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Depression has been noted to occur in approximately one in six people during their lifetime,1 and to occur in nearly a fifth of patients following myocardial infarction (MI).2 As well as the morbidity associated with the symptoms of depression, it has been associated with a raised risk of death following MI independent of cardiac disease severity.3 This has led to trials of treatment for depression in patients with heart disease. However, randomised controlled trials (RCTs) of treatment of depression post-MI, such as the ENRICHD trial, which used cognitive behavioural therapy and selective serotonin reuptake inhibitors (SSRIs) for more severe depression,4 improved symptoms of depression but did not reduce the frequency of adverse cardiac events.
In this issue of Heart, Kranz and colleagues report data from 519 women enrolled in the Women’s Ischemia Syndrome Evaluation (WISE) study (see page 1901).5 This was a prospective cohort study of women undergoing clinically indicated coronary angiography and had a median follow-up of 5.9 years. These women were found to have almost a fourfold increase in risk of adverse cardiac events over the following 6 years if they had received combined treatment with anxiolytics and antidepressants. Inevitably such a finding in an observational study invites the question—is the treatment, or are other factors, responsible?
Competing interests KJ and MJSL have undertaken a Wellcome Trust-funded case-control study of drug antecedents of sudden death. MJSL has received a fee for speaking from Bayer GmbH and has received consulting fees from Galpharm and from Procter and Gamble. Consulting fees from Merck and Co Inc have been paid to the University of Birmingham. MJSL is also an honorary consultant to the WHO Collaborative Centre for International Drug monitoring in Uppsala. MJSL’s wife holds shares in GlaxoSmithKline.