Management of Depression After Myocardial Infarction

Shapiro, Peter A.

doi:10.1007/s11886-015-0634-4

Cited by 24 publications

(11 citation statements)

References 85 publications

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“…Many physical disorders have been reported to increase the risk for developing a depressive disorder (125) and to activate the production of pro-inflammatory cytokines. Examples are autoimmune and infectious diseases (156–159), endocrine and hormonal diseases (160), cancer (161), diabetes (164), myocardial infarction (165, 196), and physical trauma (166). The treatment of physical disorders, e.g., interferon-based or virostatic treatments for hepatitis C (167, 197), chemotherapy for the treatment of cancer (168), surgery (169) or transplantation (170), can lead to additional cytokine release.…”

Section: Possible Reasons For Cytokine Alterationsmentioning

confidence: 99%

Cytokine Research in Depression: Principles, Challenges, and Open Questions

et al. 2019

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Cytokines have been implicated in the pathology of depression. Currently, the evidence is based on cross-sectional studies and meta-analytic research comparing blood concentrations of T helper type 1 (TH1), T helper type 2 (TH2), pro-inflammatory or anti-inflammatory cytokines of patients with a depressive disorder to those of healthy controls. Additionally, multiple longitudinal studies have investigated cytokine levels during antidepressant treatment. According to the current literature, it seems that peripheral levels of interleukin (IL)-6, IL-10, IL-12, IL-13, and tumor necrosis factor (TNF)-α are elevated and that interferon (IFN)-γ levels are lower in patients with depression compared to healthy controls. However, the overlap of cytokine values between acutely depressed patients, remitted and recovered patients and healthy controls is considerable. Thus, the discriminative power of cytokine concentrations between depressed and non-depressed people is likely weak. Treatment with certain antidepressants appears to decrease peripheral levels of IL-6, IL-10, and TNF-α. However, weight gain-inducing psychopharmacological substances, such as the antidepressant mirtazapine, have been reported to potentially increase the production of pro-inflammatory cytokines. Even though cytokines are often discussed as biomarkers for depression, they have also been shown to be altered in other psychiatric disorders. Moreover, many environmental, social, psychological, biological, and medical factors are also associated with cytokine changes. Thus, cytokine alterations seem extremely unspecific. The interpretation of the results of these studies remains a challenge because it is unknown which type of cells are most responsible for cytokine changes measured in the blood nor have the main target cells or target tissues been identified. The same cytokine can be produced by multiple cell types, and the same cell can produce various cytokines. Additionally, redundancy, synergy, antagonism, and signaling cascades of cytokine signaling must be considered. Cytokines might not be associated with the diagnosis of depression according to the currently used diagnostic manuals, but rather with specific subtypes of depression, or with depressive symptoms across different psychiatric diagnoses. Therefore, the currently available diagnostic systems may not be the ideal starting point for psychiatric cytokine research.

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Section: Possible Reasons For Cytokine Alterationsmentioning

confidence: 99%

Cytokine Research in Depression: Principles, Challenges, and Open Questions

et al. 2019

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“…As the classical emergent manifestation of CHD, acute myocardial ischemia (MI) is associated with an increased mortality risk (Wang et al, 2014). Depression is an important clinical issue in MI patients due to its extreme commonness, and the comorbidity complicates the depression treatment and worsens the cardiovascular prognosis (Shapiro, 2015). Although many therapeutic strategies have been used to treat CHD or MI patients with depression (Colquhoun et al, 2013), such as psychological therapy (cognitive-behavioral therapy and interpersonal psychotherapy) and pharmacological therapy (fluoxetine, sertraline, citalopram, and mirtazapine), clinical outcomes remain unsatisfied, which can be mainly attributed to the unavoidable adverse effects of these treatments.…”

Section: Introductionmentioning

confidence: 99%

Behavioral and Biochemical Effects of KXS on Postmyocardial Infarction Depression

Liu

Zhang

et al. 2020

Front. Pharmacol.

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Background: Depression and coronary heart disease (CHD) often occur together in clinical practice. As a traditional Chinese medicine, Kai-Xin-San (KXS) has been widely used for the treatment of emotion-related disorders. In the present study, we aimed to explore whether KXS had both antidepressive effects and cardioprotective functions in a rat model of myocardial ischemia (MI) with depression. Methods: A total of 50 SD rats were randomly assigned into five groups as follows: normal control (control group), celiac injection of isopropyl adrenaline (ISO) (MI group), depression (depression group), MI+ depression (model group) and MI+ depression treated with intragastric administration of 370 mg/kg KXS (KXS group). MI was induced by subcutaneous injection of 85 mg/kg ISO. Depression was developed by a 7-week chronic mild stress (CMS) challenge. Behavioral test was conducted before and during the experiment. Echocardiography and biochemical analysis were carried out after 7 weeks of CMS challenge. Results: After 7 weeks of experiment, depression-like behaviors were observed in all the groups except for control and KXS groups, and KXS treatment dramatically increased open-field test scores and sucrose consumption (P < 0.01 vs. model group). Echocardiography and biochemical analysis showed that KXS treatment could improve levels of ejection fraction (EF) and fractional shortening (FS), which were reduced by depression and ISO challenge. Meanwhile, KXS treatment significantly decreased the levels of creation kinase MB (CK-MB) and lactate dehydrogenase (LDH), which were increased in the model group. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), catalase (CAT) were increased, while the malondialdehyde (MDA) activity was significantly decreased in the KXS group. Moreover, KXS treatment reduced

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“…The comorbidity of depression and CVD, such as CSF, is associated with hyperactivity of the hypothalamic-pituitary-adrenal axis, overactivation of the sympathetic nervous system, disturbances in platelet reactivity and inflammation [ 6 , 7 ]. Although the well-recognized comorbidity worsens the cardiovascular prognosis, the beneficial effects of antidepressant treatment on cardiovascular outcomes are controversial [ 8 ]. Higher prevalence of depression and anxiety has been repeatedly observed in patients with CSF [ 3 , 4 ].…”

Section: Discussionmentioning

confidence: 99%

Alleviating Effect of Antidepressant Treatment on Psychiatric Symptoms and Cardiac Conditions in a Patient with Coronary Slow Flow Comorbid with Depression and Anxiety

Gong

Guo

et al. 2018

Am J Case Rep

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Patient: Female, 52Final Diagnosis: Coronary slow flowSymptoms: Frequent chest pain • serious TIMI grade 2 flow without any coronary stenosis • comorbid with depression and anxietyMedication: —Clinical Procedure: —Specialty: PsychiatryObjective:Rare co-existance of disease or pathologyBackground:Depressive patients are considerably more likely to suffer cardiovascular disease (CVD), and in patients with CVD, depression is a predictor of poor outcome. Recent findings suggest higher rates of depression and anxiety in patients with coronary slow flow (CSF). However, there is no research investigating whether the antidepressant treatment can mitigate psychiatric symptoms and cardiac conditions in CSF patients comorbid with depression.Case Report:The patient was a 52-year-old Chinese female with frequent chest pain. The patient had serious TIMI (thrombolysis in myocardial infarction) grade 2 flow without any coronary stenosis, but comorbid with depression and anxiety. The CSF was very likely associated with her mental health condition, given that the chest distress and intermittent chest pain followed psychological stress and disturbed sleep. Therefore, paroxetine was used under the circumstances of the poor effect of cardiovascular active drugs. We found that the adjunctive use of paroxetine not only improved the psychiatric symptoms, but also alleviated the cardiac conditions.Conclusions:Our findings strengthen the importance of the treatment of psychiatric symptoms in patients with CSF and this finding should promote randomized controlled trials in a larger population to confirm the beneficial effects of antidepressant treatment on psychiatric symptoms and cardiac conditions in CSF patients with psycho-cardiac conditions.

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Management of Depression After Myocardial Infarction

Cited by 24 publications

References 85 publications

Cytokine Research in Depression: Principles, Challenges, and Open Questions

Cytokine Research in Depression: Principles, Challenges, and Open Questions

Behavioral and Biochemical Effects of KXS on Postmyocardial Infarction Depression

Alleviating Effect of Antidepressant Treatment on Psychiatric Symptoms and Cardiac Conditions in a Patient with Coronary Slow Flow Comorbid with Depression and Anxiety

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