Depressive state on cardiac remodeling and left ventricular function in chronic heart failure: A retrospective study

Chronic heart failure (CHF) is a severe cardiovascular disease that significantly threatens human health. Depression, a common comorbidity, may substantially impact cardiac structure and function. However, the exact relationship between depression and cardiac remodeling and left ventricular functional changes remains incompletely understood. This study sets out to explore, with a clinically grounded perspective, how depressive states may subtly or profoundly influence the trajectory of cardiac remodeling and the functional dynamics of the left ventricle in individuals grappling with CHF. Beyond mere observation, it also aims to untangle the underlying physiological or neurohormonal pathways that might bridge emotional distress and cardiac dysfunction.

To delve into how depressive symptoms might shape the progression of cardiac remodeling and impair left ventricular function among individuals living with CHF. Particular attention is given to the role of inflammatory signaling and disruptions in neuroendocrine balance as possible mediating factors. By examining these intertwined physiological and psychological processes, the study seeks to shed light on the reciprocal link between emotional distress and CHF, offering insights that may inform more precise, mechanism-based treatment strategies.

In this retrospective clinical trial, 248 patients diagnosed with CHF were analyzed in the tertiary treatment center between January 2018 and December 2022. According to Hamilton's Depression Scale score, participants were classified into two cohort of depression (score 17) and no significant depression characteristics (score 17). Cardiac morphology and functional parameters were assessed using a combination of hyperechocardiocardiocardiography, heart magnetic resonance, and associated blood biomarkers.

The results of this study underscore the significant effects that depression can have on both the structure and function of the heart in patients with CHF. In particular, the individuals in the cohort with depression were 42.3% ± 6.7% of the individuals without depression vs 51.6% ± 5.9%, P < 0.01) In comparison, the left ventricular ejection fraction, an important measure of contractional performance, was significantly reduced, underlining the harmful physiological interaction between mood disorders and cardiac efficiency. The measurement of the left ventricular end-diastolic diameter showed a significant expansion of the ventricular envelope in the depression group (68.2 ± 7.5 mm vs 59.6 ± 6.3 mm, P < 0.01). Inflammatory markers, including high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor-α (TNF-α), were significantly elevated in the depressed group (hs-CRP: 8.7 ± 2.3 mg/L vs 4.5 ± 1.6 mg/L; TNF-α: 42.5 ± 7.6 pg/mL vs 28.3 ± 5.4 pg/mL). Both B-type natriuretic peptide (1256 ± 345 pg/mL vs 756 ± 234 pg/mL) and angiotensin II (86.4 ± 15.7 ng/mL vs 62.5 ± 12.3 ng/mL) levels were significantly higher in the depressed group.

Among people with CHF, the presence of depressive symptoms appears to be closely related to pronounced changes in heart structure and impaired functional abilities. It is likely that depressive states contribute to the progress of heart reform and deterioration of left stomach function, possibly due to increased inflammatory cascades and increased activation of neuroendocrine regulatory pathways.