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Depression and cardiovascular disease: have a happy day—just smile!

Bertram Pitt, Patricia J. Deldin
DOI: http://dx.doi.org/10.1093/eurheartj/ehq031 1036-1037 First published online: 17 February 2010

This editorial refers to ‘Don't worry, be happy: positive affect and reduced 10-year incident coronary heart disease: The Canadian Nova Scotia Health Survey’, by K.W. Davidson et al. on page 1065

The relationship between cardiovascular disease and depression poses intriguing research questions, particularly for co-morbid treatment. Preliminary studies have indicated that patients with early-onset depression are at a significantly increased risk for developing cardiovascular disease (CVD) after correcting for cardiovascular risk factors, and this effect occurs even in the absence of a diagnosis of major depression.1 Depression increases the risk of coronary artery disease by 1.5–2 times in otherwise physically healthy individuals.2 In addition, patients with CVD such as myocardial infarction, stroke, heart failure, and atrial fibrillation are at increased risk of developing depression and, when depression develops, cardiovascular risk is exacerbated further.2,3 Patients with treatment-resistant depression (failure to respond to a single trial of antidepressant) after an acute coronary syndrome are at even greater cardiovascular risk.4

The use of antidepressants, such as selective serotonin uptake inhibitors (SSRIs) and tricyclic antidepressants (TCAs), does not appear to mitigate cardiovascular risk associated with depression, despite altering one or more of the physiological abnormalities linking CVD to depression such as increased inflammatory cytokines, a decreased circulation of endothelial progenitor cells, and a deficiency in nitric oxide availability.57 Nor does the combination of an SSRI and n-3 fatty acids appear to reduce mood-associated cardiovascular risk.8 Instead, a recent report of >99 000 patients surviving their first hospitalization for heart failure has suggested that the use of both TCAs and SSRIs was associated with an increased risk of total and cardiovascular-related mortality.9 Surprisingly, co-administration of an SSRI and a beta-adrenergic blocking agent was also associated with an increased risk of total and cardiovascular-related mortality, prompting the authors of the study to urge further clinical study to determine the optimum antidepressant strategy in patients with heart failure.

Davidson et al.10 have examined the association between patient affect and cardiovascular events after correcting for age, gender, and cardiovascular risk factors. The researchers found that positive affect protected against the development of coronary heart disease while depressive symptoms increased the likelihood of disease onset. They point out that positive affect can easily be assessed by measures such as whether or not the patient smiles during the clinical interview and whether they appear to take pleasure or excitement in aspects of their daily life.

Since the study of Davidson et al. is non-experimental, it has not been determined whether positive affect has a direct or indirect causal role in CVD, or whether both conditions share a common, underlying third variable. This has important implications for co-morbid treatment. If positive affect is indirectly related to CVD, perhaps positive affect moderates the effects of stress and this stress reduction may decrease CVD risk. Alternatively, perhaps poor or negative affect and cardiovascular disease are influenced by an underlying third variable. For example, reductions in positive affect and CVD can both be caused by poor sleep.11,12 However. if the positive affect–CVD relationship is direct, atypical, aminoketone antidepressants such as buproprion that modulate noradrenergic and dopaminergic activity might be better candidates for improving cardiac outcome because they have been shown to enhance positive affect better than SSRIs and have the added benefits of facilitating weight loss13 and smoking cessation.14 In contrast, SSRIs may produce weight gain15 and may have less impact on positive affect.16

Another important question is whether positive affect is also related to long-term risk. For example, heart rate variability, indicative of healthy cardiac autonomic control, was found to be highly associated with positive affect over a day in an experience sampling ambulatory study.17 Yet even if reduced positive affect is shown to cause increased mortality over the long term, it may not be easily modified. Historically, theorists have believed that it is nearly impossible to institute long-term changes in the amount of positive (or negative) emotion an individual experiences and that humans have an emotional ‘set point’ that they return to regardless of intervening life events.18 More recently, however, theorists acknowledge that although much of affective experience may be genetically determined, long-term happiness may be modifiable by life experiences.19 For example, people who get divorced, on average, never return to their pre-divorce levels of happiness.20 Davidson et al.10 suggest that interventions to augment positive affect (‘behavioural activation interventions’) such as instructions to pursue hobbies or enjoyable activities on a daily basis to increase quality of life may have a beneficial effect on cardiovascular risk in patients with depression or negative affect.

Researchers in the nascent field of positive psychology have been successful in finding additional, empirically based strategies that are believed to increase happiness over the long term. These strategies fall along four, broad, inter-related domains: social, psychological, behavioural, and physiological. Strong, supportive, and safe social networks have long been associated with increased happiness and sense of well-being.21 Therefore, strategies that improve social skill and decrease social anxiety theoretically could also have an impact on cardiovascular function. Activities such as regularly expressing gratitude, choosing an optimistic framework, regularly carrying out acts of kindness, repeatedly writing or talking about negative (not positive) life events, regularly visualizing one's best possible self, savouring joyful events, attending to and learning to appreciate life's positives and practising mindfulness, forgiveness therapy, and thoughtful self-reflection are successful at increasing subjective well-being.22 Finally, regular exercise,23 and sexual activity24 and good sleep11 are all associated with increased self-reported happiness. Currently, randomized controlled trials of interventions to increase positive affect in patients with CVD are underway; they will help determine the effectiveness of increasing positive affect on cardiovascular outcome and will provide insight into the nature of the relationship between positive affect and CVD.

The ‘vicious cycle’ linking CVD to major depression and depression to CVD deserves greater attention from both cardiovascular and psychiatric investigators. The apparent failure of current antidepressive therapy with SSRIs and TCAs to break the link between depression and CVD emphasizes the importance of new approaches such as those proposed by Davidson et al.10 These new treatments could open up an exciting potential new approach for treating patients with known cardiovascular disease who develop depression. If the observations and hypotheses of Davidson et al. stimulate further investigation regarding the effect of increased positive affect on physiological abnormalities associated with cardiovascular risk, perhaps it will be time for all of us to smile.

Conflict of interest: none declared.


  • doi:10.1093/eurheartj/ehp603

  • 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.


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