Background In adults with acquired heart disease, depression is common and associated with adverse outcomes. Depression may also be important in adults with congenital heart disease ( CHD ). Methods and Results We conducted a cohort study of outpatients with CHD, aged ≥18 years, enrolled in a prospective biobank between 2012 and 2017. Clinical data were extracted from medical records. Survival analysis assessed the relationship between depression, defined by a history of clinical diagnosis of major depression, with all‐cause mortality and a composite outcome of death or nonelective cardiovascular hospitalization. A total of 1146 patients were enrolled (age, 38.5±13.8 years; 49.6% women). Depression had been diagnosed in 219 (prevalence=19.1%), and these patients were more likely to have severely complex CHD (41.3% versus 33.7%; P =0.028), cyanosis (12.1% versus 5.7%; P =0.003), and worse functional class (≥ II ; 33.3% versus 20.4%; P <0.0001), and to be taking antidepressant medication at time of enrollment (68.5% versus 5.7%; P <0.0001). Depression was associated with biomarkers indicative of inflammation (hsCRP [high‐sensitivity C‐reactive protein], 1.71 [25th–75th percentile, 0.82–4.47] versus 1.10 [0.45–2.40]; P <0.0001) and heart failure (NT‐proBNP [N‐terminal pro‐B‐type natriuretic peptide], 190 [92–501] versus 111 [45–264]; P <0.0001). During follow‐up of 605±547 days, 137 participants (12.0%) experienced the composite outcome, including 33 deaths (2.9%). Depression was associated with increased risk for both all‐cause mortality (multivariable hazard ratio, 3.0; 95% CI , 1.4–6.4; P =0.005) and the composite outcome (multivariable hazard ratio, 1.6; 95% CI, 1.1–2.5; P =0.025), adjusting for age, sex, history of atrial arrhythmia, systolic ventricular function, CHD complexity, and corrected QT interval. Conclusions In adults with CHD, major depression is associated with impaired functional status, heart failure, systemic inflammation, and increased risk for adverse outcomes.

Atrial fibrillation is the most common cardiac arrhythmia and symptoms overlap with physiological sensations of anxiety. Patients with atrial fibrillation can demonstrate anxiety sensitivity even in the absence of actual atrial fibrillation symptoms. Interoceptive exposure is effective in treating anxiety sensitivity, and recently, mindfulness has been proposed as an enhancement strategy to facilitating inhibitory learning in exposure therapy. This pragmatic study piloted a brief mindfulness and interoceptive exposure treatment for anxiety sensitivity in atrial fibrillation. Eight participants with atrial fibrillation and elevated anxiety sensitivity from a hospital cardiology department participated in the treatment. Anxiety sensitivity significantly decreased during the course of the intervention. These initial findings show proof of concept for this brief intervention in a cardiac-specific behavioral medicine setting.

The current study was undertaken to study the role of prostaglandins in regulating microglial activation. Mice were treated with indomethacin (2 microg/ml) in their drinking water to selectively inhibit cyclooxygenase activity. After 4-8 days, the effect of inhibiting prostaglandin synthesis on microglial activity was evaluated. This was accomplished by analyzing microglial expression of Mac-1 (C3 complement receptor) as an indicator of activation. Mac-1 expression was assessed by immunohistochemistry of fixed brain cryosections, and by flow cytometric analysis of immunostained single cell suspensions. Both methods demonstrated that compared to age-matched, untreated controls, brains of indomethacin-treated mice had increased levels of Mac-1 expression, suggesting an increase in the state of microglial activation. These results demonstrate the importance of prostaglandins in down regulating microglial activity, and that inhibition of prostaglandin synthesis with indomethacin may act to increase the reactivity of the brain's immune system.