Depression in Heart Failure. A Meta-Analytic Review of Prevalence, Intervention Effects, and Associations With Clinical Outcomes

San Diego State University, San Diego, California, United States
Journal of the American College of Cardiology (Impact Factor: 16.5). 11/2006; 48(8):1527-37. DOI: 10.1016/j.jacc.2006.06.055
Source: PubMed


This article describes a meta-analysis of published associations between depression and heart failure (HF) in regard to 3 questions: 1) What is the prevalence of depression among patients with HF? 2) What is the magnitude of the relationship between depression and clinical outcomes in the HF population? 3) What is the evidence for treatment effectiveness in reducing depression in HF patients? Key word searches of the Medline and PsycInfo databases, as well as reference searches in published HF and depression articles, identified 36 publications meeting our criteria. Clinically significant depression was present in 21.5% of HF patients, and varied by the use of questionnaires versus diagnostic interview (33.6% and 19.3%, respectively) and New York Heart Association-defined HF severity (11% in class I vs. 42% in class IV), among other factors. Combined results suggested higher rates of death and secondary events (risk ratio = 2.1, 95% confidence interval 1.7 to 2.6), trends toward increased health care use, and higher rates of hospitalization and emergency room visits among depressed patients. Treatment studies generally relied on small samples, but also suggested depression symptom reductions from a variety of interventions. In sum, clinically significant depression is present in at least 1 in 5 patients with HF; however, depression rates can be much higher among patients screened with questionnaires or with more advanced HF. The relationship between depression and poorer HF outcomes is consistent and strong across multiple end points. These findings reinforce the importance of psychosocial research in HF populations and identify a number of areas for future study.

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    • "Adverse effects of distress are also observed for other adverse cardiovascular health outcomes such as incident MI and post-MI mortality [14] [15] [16] [17]. These elevated cardiovascular risks are observed following prolonged psychological distress such as distress experienced during exhaustion [18] [19] and depression [13] [20] [21] as well as milder forms of chronic distress [22] [23]. However, the direction of causal pathways is complicated to discern when assessing human clinical or epidemiological studies, because it cannot be ruled out that underlying disease accounts for the association between psychosocial factors and disease progression. "
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    ABSTRACT: Background: Heart failure (HF) prognosis is negatively influenced by adverse environmental conditions associated with psychological distress and depression. The underlying mechanisms are not well understood because of insufficient experimental control in prior clinical and epidemiological studies. Using a validated animal model we examined whether distress-producing environmental manipulations (social isolation and crowding) increase HF progression following myocardial infarction (MI). Methods: MI was induced using coronary artery ligation in 8-week old male Wistar rats (N=52) and results were compared to sham surgery (N=24). Housing conditions were randomly assigned at 5days post MI or sham surgery (1/cage=isolation, 2/cage=standard reference condition, or 4/cage=crowding) and continued for 17weeks until the end of observation. The open field test was used to test behavioral responses. Echocardiograms were obtained at weeks 8 and 16, and left ventricular (LV) weight at week 17. Results: Housing conditions increased behavioral markers of distress (p=0.046) with the strongest effects for the isolated (1/cage) (p=0.022). MI did not increase distress-related behaviors compared to sham. MI-surgery resulted in characteristic HF indices (left ventricular ejection fraction (LVEF) at week 16=46±12% vs. 80±7% in sham, p<0.001). Housing condition was not related to LVEF or LV weight (p>0.10). Conclusions: Adverse environmental conditions, particularly isolated housing, produce increases in some of the behavioral indicators of distress. No effects of housing were found on post-MI progression of HF. The distress-HF associations observed in humans may therefore reflect common underlying factors rather than an independent causal pathway. Stronger environmental challenges may be needed in future animal research examining distress as related HF progression.
    Physiology & Behavior 10/2015; 152. DOI:10.1016/j.physbeh.2015.09.024 · 2.98 Impact Factor
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    • "These findings also have significant implications for other chronic illness populations in which depression is comorbid (e.g. diabetes, Anderson et al., 2001; chronic kidney disease, Palmer et al., 2013; and heart failure, Rutledge et al., 2006). Our findings suggest that not all depression questionnaires may be appropriate for assessing depressive symptomatology in chronic illness populations. "
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    ABSTRACT: Introduction: Depression is common in chronic illness, albeit prevalence can be highly variable. This variability may be a function of symptom overlap between depression and chronic illness. Using Obstructive Sleep Apnoea (OSA) as an exemplar, this meta-analysis explored whether the proportion of overlapping symptoms between OSA and depression, within different depression questionnaires, moderates prevalence estimates. Methods: A systematic search identified 13 studies meeting eligibility criteria. Results: Based on depression questionnaires, the prevalence of depression in OSA ranged from 8% to 68%, reflecting marked heterogeneity. Prevalence estimates based on questionnaires with greater symptom overlap between OSA and depression were higher, whereas questionnaires with a higher proportion of anhedonia symptoms were associated with lower prevalence estimates. Discussion: Overall, these data suggest that when using depression questionnaires to assess the prevalence of depression in OSA, questionnaires that have a lower proportion of symptom overlap between OSA and depression, as well as a higher proportion of anhedonia symptoms, reduce the likelihood of overestimating the prevalence of depression in OSA. This study has implications for other chronic illnesses with symptom overlap with depression, for example diabetes, chronic kidney disease, or heart disease, as well as suggesting that depression questionnaires are not equally appropriate for assessing depression symptomatology in chronic illness populations. (PsycINFO Database Record
    Health Psychology 08/2015; In press. DOI:10.1037/hea0000280 · 3.59 Impact Factor
    • "CRH = corticotrophin releasing hormone, AVP = arginine vasopressin, ACTH = adrenocorticotropic hormone. mortality rates have been established (Rutledge et al., 2006). The first reports of a higher incidence of CHD-related deaths in patients suffering from major depression originate from 1930 (Malzberg, 1937). "
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    ABSTRACT: Cardiovascular disease (CVD) remains a leading cause of death worldwide and identification and therapeutic modulation of all its risk factors is necessary to ensure a lower burden on the patient and on society. The physiological response to acute and chronic stress exposure has long been recognized as a potent modulator of immune, endocrine and metabolic pathways, however its direct implications for cardiovascular disease development, progression and as a therapeutic target are not completely understood. More and more attention is given to the bidirectional interaction between psychological and physical health in relation to cardiovascular disease. With atherosclerosis being a chronic disease starting already at an early age the contribution of adverse early life events in affecting adult health risk behavior, health status and disease development is receiving increased attention. In addition, experimental research into the biological pathways involved in stress-induced cardiovascular complications show important roles for metabolic and immunologic maladaptation, resulting in increased disease development and progression. Here we provide a concise overview of human and experimental animal data linking chronic and acute stress to CVD risk and increased progression of the underlying disease atherosclerosis. Copyright © 2015. Published by Elsevier Inc.
    Brain Behavior and Immunity 08/2015; DOI:10.1016/j.bbi.2015.08.007 · 5.89 Impact Factor
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