American Psychiatric Association’s *Psychiatric
News* (vol. 43, #7, April 4, 2008 ) includes an article: “Depression, Heart
Disease: A Curiously Strong Relationship” by Carolyn Robinowitz, M.D.,
president of the American Psychiatric Association, and Charles Nemeroff,
M.D., Ph.D., chair of Psychiatry at Emery U.

Here’s the article:

Over the past several years, research findings have increasingly
demonstrated that the co-occurrence of depression and heart disease has
an impact considerably greater than the comorbidity of two common
medical disorders. My colleague Charles Nemeroff, chair of the
Department of Psychiatry at Emory University School of Medicine, has
highlighted some of the findings that have major implications for not
only psychiatry but all medical specialties.

There is an unusually high prevalence rate of major depression in
patients with coronary artery disease (CAD), far higher than in the
population as a whole. The decrease in life expectancy in depressed
patients compared with that of the general population is, in part,
attributable to an increased risk for death secondary to cardiovascular

Further, patients with major depression are far more likely to die after
a myocardial infarction (MI) than are patients with equal cardiac
morbidity without major depression.

There is now a well-documented, positive correlation between depression
symptom severity and cardiovascular morbidity and mortality. The more
severe the depression, the higher the likelihood of developing
cardiovascular disease and dying post-MI.

The adverse effect of depression on cardiovascular disease outcome is
not limited to MIs, but has also been found for outcome after coronary
artery bypass graft surgery and in patients with isolated systolic
hypertension. Further, there is evidence supporting depression as an
independent risk factor for the development of CAD, perhaps as important
as tobacco use. These data are based on more than 40,000 subjects
followed for approximately 10 years. The adjusted relative risk for
development of CAD in depressed patients is 4- to 4.5-fold that of
nondepressed individuals.

Depression is a systemic illness characterized by a number of biological
alterations that likely contribute to cardiac morbidity and mortality.
Depressed patients, for example, exhibit multiple alterations in immune
function, largely in inflammatory cytokines such as interleukin-6 and C-
reactive peptide. Depressed patients also exhibit multiple defects in
the platelet clotting cascade, all contributing to a clotting diathesis.
These include alterations in platelet activation, the platelet “release”
reaction, and platelet aggregation. Decreased heart-rate variability, a
well-documented risk for MI, has repeatedly been found in patients with
major depression.

Fortunately, patients with depression and comorbid CAD respond as well
to treatment with select ive serotonin reuptake inhibitor
antidepressants as do depressed patients without CAD. Further, the
direct effects of these drugs on platelets reduce the risk of thrombus

This remarkable body of evidence linking depression and heart disease
now needs to be translated into changes in clinical practice.

Both disorders have an immense impact on individuals and families.
Depressed patients are at risk for cardiovascular and cerebrovascular
disease, requiring careful monitoring and early intervention. Similarly,
patients with cardiovascular disease should be screened for depression.

Only a partnership between psychiatry, internal medicine, family
medicine, and cardiology can successfully move these findings from the
bench to the bedside. These findings have served as a clarion call for
APA to work with the American Heart Association and American College of
Cardiology to educate our respective members on this area of paramount
importance to patients’ health and well-being.

As one of my presidential initiatives, I have begun a dialogue and have
interacted with representatives of those groups to enlist their support
in informing their physician members of the need to assess their
patients for depression (the PHQ-9 is a helpful tool). I also am
encouraging them to inform their members and their members’ patients
about the role of depression as a contributor to greater morbidity and
mortality as well as a risk factor for disease development and progression.

We hope these organizations will use their public-information efforts,
including their Web sites, to provide this information and to initiate
links to psychiatric resources such as APA’s Web site.

These organizational interactions need to be supplemented by work at the
clinician level. Of course, when we review our patients’ general medical
status, we should be alert to risk factors as well as to symptoms of
cardiovascular disease, and we should inform our patients of what we
find. But there is one more way to put our voices into action for our
patients. We need to ensure that our colleagues in internal medicine,
family medicine, and cardiovascular disease are aware of the impact of
untreated depression on patients’ cardiovascular status, as well as
informed of the positive and protective impact of treatment–or simply,
that Treatment Works!