The interface of emotion and biology in myocardial ischemia: Can we progress using the traditional paradigm?

Journal of Nuclear Cardiology, Feb 2017

Robert Soufer MD, FACC, Matthew M. Burg PhD

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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 - 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)


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Robert Soufer MD, FACC, Matthew M. Burg PhD. The interface of emotion and biology in myocardial ischemia: Can we progress using the traditional paradigm?, Journal of Nuclear Cardiology, 2017, pp. 783-787, Volume 24, Issue 3, DOI: 10.1007/s12350-016-0762-2