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Amanda Nicholson, Hannah Kuper, Mika Kivimaki, Harry Hemingway, Meta-analysis urges the development of new strategies to treat depression in order to improve cardiac prognosis: reply, European Heart Journal, Volume 28, Issue 13, July 2007, Pages 1661–1662, https://doi.org/10.1093/eurheartj/ehm128
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de Jonge and Van Melle's model, suggesting that the somatic symptoms of depression may impair prognosis in CHD independently of severity of disease, offers a useful framework for future work.1 The first step will be to confirm that such an independent effect exists. Their findings need to be confirmed in other studies which control effectively for the severity of cardiac disease and examine different dimensions of depression. A meta-analysis using individual patient data would allow systematic adjustment for confounders and severity of disease. If an independent effect of depression is confirmed by such work, some doubts about residual reverse causality in the observed effect may persist. Results of studies based on depression reports will remain open to the possibility that the somatic items on depression symptom scales are acting as a better measure of physical health than the items being used to control for severity of disease.
Failure to demonstrate reversibility in the association between depression and impaired prognosis in heart disease remains a strong argument against a causal effect. There is some evidence of an effect of selective serotonin reuptake inhibitors (SSRIs) in improving prognosis in those suffering depression after an MI,2,3 although this requires confirmation in further studies. We wonder whether pharmacogenetic studies might add extra support to a causal link if an effect of SSRIs on prognosis of CHD is confirmed. Polymorphisms in genes influencing brain monoamines, for example, 5-HTTLPR and NET, may influence the impact of SSRI or NRI antidepressants on depressive symptoms.4,5 Assuming an independent effect of depression on CHD prognosis, any improvement in CHD prognosis due to treatment should be less in subjects with the genotype associated with a poorer response of depression to medication.
