From the Behavioral Medicine Center, Department of Psychiatry, Washington
University School of Medicine, St Louis, Mo.
There
is abundant evidence that depression, anxiety, and anger increase the
risk for cardiac events in patients with coronary heart
disease. Denollet and Brutsaert1 are to be
commended for contributing a generally well-conducted study of
psychological predictors of cardiac end points to this rapidly growing
literature. They have found that the combination of "negative
affectivity" and social inhibition predicts cardiac events
independently of established medical risk factors. Prospective studies
such as theirs, in which potential confounders are adequately measured
and cardiac end points carefully documented, are needed to substantiate
the effects of psychological factors on medical outcomes after acute
myocardial infarction (MI).
Unfortunately, the authors may have gone beyond their data in
asserting that they have identified a personality trait that both
predicts cardiac events and explains why such disparate mood states as
depression, anxiety, and anger predict cardiac events as well. It is
not at all clear that they have substantiated this claim or that it is
time to abandon research on depression, anxiety, and anger in favor of
this personality trait.
Absent from the authors' discussion is any reference to an established
theory of personality. It is by no means universally accepted among
personality theorists that a single trait accounts for every negative
mood state (cf Cloninger et al2 ) or that the
combination of negative affectivity and social inhibition defines a
persistent "distressed personality type." In this light, it makes
more sense to conclude simply that patients with coronary heart
disease who are both emotionally distressed and socially inhibited are
at greater risk for cardiac events than are patients without both
characteristics. This more conservative interpretation does not
diminish the importance of the study or the need for further research
on the relationship between social inhibition and emotional distress in
cardiac patients.
The authors' argument that the distressed personality type accounts
for the relationships between cardiac events and depression, anxiety,
and anger rests, in large part, on the finding that negative
affectivity and social inhibition remained in a multiple regression
model after the negative mood state variables dropped out.
Unfortunately, this is not particularly convincing evidence, because
the statistical power of the model was too low to test the hypothesized
relationships among personality, mood state, and cardiac events.
Furthermore, the measures of negative mood states used in this study
were not the same ones that have been found in other studies to predict
post-MI mortality. For example, most previous studies of depression as
a predictor of cardiac mortality have either used standardized clinical
interviews or well-validated questionnaires such as the Beck Depression
Inventory3 4 or the Zung Depression
Scale.5 Instead of one of these established
depression measures, the authors used the Pessimism and Despair scales
from the Millon Behavioral Health Inventory as indicators of
depression. Pessimism and despair may be common features of depression,
but they are not equivalent to depression. In fact, these two Millon
scales correlate better with the authors' measure of negative
affectivity1 than they do with the Beck
Depression Inventory.6
Even if a single personality factor were found to account for a variety
of negative mood states in post-MI patients, it would not necessarily
do so for clinical depression, a known predictor of cardiac events. The
authors argue that this is unimportant because depressed mood, even in
the absence of a clinical depressive disorder, increases the risk for
the post-MI period. They cite the study by Frasure-Smith et
al4 to support this position, but this is
somewhat misleading. Although Frasure-Smith and colleagues did find
that the number and severity of depressive symptoms (as measured by the
Beck Depression Inventory) was a better predictor of 18-month mortality
than was a diagnosis of major depression, their previous
report7 showed that major depression was the
better predictor of 6-month mortality. Furthermore, they found that
patients who were free of major depression at index but who
nevertheless had high Beck Depression Inventory scores were at high
risk of developing major depression during the follow-up
period.8 This is similar to our study of patients
with stable coronary heart disease, in which nearly half of
those who had minor depression at index developed major depression in
the course of the following 12 months.9 In short,
some post-MI patients with depressed mood or minor depression will
subsequently develop major depression, and others will not. We do not
yet know whether the dysphoric or mildly depressed patients who do not
go on to develop major depression are at any higher risk for mortality
than are otherwise comparable nondepressed patients.
It may or may not be easier for clinicians to assess a single
personality factor than three separate mood states. However,
personality factors are, by definition, much more stable and much more
difficult to change than are mood states such as depression or anxiety.
There are well-established, short-term psychotherapeutic and
pharmacological treatments for the most common forms of depression,
anxiety, and pathological anger10 11 as well as
social inhibition.10 Thus, even if it were easier
to assess personality traits than mood states, this advantage would be
thoroughly offset by the challenge of changing the patient's
personality.
The authors have attempted to bypass this obstacle by proposing
clinical trials of "comprehensive treatment programs" aimed not at
changing personality but rather at reducing general emotional distress.
However, two recent randomized trials cast doubt on the wisdom of that
approach.12 13 These studies found that
nonspecific interventions for general distress failed to improve
survival in post-MI patients and may even have decreased survival in
female patients.
Finally, it is not clear that all negative emotions affect all patients
and all cardiac end points in the same way or to the same degree. For
example, although numerous studies have established a link between
hostility and anger and the development of coronary artery
disease,14 there is little evidence that anger
has prognostic significance after an MI.15 As
another example, chronic, low- to moderate-intensity anxiety, such as
that seen in generalized anxiety disorder, may have different effects
on both cardiac physiology and cardiac end points than transient,
high-intensity anxiety such as that seen in phobias and panic disorder.
Preserving such distinctions is essential if we are to identify the
mechanisms that underlie the relationships between these mood states
and cardiac end points. Identification of the specific mechanisms is,
in turn, necessary if we are to refine our ability to identify and
treat patients at risk.16 The history of research
on cholesterol as a cardiac risk factor provides an
instructive analogy. If lipid researchers had studied only total serum
cholesterol to the exclusion of specific
cholesterol fractions, much less would have been learned
about the mechanisms by which cholesterol contributes to
atherogenesis or about how to most effectively treat
hypercholesterolemia.
Again, Denollet and Brutsaert are to be commended for their work. Their
findings should stimulate a much-needed debate about the direction for
future research in this area. However, I submit that it is too early to
abandon research on specific mood states in favor of a single
personality trait. Studies of the effects of specific mood states on
specific cardiac end points are still needed. Whether successful
treatment of depression, anxiety, or pathological anger can reduce
cardiac event rates is still unknown. Clinical trials could help answer
this question, but only if these mood states are adequately
characterized.
Footnotes
Reprint requests to Robert M. Carney, PhD, Behavioral Medicine Center, Department of Psychiatry, Washington University School of Medicine, 4940 Children's Place, St Louis, MO 63110-1093.
The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.
References
1.
Denollet J, Brutsaert DL. Personality, disease
severity, and the risk of long-term cardiac events in patients with a
decreased ejection fraction after myocardial infarction.
Circulation. 1998;97:167–173.
2.
Cloninger CR, Przybeck TR, Svrakic DM, Wetzel RD.
The Temperament and Character Inventory (TCI): A Guide to Its
Development and Use. St Louis, Mo: Washington University
Press; 1994.
3.
Ahern DK, Gorkin L, Anderson JL, Tierney C, Ewart C,
Capone RJ, Schron E, Kornfeld D, Herd JA, Richardson DW, Follick
MJ. Biobehavioral variables and mortality or cardiac arrest in
the Cardiac Arrhythmia Pilot Study (CAPS). Am J
Cardiol. 1990;66:59–62.[Medline]
[Order article via Infotrieve]
4.
Frasure-Smith N, Lespérance F, Talajic M.
Depression and 18-month prognosis after myocardial infarction.
Circulation. 1995;91:999–1005.
5.
Barefoot JC, Helms MJ, Mark DB, Blumenthal JA, Califf
RM, Haney TL, O'Connor CM, Siegler IC, Williams RB. Depression and
long-term mortality risk in patients with coronary artery
disease. Am J Cardiol. 1996;78:613–617.[Medline]
[Order article via Infotrieve]
6.
Watson D, Clark LA. Negative affectivity: the
disposition to experience aversive emotional states. Psychol
Bull. 1984;96:465–490.[Medline]
[Order article via Infotrieve]
7.
Frasure-Smith N, Lespérance F, Talajic M.
Depression following myocardial infarction: impact on 6-month survival.
JAMA. 1993;270:1819–1825.
8.
Lespérance F, Frasure-Smith N, Talajic M. Major
depression before and after myocardial infarction: its nature and
consequences. Psychosom Med. 1996;58:99–110.
9.
Hance M, Carney RM, Freedland KE, Skala J. Depression
in patients with coronary heart disease. Gen Hosp
Psychiatry. 1996;18:61–65.[Medline]
[Order article via Infotrieve]
10.
Barlow DH. Clinical Handbook of Psychological
Disorders. 2nd ed. New York: Guilford Press; 1993.
11.
Hyman SE, Arana GW, Rosenbaum JF. Handbook of
Psychiatric Drug Therapy. 3rd ed. Boston: Little, Brown Co; 1995.
12.
Frasure-Smith N, Lespérance F, Prince RH, Verrier
P, Garber RA, Juneau M, Wolfson C, Bourassa MG. Randomized trial of
home-based psychosocial nursing intervention for patients recovering
from myocardial infarction. Lancet. 1997;350:473–479.[Medline]
[Order article via Infotrieve]
13.
Jones DA, West RR. Psychological rehabilitation after
myocardial infarction: multicentre randomised controlled trial.
BMJ. 1996;313:1517–1521.
14.
Williams RB. Neurobiology, cellular and molecular
biology, and psychosomatic medicine. Psychosom
Med. 1994;56:308–315.
15.
Frasure-Smith N, Lespérance F, Talajic T. The
impact of negative emotions on prognosis following myocardial
infarction: is it more than depression? Health Psychol. 1995;14:388–398.[Medline]
[Order article via Infotrieve]
16.
Carney RM, Freedland KE, Rich MW, Jaffe AS. Depression
as a risk factor for cardiac events in established coronary
heart disease: a review of possible mechanisms. Ann Behav
Med. 1995;17:142–149.[Medline]
[Order article via Infotrieve]
© 1998 American Heart Association, Inc.
Editorial
Psychological Risk Factors for Cardiac Events
Could There Be Just One?
Key Words: Editorials • depression • myocardial infarction • risk factors
This article has been cited by other articles:
 |
|
 |
|
  R. Fraguas Jr., D. V. Iosifescu, J. Alpert, S. R. Wisniewski, J. L. Barkin, M. H. Trivedi, A J. Rush, and M. Fava Major Depressive Disorder and Comorbid Cardiac Disease: Is There a Depressive Subtype With Greater Cardiovascular Morbidity? Results From the STAR*D Study Psychosomatics, October 1, 2007; 48(5): 418 - 425. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. D. Kubzansky, K. W. Davidson, and A. Rozanski The Clinical Impact of Negative Psychological States: Expanding the Spectrum of Risk for Coronary Artery Disease Psychosom Med, May 1, 2005; 67(Supplement_1): S10 - S14. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. K. Schulman, P. R. Muskin, and P. A. Shapiro Psychiatry and Cardiovascular Disease Focus, April 1, 2005; 3(2): 208 - 224. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. P. van Melle, P. de Jonge, T. A. Spijkerman, J. G. P. Tijssen, J. Ormel, D. J. van Veldhuisen, R. H. S. van den Brink, and M. P. van den Berg Prognostic Association of Depression Following Myocardial Infarction With Mortality and Cardiovascular Events: A Meta-analysis Psychosom Med, November 1, 2004; 66(6): 814 - 822. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Tiemeier, W. van Dijck, A. Hofman, J. C. M. Witteman, T. Stijnen, and M. M. B. Breteler Relationship Between Atherosclerosis and Late-Life Depression: The Rotterdam Study Arch Gen Psychiatry, April 1, 2004; 61(4): 369 - 376. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||