Depression and Anxiety as Predictors of 2-Year Cardiac Events in Patients With Stable Coronary Artery Disease
Anxiety and depression are associated with mechanisms that promote atherosclerosis. Most recent studies of emotional disturbances in coronary artery disease (CAD) have focused on depression only. To assess the 2-year cardiac prognostic importance of the DSM-IV-based diagnoses of major depressive disorder (MDD) and generalized anxiety disorder (GAD) and self-report measures of anxiety and depression and their co-occurrence. Two-year follow-up of 804 patients with stable CAD (649 men) assessed using the Beck Depression Inventory II (BDI-II), the anxiety subscale of the Hospital Anxiety and Depression Scale (HADS-A), and the Structured Clinical Interview for DSM-IV (masked to self-reports) 2 months after acute coronary syndromes. Major adverse cardiac events (MACEs) (cardiac death, myocardial infarction, cardiac arrest, or nonelective revascularization) in the 2 years after baseline. Of the 804 patients, 57 (7.1%) met the criteria for MDD and 43 (5.3%) for GAD (11 [1.4%] had comorbidity); 220 (27.4%) had elevated BDI-II scores (> or = 14), and 333 (41.4%) had elevated HADS-A scores (> or = 8), with 21.1% overlap. MDD (odds ratio [OR], 2.85; 95% confidence interval [CI], 1.62-5.01), GAD (OR, 2.09; 95% CI, 1.08-4.05), elevated BDI-II (OR, 1.75; 95% CI, 1.21-2.54), elevated HADS-A score (OR, 1.67; 95% CI, 1.18-2.37), and continuous standardized scores on the BDI-II (OR, 1.34; 95% CI, 1.11-1.62) and the HADS-A (OR, 1.38; 95% CI, 1.16-1.63) all predicted MACEs. After covariate control, only the P value associated with the continuous BDI-II score increased to above .10. Most of the risk associated with elevated symptoms was in patients with psychiatric disorders. However, patients with comorbid MDD and GAD or elevated anxiety and depression symptoms were not at greater MACE risk than those with only 1 factor. Anxiety and depression predict greater MACE risk in patients with stable CAD, supporting future research into common genetic, environmental, and pathophysiologic pathways and treatments.