The Practitioner 2007;251(1699):24
Screening for depression post-MI may not be beneficial
01 Oct 2007
AUTHORS
Dr Phillip Bland
GP, Dalton-in-Furness
Article
Depression and ischaemic heart disease (IHD) are intricately linked: depression is an independent risk factor for the development of IHD, approximately 20% of patients become depressed following a heart attack and post-MI depression more than doubles the risk of mortality.1
Screening for depression has therefore been included in the QOF (see table 1, attached), despite the lack of evidence from intervention studies that identification and treatment of post-MI depression improves outcomes.
The ENRICHD trial found that CBT improved depression but did not increase event-free survival2 and the SADHART trial was not designed to assess the effects of treatment on cardiovascular prognosis.
A recent study has looked at interventions for depression in patients following an MI.
This study recruited 2,177 patients admitted to hospital with an MI, who were then screened for depression at three-monthly intervals over an 18-month period. During this time, 375 patients (17.2%) met the ICD-10 criteria for depression and were randomised to intervention or care as usual. Patients in the intervention group who agreed to treatment were either randomised to mirtazapine/placebo, given open treatment with citalopram or given non-pharmacological or no treatment.
At 18 months post-MI, no differences were observed between the intervention and control groups, either in the prevalence of ICD-10 depression (30.5% in the intervention group and 32.1% in patients randomised to care as usual) or in the incidence of cardiac events (14% and 13% respectively).
It is possible that these negative results represent a type II error. The study was underpowered to detect differences in cardiac outcomes, in part because the observed incidence of cardiac events was much less than the expected incidence and because the authors were over-optimistic with regard to the anticipated effects of their intervention.
The study's flexible approach to treatment meant that only 90 of the 196 patients randomised to the intervention group received antidepressant treatment (46%). Data were not collected regarding the duration of antidepressant treatment.
The question as to whether identification and treatment of post-MI depression can improve cardiovascular prognosis remains unanswered: an adequately powered trial that incorporates managed care in the intervention arm is required. This trial does, however, provide further evidence for the view that we should not be screening for depression until we have set in place efficient and effective management programmes.3
REFERENCES
• van Melle JP, de Jonge P, Honig A et al. Effects of antidepressant treatment following myocardial infarction. Br J Psychiatry 2007;190:460-6
References
1 van Melle JP, de Jonge P, Spijkerman TA. Prognostic association of depression following myocardial infarction with mortality and cardiovascular events: a meta-analysis. Psychosom Med 2004;66:814-22
