Background: Depressive disorder after myocardial infarction (MI) is associated with increased cardiac morbidity and mortality. Immune activity such as inflammation might be implicated as an underlying mechanism. The purpose of this study is to investigate whether the response to an antidepressant in post-MI depression is associated with changes of inflammatory markers in serum.
View Article and Find Full Text PDFBackground: Prevalence of depressive symptoms in the post-myocardial infarction (MI) period varies from 8 to 30%. Cerebral damage after MI, caused by transient ischemia, an inflammatory response or both, may contribute to development of post-MI depression. S100B is an established protein marker of cerebral damage.
View Article and Find Full Text PDFObjective: To examine the antidepressant efficacy of a dual-acting antidepressant (mirtazapine) in patients with post-myocardial infarction (MI) depressive disorder. Antidepressants used in post MI trials with a randomized, double-blind, placebo-controlled design have been restricted to selective serotonin reuptake inhibitors (SSRIs). Antidepressant effects have been limited.
View Article and Find Full Text PDFObjective: Depression following myocardial infarction is associated with an increased risk of cardiac events, but attempts to alter cardiovascular prognosis by providing antidepressive treatment have not been successful. This may be because of the limited effects of antidepressive treatment on depression itself. The authors assessed whether nonresponse to treatment of post-myocardial infarction depression is associated with new cardiac events.
View Article and Find Full Text PDFBackground: Depression following myocardial infarction is associated with poor cardiac prognosis. It is unclear whether antidepressant treatment improves long-term depression status and cardiac prognosis.
Aims: To evaluate the effects of antidepressant treatment compared with usual care in an effectiveness study.