European Heart Journal (2010) 31, 1036–1037
Depression and cardiovascular disease: havea happy day—just smile!
University of Michigan School of Medicine, Cardiovascular Center, 1500 E. Medical Center Drive, Ann Arbor, MI 48109, USA
Online publish-ahead-of-print 17 February 2010
This editorial refers to ‘Don’t worry, be happy: positive
Davidson et al.10 have examined the association between patient
affect and reduced 10-year incident coronary heart
affect and cardiovascular events after correcting for age, gender,
disease: The Canadian Nova Scotia Health Survey’†, by
and cardiovascular risk factors. The researchers found that positive
affect protected against the development of coronary heart diseasewhile depressive symptoms increased the likelihood of disease
The relationship between cardiovascular disease and depression
onset. They point out that positive affect can easily be assessed
poses intriguing research questions, particularly for co-morbid
by measures such as whether or not the patient smiles during
treatment. Preliminary studies have indicated that patients with
the clinical interview and whether they appear to take pleasure
early-onset depression are at a significantly increased risk for
or excitement in aspects of their daily life.
developing cardiovascular disease (CVD) after correcting for cardi-
Since the study of Davidson et al. is non-experimental, it has not
ovascular risk factors, and this effect occurs even in the absence of
been determined whether positive affect has a direct or indirect
a diagnosis of major depression.1 Depression increases the risk of
causal role in CVD, or whether both conditions share a
coronary artery disease by 1.5 – 2 times in otherwise physically
common, underlying third variable. This has important implications
healthy individuals.2 In addition, patients with CVD such as myo-
for co-morbid treatment. If positive affect is indirectly related to
cardial infarction, stroke, heart failure, and atrial fibrillation are at
CVD, perhaps positive affect moderates the effects of stress and
increased risk of developing depression and, when depression
this stress reduction may decrease CVD risk. Alternatively,
develops, cardiovascular risk is exacerbated further.2,3 Patients
perhaps poor or negative affect and cardiovascular disease are
with treatment-resistant depression (failure to respond to a
influenced by an underlying third variable. For example, reductions
single trial of antidepressant) after an acute coronary syndrome
in positive affect and CVD can both be caused by poor sleep.11,12
are at even greater cardiovascular risk.4
However. if the positive affect– CVD relationship is direct, atypical,
The use of antidepressants, such as selective serotonin uptake
aminoketone antidepressants such as buproprion that modulate
inhibitors (SSRIs) and tricyclic antidepressants (TCAs), does not
noradrenergic and dopaminergic activity might be better candi-
appear to mitigate cardiovascular risk associated with depression,
dates for improving cardiac outcome because they have been
despite altering one or more of the physiological abnormalities
shown to enhance positive affect better than SSRIs and have the
linking CVD to depression such as increased inflammatory cyto-
added benefits of facilitating weight loss13 and smoking cessation.14
kines, a decreased circulation of endothelial progenitor cells, and a
In contrast, SSRIs may produce weight gain15 and may have less
deficiency in nitric oxide availability.5 – 7 Nor does the combination
of an SSRI and n-3 fatty acids appear to reduce mood-associated
Another important question is whether positive affect is also
cardiovascular risk.8 Instead, a recent report of .99 000 patients
related to long-term risk. For example, heart rate variability, indica-
surviving their first hospitalization for heart failure has suggested
tive of healthy cardiac autonomic control, was found to be highly
that the use of both TCAs and SSRIs was associated with an
associated with positive affect over a day in an experience sampling
increased risk of total and cardiovascular-related mortality.9 Surpris-
ambulatory study.17 Yet even if reduced positive affect is shown to
ingly, co-administration of an SSRI and a beta-adrenergic blocking
cause increased mortality over the long term, it may not be easily
agent was also associated with an increased risk of total and
modified. Historically, theorists have believed that it is nearly
cardiovascular-related mortality, prompting the authors of the
impossible to institute long-term changes in the amount of positive
study to urge further clinical study to determine the optimum anti-
(or negative) emotion an individual experiences and that humans
depressant strategy in patients with heart failure.
have an emotional ‘set point’ that they return to regardless of
The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.
* Corresponding author. Tel: þ1734 936-5260, Fax: þ1 734 9365256, Email: email@example.com† doi:10.1093/eurheartj/ehp603
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2010. For permissions please email: firstname.lastname@example.org.
intervening life events.18 More recently, however, theorists
acknowledge that although much of affective experience may be
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Davidson et al.10 suggest that interventions to augment positive
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Conflict of interest: none declared.
the case for a new conceptual paradigm. J Sex Marital Ther 2008;34:291 – 297.
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