Premiere Date: September 20, 2018
Expiration Date: March 20, 2020
This activity offers CE credits for:
1. Physicians (CME)
All other clinicians either will receive a CME Attendance Certificate or may choose any of the types of CE credit being offered.
To goal of this activity is to understand the bidirectional relationship between depression and cardiovascular disease.
At the end of this CE activity, participants should be able to:
• Explain the reasons for the high comorbidity between depression and cardiovascular disease
• Understand the role of the autonomic nervous system in regulating heart function
• Assess autonomic nervous system activity through measurement of heart rate variability
This continuing medical education activity is intended for psychiatrists, psychologists, primary care physicians, physician assistants, nurse practitioners, and other health care professionals who seek to improve their care for patients with mental health disorders.
CME Credit (Physicians): This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of CME Outfitters, LLC, and Psychiatric Times. CME Outfitters, LLC, is accredited by the ACCME to provide continuing medical education for physicians.
CME Outfitters designates this enduring material for a maximum of 1.5 AMA PRA Category 1 Credit™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Note to Nurse Practitioners and Physician Assistants: AANPCP and AAPA accept certificates of participation for educational activities certified for AMA PRA Category 1 Credit™.
It is the policy of CME Outfitters, LLC, to ensure independence, balance, objectivity, and scientific rigor and integrity in all of their CME/CE activities. Faculty must disclose to the participants any relationships with commercial companies whose products or devices may be mentioned in faculty presentations, or with the commercial supporter of this CME/CE activity. CME Outfitters, LLC, has evaluated, identified, and attempted to resolve any potential conflicts of interest through a rigorous content validation procedure, use of evidence-based data/research, and a multidisciplinary peer-review process.
The following information is for participant information only. It is not assumed that these relationships will have a negative impact on the presentations.
Angelos Halaris, MD, has no conflicts to report.
Ebrahim Haroon, MD (peer/content reviewer), reports that he receives funding from the NIH.
Applicable Psychiatric Times staff and CME Outfitters staff, have no disclosures to report.
UNLABELED USE DISCLOSURE
Faculty of this CME/CE activity may include discussion of products or devices that are not currently labeled for use by the FDA. The faculty have been informed of their responsibility to disclose to the audience if they will be discussing off-label or investigational uses (any uses not approved by the FDA) of products or devices. CME Outfitters, LLC, and the faculty do not endorse the use of any product outside of the FDA-labeled indications. Medical professionals should not utilize the procedures, products, or diagnosis techniques discussed during this activity without evaluation of their patient for contraindications or dangers of use.
For content-related questions, email us at [email protected]; for questions concerning CME credit – Call us at 877.CME.PROS (877.263.7767)
Dr Halaris is Professor of Psychiatry and Behavioral Neuroscience, Loyola University Stritch School of Medicine, Loyola University Medical Center, Maywood, IL.
1. Harvey W. The circulation of the blood is further confirmed by probably reasons. On the Motion of the Heart and Blood in Animals. March 2016. https://ebooks.adelaide.edu.au/h/harvey/william/motion/chapter15.html. Accessed August 1, 2018.
2. Waldman SA, Terzic A. Cardiovascular health: the global challenge. Clin Pharmacol Ther. 2011;90:483-485.
3. American Heart Association: Heart Disease and Stroke Statistics: 2004 Update. Dallas, TX: American Heart Association; 2004.
4. Demyttenaere K, Bruffaerts R, Posada-Villa J, et al. Prevalence, severity, and unmet need for treatment of mental disorders in the World Health Organization World Mental Health surveys. JAMA. 2004;291:2581-2590.
5. Barth J, Schumacher M, Herrmann-Lingen C. Depression as a risk factor for mortality in patients with coronary heart disease: a meta-analysis. Psychosom Med. 2004;66:802-813.
6. Gump BB, Matthews KA, Eberly LE, Chang YF, for the MRFIT Research Group. Depressive symptoms and mortality in men: results from multiple risk factor intervention trial. Stroke. 2005;36:98-102.
7. Thayer JF, Lane RD. The role of vagal function in the risk for cardiovascular disease and mortality. Biol Psychol. 2007;74:224-242.
8. Otte C, Neylan TC, Pipkin SS, et al. Depressive symptoms and 24-hour urinary norepinephrine excretion levels in patients with coronary disease: findings from the Heart and Soul Study. Am J Psychiatry. 2005;162:2139-2145.
9. Licht CM, de Geus EJC, Zitman FG, et al. Association between major depressive disorder and heart rate variability in the Netherlands Study of Depression and Anxiety (NESDA). Arch Gen Psychiatry. 2008;65:1358-1367.
10. Porges SW. Cardiac vagal tone; a physiological index of stress. Neurosci Biobehav Rev. 1995;19:225-233.
11. Kop WJ, Stein PK, Tracy RP, et al. Autonomic nervous system dysfunction and inflammation contribute to the increased cardiovascular mortality risk associated with expression. Psychosom Med. 2010;72:626-635.
12. Hage B, Britton B, Daniels D, et al. Low cardiac vagal tone index by heart rate variability differentiates bipolar from major depression. World J Biol Psychiat. October 2017;1-9.
13. Hage B, Britton B, Daniels D, et al. Heart Rate Variability predicts treatment outcome in major depression. J Psychiat Brain Sci. 2017;2:1-13.
14. Pavlov V, Tracey K. The cholinergic anti-inflammatory pathway. Brain Behav Immun. 2009;19:493-499.
15. Halaris A. Myint A-M, Savant V et al. 2015. Does escitalopram reduce neurotoxicity in major depression? J Psychiat Res. 2015;66-67:118-126.
16. Wichers M, Maes M. The psychoneuroimmuno-pathophysiology of cytokine-induced depression in humans. Int J Neuropsychopharmacol. 2002;5:375-388.
17. Koenig W. Inflammation and coronary heart disease: an overview. Cardiol Rev. 2001;9:31-35.
18. Mulvihill NT, Foley JB. Inflammation in acute coronary syndromes. Heart. 2002;87:201-204.
19. Connor TJ, Leonard BE. Depression, stress and immunological activation: the role of cytokines in depressive disorders. Life Sci. 1998;62:583-606.
20. Lind L. Circulating markers of inflammation and atherosclerosis. Atheroscler. 2003;169:203-214.
21. Frasure-Smith N, Lespérance F, Irwin MR, et al. Depression, C-reactive protein and two-year major adverse cardiac events in men after acute coronary syndromes. Biol Psychiat. 2007;62:302-308.
22. Pizzi C, Mancini S, Angeloni L, et al. Effects of selective serotonin reuptake inhibitor therapy on endothelial function and inflammatory markers in patients with coronary heart disease. Clin Pharmacol Therap. 2009;86:527-532.
23. Hiles SA, Baker A, de Malmanche T, et al. Interleukin-6, C-reactive protein and interleukin-10 after antidepressant treatment in people with depression: a meta-analysis. Psychol Med. 2012;42:2015-2026.
24. Chavda N, Kantharia ND, Jaykaran. Effects of fluoxetine and escitalopram on C-reactive protein in patients of depression. J Pharmacol Pharmacother. 2011;2:11-16.
25. Halaris A. Do antidepressants exert effects on the immune system? In: Mueller N, Myint A-M, Schwarz MJ, Eds. Immunology and Psychiatry, Current Topics in Neurotoxicity. Berlin: Springer Verlag; 2015:339-350.