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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:† doi:10.1093/eurheartj/ehp603 Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2010. For permissions please email:
intervening life events.18 More recently, however, theorists acknowledge that although much of affective experience may be 1. Rugulies R. Depression as a predictor for coronary heart disease. A review and genetically determined, long-term happiness may be modifiable meta-analysis. Am J Prev Med 2002;23:51 – 61.
2. Lett H, Blumenthal J, Babyak M, Sherwood A, Strauman T, Robins C, Newman MF.
by life experiences.19 For example, people who get divorced, on Depression as a risk factor for coronary artery disease: evidence, mechanisms, average, never return to their pre-divorce levels of happiness.20 and treatment. Psychosom Med 2004;66:305 – 315.
Davidson et al.10 suggest that interventions to augment positive 3. Frasure-Smith N, Lespe´rance F, Habra M, Talajic M, Khairy P, Dorian P, Roy D.
Atrial Fibrillation and Congestive Heart Failure Investigators. Elevated depression affect (‘behavioural activation interventions’) such as instructions symptoms predict long-term cardiovascular mortality in patients with atrial fibril- to pursue hobbies or enjoyable activities on a daily basis to lation and heart failure. Circulation 2009;120:134 – 340.
increase quality of life may have a beneficial effect on cardiovascu- 4. Carney R, Freedland K. Treatment-resistant depression and mortality after acute coronary syndrome. Am J Psychiatry 2009;166:410 – 417.
lar risk in patients with depression or negative affect.
5. Follath F. Depression, stress and coronary heart disease—epidemiology, progno- Researchers in the nascent field of positive psychology have sis and therapeutic sequelae. Rev Med Suisse 2009;5:515 – 516, 518 – 519.
been successful in finding additional, empirically based strategies 6. Rajagopalan S, Brook R, Rubenfire M, Pitt E, Young E, Pitt B. Abnormal brachial artery flow-mediated vasodilation in young adults with major depression. Am J that are believed to increase happiness over the long term.
These strategies fall along four, broad, inter-related domains: 7. Dome P, Teleki Z, Rihmer Z, Peter L, Dobos J, Kenessey I, Tovari J, Timar J, Paku S, social, psychological, behavioural, and physiological. Strong, sup- Kovacs G, Dome B. Circulating endothelial progenitor cells and depression: apossible novel link between heart and soul. Mol Psychiatry 2009;14:523–531.
portive, and safe social networks have long been associated with 8. Carney RM, Freedland KE, Rubin EH, Rich MW, Steinmeyer BC, Harris WS.
increased happiness and sense of well-being.21 Therefore, strat- Omega-3 augmentation of sertraline in treatment of depression in patients with egies that improve social skill and decrease social anxiety theor- coronary heart disease: a randomized controlled trial. JAMA 2009;302:1651.
9. Fosbøl E, Gislason G, Poulsen H, Hansen M, Folke F, Schramm T, Olesen JB, etically could also have an impact on cardiovascular function.
Activities such as regularly expressing gratitude, choosing an Torp-Pedersen C. Prognosis in heart failure and the value of b-blockers are optimistic framework, regularly carrying out acts of kindness, altered by the use of antidepressants and depend on the type of antidepressants used. Circulation 2009;2:582 – 590.
repeatedly writing or talking about negative (not positive) life 10. Davidson KW, Mostofsky E, Whang W. Don’t worry, be happy: positive affect and events, regularly visualizing one’s best possible self, savouring reduced 10-year incident coronary heart disease: The Canadian Nova Scotia joyful events, attending to and learning to appreciate life’s posi- Health Survey. Eur Heart J 2010;31:1065 – 1070. First published on 17 February2010. doi:10.1093/eurheartj/ehp603.
tives and practising mindfulness, forgiveness therapy, and 11. Steptoe A, O’Donnell K, Marmot M, Wardle J. Positive affect, psychological well- thoughtful self-reflection are successful at increasing subjective being, and good sleep. J Psychosom Res 2008;64:409 – 415.
well-being.22 Finally, regular exercise,23 and sexual activity24 12. Caples S, Garcia-Touchard A, Somers V. Sleep-disordered breathing and cardio- vascular risk. Sleep 2007;30:291 – 304.
and good sleep11 are all associated with increased self-reported 13. Demyttenaere K, Jaspers L. Bupropion and SSRI-induced happiness. Currently, randomized controlled trials of interven- J Psychopharmacol 2008;22:792 – 804.
tions to increase positive affect in patients with CVD are under- 14. Rigotti N, Thorndike A, Regan S, McKool K, Pasternak R, Chang Y, Swartz S, Torres-Finnerty N, Emmons KM, Singer DE. Bupropion for smokers hospitalized way; they will help determine the effectiveness of increasing with acute cardiovascular disease. Am J Med 2006;119:1080 – 1087.
positive affect on cardiovascular outcome and will provide 15. Sussman N, Ginsberg D, Bikoff J. Effects of nefazodone on body weight: a pooled insight into the nature of the relationship between positive analysis of selective serotonin reuptake inhibitor- and imipramine-controlledtrials. J Clin Psychiatry2001;62:256 – 260.
16. Nutt DJ. Relationship of neurotransmitters to the symptoms of major depressive The ‘vicious cycle’ linking CVD to major depression and disorder. J Clin Psychiatry 2008;69:4 – 7.
depression to CVD deserves greater attention from both cardio- 17. Steptoe A, Wardle J, Marmot M, McEwen B. Positive affect and health-related neuroendocrine, cardiovascular, and inflammatory processes. Proc Natl Acad Sci vascular and psychiatric investigators. The apparent failure of current antidepressive therapy with SSRIs and TCAs to break 18. Brickman P, Campbell DT. Hedonic relativism and planning the good society. In: the link between depression and CVD emphasizes the importance Appley HM, ed. Adaptation level theory: a symposium. New York: Academic Press;1971. p287 – 302.
of new approaches such as those proposed by Davidson et al.10 19. Diener E, Lucas RE, Scollon CN. Beyond the hedonic treadmill: revising the adap- These new treatments could open up an exciting potential new tation theory of well-being. Am Psychol 2006;61:305.
approach for treating patients with known cardiovascular disease 20. Lucas R, Clark A, Georgellis Y, Diener E. Reexamining adaptation and the set point model of happiness: reactions to changes in marital status. J Person Soc who develop depression. If the observations and hypotheses of Davidson et al. stimulate further investigation regarding the effect 21. Berkman L, Glass T, Brissette I, Seeman T. From social integration to health: Dur- of increased positive affect on physiological abnormalities associ- kheim in the new millennium. Soc Sci Med 2000;51:843 – 857.
22. Sin N, Lyubomirsky S. Enhancing well-being and alleviating depressive symptoms ated with cardiovascular risk, perhaps it will be time for all of us with positive psychology interventions: a practice-friendly meta-analysis. J Clin Psy- 23. Mutrie N. Healthy body, healthy mind? The Psychologist 2002;15:412 – 413.
24. Rosen R, Bachmann G. Sexual well-being, happiness, and satisfaction, in women: Conflict of interest: none declared.
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