Psychiatry - November 2008 - (Page 47)

[the interface] multiple factors, both pathophysiological and psychosocial, that mediate the complex relationshi between depression and cardiovascular phenomena—yet another complex interaction in the mind/body interface. THE ROLE OF ANTIDEPRESSANTS If depression contributes to CVD, both prospectively and concurrently, does depression treatment exert an impact on medical outcome? There is very little available research in this area. In examining the use of nontricyclic antidepressants in patients with cardiac disease, a study by de Jonge et al26 compared with antidepressant-nonresponders and untreated controls, antidepressant-responders to citalopram and mirtazapine were the least likely subgroup to develop new cardiac events following myocardial infarction. Finally, in a small study by Mohapatra et al27 of depressed postmyocardial-infarction patients, cardiac events were around three times more frequent in the nonantidepressant subgroup compared to participants on antidepressant treatment with sertraline. So, preliminary findings clearly but modestly lean in the direction of a positive effect of events in individuals with current disease. Like many other areas in medicine, this mind/body interface will clearly benefit from additional research—particularly the degree to which nontricyclic antidepressant therapy (principally treatment with SSRIs) will consistently prevent CVD in the depressed as well as stave off cardiac complications in those with comorbid depression and CVD. REFERENCES 1. Glassman AH. Depression and cardiovascular comorbidity. Dialogues Clin Neurosci. 2007;9:9–17. Collins-McNeil J, Holston EC, Edwards CL, et al. Depressive symptoms, cardiovascular risk, and diabetes self-care strategies in African American women with type 2 diabetes. Arch Psychiatr Nurs. 2007;21:201–209. Mausbach BT, Patterson TL, Rabinowitz YG, Grant I, Schulz R. Depression and distress predict time to cardiovascular disease in dementia caregivers. Health Psychol. 2007;26:539–544. Jacka FN, Pasco JA, McConnell S, et al. Self-reported depression and cardiovascular risk factors in a community sample of women. Psychosomatics. 2007;48:54–59. Janszky I, Ahlbom A, Hallqvist J, Ahnves S. Hospitalization for depression is associated with an increased risk for myocardial infarction not explained by lifestyle, lipids, coagulation, and inflammation: the SHEEP study. Biol Psychiatry. 2007;62:25–32. Ahto M, Isoaho R, Puolijoki H, Vahlberg T, Kivela SL. Stronger symptoms of depression predict high coronary heart disease in older men and women. Int J Geriatr Psychiatry. 2007;22:757–763. Kopp M, Skrabski A, Szanto Z, Siegrist J. Psychosocial determinants of premature preliminary findings clearly but modestly lean in the direction of a positive effect of nontricyclic antidepressants on cardiovascular outcome. sertraline is the most studied, but there are also studies with citalopram and mirtazapine. All three antidepressants have been well tolerated and safe in patients with cardiac disease. The two selective serotonin reuptake inhibitors (SSRIs) (i.e., sertraline and citalopram) have clearly demonstrated efficacy in treating depression in this population23 and appear to improve quality of life.24 However, the predictive effect of antidepressant treatment with regard to cardiovascular outcome remains unclear.24 Scant available data suggest that several antidepressants may modestly improve CVD outcome. For example, Glassman et al25 examined the efficacy of sertraline in preventing subsequent cardiac events in a group of depressed, hospitalized patients with myocardial infarctions.25 In this controlled study, the subgroup of patients on sertraline experienced fewer subsequent cardiac events (14.5%) compared with nontreated individuals (22.4%), but there was not a statistically significant difference. In nontricyclic antidepressants on cardiovascular outcome. If nontricyclic antidepressants, particularly SSRIs, are ultimately confirmed to be effective, their effects may not be limited to the alleviation of depression. Parissis et al17 have suggested that there are relevant SSRI effects on platelets (e.g., an inhibition of platelet activity). In addition, Paraskevaidis et al28 indicate that SSRIs may deter immune activation (i.e., prevent an inflammatory response) as well as normalize neurohormonal dysfunction (e.g., autonomic dysregulation) in patients. 2. 3. 4. 5. CONCLUSION According to available data, there is convincing evidence that depression is one of several contributory variables in the evolution of subsequent CVD. In addition, acute depression appears to influence the outcome of those with existing CVD. While the reasons remain unclear, antidepressant therapy with nontricyclics (particularly SSRIs) may modestly reduce the risk of subsequent cardiac 6. 7. [NOVEMBER] Psychiatry 2008 47

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Psychiatry - November 2008 Editor's Message Editorial Advisory Board Contents PsychRx Letters to the Editor Measuring Adverse Events in Psychiatry Nonsuicidal Self Injury in Adolescents Relative Tolerability of Alzheimer's Disease Treatments Biracial Identity Development and Recommendations in Therapy Depression and Cardiovascular Disease: Just an Urban Legend? Three Risk Management Basics Journal Watch Classified Advertising Information for Authors

Psychiatry - November 2008

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