied depressogenic vulnerabilities be rare or nonpredictive in these patients, pursuing
alternative conceptualizations of subthreshold depression
symptoms becomes urgent.
REFERENCES
1. Glassman AH, Shapiro PA. Depression and the course of coronary artery
disease. Am J Psychiatry 1998;155:4 11.
2. Anda R, Williamson D, Jones D, Macera C, Eaker E, Glassman A, Marks
J. Depressed affect, hopelessness, and the risk of ischemic heart disease
in a cohort of U. S. adults. Epidemiology 1993;4:28594.
3. Aromaa A, Raitasalo R, Reunanen A, Impivaara O, Heliovaara M, Knekt
P, Lehtinen V, Joukamaa M, Maatela J. Depression and cardiovascular
diseases. Acta Psychiatr Scand 1994;377(suppl):77 82.
4. Barefoot JC, Schroll M. Symptoms of depression, acute myocardial
infarction, and total mortality in a community sample. Circulation 1996;
93:1976 80.
5. Ford DE, Mead LA, Chang PP, Cooper-Patrick L, Wang NY, Klag MJ.
Depression is a risk factor for coronary artery disease in men: the
precursors study. Arch Intern Med 1998;158:1422 6.
6. Bush DE, Ziegelstein RC, Tayback M, Richter D, Stevens S, Zahalsky H,
Fauerbach JA. Even minimal symptoms of depression increase mortality
risk after acute myocardial infarction. Am J Cardiol 2001;88:337 41.
7. Carney RM, Freedland KE, Rich MW, Jaffe AS. Depression as a risk
factor for cardiac mortality and morbidity: a review of potential mechanisms. J Psychosom Res 2002;53:897902.
8. Denollet J, Sys SU, Brutsaert DL. Personality and mortality after myocardial infarction. Psychosom Med 1995;57:58291.
9. Frasure-Smith N, Lespe rance F, Talajic M. Depression following myocardial infarction: impact on 6-month survival. JAMA 1993;270:
1819 25.
10. Frasure-Smith N, Lespe rance F, Juneau M. Differential long-term impact
of in-hospital symptoms of psychological stress after non-q-wave and
q-wave acute myocardial infarction [published erratum]. Am J Cardiol
1994;74:639.
11. Frasure-Smith N, Lespe rance F, Talajic M. Depression and 18-month
prognosis after myocardial infarction. Circulation 1995;91:999 1005.
12. Ladwig KH, Roll G, Breithardt G, Budde T, Borggrefe M. Post-infarction
depression and incomplete recovery 6 months after acute myocardial
infarction. Lancet 1994;343:20 3.
13. Lespe rance F, Frasure-Smith N, Juneau M, Theroux P. Depression and
1-year prognosis in unstable angina. Arch Intern Med 2000;160:
1354 60.
14. Lespe rance F, Frasure-Smith N, Talajic M, Bourassa MG. Five-year risk
of cardiac mortality in relation to initial severity and 1-year changes in
depression symptoms after myocardial infarction. Circulation 2002;105:
1049 53.
15. Rugulies R. Depression as a predictor for coronary heart disease: a review
and meta-analysis. Am J Prev Med 2002;23:51 61.
16. Beck AT. Cognitive therapy: past, present, and future. J Consult Clin
Psychol 1993;61:194 8.
17. Beck AT, Rush AJ, Saw BF, Emery G. Cognitive therapy of depression.
New York: Guilford; 1979.
18. Beck JS. Cognitive therapy: basics and beyond. New York: Guilford;
1995.
19. Klerman G, Weissman M, Rounseville B, Chevron E. Interpersonal
psychotherapy of depression. New York: Basic Books; 1984.
20. Lewinsohn PM, Antonuccio DO, Steinmetz-Breckenridge JL, Teri L. The
coping with depression course: a psychoeducational intervention for
unipolar depression. Eugene, OR: Castalia Publishing; 1984.
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