Chronic heart failure: a disease of the brain

Singh, Ram B.; Hristová, Krasimira; Fedačko, Ján; Elkilany, Galal; Cornélissen, Germaine

doi:10.1007/s10741-018-9747-3

Cited by 27 publications

(19 citation statements)

References 31 publications

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“…The second important set of findings relates to the effects of RDN on the course of CHF-dependent mortality in ACF FHL and ACF FHH animals. The rationale for employing RDN as a novel tool for the treatment of CHF, particularly in individuals when CHF is combined with some form of kidney damage and/or renal dysfunction, is based on the concept of potentially beneficial effect of the removal of inappropriately activated and consequently deleterious influence of the renal sympathetic nerves (RSNA) (15)(16)(17)(18)(19)(20)27,45). This notion is based on clinical and experimental studies demonstrating that enhanced renal NE spillover and tissue turnover, the recognized markers of increased SNS activity, is associated with increased morbidity in individuals with CHF (63-66).…”

Section: Discussionmentioning

confidence: 99%

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Effects of renal sympathetic denervation on the course of congestive heart failure combined with chronic kidney disease: Insight from studies with fawn-hooded hypertensive rats with volume overload induced using aorto-caval fistula

Honetschlägerová

Škaroupková

Kikerlová

et al. 2021

Clinical and Experimental Hypertension

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Section: Discussionmentioning

confidence: 99%

“…It is recognized that inappropriate activation of the sympathetic nervous system (SNS) plays an important role in the progression of CHF (15)(16)(17)(18), contributing to the pathophysiology of hypertension (19). SNS hyperactivity occurs also in patients with CKD, probably with significant consequence on the prognosis (20)(21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

Effects of renal sympathetic denervation on the course of congestive heart failure combined with chronic kidney disease: Insight from studies with fawn-hooded hypertensive rats with volume overload induced using aorto-caval fistula

Honetschlägerová

Škaroupková

Kikerlová

et al. 2021

Clinical and Experimental Hypertension

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“…PVN is the sympathetic neural modulation center of cardiovascular function [ 21 ]. A host of studies demonstrated that many cardiovascular diseases, such as myocardial infarction, heart failure, myocardial I/R, and hypertension, were related to neuroinflammation in PVN, and inhibition of such neuroinflammation could improve the outcome of these diseases [ 9 , 22 – 25 ]. For example, previous studies suggested that there was an increase of proinflammatory cytokines and activated microglia in the PVN post-MI [ 3 , 8 , 26 , 27 ], and the inhibition of activated microglia in PVN by minocycline resulted in smaller infarct size following MI [ 8 ].…”

Section: Discussionmentioning

confidence: 99%

Light Emitting Diode Therapy Protects against Myocardial Ischemia/Reperfusion Injury through Mitigating Neuroinflammation

Wang

Luo

Chen

et al. 2020

Oxidative Medicine and Cellular Longevity

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Background. Neuroinflammation plays a key role in myocardial ischemia-reperfusion (I/R) injury. Previous studies showed that light-emitting diode (LED) therapy might improve M2 microglia activation and brain-derived neurotrophic factor (BDNF) expression, thereby exerting anti-inflammatory effects. Therefore, we hypothesized that LED therapy might reduce myocardial I/R injury by neuroinflammation modulation. Objective. To explore the effect of LED therapy on myocardial I/R-induced injury and seek the underlying mechanism. Methods. Thirty rats were randomly divided into three groups: Control group (without LED treatment or myocardial I/R, n=6), I/R group (with myocardial I/R only, n=12), and LED+I/R group (with myocardial I/R and LED therapy, n=12). Electrocardiogram was recorded continuously during the procedure. In addition, brain tissue was extracted for BDNF, Iba1, and CD206 analyses, and heart tissue for myocardial injury (ischemic size and infarct size), IL-4 and IL-10 mRNA analysis. Results. In comparison with the I/R group, the ischemia size and the infarct size were significantly attenuated by LED therapy in the LED+I/R group. Meanwhile, the microglia activation induced by I/R injury was prominently attenuated by LED treatment either. And it is apparent that there was also an increase in the beneficial neuroinflammation markers (BDNF and CD206) in the paraventricular nucleus (PVN) in the LED+I/R group. Furthermore, the anti-inflammatory cytokines, IL-4 and IL-10, were greatly decreased by I/R while improved by LED treatment in myocardium. Conclusion. LED therapy might reduce neuroinflammation in PVN and decrease myocardium injury by elevating BDNF and M2 microglia.

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“…However, patients with heart failure mainly die due to malignant arrhythmias (ventricular tachycardia or ventricular fibrillation). Previous studies reported that sympathetic activity is similar to that of AngII, and sympathetic activity can directly increase sodium retention [12]. In HF patients with excessive sympathetic activation, β-blocker dose (BBD) might be necessary to avoid cardiovascular events [13].…”

Section: Discussionmentioning

confidence: 99%

Renal Sympathetic Denervation Improves Outcomes in a Canine Myocardial Infarction Model

et al. 2019

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Background Myocardial infarction (MI) is the main cause of heart failure (HF), and sympathetic nerve activity is associated with prognosis chronic heart failure. Renal sympathetic denervation (RDN) is noted for its powerful effect on the inhibition of sympathetic nerve activity. This study investigated the effect of RDN on heart failure in dogs after myocardial infarction. Material/Methods The experimental animals were randomized into 2 groups: the MI group (n=12) and the sham operation group (n=6). In the MI group we established an MI model by permanently ligating the left anterior descending branch. After 4 weeks, the MI dogs were randomly divided into 2 groups: the MI+RDN group (MI+renal sympathetic denervation, n=6) and the simple MI group (n=6). Animals in the MI+RDN group underwent both surgical and chemical renal denervation. Results Compared with sham operation group, left ventricular fraction shortening (LVFS) and left ventricular ejection fraction (LVEF) were significantly reduced in the simple MI group, while the reduction was partly reversed in the MI+RDN group. RDN reduced sympathetic nerve activity and release of B-type natriuretic peptide (BNP) and Angiotensin II (AngII) in the MI+ RDN group but not in the simple MI group. Conclusions Canine renal sympathetic denervation prevents myocardial malignant remodeling by lowering the activity of the systemic sympathetic nerve and inhibiting renin-angiotensin-aldosterone system (RASS) activation, providing a new target and method for the treatment of heart failure.

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Chronic heart failure: a disease of the brain

Cited by 27 publications

References 31 publications

Effects of renal sympathetic denervation on the course of congestive heart failure combined with chronic kidney disease: Insight from studies with fawn-hooded hypertensive rats with volume overload induced using aorto-caval fistula

Effects of renal sympathetic denervation on the course of congestive heart failure combined with chronic kidney disease: Insight from studies with fawn-hooded hypertensive rats with volume overload induced using aorto-caval fistula

Light Emitting Diode Therapy Protects against Myocardial Ischemia/Reperfusion Injury through Mitigating Neuroinflammation

Renal Sympathetic Denervation Improves Outcomes in a Canine Myocardial Infarction Model

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