Why have we failed to show that effective treatment of depression in patients with comorbid coronary heart disease improves cardiac outcome?
Article first published online: 17 MAR 2011
© 2011 The Authors. Psychiatry and Clinical Neurosciences © 2011 Japanese Society of Psychiatry and Neurology
Psychiatry and Clinical Neurosciences
Volume 65, Issue 2, page 203, March 2011
How to Cite
Vieweg, W. V. R., Hasnain, M., Lesnefsky, E. J. and Pandurangi, A. K. (2011), Why have we failed to show that effective treatment of depression in patients with comorbid coronary heart disease improves cardiac outcome?. Psychiatry and Clinical Neurosciences, 65: 203. doi: 10.1111/j.1440-1819.2011.02187.x
- Issue published online: 17 MAR 2011
- Article first published online: 17 MAR 2011
- Received 8 June 2010; revised 16 December 2010; accepted 19 December 2010.
IN PATIENTS WITH coronary heart disease (CHD), depression following myocardial infarction (MI) is associated with a 2–2.5-fold increased risk for severe adverse cardiovascular events1 and we have highly effective treatments for major depressive disorder (MDD). Why have large-scale studies of patients with depression and comorbid CHD2–5 repeatedly failed to show that effective treatment of depression improves cardiac outcome? We believe that the mismatch between instruments used in depression and those used in CHD is the most likely explanation.
Using the Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) randomized trial6 as an example of this mismatch, the method used to assess depression was based on modified DSM-IV-TR criteria for either current MDD, minor depressive disorder with a history of past MDD, or dysthymia. The principle modification was that current symptoms of depression must be present for 7 days instead of 14 days to facilitate enrollment and start treatment early. A structured version of the 17-item Hamilton Depression Rating Scale (HDRS) was integrated with the National Institute of Mental Health Diagnostic Interview Scale as modified for cardiac patients7 to form a new instrument: the Depression Interview and Structured Hamilton (DISH). According to the ENRICHD authors, the DISH produces accurate DSM-IV diagnoses, assesses the longitudinal course of the depressive disorder, and provides a reliable HDRS.
The method used to assess CHD in the ENRICHD study focused on acute MI and required a characteristic increase in creatine kinase cardiac isoenzyme above the upper limits of the reference or an increase in other biomarkers to more than twice the upper limit. When cardiac isoenzyme values were less than twice the reference range, there was a mandatory review by the onsite cardiologist. Also, at least one of the following must have been present: (i) symptoms compatible with acute MI; or (ii) characteristic evolutionary electrocardiographic ST-T wave changes or new Q waves.
Thus, instruments used in depression are less rigorous than those used in CHD. Depression instruments largely employ scales of categorical variables, when most depressive symptoms/behaviors are better described on ordinal scales. During instrument development, subjects with comorbid medical illness were excluded during field-testing. Parametric statistics were often used to analyze non-Gaussian data. These factors may explain why treatment of depression has not been found to improve cardiovascular conditions. We propose using the objectivity of CHD parameters to assess the efficacy of psychiatric interventions in patients with comorbid depression and to define the link between depression and CHD.