Gulliksson et al1 report the results of a randomized controlled trial of cognitive behavioral therapy (CBT), measuring its effects on Cardiovascular Disease (CVD) recurrence in 362 patients with coronary artery disease. The authors found that, after 94 months, the CBT group had a 41% lower rate of fatal and nonfatal recurrent CVD events and 45% fewer recurrent acute myocardial infarctions (AMIs) after adjustment for covariates. As the authors acknowledge, a large body of evidence exists to link psychosocial factors such as depression, anxiety, and low social support to adverse cardiovascular outcomes. There is compelling evidence that up to 42% of coronary patients experience depression.2 Comorbid depression, even mild symptoms, can predict mortality,3 morbidity, and poorer clinical and well-being outcomes. Indeed, the intervention detailed by Gulliksson and colleagues, which comprised a group-based CBT program, addressed these psychosocial influences. Twenty-two–hour sessions were conducted over 1 year (plus usual medical care), with the overall goal of treatment to develop emotional and behavioral coping strategies for dealing with stress. The focus was particularly on stress reactivity and stress behaviors characterized by negative affect like hostility, anxiety, and depressive mood reactions [see eAppendix1] However, in the absence of depression, anxiety, and social support outcome measures documented in this study, ascertaining the components of this group-based CBT intervention that led to these improvements is particularly difficult. Post-AMI depression has been identified as a predictor of 1-year cardiac mortality, and moreover, high levels of social support have been found to provide a protective influence from depression on mortality.4 Because the authors have not discussed the mediating role of these variables, readers can only speculate about their influence. Furthermore, while this study highlights the benefits of a protocol-driven program, whether its effectiveness is fully explained by the CBT approach to treatment, from enhanced social support via regular, face-to-face, group-based contact with peers or via improvements in anxiety and depression as a direct consequence of therapy or as a byproduct of other behavioral modifications, remains unanswered. Unlike other trials using CBT in cardiac populations that have failed to produce significant survival benefits,5 this study demonstrates the positive effects of a CBT approach in the secondary prevention of CAD. However, we hypothesize that while the contribution of putative influences such as depression, anxiety, and social support remains unaccounted for in this study, it is likely that they are, in fact, elucidating the observed relationship between survival and treatment.
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