A

Copyright © American Psychiatric Publishing, Inc., or American Psychiatric Association, unless otherwise indicated in figure legend, All rights reserved.

Kaplan-Meier analysis of the percentage of patients in the placebo and paroxetine groups who were free of major depression (A) and of severe depression, requiring the discontinuation of IFN-c: (B).

Source.Musselman et al. 2000.

Increased platelet reactivity has been observed in individuals with depression, which may explain the increased vulnerability to IHD in this population (Musselman et al. 1996). One study demonstrated normalization of platelet activity in patients with depression, following 6 weeks of treatment with paroxetine 20 mg/day (Musselman et al. 2000). It is unclear whether the antidepressant action of paroxetine or a direct pharmacological effect of the drug on platelet activity resulted in the observed outcome, but the preponderance of evidence with other SRIs supports the latter hypothesis (Serebruany et al. 2003).

Although the physiological association between depression and IHD is still obscure, there is ample evidence that the treatment of depression and comorbid IHD with SRIs is safe and effective and that it reduces the risk of adverse cardiac events (Roose and Spatz 1999). In a landmark study, Roose et al. (1998) reported that paroxetine and nortriptyline were both effective in treating depression in elderly patients with severe heart disease but that paroxetine had a superior safety and tolerability profile. It is currently unknown whether early recognition and treatment of depression will reduce the risk of future cardiac disease.

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