Depression Increases Sympathetic Activity and Exacerbates Myocardial Remodeling after Myocardial Infarction: Evidence from an Animal Experiment

Shu, Shi; Liang, Jinjun; Liu, Tao; Yuan, Xiaoran; Ruan, Bing; Sun, Lifang; Tang, Yanhong; Yang, Bo; Hu, Dan; Huang, Congxin

doi:10.1371/journal.pone.0101734

Cited by 48 publications

(44 citation statements)

References 34 publications

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“…Myocardial infarction-induced heart failure facilitates an underlying risk for depressive-like behaviour, distinguished by elevated cardiac nr4a1 expression Models of depression have been used to investigate the effect of depression on HF after myocardial ischaemia in mice 13 and rats. 12 However, evidence regarding the impact of HF after MI on susceptibility to behavioural alterations prompted by a model of depression was missing. Here, we underpin the absence of depressive-like behaviour after MI in mice by the lack of elevated susceptibility to LH, which has been established as a clinically relevant model of depression.…”

Section: Myocardial Infarction-induced Heart Failure Is Not a Murine mentioning

confidence: 99%

“…Even though myocardial infarction (MI) and ischaemic heart disease present the leading cause of HF in Europe 1 and an important risk factor for the subsequent development of depression, 4 the pathogenesis of increased vulnerability to depression and anxiety in response to MI remains unclear. Several studies utilize a model of depression together with MI 12,13 to investigate the effects of depression on cardiac remodelling, but few publications focus on the pathogenesis of depression due to MI per se. 5,6 Pathogenetically oriented treatment options remain scarce.…”

Section: Introductionmentioning

confidence: 99%

“…And even though there is a reproducible rat model of good validity, 11 a murine model of depression after MI remains missing. Several studies utilize a model of depression together with MI 12,13 to investigate the effects of depression on cardiac remodelling, but few publications focus on the pathogenesis of depression due to MI per se. In this regard, murine anhedonia over the course of 8 weeks after MI associated with expression changes of the orphan nuclear receptor 4a1 (nr4a1) has been observed.…”

Section: Introductionmentioning

confidence: 99%

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Learned helplessness reveals a population at risk for depressive‐like behaviour after myocardial infarction in mice

et al. 2019

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Aims Myocardial infarction (MI) and heart failure (HF) are risk factors for the development of depression, additionally worsening the quality of life and patient outcome. How HF causes depression and how depression promotes HF remain mechanistically unclear, which is at least partly caused by the difficulty of in vivo modelling of psychosomatic co‐morbidity. We aimed to study the potential sequence of events with respect to different depression aspects upon HF. Methods and results Male C57BL6 mice underwent MI, followed by behavioural and echocardiographic characterization. Motility, exploration, and anxiety‐like behaviour were unaffected in mice after MI. We did not observe increased depressive‐like behaviour in the sucrose preference, tail suspension, or Porsolt forced swim test. Mice did not display signs of learned helplessness (LH) when compared to sham. Accordingly, cluster analysis revealed only a slightly higher quota of LH in HF (38%) vs. sham mice (32%). But strikingly, three‐group cluster analysis revealed an additional intermediate subpopulation at risk for LH after HF (29%). Interestingly, this population featured elevated cardiac expression of nr4a1. Conclusions The LH paradigm uncovered a subtle predisposition to depressive‐like behaviour after MI, whereas testing for anhedonia and despair was insufficient to show a behavioural shift in mice. Therefore, we suggest an accumulating risk profile and a multiple‐hits hypothesis regarding the pathogenesis of co‐morbid depression after MI. Symptoms of LH may present a marker of subclinical depression after MI, the impact of which remains to be investigated. The proposed sequence of behavioural testing enables the mechanistic dissection of cardio‐psychogenic signalling in the future.

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Section: Myocardial Infarction-induced Heart Failure Is Not a Murine mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Learned helplessness reveals a population at risk for depressive‐like behaviour after myocardial infarction in mice

et al. 2019

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“…Both ANS divisions are highly coordinated in a dynamic sympathovagal balance aimed at maintaining physiological homeostasis. Disruption in ANS homeostasis, characterized by sympathetic overactivity and/or vagal underactivity, is an important contributor to adverse cardiac outcomes associated with depression [70,71]. Heart rate variability (HRV), that is, spontaneous oscillations of heart rate around its mean value, is determined by the dynamic interaction of the acceleratory sympathetic nervous system and deceleratory parasympathetic nervous system, indicating a healthy and adaptive organism.…”

Section: Role Of Autonomic Nervous System In Depressive Disordermentioning

confidence: 99%

Novel Insight into Neuroimmune Regulatory Mechanisms and Biomarkers Linking Major Depression and Vascular Diseases: The Dilemma Continues

Tonhajzerová

Sekaninova

Olexova

et al. 2020

IJMS

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Major depressive disorder (MDD) represents a serious health problem estimated to affect 350 million people globally. Importantly, MDD has repeatedly emerged as an etiological or prognostic factor in cardiovascular disease (CVD) development, including vascular pathology. Several linking pathomechanisms between MDD and CVD involve abnormal autonomic regulation, inflammation, and endothelial dysfunction as an early preclinical stage of atherosclerosis. However, the cause of accelerated atherosclerosis in MDD patients remains unclear. Recently, the causal relationships between MDD and mediator (e.g., inflammation and/or endothelial dysfunction), as well as the causal pathways from the mediator to atherosclerosis, were discussed. Specifically, MDD is accompanied by immune dysregulation, resulting in increased production of proinflammatory cytokines (e.g., interleukin (IL)-6 and tumor necrosis factor (TNF)-α), which could lead to depression-linked abnormalities in brain function. Further, MDD has an adverse effect on endothelial function; for example, circulating markers of endothelial dysfunction (e.g., soluble adhesion molecules, von Willebrand factor) have been linked with depression. Additionally, MDD-linked autonomic dysregulation, which is characterized by disrupted sympathovagal balance associated with excessive circulating catecholamines, can contribute to CVD. Taken together, activated inflammatory response, endothelial dysfunction, and autonomic dysregulation could affect gradual atherosclerosis progression, resulting in a higher risk of developing CVD in MDD. This review focused on the pathomechanisms linking MDD and CVD with respect to neuroimmune regulation, and the description of promising biomarkers, which is important for the early diagnosis and personalized prevention of CVD in major depression.

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“…There is evidence of the relationship between psychosocial factors and mortality and morbidity due to cardiovascular diseases or the autonomic nervous response [19,20]. Patient with psychiatric disorders are known to have an increased cardiovascular morbidity [21][22][23][24][25][26][27][28][29][30][31]. Patients with major depression display significantly increased RHR relative to controls [32], possibly due to sympathetic hyperactivation, as some studies presume [27,28,30].…”

Section: Cardiovascular Risk and Psychiatric Disorders ▼mentioning

confidence: 99%

Elevated Rest Heart Rate in Psychiatric Patients and Different Effects of Psychotropic Medication

2015

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Depression Increases Sympathetic Activity and Exacerbates Myocardial Remodeling after Myocardial Infarction: Evidence from an Animal Experiment

Cited by 48 publications

References 34 publications

Learned helplessness reveals a population at risk for depressive‐like behaviour after myocardial infarction in mice

Learned helplessness reveals a population at risk for depressive‐like behaviour after myocardial infarction in mice

Novel Insight into Neuroimmune Regulatory Mechanisms and Biomarkers Linking Major Depression and Vascular Diseases: The Dilemma Continues

Elevated Rest Heart Rate in Psychiatric Patients and Different Effects of Psychotropic Medication

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