Background: Major depression and inadequate self-care are common in patients with heart failure (HF). Little is known about how to intervene when both problems are present. This study examined the efficacy of a sequential approach to treating these problems. Methods: Stepped Care for Depression in HF was a single-site, single-blind, randomized controlled trial of cognitive behavior therapy (CBT) versus usual care (UC) for major depression in patients with HF. The intensive phase of the CBT intervention lasted between 8 and 16 weeks, depending upon the rate of improvement in depression. All participants received a tailored HF self-care intervention that began 8 weeks after randomization. The intensive phase of the self-care intervention ended at 16 weeks post-randomization. The coprimary outcome measures were the Beck Depression Inventory (version 2) and the Maintenance scale of the Self-Care of HF Index (v6.2) at week 16. Results: One hundred thirty-nine patients with HF and major depression were enrolled; 70 were randomized to UC and 69 to CBT. At week 16, the patients in the CBT arm scored 4.0 points ([95% CI, −7.3 to −0.8]; P =0.02) lower on the Beck Depression Inventory, version 2 than those in the usual care arm. Mean scores on the Self-Care of HF Index Maintenance scale were not significantly different between the groups ([95% CI, −6.5 to 1.5]; P =0.22). Conclusions: CBT is more effective than usual care for major depression in patients with HF. However, initiating CBT before starting a tailored HF self-care intervention does not increase the benefit of the self-care intervention. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02997865.

• Ketamine is increasingly being used in the treatment of depression. • In such situations, ketamine use may be associated with a "high". • The high resembles that resulting from alcohol use. • Some patients, consequently, may experience alcohol craving. • Previously abstinent alcoholic patients may relapse into drinking.

Objective: This study evaluated agreement between the Patient-Reported Outcomes Measurement Information System® (PROMIS®) Depression scale and the Beck Depression Inventory (BDI-II) in patients with heart failure and comorbid major depression. Method: The BDI-II and the computerized adaptive test version of the PROMIS® Depression scale were administered at baseline to 158 participants in a randomized controlled trial of cognitive behavior therapy for major depression in patients with heart failure. A crosswalk table (Choi, Schalet, Cook, & Cella, 2014) was used to transform the PROMIS® scores into “linked” BDI-II equivalent scores. Bland-Altman plots, histograms, and scatterplots were used to visualize the agreement between these scores at baseline and 6 months, and intraclass correlation coefficients (ICCs) were calculated for each occasion to quantify the agreement. Treatment effects and change scores were also examined. Results: The measures agreed moderately at baseline (ICC = 0.52, p < .0001) and strongly at 6 months (ICC = 0.77, p < .0001), but on average, the linked and observed BDI-II scores differed by 3.1 points at baseline (p < .0001) and −0.17 points at 6 months (p = .78). The discrepancies were considerably larger in many individual cases on both occasions. Conclusions: The PROMIS® Depression scale is likely to play an important role in research on depression in patients with heart failure, but for now, it should be used in addition to rather than instead of the BDI-II in studies in which the BDI-II would ordinarily be used. Additional research is needed to evaluate the validity and utility of the PROMIS® Depression scale in patients with heart failure.

ABSTRACT Objective Depression is associated with an increased risk of mortality in patients with coronary heart disease (CHD). The risk may be reduced in patients who remit with adequate treatment, but few patients achieve complete remission. The purpose of this study was to identify the symptoms that persist despite aggressive treatment for depression in patients with CHD. Methods One hundred twenty-five patients with stable CHD who met the DSM-IV criteria for a moderate-to-severe major depressive episode completed treatment with cognitive behavior therapy, either alone or combined with an antidepressant, for up to 16 weeks. Depression symptoms were assessed at baseline and after 16 weeks of treatment. Results The M (SD) Beck Depression Inventory scores were 30.0 (8.6) at baseline and 8.3 (7.5) at 16 weeks. Seventy seven (61%) of the participants who completed treatment met remission criteria (Hamilton Rating Scale for Depression ≤7) at 16 weeks. Loss of energy and fatigue were the most common posttreatment symptoms both in remitters (n = 44, 57%; n = 34, 44.2%) and nonremitters (n = 42, 87.5%; n = 35, 72.9%). These symptoms were not predicted by baseline depression severity, anxiety, demographic, or medical variables including inflammatory markers or cardiac functioning or by medical events during depression treatment. Conclusions Fatigue and loss of energy often persist in patients with CHD even after otherwise successful treatment for major depression. These residual symptoms may increase the risks of relapse and mortality. Development of effective interventions for these persistent symptoms is a priority for future research.

BACKGROUND:Depression is a risk factor for morbidity and mortality in patients with coronary heart disease. Finding effective methods for identifying and treating depression in these patients is a high priority. The purpose of this study was to determine whether collaborative care (CC) for patients who screen positive for depression during an outpatient cardiology visit results in greater improvement in depression symptoms and better medical outcomes than seen in patients who screen positive for depression but receive only usual care (UC).METHODS:Two hundred-one patients seen in an outpatient cardiology clinic who screened positive for depression during an outpatient visit were randomized to receive either CC or UC. Recommendations for depression treatment and ongoing support and monitoring of depression symptoms were provided to CC patients and their primary care physicians (PCPs) for up to 6months.RESULTS:There were no differences between the arms in mean Beck Depression Inventory-II scores(CC, 15.9; UC, 17.4; p=.45) or in depression remission rates(CC, 32.5%; UC, 26.2%; p=0.34) after 6months, or in the number of hospitalizations after 12months (p=0.73). There were fewer deaths among the CC (1/100) than UC patients (8/101) (p=0.03).CONCLUSIONS:This trial did not show that CC produces better depression outcomes than UC. Screening led to a higher rate of depression treatment than was expected in the UC group, and delays in obtaining depression treatment from PCPs may have reduced treatment effectiveness for the CC patients. A different strategy for depression treatment following screening in outpatient cardiology services is needed.

Background: Previous studies suggest that patients with coronary heart disease (CHD) who do not respond to treatment for depression are at higher risk of mortality than are treatment responders. The purpose of this study was to determine whether elevated nighttime heart rate (HR) and low heart rate variability (HRV), both of which have been associated with depression and with cardiac events in patients with CHD, predict poor response to depression treatment in patients with CHD.Methods: Patients with stable CHD and a current major depressive episode completed 24 h ambulatory ECG monitoring and were then treated for up to 16 weeks with cognitive behavior therapy (CBT), either alone or in combination with an antidepressant. Pre-treatment HR and HRV were calculated for 124 patients who had continuous ECG from early evening to mid-morning.Results: Following treatment, 64 of the 124 patients (52%) met study criteria for remission (Hamilton Rating Scale for Depression score < 7). Prior to treatment, non-remitters had higher nighttime HR (p=0.03) and lower nighttime HRV (p=0.01) than did the remitters, even after adjusting for potential confounds.Limitations: Polysomnography would have provided information about objective sleep characteristics and sleep disorders. More CBT sessions and higher doses of antidepressants may have resulted in more participants in remission.Conclusions: High nighttime HR and low nighttime HRV predict a poor response to treatment of major depression in patients with stable CHD. These findings may help explain why patients with CHD who do not respond to treatment are at higher risk for mortality. (C) 2016 Elsevier B.V. All rights reserved.

Objectives: Patients with coronary heart disease (CHD) who respond to treatment for depression are at lower risk of mortality than are nonresponders. This study sought to determine whether variables that have been shown to predict both depression treatment outcomes in psychiatric patients and cardiac events in patients with CHD, also predict poor response to depression treatment in patients with CHD.Methods: One hundred fifty-seven patients with stable CHD who met the DSM-IV criteria for a major depressive episode were treated with cognitive behavior therapy (CBT) for 16 weeks, either alone or in combination with an antidepressant.Results: The mean Beck Depression Inventory (BDI-II) score was 30.2 +/- 8.5 at baseline and 85 +/- 7.8 at 16 weeks. Over 50% of the participants were in remission (HAM-D-17 score <= 7) at the end of treatment. Of the hypothesized predictors, severe depression at baseline (p = 0.02), stressful life events during the first (p = 0.03) and last (p < 0.0001) 8 weeks of treatment, and the completion of CBT homework assignments (p = 0.001) predicted depression outcomes. History of prior episodes, anxiety symptoms, antidepressant therapy at study enrollment, and medical hospitalizations or emergency department visits during treatment did not predict treatment outcome.Conclusions: Patients who are under considerable stress do not respond as well to evidence-based treatments for depression as do patients with less stress. If future studies support these findings, more work will be needed to better address stressful life events in patients who may otherwise remain at high risk for mortality and medical morbidity following depression treatment. (C) 2016 Elsevier Inc. All rights reserved.

BACKGROUND:Depression is associated with an increased risk of mortality in patients with coronary heart disease. There is evidence that this risk may be reduced in patients who respond to depression treatment. The purpose of this study was to determine whether cardiac risk markers predict poor response to depression treatment and, second, whether they improve with successful treatment.METHODS:One hundred fifty-seven patients with stable coronary heart disease who met the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria for a moderate to severe major depressive episode were treated with cognitive behavior therapy, either alone or combined with an antidepressant, for up to 16 weeks. Depression, physical activity, sleep quality, thyroid hormones (total thyroxine [T4] and free T4), and inflammatory blood markers (C-reactive protein, interleukin-6, tumor necrosis factor) were assessed at baseline and after 16 weeks of treatment.RESULTS:The mean (SD) Beck Depression Inventory scores were 30.2 (8.5) at baseline and 8.5 (7.8) at 16 weeks. More than 50% of the participants met the criteria for depression remission (17-item Hamilton Rating Scale for Depression ≤ 7) at 16 weeks. Only free T4 thyroid hormone at baseline predicted poor response to depression treatment after adjustment for potential confounders (p = .004). Improvement in sleep quality (p = .012) and physical activity level (p = .041) correlated with improvement in depression. None of the inflammatory markers predicted posttreatment depression or changed with depression.CONCLUSIONS:Thyroid hormone (T4) level predicted depression treatment outcome, and improvement in depression correlated with improvement in sleep and physical activity. More detailed studies of thyroid function and objective assessments of sleep and physical activity in relation to depression improvement and cardiac outcomes are needed.

OBJECTIVE:Depression is associated with low red blood cell (RBC) levels of 2 omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), suggesting that omega-3 supplements might improve depression. However, clinical trials have produced mixed results. The purpose of this secondary analysis of data from a randomized controlled trial was to determine whether baseline blood levels of omega-3, which are known to vary widely among individuals, predict depression outcomes.METHOD:The percentages of EPA, DHA, and the omega-6 arachidonic acid (AA) were measured in RBCs at baseline and posttreatment in 122 participants with DSM-IV major depression who were randomly assigned between May 2005 and December 2008 to receive either 50 mg/d of sertraline and a daily dosage of 930 mg EPA/750 mg DHA or sertraline plus placebo. Associations between baseline omega-3 RBC levels and remission of depression (17-item Hamilton Depression Rating Scale score ≤ 7) were analyzed by treatment arm.RESULTS:Among participants in the omega-3 arm, baseline RBC levels of EPA + DHA (P = .002) and the EPA + DHA:AA ratio (P = .003) were significantly higher among those whose depression subsequently remitted compared with those whose depression did not remit. No associations were detected in the sertraline plus placebo arm. Baseline levels of EPA (P = .03) and the EPA + DHA:AA ratio (P = .04) moderated the relationship between treatment arm and depression outcomes.CONCLUSIONS:High baseline RBC levels of EPA and DHA and a high EPA + DHA:AA ratio predict favorable depression outcomes in patients receiving omega-3 supplements. Omega-3 supplementation may be an effective treatment for depression, but the requisite dosage and duration of treatment may depend on the patient's baseline level of omega-3 fatty acids.TRIAL REGISTRATION:ClinicalTrials.gov identifier: NCT00116857.

IMPORTANCE Depression and inadequate self-care are common and interrelated problems that increase the risks of hospitalization and mortality in patients with heart failure (HF). OBJECTIVE To determine the efficacy of an integrative cognitive behavior therapy (CBT) intervention for depression and HF self-care. DESIGN, SETTING, AND PARTICIPANTS Randomized clinical trial with single-blind outcome assessments. Eligible patients were enrolled at Washington University Medical Center in St Louis between January 4, 2010, and June 28, 2013. The primary data analyses were conducted in February 2015. The participants were 158 outpatients in New York Heart Association Class I, II, and III heart failure with comorbid major depression. INTERVENTIONS Cognitive behavior therapy delivered by experienced therapists plus usual care (UC), or UC alone. Usual care was enhanced in both groups with a structured HF education program delivered by a cardiac nurse. MAIN OUTCOMES AND MEASURES The primary outcome was severity of depression at 6 months as measured by the Beck Depression Inventory. The Self-Care of Heart Failure Index Confidence and Maintenance subscales were coprimary outcomes. Secondary outcomes included measures of anxiety, depression, physical functioning, fatigue, social roles and activities, and quality of life. Hospitalizations and deaths were exploratory outcomes. RESULTS One hundred fifty-eight patients were randomized to UC (n = 79) or CBT (n = 79). Within each arm, 26 (33%) of the patients were taking an antidepressant at baseline. One hundred thirty-two (84%) of the participants completed the 6-month posttreatment assessments; 60 (76%) of the UC and 58 (73%) of the CBT participants completed every follow-up assessment (P = .88). Six-month depression scores were lower in the CBT than the UC arm on the Beck Depression Inventory (BDI-II) (12.8 [10.6] vs 17.3 [10.7]; P = .008). Remission rates differed on the BDI-II (46% vs 19%; number needed to treat [NNT] = 3.76; 95% CI, 3.62-3.90; P < .001) and the Hamilton Depression Scale (51% vs 20%; NNT = 3.29; 95% CI, 3.15-3.43; P < .001). The groups did not differ on the Self-Care Maintenance or Confidence subscales. The mean (SD) Beck Depression Inventory scores 6 months after randomization were lower in the CBT (12.8 [10.6]) than the UC arm (17.3 [10.7]), P = .008. There were no statistically significant differences between the groups on the Self-Care Maintenance or Confidence subscale scores or on physical functioning measures. Anxiety and fatigue scores were lower and mental- and HF-related quality of life and social functioning scores were higher at 6 months in the CBT than the UC arm, and there were fewer hospitalizations in the intervention than the UC arm. CONCLUSIONS AND RELEVANCE A CBT intervention that targets both depression and heart failure self-care is effective for depression but not for HF self-care or physical functioning relative to enhanced UC. Additional benefits include reduced anxiety and fatigue, improved social functioning, and better health-related quality of life. TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT01028625.

This study assessed the relationships between older patients’ social support resources and depressive symptoms and psychosocial functioning at 6 months following a psychiatric hospital discharge. The data used in this study were extracted from a prospective study titled “Service Use of Depressed Elders after Acute Care” (National Institute of Mental Health-56208). This sample included 148 older patients who participated in the initial and the 6-month follow-up assessment. Ordinary Least Squares regression (OLS) was used to examine important social support resources in relation to older patients’ depressive symptoms and psychosocial functioning. A vast majority of patients were embedded in a social support network that consisted of acquaintances and confidants. Patients’ depressive symptoms were related to availability of a confidant and the extent to which they spent time with others. However, patients’ psychosocial functioning was not related to social support resources assessed in this study.

Psychiatry is facing a crisis fueled by a fragmented and inefficient system of care delivery and a disconnection between the state of research and the state of psychiatry education and practice. Many factors contribute to the current state of psychiatric care. Psychiatry is a shortage specialty, and this will become worse in the near future. In addition, financial pressures have led to decreases in psychiatric inpatient and outpatient services and to shorter lengths of hospitalization for even the sickest patients. This has resulted in fragmented care and an overreliance on polypharmacy. To reach the large number of patients needing psychiatric services, health care systems must change and take advantage of collaborative and integrative care models and new technologies. Psychiatrists must learn to partner more effectively with primary care providers to extend their expertise to the greatest number of patients. Currently, psychiatric diagnosis is based on a criteria-based system that was developed in the 1970s. Advances in systems and molecular neuroscience are beginning to elucidate specific brain systems that are dysfunctional in psychiatric illness. This has the potential to revolutionize psychiatric diagnosis and treatment in the future. However, psychiatry has not yet been successful in incorporating the language of this research into clinically meaningful terminology. If neuroscientific progress is to be translated into clinical advances, this must change. Residency programs must better prepare their graduates to keep up with a psychiatry literature that will increasingly use the language of neural circuits to describe psychiatric symptomatology and treatments.

This resource examines recent developments in the field of network neuroscience and their potential impact on clinical psychiatry, including the way that psychiatrists are trained and interact with other medical specialties and mental health professionals. It discusses how research in neuroscience is revolutionizing how we think about psychiatric diagnosis and treatment, and how understanding how the neural networks that underlie these mental functions become dysfunctional holds great promise for devising innovative approaches to diagnosis and treatment. It covers recent advances in human functional neuroimaging, which is being used to characterize the activity of specific brain circuits at rest and during the performance of specific tasks, as well as advances in clinical neuroscience that are being coupled with expanding knowledge about genetics and cellular and synaptic neuroscience. Taken together, these advancements offer the hope of much more mechanism-based approaches to treatment in the future.

OBJECTIVE Evidence from several clinical trials in patients with coronary heart disease suggests that depression that does not respond to treatment is associated with a particularly high risk of adverse cardiac outcomes. The purpose of this study was to determine whether obstructive sleep apnea/hypopnea syndrome (OSAHS) is associated with a poor response to antidepressant medication in patients with coronary heart disease. METHOD This was a secondary analysis of data from a randomized, double-blind, placebo-controlled clinical trial of omega-3 fatty-acid augmentation of sertraline for depression in patients with coronary heart disease. Patients with documented coronary heart disease were recruited between May 2005 and December 2008 from cardiology practices in St Louis, Missouri, and through cardiac diagnostic laboratories affiliated with Washington University School of Medicine, St Louis, Missouri. One hundred five patients (mean age = 58 years) with coronary heart disease and current major depressive disorder (DSM-IV) were randomized to receive sertraline plus either omega-3 or placebo for 10 weeks. Cyclical heart-rate patterns associated with OSAHS were detected via ambulatory electrocardiography prior to treatment. Symptoms of depression were measured at baseline and follow-up with the Beck Depression Inventory-II (BDI-II) and the 17-item Hamilton Depression Rating Scale (HDRS-17). The primary endpoint was the BDI-II score at 10 weeks. RESULTS Thirty of the 105 patients (29%) were classified as having probable moderate to severe OSAHS on the basis of nighttime heart-rate patterns. These OSAHS patients had significantly higher scores on both the BDI-II (t = -2.78, P = .01) and the HDRS-17 (t = -2.33, P = .02) at follow-up as compared to the reference group. Adjustment for baseline depression score, treatment arm (omega-3 vs placebo), body mass index, and inflammatory markers did not change the results. Patients with OSAHS reported higher item scores at follow-up on all depressive symptoms measured with the BDI-II compared to those without OSAHS. CONCLUSIONS Obstructive sleep apnea/hypopnea syndrome is associated with a relatively poor response to sertraline treatment for depression. Future research should determine the contribution of OSAHS to the increased risk of adverse cardiac outcome associated with treatment-resistant depression.

Objective: To determine whether omega-3 fatty acid (FA) increases the natural log of very low frequency (InVLF) power, an index of heart rate variability (HRV), and reduces 24-hour heart rate (HR) in depressed patients with coronary heart disease (CHD). Low intake of omega-3 FAs is associated with depression and with low HRV, and all three are associated with an increased risk of death in patients with CHD. Methods: Thirty-six depressed patients with CHD randomized to receive 50 mg of sertraline and 2 g of omega-3/day, and 36 randomized to sertraline and a placebo, had 24-hour HRV measured at baseline and after 10 weeks of treatment. Results: There was a significant treatment x time interaction for covariate adjusted InVLF (p =.009), for mean 24-hour HR (p = .03), and for 1-minute resting HR (p = .02). The interaction was not significant for three other measures of H RV. LnVLF did not change over time in the omega-3 arm but decreased in the placebo arm (p = .002), suggesting that omega-3 may have prevented or slowed deterioration in cardiac autonomic function. Conclusions: The effects of omega-3 FAs on InVLF and HR, although modest, were detected after only 10 weeks of treatment with 2 g per day of omega-3. Whether a longer course of treatment or a higher dose of omega-3 would further decrease HR, improve other indices of HRV, or reduce mortality in depressed CHD patients should be investigated.

Abstract This chapter is about psychiatrists themselves—about how they are trained and how their training clearly distinguishes them from other mental health professionals, such as clinical psychologists or social workers, and prepares them for their practice as physicians who specialize in the diagnosis and treatment of mental disorders. We will also describe the nature of that practice and the various challenges and complications that psychiatrists encounter in the care of patients with psychiatric illness. In other words, because there is considerable misunderstanding in the general public, including among many patients and families, about the role that psychiatrists play in the mental health world, we believe it will be helpful to describe in some detail who they are and what they do.

Abstract What are the early signs of a psychiatric disorder? How can a person recognize early symptoms of a relapse of a preexisting illness? What symptoms should lead someone to seek psychiatric care? Psychiatrists are asked these questions regularly, often by people who are concerned about the behaviour of a friend or family member. Some psychiatric disorders are associated with loss of insight, and those afficted by these illnesses may accept changes in their thinking, mood, and behavior as “normal” or “understandable” under the circumstances of their lives. It frequently falls to friends and family members to recognize that something is wrong and to encourage the person to seek help. In this chapter, we will discuss warning signs that indicate that an individual has or may be developing a serious psychiatric disorder.

Abstract The Holy Grail of psychiatric science is to understand the biological mechanisms underlying mental illnesses. It is hoped that once we are armed with this information, we will be able to devise new strategies that target the primary brain dysfunctions and that possibly prevent these complex and devastating disorders from occurring in the first place. Realistically, we are a long way from these goals. However, rapid advances in neuroimaging, neuroscience, and genetics over the latter part of the last century give us strong reasons for optimism. Some of the research techniques that are now routinely used in neurobiology laboratories on a daily basis were considered “Star Wars” science 15 or 20 years ago.

Abstract A recurring theme in this book has been that psychiatric disorders involve abnormal brain function and are serious medical problems. Complications from these disorders can be devastating for individuals, families, and society, and can include suicide, violence, physical abuse, premature death from a variety of causes, job loss, and discord in relationships. Thus, we believe that psychiatric disorders merit the highest level of attention from the highest quality providers in our health care delivery system.