Retrospective Study
Copyright ©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Psychiatry. Sep 19, 2025; 15(9): 106906
Published online Sep 19, 2025. doi: 10.5498/wjp.v15.i9.106906
Depressive state on cardiac remodeling and left ventricular function in chronic heart failure: A retrospective study
Bo Gao, Yun-Fan Gao, Meng-Ting Chu, Ke-Fang Yuan
Bo Gao, Department of Cardiology, Suizhou Central Hospital, Affiliated Hospital of Hubei University of Medicine, Suizhou 441300, Hubei Province, China
Yun-Fan Gao, Department of Emergency, Suizhou Central Hospital, Affiliated Hospital of Hubei University of Medicine, Suizhou 441300, Hubei Province, China
Meng-Ting Chu, Department of Pain and Rehabilitation, Suizhou Central Hospital, Affiliated Hospital of Hubei University of Medicine, Suizhou 441300, Hubei Province, China
Ke-Fang Yuan, Department of Cardiovascular Surgery, Hebei Petro China Central Hospital, Langfang 065000, Hebei Province, China
Co-first authors: Bo Gao and Yun-Fan Gao.
Author contributions: Gao B, Gao YF, Chu MT conceived and designed the study, performed the statistical analysis, and wrote the manuscript; Yuan KF collected and processed the data, conducted literature research, and critically revised the manuscript for important intellectual content. Both authors reviewed and approved the final version of the manuscript. Gao B and Gao YF contributed equally to this work as co-first authors.
Institutional review board statement: This study was reviewed and approved by the Ethics Committee of Suizhou Central Hospital, Hubei Province, China (Approval No. KY-2025-002-01). The study was conducted in accordance with the principles outlined in the Declaration of Helsinki.
Informed consent statement: Informed consent was waived by the Medical Ethics Committee of Suizhou Central Hospital (KY-2025-002-01) due to the retrospective design and use of de-identified data.
Conflict-of-interest statement: The authors declare no conflicts of interest related to this study.
Data sharing statement: The data supporting the findings of this study are available from the corresponding author upon reasonable request.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Ke-Fang Yuan, Department of Cardiovascular Surgery, Hebei Petro China Central Hospital, No. 51 Xinkai Road, Langfang 065000, Hebei Province, China. yuankf198301@163.com
Received: April 15, 2025
Revised: June 2, 2025
Accepted: July 9, 2025
Published online: September 19, 2025
Processing time: 133 Days and 1.4 Hours
Abstract
BACKGROUND

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.

AIM

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.

METHODS

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.

RESULTS

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.

CONCLUSION

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.

Keywords: Chronic heart failure; Depression; Cardiac remodeling; Left ventricular function; Inflammatory response

Core Tip: This study highlights a significant link between depression and cardiac remodeling in chronic heart failure (CHF) patients. Depression was associated with lower left ventricular ejection fraction, larger end-diastolic diameter, increased myocardial fibrosis, and elevated inflammatory and neuroendocrine markers. These findings suggest that depressive states exacerbate structural and functional cardiac abnormalities through inflammatory activation, neuroendocrine dysregulation, and enhanced oxidative stress. The results underscore the importance of psychological assessment and targeted management of depression in CHF patients. Addressing depression may mitigate its detrimental cardiovascular effects, offering a potential avenue to improve clinical outcomes and quality of life for patients with heart failure.