The interface of emotion and biology in myocardial ischemia: Can we progress using the traditional paradigm?
Received Aug
The interface of emotion and biology in myocardial ischemia: Can we progress using the traditional paradigm?
Robert Soufer 0
Matthew M. Burg 0
0 Reprint requests: Robert Soufer, Department of Cardiology, Yale University , 950 Campbell Avenue, West Haven, CT 06516; J Nucl Cardiol 2017;24:783-7. 1071-3581/ $34.00 Copyright 2017 American Society of Nuclear Cardiology
1 Department of Cardiology, Yale University , West Haven, CT , USA
DEPRESSION AND CHD
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Programmatic research conducted over the past
30 years has consistently found depression to be
common in patients with coronary heart disease (CHD), yet
it is often unrecognized. Furthermore, depression in this
group has been shown to increase risk for recurrent
cardiac events and mortality. The threshold of
depression severity at which risk is conferred can be quite low
and substantially below the threshold associated with a
diagnosis of major depression, and the pathway(s) by
which depression confers risk may involve physiologic
and/or behavioral factors. A higher than expected
prevalence of depression is also characteristic of the
patient group with diabetes, and similarly is associated
with an elevated risk of medical complications and early
mortality. Here too, the pathways linking depression to
outcomes in this patient group appear to involve both
physiologic and behavioral factors.
The current article by Haaf et al.1 adds to this
literature by focusing specifically on incident CHD risk—
evidenced by a new myocardial perfusion defect—in
diabetic patients with depression. In a sub-study of the
BARDOT trial, patients with type 2 diabetes and free
from coronary disease manifestations or symptoms at
baseline underwent assessment that included myocardial
perfusion imaging (MPI) with SPECT and either
exercise or pharmacologic stress, along with assessment of
psychosocial functioning, including depression. These
assessments were repeated 2 years later, and the
predictors of new onset MPI defect were tested. Of many
variables—including both biologic and psychologic—it
was only the psychological measures—depression in
particular—that predicted new onset MPI defect. While
the sample was not large for a population study, and the
number of new ‘events’ small—in part due perhaps to
the length of follow-up—the findings of this paper
nonetheless raise important questions regarding risk
assessment and surveillance in this high-risk patient
group.
Several large, prospective epidemiological studies
of initially healthy individuals have shown that a history
of major depression disorder (MDD) carries up to a
fourfold elevated risk of incident CHD,2 with
metaanalyses3 showing depression to carry a relative risk of
1.64 for incident CHD, independent of standard risk
factors and markers including poor diet, tobacco use,
and lack of physical activity. In patients with CHD,
defined as chronic, stable coronary disease, unstable
angina, or a history of prior acute coronary syndrome (ACS)
event, up to 40% evidence clinically meaningful
depression symptomatology, and overall, 15% to 20% meet
criteria for MDD,4 a rate three times greater than in the
general population.5 Hospitalized ACS patients with
depression during hospital admission are highly likely to
have had depression prior to their cardiac event,6 which
should not be surprising, as depression is a recurring,
remitting disorder.
DEPRESSION AND DIABETES
Overall, the comorbidity of depression and CHD
mirrors that of depression and diabetes. Approximately
25% of patients with either type 1 or type 2 diabetes
report significant depression symptom elevation, while
10% to 15% meet diagnostic criteria for MDD.7 The
incidence of depression in type 2 diabetics is 24% higher
than in non-diabetics,8 depression in both type 1 and 2
diabetics can be persistent for a great majority, and over
75% of those whose depression remits experience a
recurrence over 5 years.9 As with CHD, the relationship
appears bi-directional in those adults with depression,
and they are also at up to 37% elevated risk of
developing diabetes.10
MECHANISMS IN DEPRESSION AND CHD
The mechanisms underlying the link between
depression and CHD are many and involve both
biological and behavioral components.11 These include:
autonomic dysregulation—e.g., chronically elevated
sympathetic nervous system (SNS) activity and reduced
cardiac vagal control; chronically elevated activity of
the hypothalamic–pituitary–adrenal cortex (HPA) axis;
endothelial dysfunction; increased likelihood of
experiencing myocardial ischemia during psychological stress;
ongoing inflammatory processes; platelet activation;
smoking and physical inactivity; and overall health risk
behavior and medication non-adherence.
Otherwise healthy individuals with MDD have
elevations in circulating catecholamines and cortisol
that have been shown to predispose CHD patients to
myocardial ischemia, ventricular tachycardia, and
fibrillation, thus leading to sudden cardiac death.11
Depress (...truncated)