Redefining psychocardiology: Integrating depression management into heart failure care for enhanced long-term recovery and prognosis

Abstract

Depression is a highly prevalent and often under-recognized comorbidity in heart failure (HF), contributing to worse symptoms, impaired self-care, increased rehospitalization risk, and reduced quality of life. Nowadays, some studies link depression severity with poorer ventricular function, lower medication adherence, and increased readmission rates. This suggests that depression management should be treated as a core component of HF care rather than an optional add-on. In this paper, we briefly summarize the bidirectional links between HF and depression and highlight that, although depression strongly predicts adverse outcomes, large randomized trials of antidepressants and collaborative care have not been shown to reduce HF hospitalizations or mortality. These sobering data call for a cautious approach, reframing depression as a risk marker rather than a risk factor. We then outline a pragmatic psychocardiology agenda: Routine screening; stepped collaborative care embedded in HF services; and judicious use of digital tools to support—not replace—human care. Rather than promising a new cure, we propose a realistic redefinition of psychocardiology that focuses on protecting patients from the clinical consequences of untreated depression while acknowledging the current limits of evidence for hard cardiovascular endpoints.

Key Words: Heart failure; Depression; Psychocardiology; Integrated care; Collaborative care; Digital health; Psychosocial interventions

Core Tip: Depression is common in heart failure (HF) and reliably identifies patients at higher risk of poor self-care, rehospitalization, and death, yet treating depression has not consistently improved hard HF outcomes. Using new data from a retrospective cohort study, this review calls for a pragmatic form of “psychocardiology”: Routinely screening for depression; embedding simple collaborative-care models into HF services; and using digital tools cautiously as supports rather than standalone solutions. The goal is not to promise fewer HF events, but to reduce the avoidable suffering associated with living with both HF and depression.

INTRODUCTION

Heart failure (HF) and depression often coexist, worsening outcomes in both conditions[1-4]. About 41.9% of HF patients are depressed, with 28.1% experiencing moderate to severe symptoms, a prevalence significantly higher than that in the general population[1,5,6]. Depressive symptoms are particularly prominent in elderly hospitalized patients with HF[7]. A meta-analysis of 149 studies including 305407 patients with HF estimated the global prevalence of depression at 41.9% for any severity and 28.1% for moderate-to-severe symptoms[1,4]. In low- and middle-income countries, a systematic review and meta-analysis of 21 studies involving 5074 participants found a pooled depression prevalence of 51.5% (95% confidence interval: 39.7%-63.3%) and a significant association between depressive symptoms and poorer health-related quality of life[8]. Further studies have showed that depressive symptoms in HF are associated with persistently poorer health status in advanced HF, reduced quality of life in chronic systolic HF, and a higher burden of depressive symptoms in elderly HF populations compared with matched community controls[9-11].

This comorbidity is not simply additive. In addition to increased mortality and rehospitalization risk, depressive symptoms in HF have been associated with functional decline and greater healthcare utilization[12,13]. Consistent with this, in a 3-year retrospective cohort of 1098 patients after their first hospitalization for HF, median annualized healthcare costs were 7474 dollars in patients without depression, 11012 dollars in those with antidepressant prescriptions only, and 9550 dollars in those with both a recorded depression diagnosis and antidepressant treatment[11,14]. In 374 hospitalized patients with congestive HF, 35.3% had a Beck Depression Inventory score ≥ 10 and 13.9% met the criteria for major depressive disorder; major depression was associated with an approximately twofold higher risk of death or rehospitalization within 1 year[15]. Depression is also an important and independent predictor of all-cause mortality in HF[3,16]. Moreover, a large national cohort study showed that the risks of both depression and suicide were highest within the first 3 months after HF diagnosis, highlighting the vicious cycle between cardiac and mental health[17,18].

Mao et al[19] further reported, in a real-world retrospective cohort of 160 hospitalized patients with HF, that greater depression severity is associated with poorer medication adherence, worse ventricular function, and higher readmission risk, reinforcing the need for integrated care. The 2022 American Heart Association/American College of Cardiology/Heart Failure Society of America guidelines provide patient-centered recommendations for the prevention, diagnosis, and management of HF, while the 2021 American Heart Association scientific statement highlights the broader importance of psychological health in cardiovascular care[20,21]. Recent reviews and related cardiovascular studies further identify depression as a clinically important comorbidity in HF and support the practical use of Patient Health Questionnaire (PHQ) 2/PHQ 9-based screening strategies, although the key validation data for these tools were derived mainly from patients with coronary heart disease rather than HF-specific cohorts[22-25]. Despite this, mental health care remains underintegrated in HF management, with depression and HF often treated separately. At the same time, an important clinical and conceptual tension remains: Although depression consistently predicts worse HF outcomes[17,20,23,26], interventions that improve depressive symptoms have not yet shown consistent benefits for HF hospitalization or mortality[26-30]. This review discusses why depression should be central to HF care and explores strategies for its management, including pathophysiological mechanisms, clinical evidence, digital health innovations, and interdisciplinary care models, while also addressing current controversies and future research directions in psychocardiology for HF.

PSYCHOBIOLOGICAL MECHANISMS LINKING DEPRESSION AND HF

Depression accelerates HF progression through complex neurobiological and behavioral mechanisms[17,31-34]. A key pathway is neurohormonal activation: Depression induces sustained sympathetic nervous system hyperactivity and hypothalamic-pituitary-adrenal axis dysregulation, increasing catecholamines and cortisol levels[33,35]. Elevated catecholamines promote cardiac fibrosis and ventricular hypertrophy, while cortisol exacerbates endothelial dysfunction, impeding vasodilation and contributing to atherosclerosis[32,34,35]. Systemic inflammation, marked by elevated interleukin-6, tumor necrosis factor-α, and C-reactive protein levels, further worsens vascular health[31,34]. Depression also enhances platelet activation, raising thrombotic risk, and exacerbates autonomic dysregulation, manifested by reduced heart rate variability and increased sympathetic tone, both associated with a higher risk of sudden cardiac death and arrhythmias[31,33]. Although these pathways are biologically plausible, their relative causal contribution to adverse HF outcomes in depressed patients remains incompletely defined[17,33,34].

Beyond biological disruptions, depression impairs patient behavior, particularly self-care. Depressed HF patients exhibit poorer adherence to medications, inconsistent dietary habits, and reduced physical activity[28,29,36,37]. As self-care—such as monitoring weight, restricting sodium, and adhering to medications—is crucial for HF management, depression compromises motivation and executive function, leading to lapses that can precipitate disease decompensation[38]. Higher depression scores correlate with poorer self-care outcomes, often mediated by reduced self-care confidence[39,40]. Additionally, social isolation and lack of support exacerbate adherence issues, increasing stress and reinforcing the cycle of both psychological and cardiac dysfunction. This bidirectional relationship between depression and HF undermines patient health, influencing cardiac function, self-care, and overall well-being, as illustrated in Figure 1. Recent symptom-network data further suggest that sleep quality may serve as an important bridge linking depressive and anxiety symptoms in patients with chronic HF[41].

Figure 1 Bidirectional relationship between heart failure and depression and their impact on clinical outcomes. This figure illustrates the bidirectional relationship between heart failure and depression, where heart failure worsens depression by reducing left ventricular function, increasing hospitalization rates, and impairing exercise capacity, while depression in turn impairs self-care, increases inflammation, and reduces physical activity, leading to poorer outcomes and increased mortality risk.

EVIDENCE FROM CLINICAL STUDIES

A growing body of evidence confirms that depression significantly worsens outcomes in HF[3,4,16,31,42]. Even mild depressive symptoms are prognostically important[2,43]. In patients with HF, greater depressive symptom burden has been associated with poorer health status, greater illness severity, and lower self-care confidence[9,10,35,43,44]. More severe depression correlates with a 1.5-fold to 2-fold increase in mortality risk and higher hospitalization rates[2,4,16]. A global meta-analysis demonstrated that depression increases the risk of readmission by 54%, with a hazard ratio of 1.54, and this risk persists in both short-term (≤ 90 days post-discharge) and long-term follow-up[4,31]

Depression complicates HF management by reducing medication adherence and hindering optimal dose titration of HF therapies. Depressed patients are less likely to meet guideline-recommended targets for β-blockers and angiotensin-converting enzyme inhibitors, contributing to worse clinical outcomes[36,45,46]. Notably, depression impairs self-care, further exacerbating disease progression[28,29,35,39].

Current evidence suggests that treating depression in patients with HF may improve patient-centered outcomes such as mood, quality of life, and self-care[26,27,37]. However, randomized trials have not shown consistent benefits with respect to major cardiovascular endpoints such as HF hospitalization or mortality[26,37,47]. The MOOD-HF trial, which tested escitalopram in patients with HF and depression, showed no significant reduction in all-cause mortality or hospitalization and no significant improvement in depressive symptoms[26]. Similarly, reviews and HF-focused trials/meta-analyses suggest that psychological interventions, particularly cognitive behavioral therapy, may improve depressive symptoms, self-care, and quality of life, whereas their effects on HF hospitalization and mortality remain uncertain[25,28,48,49]. Consistent with the broader literature identifying depression as an adverse prognostic marker in HF[3], Burg[47] underscored the persistent gap between prognostic evidence and effective management strategies, while Xing et al[50] further showed, in a secondary analysis of the TOPCAT trial, that unfavorable depression trajectories are associated with worse outcomes in patients with HF.

Despite these challenges, depression remains a powerful prognostic indicator for HF. It is associated with poorer survival, more frequent hospitalizations, and lower treatment adherence[3,4,36,42]. Therefore, depression management should be central to HF care. Guidelines and scientific statements increasingly recognize psychological health as an important component of cardiovascular care, and recent studies further support the use of practical screening and management approaches to identify depressive symptoms and high-risk patients in HF, although evidence that such strategies improve HF hospitalization or mortality remains limited[4,20-22]. Patients with high depression scores should be treated as high-risk, warranting close monitoring and tailored interventions[22]. Representative studies on the prevalence, prognostic significance, and intervention outcomes of depression in HF are summarized in Table 1. Collectively, current evidence supports depression management primarily as a strategy to reduce psychological distress and improve self-care and quality of life[27-29,37,48], whereas reductions in HF hospitalization or mortality remain unproven[26,48].

Table 1 Representative studies on depression and heart failure: Prevalence, prognosis, and intervention outcomes.

Ref.	Design/population	Main focus	Key findings	Main implication
Rutledge et al[1], 2006	Meta-analysis of HF studies	Prevalence and outcomes	Depression is highly prevalent in HF and associated with poorer clinical outcomes	Depression is a highly relevant comorbidity in HF
Jiang et al[15], 2001	Prospective cohort, CHF patients	Mortality and rehospitalization	Depression is associated with increased mortality and rehospitalization risk	Prognostic relevance of depression
Sherwood et al[42], 2007	Prospective cohort, HF patients	Death or hospitalization	Depression predicts death or hospitalization	Depression is a marker of adverse HF prognosis
Sokoreli et al[3], 2016	Systematic review and meta-analysis	Depression/anxiety and mortality	Depression and anxiety predict higher mortality in HF	Supports routine psychosocial risk assessment
Mao et al[19], 2025	Retrospective cohort, HF patients	Ventricular function, adherence, readmission	Greater depression severity is associated with poorer ventricular function, reduced medication adherence, and higher readmission	Supports integration of depression management into HF care
O'Connor et al[30], 2010	Randomized clinical trial	Sertraline in HF with depression	Sertraline does not significantly improve depressive symptoms compared with placebo, and no clear cardiovascular benefit was demonstrated	Antidepressant therapy does not translate into clear HF-specific clinical benefit
Angermann et al[26], 2016	Randomized clinical trial	Escitalopram in HF with depression	No significant reduction in all-cause mortality or hospitalization, and no significant improvement in depressive symptoms	Challenges the assumption that treating depression improves hard HF endpoints
Rollman et al[37], 2021	Randomized clinical trial	Blended collaborative care	Improved mood and mental health-related quality of life, but not rehospitalization or physical function	Collaborative care benefits patient-centered outcomes more than hard endpoints
Freedland et al[28], 2015	Randomized clinical trial	Cognitive behavioral therapy in HF	Benefits for depression and self-care persist at 1 year	Nonpharmacological intervention may improve self-management
Freedland et al[29], 2023	Randomized clinical trial	Depression treatment and self-care	Benefits on depression/self-care persist, but cardiovascular outcome effects remain limited	Supports continued interest in patient-centered outcomes after depression treatment

HF: Heart failure; CHF: Congestive heart failure.

DIGITAL TOOLS AND INNOVATIONS IN PSYCHOCARDIOLOGY

Digital health innovations are increasingly being incorporated into HF care and may provide practical support for depression management. Mobile health systems that monitor HF symptoms may also create opportunities for broader psychosocial assessment and longitudinal follow-up. For example, the “Medly” telemonitoring HF program enables patients to report daily weight, blood pressure, and symptoms through a mobile application; although depression screening is not yet embedded in this program, patients can access mental health services when needed, and the program has been associated with reduced HF-related hospitalizations as well as improvements in quality of life and self-care[51]. Similarly, in the European Union-funded HeartMan trial, a smartphone application combined with a wristband system improved mental and sexual health and enhanced self-care behaviors in patients with HF, although no significant improvements were observed in health-related quality of life or exercise capacity[38].

Digital therapeutics, including Internet-based cognitive-behavioral therapy (CBT) and smartphone-delivered interventions, are also emerging as potentially scalable approaches. Although evidence from diabetes suggests that CBT-based interventions can improve depressive symptoms and quality of life[52], HF-specific evidence more directly supports the benefits of CBT and related psychological interventions for depressive symptoms, self-care, and quality of life, rather than specifically for digital CBT[28,29,48,49,53]. Artificial intelligence-based prediction models may further expand this field. In one study, a stacking model predicted comorbid depression in patients with HF with an accuracy of 77%[54]. A recent systematic review and network meta-analysis has further synthesized the comparative effects of non-pharmacological interventions on anxiety and depressive symptoms in HF, underscoring growing interest in scalable adjunctive approaches in psychocardiology[55]. Taken together, these findings suggest that digital tools may serve as useful adjuncts to psychocardiological care, but current evidence remains insufficient to support their use as stand-alone substitutes for integrated multidisciplinary management[38,51,54]. Nevertheless, clinical utility, generalizability, and implementation feasibility require further validation before widespread adoption[17,21,54].

INTEGRATION CHALLENGES AND INTERDISCIPLINARY CARE

Although the benefits of addressing depression in HF are well documented, integrating psychiatric and cardiac care in routine practice remains difficult[17,21,37,40]. Cardiology and mental health services have largely developed in parallel, with limited day-to-day communication; cardiologists often regard depression management as outside their remit, and mental health professionals are seldom embedded in HF clinics, resulting in underdiagnosed and undertreated depression in this population[37,56]. A qualitative study from Canada further highlighted fragmented coordination, lack of comprehensive care, and restricted access to counselling, particularly in rural settings[40]. In many health systems, reimbursement structures that prioritize procedures and volume over psychosocial care also discourage investment in collaborative models.

Even when depression is recognized, treatment gaps are common. Patients may decline mental health referrals because of stigma or the perceived burden of additional visits, or may start antidepressant therapy without adequate follow-up for titration and side-effect monitoring. Core depressive symptoms—fatigue, cognitive impairment, and hopelessness—make it harder for patients to navigate the healthcare system and maintain self-care, creating a cycle in which depression itself limits access to appropriate treatment. Caregiver burnout, often overlooked, further exacerbates this situation, as family members who support HF patients may become overwhelmed and under-resourced, leading to suboptimal care at home.

Despite these challenges, collaborative care models that incorporate depression care managers or psychiatric consultants into chronic disease programmed demonstrate that integrated management is feasible. In cardiovascular and other chronic illness populations, such models significantly reduce depressive symptoms and improve mental health-related quality of life, although effects on major cardiovascular outcomes are often neutral or inconsistent[27,37,57,58].

The randomized clinical trial by Rollman et al[37] combined HF disease management with antidepressant therapy and psychotherapy over 12 months and, while it improved mood and mental health-related quality of life, it did not significantly reduce rehospitalization or improve physical function compared with enhanced usual care. These findings suggest that depression treatment embedded within HF care reliably improves psychological outcomes, yet may need to be coupled with optimized HF therapy and longer follow-up to influence hard endpoints[27-29,37].

Scaling such models beyond academic centers remains challenging. Many cardiology clinics lack on-site mental health professionals, and training cardiac nurses in screening and basic counselling requires time and resources. Clinicians may be reluctant to raise mental health issues, fearing that this will complicate or prolong consultations[40]. Digital health technologies, such as mobile applications and artificial intelligence-driven mood-tracking tools (Figure 2), may help bridge these gaps by supporting collaboration between cardiologists and mental health professionals and enabling longitudinal monitoring of mood and self-care. Overall, integrated psychocardiological interventions consistently improve mood and quality of life[27-29,37,59], whereas effects on rehospitalization or mortality remain modest and inconsistent[26,48,49,59], underscoring the need for models that can translate psychological gains into durable cardiovascular benefits.

Figure 2 Role of digital health technologies in managing depression and self-care in heart failure patients. This figure illustrates the integration of digital health technologies, such as mobile applications, remote monitoring, and artificial intelligence-driven mood tracking, into depression management for heart failure patients. These technologies support personalized care plans by facilitating collaboration between cardiologists and mental health professionals, ultimately improving long-term recovery, prognosis, and quality of life. The figure was created using BioRender (Supplementary material).

CURRENT CONTROVERSIES IN PSYCHOCARDIOLOGY FOR HF

A central controversy is whether depression in HF should be viewed primarily as a modifiable causal risk factor for adverse cardiovascular outcomes or as a robust marker of disease burden, vulnerability[1,3,17], and poor self-management[35,36,39]. Studies consistently demonstrate associations between depression and worse prognosis[2,3,15,16,42], yet randomized trials have not shown parallel reductions in hospitalization or mortality after treatment of depression[26,30,37,59]. This discrepancy suggests that depression may operate through both causal and non-causal pathways, and that currently available interventions may be more effective at improving psychological suffering than altering cardiovascular trajectories[17,25,37,59].

A second controversy concerns screening. Routine use of instruments such as the PHQ-2 and PHQ-9 is clinically attractive, but screening alone does not improve outcomes unless it is linked to feasible referral pathways, follow-up, and treatment capacity[21,22,56]. In busy HF clinics, identifying depressive symptoms without providing integrated management may have limited practical value[40].

A third controversy involves digital innovation. Telemonitoring, application-based support, and artificial intelligence-assisted risk stratification may enhance longitudinal assessment and access to care, but evidence remains insufficient to support their use as stand-alone substitutes for multidisciplinary psychocardiological care[17,21,38,51,54]. Accordingly, digital tools should currently be positioned as adjuncts that extend human care, not replacements for it[17,21]. The major controversies discussed in this review are summarized in Table 2.

Table 2 Current controversies in psychocardiology for heart failure.

Controversy	Supporting rationale	Counterpoint/Limitation	Practical interpretation
Is depression a modifiable causal risk factor or mainly a prognostic marker in HF?	Observational studies consistently show associations with mortality, hospitalization, poor self-care, and reduced quality of life	Randomized trials have not consistently shown reductions in HF hospitalization or mortality after depression treatment	At present, depression in HF may be most appropriately framed as a clinically important prognostic marker and treatment target for symptom burden and self-management
Should routine depression screening be implemented in all HF settings?	Depression is common, under-recognized, and clinically meaningful; tools such as PHQ-2/PHQ-9 are feasible	Screening alone is insufficient if referral pathways, psychiatric support, and follow-up capacity are lacking; moreover, key validation data for common screening strategies were derived mainly from non-HF cardiovascular cohorts	Screening is reasonable only when linked to an actionable care pathway
Do antidepressants improve HF prognosis?	They may be appropriate for selected psychiatric indications, but evidence for HF-specific benefit remains limited	Large trials such as SADHART-CHF and MOOD-HF did not show reduced hard cardiovascular endpoints	Antidepressants should be used cautiously for psychiatric indications, not as established HF outcome-modifying therapy
Can collaborative care improve cardiovascular outcomes?	Collaborative models improve depressive symptoms and mental health-related quality of life	Effects on rehospitalization, physical function, and mortality remain inconsistent	Collaborative care is justified mainly for patient-centered benefits
Can digital health replace face-to-face psychocardiological care?	Telemonitoring, mobile applications, and AI may improve access, monitoring, and longitudinal follow-up	Evidence remains limited, and clinical utility, generalizability, equity, and implementation feasibility are not yet fully established	Digital tools should support, not replace, multidisciplinary human care
Are all HF phenotypes equally affected by depression?	Depression appears relevant across HF populations, including vulnerable and preserved EF groups	Mechanisms and effect sizes may differ by phenotype, socioeconomic context, and comorbidity burden	Precision-oriented psychocardiology is needed

HF: Heart failure; PHQ: Patient Health Questionnaire; AI: Artificial intelligence; CHF: Congestive heart failure.

FUTURE RESEARCH DIRECTIONS

Outcome-focused trials of integrated, stepped care

Randomized trials are needed to determine whether integrated depression treatment can improve HF outcomes when embedded in optimized HF care. A pragmatic, multicenter trial could compare usual HF management with a nurse-led, application-supported stepped-care program for depression (screening with PHQ-2 and PHQ-9, brief behavioral activation, and stepped escalation to psychotherapy and antidepressants) and use 12-month HF hospitalization or death as the primary endpoint, with depression remission and quality of life as key secondary outcomes. This stepped-care model would directly test the hypothesis that treating depression within HF pathways reduces recurrent decompensation, rather than assuming benefit from mood improvement alone.

Implementation and equity in real-world HF care

Even effective models will fail to change practice if they cannot be implemented in routine settings. Hybrid effectiveness-implementation or cluster-randomized studies should evaluate how depression screening and brief interventions can be integrated into existing HF clinics, including community and rural services. Key outcomes should include reach, fidelity, costs, and effects on disparities (e.g., socioeconomically disadvantaged or geographically remote patients), in addition to mood and HF events. This work would inform payers and health systems about which psychocardiological strategies are both clinically meaningful and sustainable.

Mechanistic and precision-oriented psychocardiology

A third priority is to refine psychocardiological phenotypes and identify patients in whom targeting depression is most likely to modify HF trajectories. Combining digital phenotyping (applications, wearables, remote symptom and activity monitoring) with physiological markers such as inflammatory cytokines and heart rate variability could help define subgroups in whom depressive symptoms and HF decompensation are tightly coupled. Recent network-analytic findings further suggest that subjective sleep quality may function as a bridge symptom linking sleep disturbance with anxiety and depressive symptoms in chronic HF[41]. Within these phenotypes, randomized trials could evaluate targeted interventions—including exercise-based cardiac rehabilitation, mind-body programs, and positive psychology or resilience-building strategies—to determine whether enhancing psychological well-being translates into sustained improvements in self-care, functional capacity, and HF outcomes. This priority is supported by prior evidence from exercise training, nurse-led CBT, mind-body interventions, and recent evidence syntheses of non-pharmacological treatment strategies in HF, although the overall certainty of evidence remains limited[55,60-62]. Key priorities for future research are summarized in Table 3.

Table 3 Future research priorities for integrated depression management in heart failure.

Priority area	Key research question	Suggested study design	Core outcomes	Why it matters
Integrated stepped-care models	Can embedding depression treatment into optimized HF care reduce recurrent decompensation?	Pragmatic multicenter randomized trial embedded in optimized HF care	Recurrent HF hospitalization or composite HF hospitalization/all-cause death, with depression remission, self-care, and quality of life as key secondary outcomes	Directly tests whether integrated care affects both clinical and patient-centered outcomes
Implementation in real-world settings	How can screening and treatment be integrated into routine HF clinics, including rural and community settings?	Hybrid effectiveness-implementation studies; cluster-randomized trials	Reach, fidelity, feasibility, cost, equity, sustainability, and uptake	Determines whether promising models can be scaled in practice
Precision psychocardiology	Which HF patients are most likely to benefit from targeted depression interventions?	Phenotype-based prospective cohorts and stratified trials	Phenotype stability, symptom trajectories, self-care, functional status, biomarker profiles, and cardiovascular events	Moves the field beyond a one-size-fits-all approach
Digital augmentation of care	Can digital tools improve monitoring, adherence, and early symptom detection when added to standard care?	Randomized pragmatic trials or hybrid effectiveness-implementation studies	Engagement, symptom detection, adherence, self-care, quality of life, readmission	Clarifies the role of digital tools as adjuncts to care
Mechanistic research	Which biological and behavioral pathways most strongly link depression with HF progression?	Translational cohort studies with repeated biomarker and behavioral assessment	Inflammatory markers, autonomic function, sleep disturbance, physical activity, and medication adherence	Helps distinguish causal pathways from epiphenomena
Nonpharmacological intervention strategies	Which psychological or behavioral interventions are most effective in HF?	Comparative effectiveness trials	Depression severity, resilience, exercise tolerance, self-care, quality of life	Helps identify realistic, scalable, and phenotype-sensitive intervention packages

HF: Heart failure.

CONCLUSION

Depression should be recognized as a core component of HF care, as its bidirectional relationship with HF exacerbates both conditions. Integrated care, involving cardiologists, nurses, and mental health professionals, is essential for improving both mental and physical health. Failure to address depression in HF patients leads to worse outcomes, including higher mortality and readmission rates. By integrating depression management, patient-centered outcomes may be improved, particularly with respect to psychological distress, self-care, and quality of life. This shift toward “psychocardiology”—aligning mental and physical health—holds promise for better long-term recovery and quality of life. Stakeholders must collaborate to make depression management standard practice in HF care, breaking the cycle of mutual exacerbation and improving overall patient outcomes.