Skip to main page content

• HOME
• Current
• Archive
• Feedback
• Subscribe
• Help

The British Journal of Psychiatry (2007) 191: 456-457. doi: 10.1192/bjp.191.5.456a
© 2007 The Royal College of Psychiatrists

This Article Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by de Jonge, P. Articles by Ormel, J. Search for Related Content PubMed Articles by de Jonge, P. Articles by Ormel, J.

Correspondence

Authors’ reply:

P. de Jonge

Department of Internal Medicine and Department of Psychiatry, University Medical Center Groningen, The Netherlands. Email: p.d.jonge{at}med.umcg.nl

J. P. van Melle

Department of Cardiology, Thoraxcenter, University Medical Center Groningen, The Netherlands

J. Ormel

Department of Social Psychiatry and Psychiatric Epidemiology, University Medical Center Groningen, The Netherlands

EDITED BY KIRIAKOS XENITIDIS and COLIN CAMPBELL

To explain why anti-depressant treatment with selective serotonin reuptake inhibitors (SSRIs) does not improve cardiac prognosis, Korszun et al suggest that SSRIs may not alter the mechanisms through which depression leads to increased cardiovascular morbidity and mortality. However, two other explanations may be more plausible. First, the effects of antidepressant treatment on depression itself are not strong enough. In both the ENRICHD and SADHART trials, the response rates of patients in the active treatment arm hardly exceeded those of patients receiving usual care or placebo. Second, the cardiotoxic effects of depression are limited to patients for whom antidepressant treatment is not effective (Grace et al, 2005; de Jonge et al, 2006a). We have shown that the cardiotoxic effects of depression are concentrated in incident post-myocardial infarction depression, whereas results from the SADHART study have indicated that sertraline is only effective in non-incident depression (of interest, Korszun et al mention mechanisms related to recurrent depression, which appears not be to cardiotoxic). If antidepressant treatment is only effective in non-cardiotoxic depression, no effects on cardiovascular prognosis can be expected.

Shetty raises ethical concerns about our study, because we used Zelen’s method of randomisation. Controls were not told about their diagnosis of depression and, as argued by Shetty, therefore may have ‘missed’ an offer of adequate treatment. However, we feel that in 1999, when the study started, Zelen’s method was both scientifically useful and ethical because no controlled comparative studies had yet investigated the clinical efficacy and safety of antidepressant drugs in depression post-myocardial infarction. At that time, the proportion of myocardial infarction patients with depression who were treated for their post-myocardial infarction depression was negligible. In addition, serious concerns existed about the safety of antidepressant drugs in cardiac patients. Moreover, in our study patients with a significant risk of suicide or severe depression were excluded from randomisation and referred for psychiatric treatment outside the study. Finally, all patients received usual care, i.e. had cost-free access to all usual treatment facilities such as normal cardiac rehabilitation programmes and healthcare from family physicians. We therefore feel it was ethical to use Zelen’s method in our study and scientifically useful as our control patients were truly representative of patients receiving usual care.

We agree with Dr Kho that we need to develop new treatments for depression post-myocardial infarction, but believe it is premature to consider electroconvulsive therapy (ECT) as an effective alternative. In our experience those types of depression that are least similar to those seen in general psychiatry (i.e. incident depression occurring for the first time after myocardial infarction; de Jonge et al, 2006b) and those that are dominated by feelings of exhaustion rather than negative self-esteem or suicidality (de Jonge et al, 2006a) are the most cardiotoxic. To our knowledge the mechanism(s) explaining this remain unclear. Similarly, it is not known whether ECT is effective in these subtypes (although it appears that antidepressive medication is not). In fact, the studies mentioned by Dr Kho suggest increased rather than decreased cardiovascular events.

New, effective treatments for depression post-myocardial infarction will improve quality of life but perhaps also survival, as rightfully argued by Dr Kho. Carney et al (2004) showed that responders to anti-depressive medication had a better cardiovascular prognosis than non-responders, using data from the ENRICHD trial. In the MIND–IT study we recently confirmed that non-response to mirtazapine and citalopram was associated with more cardiovascular events compared with responders and even untreated controls, a finding that remained after controlling for several confounders, including early cardiovascular events (de Jonge et al, 2007). However, as it is unclear what factors are related to response to antidepressive medication (these may well include the presence of somatic symptoms of depression; Tylee & Gandhi, 2005), it also remains uncertain whether it might be an improved state of the heart disease that influences depression or reversely that treatment of depression results in an improved cardiovascular prognosis. However, although causality remains unproven it suggests that more effective treatments may have cardiovascular effects as well. We are not yet convinced that this will be ECT but we encourage researchers to explore this possibility.

REFERENCES

1. Carney, R. M., Blumenthal, J. A., Freedland, K. E., et al (2004) Depression and late mortality after myocardial infarction in the Enhancing Recovery in Coronary Heart Disease (ENRICHD) Study. Psychosomatic Medicine, 66, 466 –474.[Abstract/Free Full Text]
2. De Jonge, P., van den Brink, R. H. S., Spijkerman, T. A., et al (2006a) Only incident depressive episodes following myocardial infarction are associated with new cardiovascular events. Journal of the American College of Cardiology, 48, 2204 –2208.[Abstract/Free Full Text]
3. De Jonge, P., Ormel, J., van den Brink, R. H. S., et al (2006b) Symptom dimensions of depression following myocardial infarction and their relationship with somatic health status and cardiovascular prognosis. American Journal of Psychiatry, 163, 138 –144.[Abstract/Free Full Text]
4. De Jonge, P., Honig, A., van Melle, J. P., et al (2007) Non-response to treatment for depression following myocardial infarction is associated with subsequent cardiac events. American Journal of Psychiatry, 164, 1371 –1378.[Abstract/Free Full Text]
5. Grace, S. L., Abbey, S. E., Kapral, M. K., et al (2005) Effect of depression on five-year mortality after an acute coronary syndrome. American Journal of Cardiology, 96, 1179 –1185.[CrossRef][Medline]
6. Tylee, A. & Gandhi, P. (2005) The importance of somatic symptoms in depression in primary care. Journal of Clinical Psychiatry, 7, 167 –176.

This Article Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by de Jonge, P. Articles by Ormel, J. Search for Related Content PubMed Articles by de Jonge, P. Articles by Ormel, J.