Depression In Cardiovascular Disease Research Articles

Incidence of depression in patients with cardiovascular disease and type 2 diabetes: a nationwide cohort study.

Estimating how type 2 diabetes (T2D) affects the rate of depression in cardiovascular disease (CVD) can help identify high-risk patients. The aim is to investigate how T2D affects the rate of depression according to specific subtypes of CVD. Incident CVD patients, free of psychiatric disease, with and without T2D, were included from nationwide registries between 2010 and 2020. We followed patients from CVD diagnosis until the first occurrence of depression, emigration, death, 5years, or end of study (December 31, 2021). We used time-dependent Poisson regression to estimate the incidence rates and rate ratios (IRR) of depression following subtypes of CVD with and without T2D. The model included age, sex, comorbidities, calendar year, T2D duration, educational level, and living situation as covariates. A total of 165,096 patients were included; 45,845 had a myocardial infarction (MI), 63,691 had a stroke, 19,959 had peripheral artery disease (PAD), 35,568 had heart failure (HF), and 979 were diagnosed with 2 or more CVD subtypes (= > 2 CVD's). Baseline T2D in each CVD subtype ranged from 11 to 17%. The crude incidence rate of depression per 1000 person-years (95% confidence intervals) was: MI + T2D: 131.1 (109.6;155.6), MI: 82.1 (65.3;101.9), stroke + T2D: 287.4 (255.1;322.6), stroke: 222.4(194.1;253.6), PAD + T2D: 173.6 (148.7;201.4), PAD:137.5 (115.5;162.5), HF + T2D: 244.3 (214.6;276.9), HF: 199.2 (172.5;228.9), = > 2 CVD's + T2D: 427.7 (388.1;470.2), = > 2 CVD's: 372.1 (335.2;411.9). The adjusted IRR of depression in MI, stroke, PAD, HF, and = > 2 CVD's with T2D compared to those free of T2D was: 1.29 (1.23;1.35), 1.09 (1.06;1.12), 1.18 (1.13;1.24), 1.05 (1.02;1.09), and 1.04 (0.85;1.27) (p-value for interaction < 0.001). The presence of T2D increased the rate of depression differently among CVD subtypes, most notable in patients with MI and PAD.

The effects of internet-based cognitive behaviour therapy for depression in cardiovascular disease on symptoms of anxiety: a secondary analysis of a randomized trial.

The aims of this study were to evaluate: (i) the short- and long-term effects of the internet-based cognitive behaviour (iCBT) programme on symptoms of distress and fear disorder in cardiovascular disease (CVD) patients, and (ii) the association between changes in depression and changes in symptoms of distress and fear disorder from baseline to 12-month follow-up. Secondary analysis of data collected in a randomized controlled study evaluating the effects on depression of an iCBT programme compared to an online discussion forum (ODF) in CVD patients (n = 144). Data were collected at baseline, at post-intervention (9 weeks), and at 6- and 12-month follow-ups.The results showed that symptoms of distress disorder were statistically significantly more reduced in the iCBT group than in the ODF group. For symptoms of the fear disorder, no differences were found except for avoidance, which showed a statistically significant reduction in the iCBT group. The long-term analysis in the iCBT group showed that CAQ total score and fear decreased from baseline to 6- and 12-month follow-ups, respectively. Avoidance and attention both decreased statistically significantly from baseline to post-intervention, but not between post-intervention and 12-month follow-up. The results suggest that the iCBT programme targeted depression in CVD patients successfully reduced symptoms of distress disorder and to a lesser extent symptoms of fear disorder. Change in depression was more strongly associated with a change in distress than a change in fear disorder. ClinicalTrials.gov: NCT02778074.

A Comparative Study on Assessment of Depression in Cardiovascular Disease Patients

Aim: To assess depression level in cardiovascular disease patients and compare it with the individual without cardiovascular disease. Methods: A comparative study was conducted to assess the level of depression in cardiovascular disease (CVD) patients. The sample size was 200 (100 CVD patients and 100 non-CVD participants) with a random sampling technique. The Depression, Anxiety, and Stress Scale (DASS-42) was used to assess the level of depression of the study participants. Results: Cardiovascular disease patients recorded significantly higher depression levels than the control group (without CVD). The impact of demographic variables such as gender, age, education and socioeconomic also revealed significant differences in depression level among them. Both, females and elderly CVD patients reported higher depression scores on DASS-42. Depressive level was also higher in CVD patients who had lower levels of education and socioeconomic status. Conclusion: The results of the study revealed that depression is a psychological risk factor and CVD patients. Females, less educated, elderly and with low socioeconomic status CVD patients were more affected. Understanding the complex relationship between mental health issues like depression and cardiovascular disease and impact of gender, education, age and socioeconomic status socioeconomic status has not been researched extensively. Further studies are needed to understand the complexity of these interrelationships Keywords: Depression, Cardiovascular disease, Gender, Age, Education and Socioeconomic status.

Evaluating Metacognitive Therapy to Improve Treatment of Anxiety and Depression in Cardiovascular Disease: The NIHR Funded PATHWAY Research Programme.

BackgroundAnxiety and depression contribute to poorer physical and mental health outcomes in cardiac patients. Psychological treatments are not routinely offered in cardiac care and have mixed and small effects. We conducted a series of studies under the PATHWAY research programme aimed at understanding and improving mental health outcomes for patients undergoing cardiac rehabilitation (CR) through provision of metacognitive therapy (MCT).MethodsPATHWAY was a series of feasibility trials, single-blind, multicenter, randomized controlled trials (RCTs), qualitative, stated preferences for therapy and health economics studies.FindingsPatients felt their psychological needs were not met in CR and their narratives of distress could be parsimoniously explained by the metacognitive model. Patients reported they would prefer therapy over no therapy as part of CR, which included delivery by a cardiac professional. Two feasibility studies demonstrated that RCTs of group-based and self-help MCT were acceptable, could be embedded in CR services, and that RCTs of these interventions were feasible. A definitive RCT of group-MCT within CR (n = 332) demonstrated significantly greater reductions in the severity of anxiety and depression, exceeding CR alone, with gains maintained at 12 month follow-up (SMD HADS total score = 0.52 at 4 months and 0.33 at 12 months). A definitive trial of self-help MCT is ongoing.ConclusionThere is a need to better meet the psychological needs of CR patients. Embedding MCT into CR demonstrated high acceptability and improved efficacy on psychological outcomes. Results support roll-out of MCT in CR with evaluation of national implementation.RegistrationURL: NCT02420431; ISRCTN74643496; NCT03129282.

Screening, Referral and Treatment of Depression by Australian Cardiologists

Depression is common in cardiovascular disease (CVD). Clinical practice guidelines recommend routine depression screening by cardiologists. The aim of the study was to undertake a national survey of Australian cardiologists' clinical practice behaviours in relation to depression screening, referral, and treatment. The Cardiovascular Disease and Depression Questionnaire was sent to 827 eligible cardiologist members of Cardiac Society of Australia and New Zealand, of which a total of 524 were returned (63%). Most Australian cardiologists do not routinely ask their patients about depression and only 3% routinely use depression screening instruments. Most cardiologists (>70%) think that General Practitioners (Primary Care Physicians) are primarily responsible for identifying and treating depression in CVD. Cardiologists, who understand the prognostic risks of depression in CVD and feel confident to identify and treat depression, were more likely to screen, refer and/or treat patients for depression. Australian cardiologists rarely use validated depression screening measures. Several brief instruments are available for use and can be easily integrated into routine patient care without taking additional consultation time.

Grand Coeur, Grand Ecoeurement! Depression and the Heart!

Sir, The prevalence rates of depression in cardiovascular disease (CVD) range from 17% to 27%. It is three times more common in patients after myocardial infarction (MI). Women are particularly at high risk. Depression is a risk factor for CVD; it approximately doubles the risk. Depression, especially treatment-resistant (TRD), independently portends poor prognosis in patients with CVD.[1] As such, there seems to be a dose–response relationship between severity of depression and cardiac mortality. Post-MI depression increases mortality by two to three times. It has been shown that somatic/neurovegetative symptom cluster of depression has a stronger association with CVD prognosis than the cognitive cluster. Possible mechanisms for this bidirectional relationship include both biological and behavioral links. Biological links include shared risk factors, metabolic syndrome, increased platelet activation, procoagulant states, hypothalamic–pituitary–adrenal axis dysregulation, dysautonomia, impaired immune function, vascular dysfunction, and inflammation.[2] Moreover, shared genetic effects might be contributory as demonstrated in a Swedish twin study,[3] with age-adjusted hazard ratio of 1.3. Recently, a systematic review and meta-analysis found a 27% increase in the risk of venous thromboembolism with antidepressant use class effect.[4] Psycho-social links include unhealthy lifestyle and treatment nonadherence. The relationship between depressive symptoms and multiple health risk factors begins in the adolescence calling for early intervention long before CVD sets in the middle age. Furthermore, a growing body of evidence connects childhood abuse to depression and other health outcomes including CVD in later years, mediated chiefly through inflammatory process.[5] Screening for depression for patients with CVD is recommended by American Heart Association. The Patient Health Questionnaire (PHQ)-2 provides two screening questions and can be followed by PHQ-9 if either answer is positive. Likewise, patients with depression should be closely monitored and treated for risk factors for CVD. Despite this link, studies failed to demonstrate reduced CVD by treating depression.[6] The major trials for treating depression in the setting of CVS include the following[7]: SADHART – demonstrated safety of sertraline ENRICHD – cognitive behavioural therapy improved depression and social isolation CREATE – citalopram was efficacious MIND-IT – mirtazapine was safe in patients after MI K-DEPACS – escitalopram was effective. Selective serotonin reuptake inhibitors are generally considered first-line treatment for demonstrated safety. Besides, they might be advantageous for blood-thinning actions. Sertraline and escitalopram are commonly preferred due to minimal pharmacokinetic interactions. Food and Drug Administration recommended a ceiling dose of 40 mg of citalopram due to concerns of dose-dependent QTc prolongation. Tricyclic antidepressants (e.g., nortriptyline) are best avoided due to quinidine-like action, prolongation of QTc interval, and possible torsadogenecity. Serotonin-norepinephrine reuptake inhibitors (e.g., venlafaxine) and norepinephrine reuptake inhibitors (e.g., reboxetine) are notorious for hypertension as these agents boost norepinephrine drive. Cases of Takotsubo cardiomyopathy have been reported in literature.[8] Bupropion (norepinephrine–dopamine reuptake inhibitor) has been associated with supine hypertension. Monoamine oxidase inhibitors (e.g., tranylcypromine) cause orthostasis and use is fraught with potential cheese reaction (hypertensive crisis) and serotonin syndrome. Finally, electro-convulsive therapy (ECT) generally can be performed safely in most patients with underlying cardiac conditions, whenever indicated (e.g., failed pharmacotherapy, depressive symptoms pose a significant barrier to care, patient's preference), as long as these patients are identified ahead of time and are closely monitored for potential complications.[9] Interestingly, Magid et al.[10] have reported on a successful ECT in a patient 10 days after MI. Of note, suggestions of psychiatric adversity with commonly prescribed cardiac medications generally have not been substantiated. B-blockers are not depressogenic (even pindolol has been anecdotally deployed to augment antidepressants in TRD) and statins do not appear to increase suicidality, as was once thought.[11] Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

The Influence of Somatic Symptoms on Beck Depression Inventory Scores in Hospitalized Postmyocardial Infarction Patients

The Beck Depression Inventory (BDI) has been used more than any other self-report questionnaire in research on depression in cardiovascular disease. However, no studies have examined whether BDI scores may be influenced by somatic symptoms common after myocardial infarction (MI) that may overlap with symptoms of depression. The objective of this study was to examine whether BDI scores of post-MI patients may be influenced by somatic symptoms that commonly occur after MI, but may not be related to depression. Post-MI patients and psychiatric outpatients were matched on BDI cognitive-affective symptom scores, sex, and age, and their BDI somatic symptom scores were compared using independent samples t tests. Somatic symptoms accounted for 57% of BDI total scores for 296 post-MI patients (mean total BDI = 8.8), compared with 50% for 296 matched psychiatric outpatients (mean total BDI = 7.6). Overall, BDI somatic scores of post-MI patients were 1.3 points higher than for psychiatric outpatients (95% CI 0.68 to 1.82; P < 0.001), equivalent to 14% of total scores of post-MI patients. The relative influence of somatic symptoms on BDI total scores was higher for post-MI patients than for psychiatric outpatients matched on cognitive-affective scores, sex, and age. This finding stands in contrast to that from a previous study that used similar methods and sample comparisons and found that post-MI and psychiatric outpatients did not differ in their endorsement of somatic symptoms on the BDI-II. The BDI-II may be preferable to the BDI in post-MI patients.

P-1481 - Sex differences in depression and cardiovascular disease

It has been long established that depression is an independent risk factor for cardiovascular disease (CVD) and that CVD is a risk factor for depression. Three lines of evidence have been proposed to date in an effort to explain the comorbidity of CVD and mood, as well as anxiety disorders: (1) the epidemiological evidence for a causal role of depression in the evolution and progression of CVD; (2) the biological evidence for the plausibility of an etiologic role of depression in CVD and (3) both depression and CVD are manifestations of a common underlying pathophysiological process. The goal of this presentation is to briefly review and synthesize the evidence for the above proposed explanations with a special focus on the roles of serotonin, platelets and the immune system. Sex and gender differences in both depression/anxiety and CVD and the relevance of these differences as they pertain to women will be emphasized.

Platelets and depression in cardiovascular disease: A brief review of the current literature

Major depression is an independent risk factor for cardiovascular mortality and morbidity. The exact mechanisms linking depression and increased cardiovascular risk remain poorly understood. Several mechanisms have been proposed including increased platelet reactivity. This review focuses on the current literature that examines the platelet hypothesis of depression. To date studies show increased serotonin response, increased platelet serotonin receptor density, decreased serotonin transporter binding, and decreased platelet serotonin levels in individuals with depression. However other studies have shown no change in serotonin uptake. In addition to platelet serotonin specific pathways, other platelet pathways that have shown significant changes in depressed individuals include blunting of the platelet adenosine response, increased platelet thrombin response, increased glycoprotein Ib expression, increased P-selectin, β thromboglobulin, and platelet factor four, as well as decreased platelet brain derived neurotrophic factor. However there are other studies that show conflicting evidence of increased platelet activation as measured by integrin receptor α2b β3. Other conflicting data include α adrenergic density and platelet response to augmented serotonin. The direction of future research in platelet functional changes in depression and coronary artery disease should continue to focus on serotonin specific pathways with emphasis on potential mechanisms of specific pathway changes.

Cardiovascular disease risk factors and depression in Korean women: Results from the fourth Korean National Health and Nutrition Examination Survey

Depression is the fourth leading factor of disease burden for the global female population, but while increasing evidence has supported a contributing role of depression in cardiovascular disease, little is known about this association within the female population of Korea. We examined the association in a study of 5658 Korean women who participated in the fourth Korean National Health and Nutrition Examination Survey. A logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). A total of 279 cases of depression were included. Cardiovascular disease risk factors were associated with higher odds of depression: ORs (95% CIs) were 3.99 (2.25–7.05) for current smokers with <5 pack-years vs. never-smokers, 1.97 (1.18–3.30) for ≥28 vs. <20kg/m2 of body mass index, 1.42 (1.03–1.95) for 100–125 vs. <100mg/dL of fasting serum glucose levels, and 2.10 (1.46–3.03) for a history of hyperlipidemia. Women with a history of two or three comorbid disorders (diabetes, hypertension, and cardiovascular disease) had a 1.63-fold higher OR for depression than women without any of these diseases. Korean women with depression had a greater prevalence of major risk factors for cardiovascular disease than women without depression.

Serotonin, depression, and cardiovascular disease: sex-specific issues

The comorbidity of cardiovascular disease (CVD) and depression/anxiety disorders is well established, but the mechanisms are not well understood. This paper will review the epidemiological and biological evidence for the role of depression in CVD, as well as the pathophysiological process underlying both depression and CVD. The focus will be on the roles of serotonin, platelets, and the immune system, with an emphasis on the relevance of sex differences in both depression/anxiety and CVD as they pertain to women.

Depression

The aim of this article is to provide an overview on depression as a risk factor for the onset and follow-up of cardiovascular disease (CVD). In brief, the current state of psychobiological mechanisms bridging the gap between affective states and somatic consequences are presented. Four meta-analyses dealing with depression as a CVD risk factor in apparently healthy populations with >100,000 participants included, extracted an adjusted effect estimator of 1.60-1.90. Depressed subjects present with an unhealthier lifestyle (nutrition, smoking, physical activity). Three major psychobiological pathways directly acting on the circulatory system are under discussion: (1) hyperregulation of the autonomic nervous system (e.g., increased mean heart rate, increased heart rate responses, impaired heart rate variability), (2) overshooting stress responses of the endocrine system with impaired feedback mechanisms (e.g., for cortisol release), and (3) the immune system with dysregulated release of acute phase proteins and proinflammatory cytokines, all involved in a bidirectional crosstalk with the patient's affective state and leading to platelet activation and flow mediated endothelial (dys-)function. Nonadherence and adverse side effects of medications also contribute to the lethal properties of depression in CVD.

Data Reveal More About Link of Depression, Heart Disease

Data Reveal More About Link of Depression, Heart Disease

Impact of Depression and Cardiovascular Disease

&lt;p&gt;Psychiatric and physical illnesses frequently coexist. Depression is associated clinically with heart disease in several ways, including risk of arrhythmia, alteration of the amount of blood flowing to the coronary arteries, increased risk of blood clots, and increased risk of cardiac arrest. Depression may even be an independent risk factor for mortality in individuals with cardiovascular disease (CVD), something that should concern those involved in the treatment of those patients.&lt;/p&gt; &lt;h4&gt;ABOUT THE AUTHORS&lt;/h4&gt; &lt;p&gt;Nazmie F. Ibishi, MD, is a Psychiatrist with the University Clinical Center of Kosova, Clinic of Psychiatry, Prishtina, Kosova. Nebi R. Musliu, MD, is a Cardiologist with the University Clinical Center of Kosova, Clinic of Cardiology. Ahmet Kamberi, PhD; Spiro Qirko, PhD; Sabit Brokaj, PhD; and Mimoza Lezha, PhD, are with University Hospital Center of Tirana, Clinic of Cardiology, Albania. Bekim Haxhiu, MD, is with Primary Care Service, Prishtina, Kosova, John Masala, MD, is a Psychiatrist with Dubrava Prison Hospital, Kosova.&lt;/p&gt; &lt;p&gt;Address correspondence to: Nazmie F. Ibishi, MD, University Clinical Center of Kosova-Clinic of Psychiatry, Prishtina, (Kosova); or e-mail &lt;a href="mailto:nazmiemb3@hotmail.com"&gt;nazmiemb3@hotmail.com&lt;/a&gt;.&lt;/p&gt; &lt;p&gt;Dr. Ibishi, Dr. Musliu, Dr. Kamberi, Dr. Qirko, Dr. Brokaj, Dr. Lezha, Dr. Haxhiu, and Dr. Masala have disclosed no relevant financial relationships.&lt;/p&gt; &lt;h4&gt;EDUCATIONAL OBJECTIVES&lt;/h4&gt; &lt;ol&gt;&lt;li&gt; Assess the impact of depression in cardiovascular disease (CVD) patients. &lt;/li&gt; &lt;li&gt; Determine the relationship of depression and CVD, including biological and behavioral factors. &lt;/li&gt; &lt;li&gt; Explain the signifi cance of early recognition of depression in CVD patients and the role of indirect self-destructive behavior as an independent risk factor for morbidity and mortality in these patients. &lt;/li&gt;&lt;/ol&gt;

S40-01 New developments in diagnosis and therapy of depression in cardiovascular disease

Introduction:Repeatedly, it has been demonstrated that depression increases the risk of developing cardiovascular disorders; vice versa, in subjects with pre-existing heart disease, comorbid depression was found to predict an unfavourable cardiovascular prognosis. However, several studies failed to observe that treatment of depression positively influences cardiac risk. Therefore, focus of research has shifted to identification of subjects, who would benefit from antidepressant therapy that is tailored to their individual needs.Method:Search of literature databases, focusing latest goals and advances in diagnosis and therapy of depression in subjects with cardiovascular disease.Results and discussion:Screening cardiac patients for depression seems to result in a different population of depressed patients, as compared with most trials testing antidepressant agents. This different inclusion process obviously favoured oversampling of subjects with minor or reversible depressive syndromes such as adjustment disorders. It is known that in these conditions placebo treatment is powerful, sometimes equalling verum condition in effectiveness.This hypothesis is supported by re-analysis of former studies revealing selective serotonin reuptake inhibitors (SSRI) to be more effective in subjects with severe or recurrent depression or in patients, in whom depression had begun prior to the onset of cardiovascular disease (e.g., myocardial infarction). Surprisingly, some data support the notion that treatment with SSRIs ameliorates cardiac prognosis irrespective of their antidepressant action. Ongoing studies deal with treatment of depression in patients with heart failure or stroke, and with psychotherapy aimed at reducing cardiac risk factors.

Depression and cardiovascular disease: does antidepressant treatment improve cardiac outcome?

The association between depression and cardiovascular disease has been well documented but the nature of this relationship continues to be defined. Given the accumulation of epidemiological evidence linking these diseases a number of interventional studies have been undertaken to assess the issue of whether antidepressant treatment in depressed patients with cardiovascular disease improves cardiac outcome. The objective of this paper is to review recent randomised controlled trials on this topic and to explore the implications that these may have for future research in this area. This review is derived from a MEDLINE search using the search terms 'depressive disorder' and 'cardiovascular diseases'. Only randomised controlled trials published in English with clearly defined methods and interventions are included here. Reference sections from the articles were used to identify additional relevant studies. A small number of high quality trials were uncovered which indicated mixed results in terms of the treatment of depression in cardiovascular disease. None indicated a statistically significant difference in cardiac outcome. It is not possible at this time to recommend treatment for depression to reduce cardiovascular risk. However depression remains prevalent in patients with cardiovascular disease and is a treatable cause of morbidity in its own right.

Broken heart: depression in cardiovascular disease

Heart disease and depression are among the most common diseases seen in developed countries. The relation-ship between heart disease and depression has been the subject of both popular interest and scientific research. Sadness is often portrayed as a feeling of heaviness in the chest or as a "broken heart." Interestingly as we learn more about the expression of emotions, it appears that these perceptions may simply be the language representation of somatic feelings. Large, prospective, longitudinal studies that have examined the relationship between depression and development of coronary artery disease (CAD) have shown that depression is a risk factor for the development of CAD. Depression also increases mortality in patients with stable CAD or myocardial infarction compared with patients without depression. The recent Sertraline AntiDepressant HeARt attack Trial (SADHART) has shown that selective serotonin reuptake inhibitors like sertraline can be safely used in patients with depression following myocardial infarction. There is also intriguing evidence that treating depression with antidepressants may improve outcomes, including mortality.

Depression and the heart: a systematic overview of definition, measurement, consequences and treatment of depression in cardiovascular disease.

Depression is an independent risk factor in the pathogenesis of cardiovascular disease and it is a prevalent disorder after cardiovascular disease associated with negative outcome in terms of mortality and morbidity. It is a dangerous condition requiring adequate screening and treatment, however, it often remains undiagnosed and thus untreated. Non-psychiatric healthcare workers, like nurses, general practitioners, physiotherapists and cardiologists are the health providers most closely involved in the management of patients with cardiovascular disease. They can play an important role in screening cardiovascular patients for depressive symptoms and in referring them for treatment. The purpose of this article therefore is to provide an evidence-based framework, aiming to educate non-psychiatric healthcare providers on depressive disorder in the context of chronic cardiovascular disease. In this paper, an overview of the definition, prevalence and consequences of depression will be discussed. Moreover, an overview of measurement methods and treatment modalities for depression will be provided. In addition, a step-by-step guide is provided in order to help non-psychiatric healthcare providers in dealing with depressed patients.