Effect of Renal Denervation on Cardiac Function and Inflammatory Factors in Heart Failure After Myocardial Infarction

Li, Chao; Xia, Wei; Wang, Li; Zhang, Jin; He, Qiang; Yin, Liu; Xia, Dasheng; Lu, Chengzhi

doi:10.1097/fjc.0000000000000899

Cited by 4 publications

(3 citation statements)

References 36 publications

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“…Compared with RDN-1d + AMI group, NGF decreased more significantly in RDN-2 W + AMI group, suggesting that RDN may not change the expression of Th and NGF immediately, with a hysteresis. Wanying Jiang et al [ 31 ] found that RDN significantly reduced the expression of Th and connexin 43 in the infarct zone of AMI rats compared with metoprolol, which suggests that RDN may not only decrease myocardial sympathetic activity in AMI via NE/β receptor signaling pathway, but may also be associated with the inhibition of inflammation, the RASS system [ 27 , 32 ].However, the mechanism by which RDN weakens the sympathetic activity of myocardial tissue is not clear.…”

Section: Discussionmentioning

confidence: 99%

Effects and mechanism of renal denervation on ventricular arrhythmia after acute myocardial infarction in rats

Xiao

Wang

et al. 2022

BMC Cardiovasc Disord

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Background Renal denervation (RDN) can reduce ventricular arrhythmia after acute myocardial infarction (AMI), but the mechanism is not clear. The purpose of this study is to study its mechanism. Methods Thirty-two Sprague–Dawley rats were divided into four groups: control group, AMI group, RDN-1d + AMI group, RDN-2w + AMI group. The AMI model was established 1 day after RDN in the RDN-1d + AMI group and 2 weeks after RDN in the RDN-2w + AMI group. At the same time, 8 normal rats were subjected to AMI modelling (the AMI group). The control group consisted of 8 rats without RDN intervention or AMI modelling. Results The study confirmed that RDN can reduce the occurrence of ventricular tachycardia in AMI rats, reduce renal sympathetic nerve discharge, and inhibit the activity of local sympathetic nerves and cell growth factor (NGF) protein expression in the heart after AMI. In addition, RDN decreased the expression of norepinephrine (NE) and glutamate in the hypothalamus,and NE in cerebrospinal fluid, and increased the expression level of γ aminobutyric acid (GABA) in the hypothalamus after AMI. Conclusion RDN can effectively reduce the occurrence of ventricular arrhythmia after AMI, and its main mechanism may be via the inhibition of central sympathetic nerve discharge.

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Section: Discussionmentioning

confidence: 99%

Effects and mechanism of renal denervation on ventricular arrhythmia after acute myocardial infarction in rats

Xiao

Wang

et al. 2022

BMC Cardiovasc Disord

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“…Importantly, RSD significantly reduced LV end-diastolic volume and improved LVEF [ 218 ]. Cardioprotection by RSD was also reported in a canine HF model induced by intra-coronary injection with ethanol to induce embolization [ 219 ]. At four weeks after coronary embolism, dogs with RSD showed significantly attenuated LV dilatation and better preservation of LV function.…”

Section: Recent Research Progressmentioning

confidence: 95%

“…At four weeks after coronary embolism, dogs with RSD showed significantly attenuated LV dilatation and better preservation of LV function. Interestingly, expression in the myocardium and hypothalamus of several inflammatory factors, like IL-6, MCP-1 (monocyte chemoattractant protein-1), tumour necrosis factor-α (TNFα) and NF-κB (nuclear factor κ-light chain-enhancer of activated B cells), was significantly lower in RSD relative to sham-procedure controlled HF animals, indicating attenuated cardiac and central inflammatory signaling by RSD [ 219 ]. Similar beneficial effects by RSD was also reported in a very recent canine study with HF induced by rapid ventricular pacing [ 220 ].…”

Section: Recent Research Progressmentioning

confidence: 99%

Sympatho-adrenergic mechanisms in heart failure: new insights into pathophysiology

2021

Medical Review

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The sympathetic nervous system is activated in the setting of heart failure (HF) to compensate for hemodynamic instability. However, acute sympathetic surge or sustained high neuronal firing rates activates β-adrenergic receptor (βAR) signaling contributing to myocardial remodeling, dysfunction and electrical instability. Thus, sympatho-βAR activation is regarded as a hallmark of HF and forms pathophysiological basis for β-blocking therapy. Building upon earlier research findings, studies conducted in the recent decades have significantly advanced our understanding on the sympatho-adrenergic mechanism in HF, which forms the focus of this article. This review notes recent research progress regarding the roles of cardiac β2AR or α1AR in the failing heart, significance of β1AR-autoantibodies, and βAR signaling through G-protein independent signaling pathways. Sympatho-βAR regulation of immune cells or fibroblasts is specifically discussed. On the neuronal aspects, knowledge is assembled on the remodeling of sympathetic nerves of the failing heart, regulation by presynaptic α2AR of NE release, and findings on device-based neuromodulation of the sympathetic nervous system. The review ends with highlighting areas where significant knowledge gaps exist but hold promise for new breakthroughs.

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Effects of renal denervation on the incidence and severity of cardiovascular diseases

Katsurada,

Kario

2024

Hypertens Res

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Effect of Renal Denervation on Cardiac Function and Inflammatory Factors in Heart Failure After Myocardial Infarction

Abstract: Supplemental Digital Content is Available in the Text.

Cited by 4 publications

References 36 publications

Effects and mechanism of renal denervation on ventricular arrhythmia after acute myocardial infarction in rats

Effects and mechanism of renal denervation on ventricular arrhythmia after acute myocardial infarction in rats

Sympatho-adrenergic mechanisms in heart failure: new insights into pathophysiology

Effects of renal denervation on the incidence and severity of cardiovascular diseases

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