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Psychiatric Times. Vol. 24 No. 7
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Depression With Coronary Disease: Therapy Adds No Benefit to SSRI

By Kenneth J. Bender, PharmD, MA | June 1, 2007

The investigators reported in the Journal of the American Medical Association (JAMA) that the antidepressant was superior to placebo in reducing depressive symptoms from baseline to the 12-week end point, by a mean 3.3 points on the HAM-D, a small to medium effect size of 0.33. Patients improved with both IPT and clinical management, with no statistical evidence of superiority for IPT. All treatments were well tolerated by the patients with CAD, with the antidepressant similar to placebo in blood pressure and ECG measures.

The CREATE trial found, as did SADHART, a greater benefit of the SSRI for patients with recurrent rather than first episode depression. This emerged from both more pronounced drug effect and reduced response to placebo in patients with a history of depression.

"It is . . . possible that SSRIs may actually have less impact in comparison with placebo among persons experiencing first episodes of major depression late in life, in the context of CAD or other cardiovascular diseases," the CREATE investigators suggested.

Although IPT did not evidence superiority over clinical management, the investigators pointed out that the clinical management protocol is not an "inert intervention." Clinical management involved semistructured 20- to 25-minute visits including information about depression and medication use, reassurance, and encouragement of adherence to medication and the study protocol.

The investigators suggested that clinical management may be particularly useful for this population. "CAD patients with low levels of support or poor daily functioning may have difficulty in dealing directly with the combination of cardiac and interpersonal issues that IPT sessions entail, and may do better with the lower demands of regular medical management," the investigators suggested.

Recognizing depression as cardiac risk factor

Lespérance and Frasure-Smith were among the first researchers to associate depression with increased mortality from MI6 and have understandably taken exception to the omission of major depression from recent lists of cardiac risk factors. "Are cardiologists particularly hard to convince, or is there something wrong with the data that has led many behavioral medicine specialists to believe that depression is a cardiac risk factor?" they asked.6

In their own review of the literature, Frasure-Smith and Lespérance did find great heterogeneity in study designs, definitions of depression, and outcome measures. Their analysis determined, however, that there is compelling evidence from adequately powered prospective etiologic studies, and from prospective studies with objective outcome measures and recognized indices of depression.

These studies, they indicated, "are remarkably consistent in their support of depression as a risk factor for both the development of and the worsening of [coronary heart disease]."2

Despite evidence of the detrimental impact of depression in cardiac patients, only 1 large randomized trial has sought to determine whether treating depression can improve CAD outcomes. The National Heart, Lung, and Blood Institute's ENRICHD (Enhancing Recovery in Coronary Heart Disease) trial demonstrated that a combination of short-term CBT and an SSRI, when necessary, was significantly better than usual care for reducing depressive symptoms.7 The study was insufficiently statistically powered, however, to determine whether the ENRICHD regimen was superior to usual care in reducing all-cause mortality or recurrent MI over a mean 29-month follow-up.

Frasure-Smith and Lespérance credit the ENRICHD trial, however, for breaking necessary ground before the CREATE trial. "The [ENRICHD] study . . . demonstrated that psychologists, psychiatrists, and cardiologists can successfully collaborate to test complicated intervention protocols with large numbers of patients from multiple sites," they pointed out.8 The CREATE trial would follow because, as Frasure-Smith and Lespérance described in a JAMA editorial, the ENRICHD study and others had left major depression as a CAD risk factor in search of a successful intervention.8 They noted further, "Regardless of whether rigorous studies will convincingly show that treating depression can influence cardiac prognosis, more trials are needed to find the best ways to improve care for patients with depression and CAD."

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References
1. Lespérance F, Frasure-Smith N, Koszycki D, et al. Effects of citalopram and interpersonal psychotherapy on depression in patients with coronary artery disease: the Canadian Cardiac Randomized Evaluation of Antidepressant and Psychotherapy Efficacy (CREATE) trial. JAMA. 2007;297:367-379.
2. Frasure-Smith N, Lespérance F. Reflections on depression as a cardiac risk factor. Psychosom Med. 2005; 67:S19-S25.
3. Glassman AH, O'Connor CM, Califf RM, et al. Sertraline treatment of major depression in patients with acute MI or unstable angina. JAMA. 2002;288:701-709.
4. Fawcett J, Epstein P, Fiester SJ, et al. Clinical management-imipramine/placebo administration manual. NIMH Treatment of Depression Collaborative Research Program. Psychopharmacol Bull. 1987;23:309-324.
5. Markowitz JC, Kocsis JH, Fishman B, et al. Treatment of depressive symptoms in human immunodeficiency virus-positive patients. Arch Gen Psychiatry. 1998;55: 452-457.
6. Frasure-Smith N, Lespérance F, Talajic M. Depression following myocardial infarction. Impact on 6-month survival. JAMA. 1993;270:1819-1825.
7. Berkman LF, Blumenthal J, Burg M, et al, and the Enhancing Recovery in Coronary Heart Disease Patients Investigators. Effects of treating depression and low perceived social support on clinical events after myocardial infarction: the Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) Randomized Trial. JAMA. 2003;289:3106-3116.
8. Frasure-Smith N, Lespérance F. Depression—a cardiac risk factor in search of a treatment. JAMA. 2003; 289:3171-3173.


 
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