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Depression in chronic heart failure: novel pathophysiological mechanisms and therapeutic approaches
John T Parissis1, Katerina Fountoulaki, Ioannis Paraskevaidis
1Attikon University Hospital Heart Failure Clinic, Aftocratoros Irakliou 17, 15122, Maroussi, Athens, Greece. jparissis@yahoo.com
Insights
Depression is common in chronic heart failure (CHF) patients, increasing hospital readmissions and mortality. Treating this comorbidity may improve outcomes and survival in CHF patients.
Area of Science:
- Cardiology
- Psychiatry
- Immunology
Background:
- Depression is highly prevalent in chronic heart failure (CHF) patients, significantly increasing mortality and hospital readmissions.
- Shared pathophysiological mechanisms link CHF and depression, including HPA axis dysfunction, sympathoadrenal hyperactivity, reduced heart-rate variability, and elevated pro-inflammatory cytokines.
Purpose of the Study:
- To review the interplay between depression and CHF.
- To explore therapeutic targets for managing depression in CHF patients.
Main Methods:
- Review of recent investigational observations.
- Analysis of antidepressant effects on immune functions.
- Assessment of anticytokine agents' effects on depressive symptoms in CHF.
Main Results:
- Antidepressants, particularly selective serotonin re-uptake inhibitors (SSRIs), may improve survival post-myocardial infarction in depressed patients.
- Targeting shared pathophysiological pathways offers potential therapeutic strategies.
Conclusions:
- Diagnosis and treatment of depression in CHF patients can positively impact functional capacity and prognosis.
- Further research into pharmacological interventions targeting immune pathways is warranted for CHF management.
Abstract:
Depression is four to five times as common in chronic heart failure (CHF) patients as in the general population, may confer a higher risk of developing CHF in susceptible populations, and is significantly related to higher hospital readmission rates and increased mortality in established CHF. This effect may be mediated via the pathophysiological mechanisms that are shared between CHF and depression, including increased hypothalamic-pituitary-adrenal function, sympathoadrenal hyperactivity, diminished heart-rate variability and excessive pro-inflammatory cytokine activation. Each of these pathways of linkage represents a potential therapeutic target to improve outcome in CHF. This paper reviews the recent investigational observations that clarify the direct effects of antidepressants on immune functions, as well as the indirect effects of anticytokine pharmacological agents on depressive symptoms in CHF. With recent evidence suggesting that selective serotonin re-uptake inhibitors improve survival after myocardial infarction in patients with depression, diagnosis and treatment of this comorbidity may beneficially affect the functional capacity and prognosis of CHF patients.
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