Depression is a common comorbidity in patients with heart failure with preserved ejection fraction (HFpEF), suggesting potential epidemiological and pathophysiological connections between these two age-related chronic diseases. Extensive clinical evidence demonstrates that depression is closely associated with both the incidence and prognosis of HFpEF. It is currently believed that depression may contribute to the pathogenesis of HFpEF through various interconnected mechanisms, including intestinal dysfunction, endothelial dysfunction, disturbances in fat and energy metabolism, autonomic nervous system dysfunction, hypothalamic-pituitary-adrenal (HPA) axis imbalance, and sex differences. Both conditions often share common comorbidities and genetic predispositions. Notably, inflammation is implicated in all these mechanisms and processes, playing a key role at different stages and facilitating the interaction between the two diseases during their onset and progression. However, the connections between depression and HFpEF have not yet been systematically and thoroughly elucidated. This review aims to comprehensively summarize the associations between depression and HFpEF, focusing particularly on elucidating their interplay in pathogenesis from an inflammation perspective, with special emphasis on the adverse effects of depression on the development of HFpEF. Additionally, we evaluate the management approaches for patients with comorbid depression and HFpEF, which include both pharmacological and nonpharmacological treatments, highlighting that personalized and integrated interventions may offer significant benefits. The review underscores the importance of increased attention and early identification of patients with comorbid depression and HFpEF and is expected to provide valuable insights and guidance for the clinical management of this significant patient population.

Inhibitory control deficits are central to cognitive dysfunction in major depressive disorder (MDD), yet how such deficits vary across subclinical depression and MDD remains unclear. Childhood trauma may further contribute to variability in inhibitory control. This study examined behavioral and computational markers of inhibitory control across nonemotional and emotional contexts in healthy, subclinical depression, and MDD groups and explored associations with childhood trauma. Thirty individuals with subclinical depression, 33 patients with MDD, and 36 healthy controls (HCs) completed three Stroop tasks (color-word, emotion, and face-word), during which reaction times (RTs) were recorded. Latent cognitive parameters were estimated using the drift diffusion model (DDM) and diffusion model for conflict tasks (DMCs). Associations between these indicators and childhood trauma were examined. Patients with MDD showed significantly longer RTs than subclinical individuals in emotion and face-word Stroop tasks. Computational modeling revealed prolonged nondecision time in MDD, relative to subclinical depression (color-word Stroop task) and HCs (emotion Stroop task). In the subclinical group, greater childhood trauma was associated with faster RTs in incongruent face-word trials and shorter nondecision time in the color-word Stroop task. Our findings support a possible inverted U-shaped pattern of inhibitory control across depressive severity, with enhanced performance in subclinical depression but poorer performance in MDD. Enhanced inhibitory control in subclinical depression may reflect compensatory adaptation linked to early adversity. These findings provide novel insights into stage-related differences of inhibitory control in depression.

Obsessive-compulsive disorder (OCD) is a chronic and disabling condition, and although exposure and response prevention (ERP) is the first-line psychological treatment, many patients decline it, drop out, or retain residual symptoms. According to Wells' metacognitive model, OCD is maintained less by intrusive thoughts themselves than by metacognitive beliefs about the significance, danger, and control of thoughts, which metacognitive therapy (MCT) targets directly. However, individual MCT has been evaluated almost exclusively in high-income Western settings, and whether metacognitive belief change temporally precedes symptom improvement remains untested. This multisite, assessor-blinded randomized controlled trial (RCT) addressed both gaps in Pakistani outpatient services. Seventy-six adults with OCD were randomized to 12 weekly sessions of individual MCT (n = 38) or documented treatment as usual (TAU; n = 38) and assessed at baseline, post-treatment, and 6-month follow-up; outcomes were analyzed with intention-to-treat (ITT) mixed-effects models and an exploratory three-wave panel mediation model. MCT produced greater reductions in clinician-rated Yale-Brown Obsessive-Compulsive Scale severity than TAU, F(1.81, 134) = 11.30, p < 0.001, with mean differences of -4.00 at post-treatment and -6.92 at follow-up (both p < 0.001) and more frequent treatment response. MCT also reduced Metacognitions Questionnaire-30 belief domains, with gains maintained at follow-up. However, the prespecified lagged indirect effect through post-treatment beliefs was not supported (β = -0.01). Findings extend the evidence for MCT to a non-Western clinical context and suggest that broad metacognitive belief domains behave as markers of clinical state rather than proximal mechanisms, underscoring the need for temporally fine-grained mechanism research.