|
Editorial
(Mayo Clinic Proceedings. 1996; 71:817-819)
(Accompanying my lead article on pages
729-734)
Identification and Treatment of
Psychosocial Risk Factors for Coronary Artery Disease
Since the introduction of the concept of
the type A behavior pattern by Friedman and Roseman in 1959,
investigators have had an ongoing interest in the relationship
between psychosocial risk factors and the epidemiologic
and pathophysiologic features of coronary artery disease.
In recent years, emphasis has shifted from attempting to
predict the development of coronary artery disease in healthy
subjects to evaluating the influence of psychosocial factors
on secondary events, health-care costs, and survival in
patients with established coronary artery disease. Moreover,
the hegemony of the type A behavior pattern as the primary
psychosocial risk factor had yielded to a variety of definitions
of psychosocial risk. The concept of type A behavior itself
has been further refined into a “hostility complex,”
shown to be the critical part of the type A behavior pattern
responsible for increasing coronary risk[1]. Hostility is
the particular characterization of psychosocial risk used
by Goodman and associates in their article
in this issue of the Mayo Clinic Proceedings (pages
729 to 734).
Although the conclusion that hostility predicts restenosis
after percutaneous transluminal coronary angioplasty (PTCA),
based on the data of Goodman and colleagues,
could be best described as preliminary (because of the small
and diverse sample size and some methodological limitations
appropriately acknowledged by the authors),
|
the article adds yet one more piece of evidence that
psychosocial factors have a major role in destabilizing
coronary artery disease and leading to new coroney events
in some fashion. The article is also valuable in that it
is only the second published study of psychosocial risk
factors to assess PTCA-treated patients, an increasingly
large group of patients with a high risk of recurrence of
coronary artery disease that is potentially available for
future prospective studies.
Despite the now overwhelming evidence of the importance
of psychosocial risk factors in coronary artery disease,
the practical questions of how to identify patients at risk
and how to intervene remain incompletely answered. Recently,
considerable interest has also been generated in the elucidation
of the physiologic mechanisms underlying psychosocial risk
factors, although this subject is beyond the scope of this
editorial.
Characterization of Risk. – Psychosocial risk
has been characterized along multiple dimensions, including
marital status,[2] social isolation,[3],[4] and low socioeconomic
status.[2] The mechanism by which social isolation increases
risk has not been established however. For example, socially
isolated persons may experience negative emotional states
such as depression and anxiety more frequently than those
with a social support structure. More directly, however,
such persons may have no one to call 911 in case of cardiac
arrest, help initiate the decision to seek medical assistance
for chest pain, or help prepare special diets, keep track
of proper dosing of medications, and encourage other patient-directed
aspects of secondary
|
Page 2
prevention. Low socioeconomic status may create further
direct problems with receiving proper medical care.
Psychosocial risk has been identified by self-report inventories
used to assess the symptoms that accompany negative emotional
states. In our work, my colleagues and I have used SCL-90-R
(formally, the Symptom Checklist-90-Revised),[5] a 90-question
self-report inventory that takes approximately 15 to 20
minutes to complete and has been well accepted among our
cardiac rehabilitation patients. Patients with increased
scores on the SCL-90-R were found to have approximately
a 2.5-fold risk for rehospitalization for cardiac symptoms
and a more than fivefold risk of a new “hard”
event (myocardial infarction, cardiac death, or out-of-hospital
cardiac arrest) within 6 months after their index events.[6]
Frasure-Smith and colleagues [7],[8] used a shortened, 20
item version of a similar self-report inventory, the General
Health Questionnaire (GHQ-20), and similarly found that
patients with increased scores were at significantly increased
risk; in their analysis, the 5-year mortality was increased.
Other studies have more specifically assessed depression
in coronary patients by using their patient-completed Beck
Depression Scale[9] or the Diagnostic Interview Schedule[10]
(a brief interview technique).
Behavioral assessment such as the Structured Interview[11]
used by Goodman and coworkers has the obvious
advantage of being somewhat “blind” to the patient.
The current, preliminary results, however, need to be replicated
in a larger study before we can be certain of the ability
of hostility, determined from the structured interview,
to predict outcome in coronary patients.
|
Furthermore, use of the Structured Interview in the
routine clinical setting has some limitations-specialized
training is needed, and the interview and scoring necessitate
more time and expertise than self-report questionnaires
such as the SCL-90-R.
Unfortunately, no study to date has systematically used
multiple assessments of psychosocial risk and examined their
intercorrelation or compared their predictability in terms
of recurrent events. Most likely, multiple dimensions of
psychosocial risk represent one or at most a few common
psychologic and physiologic states.
Although space restrictions prohibit a discussion of various
theories of the underlying physiologic mechanisms, the limited
available studies clearly support the hypothesis that psychologic
stress may trigger acute coronary events. Mittleman and
associates[12] have shown that acute myocardial infarction
can be triggered by episodes of anger, and Leor and colleagues[13]
have shown that acute psychologic stress (the 1994 earthquake
in Los Angles County) can trigger sudden cardiac death.
Presumably, patients with psychosocial risk factors such
as depression or hostility would be most vulnerable to the
effects of anger (or have more anger) and stress, although
neither study presented data to address that presumption.
Studies of Intervention. – To date, two large
studies have attempted to intervene for psychosocial risk
in coronary patients. In a 4.5-year follow-up study of 1,013
patients who had had myocardial infarction, Friedman and
coworkers[14] attempted to determine whether group counseling
to modify type A behavior would reduce recurrent events.
Of
|
Page 3
the total group, 862 patients were randomized to either
a “cardiac counseling” group (N=270) or a “type
A counseling” group (N=592). The other 151 patients,
who did not volunteer for randomization, received usual
care. The 4.5-year recurrence rates were 12.9% for patients
in type A counseling in comparison with 21.2% for those
in cardiac counseling and 28.2% for those receiving usual
care.
The second large study of the benefits of intervention for
psychosocial risk was reported by Frasure-Smith and associates.[8]
Patients who had had myocardial infarction (N = 461) were
randomly assigned to a control group or treatment with a
life stress monitoring program that consisted of a telephone
interview 1 week after dismissal and every month thereafter.
Patients were given the GHQ-20 over the telephone. Patients
with five or more positive responses were visited by a nurse,
who provided individualized intervention including support,
education, and referral. All patients initially underwent
in-hospital assessment of risk with use of the GHQ-20. Initially
high-stress men with the non-Q-wave myocardial infarctions
who were in the control group exhibited a 5-year cardiac
mortality of more than 50% versus 14% in initially low-stress
control patients. In the treatment group of patients with
non-Q-wave myocardial infarction, both initially high- and
low-stress patients had a low (12%) 5-year cardiac mortality.
Among patients with Q-wave myocardial infarction, differences
between initially high-versus low-stress patients and treatment
versus control patients (and the interaction) were small
and non-significant.
|
An additional 16 intervention trials involving smaller
numbers of patients with coronary artery disease have measured
either mortality or recurrent events. These results have
recently been reported in a meta-analysis by Linden and
associates.[15] Interventions have included such varied
techniques as group psychotherapy, stress management training,
music therapy, and relaxation training. Linden and colleagues
calculated a statistically significant odds ratio (control/treatment)
of 1.84 for 2-year morbidity and 1.70 for 2-year mortality
for all fully randomized, controlled trials.
The potential benefit of psychoactive agents, such as selective
serotonin reuptake inhibitors, traditional cardioprotective
agents (ß-adrenergic blockers, angiotensin-converting
enzyme inhibitors, anticoagulants, and antiplatelet drugs),
or vasoactive agents (calcium channel blockers and nitrates),
on the excess morbidity and mortality in coronary patients
with psychosocial risk factors has not been specifically
evaluated. The National Institutes of Health had recently
embarked on a large, multicenter trial-Enhancing Recovery
in Coronary Heart Disease of ENRICHD; the intent is to randomize
3,000 patients who had had myocardial infarction to usual
care versus psychosocial intervention that would include
the use of selective serotonin reuptake inhibitors if 6
weeks of counseling failed to resolve depression. In addition,
at least one other multicenter trial is being planned by
the pharmaceutical industry to evaluate the benefits of
a selective serotonin reuptake inhibitor on the coronary
recurrence rate in patients with depression after myocardial
infarction.
|
Page 4
Recommendations – In this brief discussion
of the topic of psychosocial risk factors in coronary patients,
especially those who have had myocardial infarction, recommendations
for current practice should be addressed. Clearly, the theory
that psychosocial risk factors constitute a tangible problem
for coronary patients has been well established in the literature.
Although many potential types of evaluation of psychosocial
risk are available, a self-report inventory is probably
sufficient to identify a subgroup at high risk. Various
types of self-report inventories are available, including
the SCL-90-R that is used in psychosocial screening procedures
at Mayo. Screening should probably be done as early as
possible after the acute event, either just before dismissal
or early in the outpatient rehabilitation program, inasmuch
as our own and other studies have shown that the divergence
in recurrent events between distressed and nondistressed
patients begins almost immediately after dismissal from
the index hospitalization. The data on intervention
do not currently favor one strategy over another. In fact,
they are instead suggestive of a “Hawthorne effect,”
in that any sincere attempt at reducing distress in these
high-risk patients seems to result in a favorable influence
on their recurrent event rates. Thus, the intervention used
in a particular clinical setting may, at least for the present,
best be determined by available resources. Small rehabilitation
programs may be limited to individualized treatment-referral
to psychiatry, psychology, or social work assistance or
perhaps just extra attention and care from nursing, if that
is the only resource readily available.
|
Larger programs may be able to use groups to reduce the
cost and resource utilization for dealing with psychosocial
risk factors. In areas where cardiac rehabilitation programs
do not exist or in cases in which patients are unable or
unwilling to participate, individual physicians will
have to assume responsibility for screening and intervention
for this important component of secondary prevention.
Just as cigarette smoking and hyperlipidemia must be addressed
in the coronary patient, likewise depression and other manifestations
of heightened distress should be evaluated and treated.
Whether selective serotonin reuptake inhibitors will become
the “magic potion” for treating psychosocial
risk in coronary disease, as hydroxylmethyl-glutaryl-coenzyme
A reductase inhibitors have become for treating hyperlipidemia,
remains to be demonstrated. Until such data are available,
we can at least rely on conventional group and individual
therapy for these patients.
Thomas G. Allison, Ph.D., M.P.H.
Division of Cardiovascular Diseases and Internal Medicine
Mayo Clinic Rochester
Rochester, Minnesota
REFERENCES
1. Dembroski TM, MacDougall JM, Williams RB, Haney TL, Blumenthal
JA. Components of type A hostility, and anger in: relationship
to angiographic findings. Psychosom Med 1985; 47:219-233
|
Page 5
2. Williams RB, Barefoot JC, Califf RM, Haney TL, Saunders
WB, Pryor DB, et al. Prognostic importance of social and
economic resources among medically treated patients with
angiographically documented coronary artery disease. JAMA
1992; 267:520-524
3. Ruberman W, Weinblatt E, Goldberg JD, Chaudhary BS. Psychosocial
influences on mortality after myocardial infarction. N Engl
J Med 1984; 311:552-559
4. Case RB, Moss AJ, Case N, McDermott M, Eberly S. Living
alone after myocardial infarction: impact on prognosis.
JAMA 1992; 267:515-519
5. Derogatis LR. SCL-90-R: Administration, Scoring and Procedure
Manual II Baltimore: Clinical Psychometrics Research, 1983
6. Allison TG, Williams DE, Miller TD, Patten CA, Baily
KR, Squires RW, et al. Medical and economic costs of psychologic
distress in patients with coronary artery disease. Mayo
Clin Proc 1995; 70:734-742
7. Frasure-Smith N. In-hospital symptoms of psychological
stress as predictors of long-term outcome after acute myocardial
infarction in men. Am J Cardiol 1991; 67:121-127
8. Frasure-Smith N. Lesperance F, Juneau M. Differential
long-term impact of in-hospital symptoms of psychological
stress after non-Q-wave and Q-wave myocardial infarction.
Am J Cardiol 1992; 69 :1128-1134
9. Ahern DK, Gorkin L, Anderson JL, Tierney C, Hallstrom
A. Ewart C, et al. Biobehavioral variables and mortality
or cardiac arrest in the Cardiac Arrhythmia Pilot Study
(CAPS). Am J Cardiol 1990; 66:59-62
|
10. Frasure-Smith N, Lesperance F, Talajic M. Depression
following myocardial infarction: impact on 6-month survival.
JAMA 1993; 270:1819-1825
11. Rosenman RH. The Interview method of assessment of the
coronary-prone behavior pattern. In: Dembroski TM, Weiss
SM, Shields JL, Haynes SG, Feinleib M, editors. Coronary-Prone
Behavior. New York: Springer-Verlag, 1978:55-70
12. Mittleman MA, Maclure M, Sherwood JB, Mulry RP, Tofler
GH, Jacobs SC, et al (for the Determinants of Myocardial
Infarction Onset Study Investigators). Triggering of acute
myocardial infarction onset by episodes of anger. Circulation
1995; 92:1720-1725
13. Leor J, Poole WK, Kloner RA. Sudden cardiac death triggerd
by an earthquake. N Engl J Med 1996; 334:413-419
14. Friedman M, Thoresen CE, Gill JJ Ulmer D, Powell LH,
Price VA, et al. Alteration of type A behavior and its effect
on cardiac recurrences in post myocardial infarction patients:
summary results of the Recurrent Coronary Prevention Project.
Am Heart J 1986; 112:653-665
15. Linden W, Stossel C, Maurice J. Psychosocial interventions
for patients with coronary artery disease: a meta-analysis.
Arch Intern Med 1996; 156:745-752
|
|