ABSTRACT
OBJECTIVE: This study aimed to explore the association between electrophysiological markers of early recurrence after defibrillation in post-myocardial infarction ventricular fibrillation and the therapeutic effects of sympathetic renal denervation, as well as to investigate the potential underlying mechanisms. METHODS: Experimental research was conducted using an animal model. Myocardial infarction was induced, followed by defibrillation treatment for ventricular fibrillation cases, and the electrophysiological markers of early recurrence were recorded. Subsequently, a subset of animals underwent sympathetic renal denervation intervention, and the therapeutic effects were compared between the sympathetic renal denervation group and the control group. Electrocardiogram monitoring, histological analysis of myocardial tissue, and neurotransmitter measurements were also performed. RESULTS: Following defibrillation treatment, early recurrence was observed in ventricular fibrillation cases. The electrophysiological markers revealed significantly higher ST segment elevation and T wave changes in the early recurrence group. However, in the sympathetic renal denervation intervention group, the early recurrence rate was significantly reduced, and the electrocardiogram showed improved stability and regularity. Additionally, histological analysis of myocardial tissue demonstrated less cellular damage and lower levels of myocardial fibrosis in the sympathetic renal denervation group. Neurotransmitter measurements revealed a significant decrease in sympathetic nerve activity in the sympathetic renal denervation intervention group. CONCLUSION: The results of this study indicate an association between electrophysiological markers of early recurrence after defibrillation in post-myocardial infarction ventricular fibrillation and the therapeutic effects of sympathetic renal denervation. Sympathetic renal denervation intervention can significantly reduce the early recurrence rate, improve electrocardiogram characteristics, and alleviate myocardial damage and fibrosis. Furthermore, the reduction in sympathetic nerve activity may be one of the potential underlying mechanisms of sympathetic renal denervation intervention.
Subject(s)
Disease Models, Animal , Electric Countershock , Kidney , Myocardial Infarction , Recurrence , Sympathectomy , Ventricular Fibrillation , Animals , Ventricular Fibrillation/physiopathology , Ventricular Fibrillation/diagnosis , Ventricular Fibrillation/etiology , Ventricular Fibrillation/therapy , Kidney/innervation , Kidney/blood supply , Myocardial Infarction/physiopathology , Myocardial Infarction/complications , Male , Time Factors , Myocardium/pathology , Action Potentials , Electrocardiography , Heart Rate , Sympathetic Nervous System/physiopathology , Sympathetic Nervous System/surgery , Neurotransmitter Agents/metabolism , Rats, Sprague-Dawley , FibrosisABSTRACT
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.
Subject(s)
Myocardial Infarction , Rats , Animals , Rats, Sprague-Dawley , Kidney , Arrhythmias, Cardiac/etiology , Arrhythmias, Cardiac/prevention & control , Arrhythmias, Cardiac/metabolism , Sympathetic Nervous System/surgery , Sympathetic Nervous System/metabolism , SympathectomyABSTRACT
Sympathectomy of arteries has been adopted for the treatment of peripheral arterial disease and Raynaud's disease. However, the exact route for sympathetic axons to reach peripheral arteries awaits further investigation that could pave the way for development of new surgical strategies. In this study, saphenous neurovascular bundles from 10 neonatal Sprague-Dawley rats first were harvested for whole-mount immunostaining to show sympathetic innervation pattern of the artery. Secondly, 40 Sprague-Dawley male rats weighing 350 to 400 g were assigned to five groups, receiving either sham, perivascular sympathectomy, nerve-artery separation, nerve transection in the saphenous neurovascular bundle, or lumbar sympathectomy surgery that removes the lumbar sympathetic trunks. Immediately after surgery, the arterial perfusion and diameter were measured using laser speckling contrast imaging, and 1 week later the saphenous neurovascular bundles were harvested for immunostaining using antibodies against TH, neuron-specific ß-tubulin (Tuj 1), and α-SMA to show the presence or absence of the TH-immuopositive staining in the adventitia. The differences among the five groups were determined using one-way analysis of variance (ANOVA). We found that an average of 2.8 ± 0.8 branches with a diameter of 4.8 ± 1.2 µm derived from the saphenous nerve that morphed into a primary and a secondary sympathetic trunk for innervation of the saphenous artery. Nerve-artery separation, nerve transection, and lumbar sympathectomy could eradicate TH-immunopositive staining of the artery, resulting, respectively, in a 12%, 36%, and 59% increase in diameter (P < .05), and a 52%, 63%, and 201% increase in perfusion compared with sham surgery (P < .01). In contrast, perivascular sympathectomy did not have a significant impact on the TH-immunopositive staining, the diameter, and perfusion of the distal part of the artery (P > .05). We conclude that the sympathetic innervation of an artery derives from segmental branches given off from its accompanying nerve. Nerve-artery disconnection is a theoretic option in sympathectomy of an artery.
Subject(s)
Sympathectomy , Sympathetic Nervous System , Animals , Arteries , Male , Rats , Rats, Sprague-Dawley , Sympathetic Nervous System/surgeryABSTRACT
Elevated sympathetic vasomotor activity is a common feature of cardiorenal diseases. Therefore, the sympathetic nervous system is an important therapeutic target, particularly the fibers innervating the kidneys. In fact, renal denervation has been applied clinically and shown promising results in patients with hypertension and chronic kidney disease. However, the underlying mechanisms involved in the cardiorenal protection induced by renal denervation have not yet been fully clarified. This mini-review highlights historical and recent aspects related to the role of renal sensory fibers in the control of cardiorenal function under normal conditions and in experimental models of cardiovascular disease. Results have demonstrated that alterations in renal sensory function participate in the maintenance of elevated sympathetic vasomotor activity and cardiorenal changes; as such, renal sensory fibers may be a potential therapeutic target for the treatment of cardiorenal diseases. Although it has not yet been applied in clinical practice, selective afferent renal denervation may be promising, since such an approach maintains efferent activity and can provide more refined control of renal function compared with total renal denervation. However, more studies are needed to understand the mechanisms by which renal afferents partially contribute to such changes, in addition to the need to evaluate the safety and advantages of the approach for application in the clinical practice.
Subject(s)
Afferent Pathways/physiopathology , Cardio-Renal Syndrome/physiopathology , Hypertension, Renovascular/physiopathology , Kidney/innervation , Renal Insufficiency, Chronic/physiopathology , Sympathetic Nervous System/physiopathology , Afferent Pathways/surgery , Animals , Cardio-Renal Syndrome/surgery , Humans , Hypertension, Renovascular/surgery , Renal Insufficiency, Chronic/surgery , Sympathectomy , Sympathetic Nervous System/surgeryABSTRACT
ABSTRACT: The efficacy of renal sympathetic denervation (RSD) in the treatment of uncontrolled hypertension (HTN) remains uncertain. A systematic review of randomized controlled trials was performed to evaluate the efficacy and safety of RSD for resistant HTN. PubMed, EMBASE, MEDLINE, Cochrane, Directory of Open Access Journals, CINAHL, and Google Scholar were searched from January 01, 2001, through July 30, 2020. Randomized controlled trials comparing RSD with the sham procedure for uncontrolled HTN were selected. The primary efficacy outcome was the reduction in ambulatory systolic blood pressure. We used random-effects models. Nine prospective clinical trials met the inclusion criteria. The ReSet and Symplicity HTN-3 Trial showed no significant changes because of discrepancies in complete circumferential ablation during RSD. The Relief study, The Radiance HTN solo, and the SPYRAL HTN OFF medical trials showed a significant reduction in systolic blood pressure in the group that had undergone the intervention compared with the sham group attributed to rigorous trial design. In conclusion, our systematic review suggests that efficacy of RSD seems to be superior to sham-controlled interventions provided circumferential denervation is performed. However, difference in efficacy is marginal.
Subject(s)
Blood Pressure , Catheter Ablation , Hypertension/surgery , Kidney/blood supply , Renal Artery/innervation , Sympathectomy , Sympathetic Nervous System/surgery , Adolescent , Adult , Aged , Aged, 80 and over , Antihypertensive Agents/therapeutic use , Blood Pressure/drug effects , Catheter Ablation/adverse effects , Drug Resistance , Female , Humans , Hypertension/diagnosis , Hypertension/physiopathology , Male , Middle Aged , Randomized Controlled Trials as Topic , Sympathetic Nervous System/physiopathology , Treatment Outcome , Young AdultABSTRACT
Myocardial ischemia-reperfusion (I/R) injury leads to intensive sympathetic nervous system (SNS) activation and inflammatory reactions. Whether renal sympathetic denervation (RDN) could be a new therapeutic strategy to modulate I/R inflammation and reduce infarct size after myocardial I/R injury needs to be explored. First, we investigated the correlation between plasma norepinephrine concentrations and circulating myeloid cell numbers in patients with acute myocardial infarction. And then, C57BL/6 mice underwent a "two-hit" operation, with 10% phenol applied to bilateral renal nerves to abrogate sympathoexcitation, and a 45-min ligation of the left coronary artery to induce myocardial I/R injury. The effects of RDN on the mobilization of immune cells in mice following myocardial I/R injury were explored. We observed a strong association between SNS overactivation and myeloid cell excessive accumulation in patients. In animal experiments, there was a significant reduction in infarct size per area at risk in the denervated-I/R group when compared to that of the innervated-I/R group (39.2% versus 49.8%; p < 0.005), and RDN also improved the left ventricular ejection fraction by 20% after 1 week. Furthermore, the denervated-I/R group showed a decrease in the number of neutrophils and macrophages in the blood and the myocardium as reflected by immunohistochemical staining and flow cytometry analysis (p < 0.05); the decrease was associated with a significant reduction in the circulating production of IL-1, IL-6 and TNF-α (p < 0.05). In summary, our study reveals a novel link between the SNS activity and inflammatory response undergoing myocardium I/R injury and identifies RDN as a potential therapeutic strategy against myocardium I/R injury via preserving the spleen immune cells mobilization.
Subject(s)
Inflammation/prevention & control , Kidney/blood supply , Myeloid Cells/immunology , Myocardial Reperfusion Injury/prevention & control , Renal Artery/innervation , Spleen/immunology , Sympathectomy , Sympathetic Nervous System/surgery , Adult , Aged , Animals , Cytokines/blood , Disease Models, Animal , Female , Humans , Inflammation/immunology , Inflammation/metabolism , Inflammation/physiopathology , Inflammation Mediators/blood , Male , Mice, Inbred C57BL , Middle Aged , Myeloid Cells/metabolism , Myocardial Reperfusion Injury/immunology , Myocardial Reperfusion Injury/metabolism , Myocardial Reperfusion Injury/physiopathology , Norepinephrine/blood , Spleen/metabolism , Stroke Volume , Sympathetic Nervous System/metabolism , Sympathetic Nervous System/physiopathology , Ventricular Function, LeftABSTRACT
PURPOSE OF REVIEW: To review the data about the use of renal denervation (RDN), a minimally invasive surgery, for resistant hypertension (RH) and to provide practical guidance for practitioners who are establishing an RDN service. RECENT FINDINGS: RDN can selectively ablate renal sympathetic nerve fibres, block the transmission of nerve impulses between central sympathetic nerve and kidney, to control blood pressure to as a novel promising non-drug treatment option for RH. At present, there are many researches on the treatment of RH by RDN, but there are some controversies. This review summarises and critically examines the evidence for RDN in the treatment of RH and identifies areas for future research. With the development of RDN, the continuous innovation of RDN technology and methods, the development about better evaluating the real-time success of RDN and the improvement for identifying individuals who are most likely to benefit from RDN will ultimately determine whether RDN represents a feasible way to manage RH in the future.
Subject(s)
Hypertension , Blood Pressure , Denervation , Humans , Hypertension/surgery , Kidney , Sympathectomy , Sympathetic Nervous System/surgery , Treatment OutcomeABSTRACT
Heart failure (HF) affects around 100 million people and is a staggering burden for health care system worldwide. Rapid and sustained activation of inflammatory response is an important feature of HF after myocardial infarction. Sympathetic overactivation is also an important factor in the occurrence and progression of HF. The beneficial effect of renal denervation (RDN) has been demonstrated in HF. In the current study, we hypothesized that RDN improves cardiac function in HF canine models due to acute myocardial infarction (AMI) and reduced inflammation might be involved. Twenty-four beagles were randomized into the control (n = 8), HF (n = 8), and HF + RDN group (n = 8). The HF model after AMI was established by embolization the anterior descending distal artery with anhydrous ethanol in the HF and HF + RDN group. Bilateral renal artery ablation was performed in the HF + RDN group. Cardiac function, serum creatine kinase, creatine kinase-MB and NT-Pro BNP level, and expression of inflammation-related proteins in myocardial were examined. Because the paraventricular nucleus of the hypothalamus might be involved in inflammation-induced central neural excitation in HF and plays an important role in regulating extracellular fluid volume and sympathetic activity, expression of inflammation-related proteins in hypothalamus was also examined. AMI and post-AMI HF model was created successfully. Compared with the HF group, dogs in the HF + RDN group showed better cardiac function 4 weeks after AMI: lower left ventricular end-diastolic pressure, left ventricular end-diastolic dimension, and left ventricular end-systolic dimension and higher LEVF and left ventricular systolic pressure (P < 0.05 for all) were observed in the HF + RDN group. In addition, dogs in the HF + RDN group had slightly less ventricular fibrosis. Interestingly, RDN had lower expression of inflammation-related proteins including interleukin-6, tumor necrosis factors-α, nuclear factor κB, and monocyte chemotactic protein 1 (P < 0.05 for all) in both myocardial tissue and hypothalamus. RDN can improve cardiac function in dogs with HF after myocardial infarction. Our results suggested that RDN might affect cytokine-induced central neural excitation in HF and later affect sympathetic activity. Our results suggested a potential beneficial mechanism of RDN independent of mechanism involving renal afferent and efferent sympathetic nerves.
Subject(s)
Catheter Ablation , Heart Failure/surgery , Hypothalamus/metabolism , Inflammation Mediators/metabolism , Kidney/blood supply , Myocardial Infarction/complications , Myocardium/metabolism , Renal Artery/innervation , Sympathectomy , Sympathetic Nervous System/surgery , Ventricular Function, Left , Animals , Disease Models, Animal , Dogs , Female , Fibrosis , Heart Failure/etiology , Heart Failure/metabolism , Heart Failure/physiopathology , Hypothalamus/physiopathology , Male , Myocardium/pathology , Stroke Volume , Sympathetic Nervous System/metabolism , Sympathetic Nervous System/physiopathology , Ventricular Pressure , Ventricular RemodelingABSTRACT
BACKGROUND: Several factors that could influence the efficacy and satisfaction of patients after bilateral thoracic sympathectomy (video-assisted thoracoscopic sympathectomy [VATS]) in the treatment of hyperhidrosis (HH) have been studied, but no studies in the literature have specifically analyzed the effectiveness of treatment and variations in the quality of life of patients aged 40 years or older compared with those of young adult patients (19-40 years). METHODS: We retrospectively analyzed 2,431 HH patients who underwent bilateral VATS and divided the patients into the following groups: a group younger than 40 years old (1,760 patients) and a group 40 years and older (142 patients). Variables included quality of life before surgery, improvement in quality of life after surgery, clinical improvement in sweating, the presence of severe compensatory hyperhidrosis (CH), and general satisfaction at 1 month after surgery. RESULTS: We observed that all surgical patients presented with poor or very poor quality of life before surgery, with similar proportions in both groups. In the postoperative period, we observed improvement in quality of life in more than 90% of the patients, with no significant difference noted between the 2 groups of patients. More than 90% of the patients in this series had great clinical improvement in the main HH site, with no significant difference between the 2 groups. Severe CH occurred in 23.8% of the patients in this series, with no significant difference between the 2 groups. CONCLUSIONS: Patients 40 years of age or older benefit just as much as younger patients from VATS performed to treat primary HH, presenting excellent significant surgical results.
Subject(s)
Hyperhidrosis/surgery , Sweating , Sympathectomy/methods , Sympathetic Nervous System/surgery , Thoracic Surgery, Video-Assisted , Adult , Age Factors , Aged , Female , Humans , Hyperhidrosis/diagnosis , Hyperhidrosis/physiopathology , Male , Middle Aged , Patient Satisfaction , Quality of Life , Retrospective Studies , Sympathectomy/adverse effects , Sympathetic Nervous System/physiopathology , Thoracic Surgery, Video-Assisted/adverse effects , Time Factors , Treatment Outcome , Young AdultABSTRACT
PURPOSE OF REVIEW: Sympathetic overactivity plays an important role in the progression of pulmonary arterial hypertension (PAH). The purpose of this review is to illustrate localization of pulmonary arterial sympathetic nerves, the key steps of pulmonary artery denervation (PADN) procedure, and to highlight clinical outcomes. RECENT FINDINGS: Sympathetic nerves mostly occurred in the posterior region of the bifurcation and pulmonary trunk. Emerging preclinical data provided the potential of PADN for PAH. PADN, produced at bifurcation area, improved a profound reduction of pulmonary arterial pressure and ameliorated clinical outcomes with an exclusive ablation catheter. The application of PADN in the patients of PAH or combined pre-capillary and post-capillary PH (CpcPH) improved the hemodynamic parameters and increased 6MWD. Sympathetic overactivity aggravates PAH. PADN is a promising interventional treatment for PAH and CpcPH. Additional clinical trials are warranted to confirm the efficacy of PADN.
Subject(s)
Denervation , Hemodynamics/physiology , Pulmonary Arterial Hypertension/surgery , Pulmonary Artery/innervation , Sympathectomy/methods , Sympathetic Nervous System/surgery , Humans , Hypertension, Pulmonary , Pressoreceptors/physiopathology , Pressoreceptors/surgery , Pulmonary Arterial Hypertension/diagnostic imaging , Pulmonary Artery/diagnostic imaging , Pulmonary Artery/surgery , Sympathetic Nervous System/physiopathology , Treatment OutcomeABSTRACT
Consumption of food high in fructose is prevalent in modern diets. One week of moderately high fructose intake combined with high salt diet has been shown to increase blood pressure and failed to suppress plasma renin activity (PRA). We tested the hypothesis that the hypertension and high PRA are consequences of elevated renal sympathetic nerve activity (RSNA). In protocol 1, we assessed RSNA by telemetry in conscious Sprague-Dawley rats given 20% fructose or 20% glucose in drinking water on a 0.4% NaCl diet (NS) for 1 wk and then transitioned to a 4% NaCl diet (HS). After an additional week, mean arterial pressure (MAP) and RSNA increased significantly in fructose-fed but not glucose-fed HS rats. In protocol 2, fructose (Fruc)- or glucose (Glu)-fed rats on NS or HS diet for 3 wk underwent sham denervation (shamDNX) or bilateral renal denervation using cryoablation (cryoDNX). MAP was higher in Fruc-HS rats compared with Glu-NS, Glu-HS, or Fruc-NS rats and decreased after cryoDNX ( P < 0.01). MAP did not change in Fruc-HS shamDNX rats. Renal norepinephrine content decreased by 85% in cryoDNX ( P < 0.01 vs. shamDNX). PRA significantly decreased after cryoDNX in both Fruc-NS and Fruc-HS rats. Nonfasting blood glucose levels were similar among the four groups. Glucose-to-insulin ratio significantly increased in Fruc-HS cryoDNX rats, consistent with greater insulin sensitivity. Taken together, these studies show that renal sympathoexcitation is, at least in part, responsible for salt-dependent increases in MAP, increased PRA, and decreased insulin sensitivity in rats fed a moderately high fructose diet for as little as 3 wk.
Subject(s)
Arterial Pressure , Cryosurgery , Dietary Sugars , Fructose , Hypertension/prevention & control , Insulin Resistance , Kidney/innervation , Sympathectomy/methods , Sympathetic Nervous System/surgery , Animals , Biomarkers/blood , Blood Glucose/metabolism , Disease Models, Animal , Hypertension/etiology , Hypertension/physiopathology , Insulin/blood , Male , Rats, Sprague-Dawley , Renin/blood , Sodium, Dietary , Sympathetic Nervous System/physiopathology , Time FactorsABSTRACT
Recently, the influence of adrenergic activity over ovarian function, and thus fertility, has begun to gain importance. Previous studies have shown that adrenergic activity through norepinephrine (NE) participates in the control of follicular development and steroidal secretion from the ovary, among other functions. To examine this phenomenon, the denervation of the gonad has been widely used to observe changes in the ovary's performance. Nevertheless, the effect of the absence of adrenergic nerves in the ovary has only been studied in short times periods. In the present work, we used guanethidine (a drug that produces an irreversible sympathectomy) during the infantile period of rats, and we observed its effects in the adult rat (6 months old). Our results indicate that ovarian NE content is recovered at 6 months old, alongside with an increase of the adrenal content of NE and a dysfunctional celiac ganglion. Together, these results suggest that the recovery of ovarian NE does not come from a neural origin. In addition, ovarian performance was impaired because the changes in follicular development and steroidal secretion are not recovered despite the recovery of ovarian NE content. In conclusion, these results suggest that the nerve-ovarian connections, which are established during infantile development, are necessary for the accurate response of the ovary to sympathetic stimulation.
Subject(s)
Estradiol/metabolism , Norepinephrine/metabolism , Ovarian Follicle/cytology , Sympathectomy , Sympathetic Nervous System/surgery , Animals , Female , Guanethidine/pharmacology , Ovarian Follicle/drug effects , Ovarian Follicle/surgery , Rats , Rats, Sprague-Dawley , Sympatholytics/pharmacologyABSTRACT
PURPOSE OF REVIEW: Renal sympathetic denervation (RDN) as treatment option for hypertension has a strong rationale; however, variable effects on blood pressure (BP) have been reported ranging from non-response to marked reductions in BP. The absence of a procedural end point for RDN is one of the potential factors associated with the variable response. Studies have suggested the use of renal nerve stimulation (RNS) to adequately address this issue. This review aims to provide an overview of the clinical and experimental data available regarding the effects of RNS in the setting of RDN. RECENT FINDINGS: Animal studies have shown that high-frequency electrical stimulation of the sympathetic nerves in the adventitia of the renal arteries elicits an increase in BP and leads to an increased norepinephrine spillover as a marker of increased sympathetic activity and these effects of stimulation were attenuated or blunted after RDN. In a human feasibility study using RNS both before and after RDN, similar BP responses were observed. Moreover, in patients with resistant hypertension, RNS-induced changes in BP appeared to be correlated with 24-h BP response after RDN. These data suggest that RNS is a useful tool to identify renal sympathetic nerve fibers in patients with treatment-resistant hypertension undergoing RDN, and to predict the likely effectiveness of RDN treatments. In acute procedural settings both in animal and human models, RNS elicits increase in BP and HR before RDN and these effects are blunted after RDN. Up to now, there is preliminary evidence that the RNS-induced BP changes predict 24-h ABPM outcome at follow-up in patients with resistant hypertension. Of note, studies are small sized and results of large trials comparing conventional RDN to RNS-guided RDN are warranted.
Subject(s)
Blood Pressure/physiology , Electric Stimulation/methods , Hypertension/therapy , Kidney/innervation , Sympathectomy/methods , Animals , Humans , Hypertension/physiopathology , Kidney/physiopathology , Renal Artery/physiopathology , Renal Artery/surgery , Sympathetic Nervous System/physiopathology , Sympathetic Nervous System/surgeryABSTRACT
PURPOSE OF REVIEW: To summarize the evidence regarding the distribution of renal nerves and their patterns of anatomic variations in animal and human settings. Moreover, the methodology and results of studies regarding renal nerve stimulation (RNS) in both preclinical and clinical models are presented. RECENT FINDINGS: There are differences regarding the number and the size of renal fibers, as well as their distance from the lumen in the diverse parts of the main renal arteries and the branches. In both animals and humans, RNS is safe and results in an increase of blood pressure (BP) while the effect on heart rate varies. In this context, the ConfidenHT™ system constitutes an integrated solution for effective RNS in humans. Due to the diversity of renal nerve anatomy in humans, arterial areas for more effective renal denervation cannot be homogenously defined. The concept of mapping of renal nerves can improve completeness of renal denervation therapies by means of integrated RNS solutions such as the ConfidenHT™ system.
Subject(s)
Blood Pressure/physiology , Heart Rate/physiology , Hypertension/diagnosis , Kidney/innervation , Sympathectomy/methods , Sympathetic Nervous System/diagnostic imaging , Animals , Humans , Hypertension/physiopathology , Hypertension/surgery , Sympathetic Nervous System/physiopathology , Sympathetic Nervous System/surgeryABSTRACT
INTRODUCTION: Sympathetic clipping in the presence of an azygos lobe is a rare combination. Anatomical relations between the sympathetic trunk and the mesoazygos impede surgical handling and can be associated with potential complications. INDICATION: We report the case of a 25-year old woman with grade III palmoplantar and axillary hyperhidrosis with azygos lobe incidentally found on preoperative chest X-ray. METHOD: Our intraoperative video shows a step-by-step approach to the sympathetic trunk in the presence of the azygos lobe, involving thoracoscopic looping and precise clip application onto the sympathetic trunk. Video-assisted reposition and expansion of the accessory lobe to avoid potential complications have been demonstrated. CONCLUSION: Videothoracoscopic sympathetic clipping in patients with lobus azygos is technically challenging. Potential complications can be avoided by coordinated surgical management.
Subject(s)
Hyperhidrosis , Lung , Postoperative Complications/prevention & control , Sympathetic Nervous System , Thoracic Surgery, Video-Assisted/methods , Adult , Female , Humans , Hyperhidrosis/diagnostic imaging , Hyperhidrosis/surgery , Lung/abnormalities , Lung/diagnostic imaging , Sympathetic Nervous System/diagnostic imaging , Sympathetic Nervous System/surgeryABSTRACT
Treatment-resistant hypertension, or resistant hypertension, is defined as blood pressure that remains above target despite concurrent use of at least three antihypertensive agents from different classes at optimal doses, one of which should be a diuretic. Important considerations in the diagnosis of treatment-resistant hypertension include the exclusion of pseudoresistance and the evaluation of potential secondary causes of hypertension and of concomitant conditions that maintain high blood pressure. The ability to diagnose true treatment-resistant hypertension is important for selection of patients who may be appropriately treated with an invasive therapy. Currently, there are three interventional approaches to treat resistant hypertension, namely: (1) reduction of the activity of the sympathetic nervous system by renal nerve ablation, (2) stimulation of baroreceptors and (3) creation of a peripheral arterial venous anastomosis. This review focuses on the rationale behind these invasive approaches and the clinical results.
Subject(s)
Hypertension , Antihypertensive Agents/therapeutic use , Humans , Hypertension/physiopathology , Hypertension/therapy , Sympathetic Nervous System/physiopathology , Sympathetic Nervous System/surgery , Treatment FailureABSTRACT
Cardiac sympathetic denervation (CSD) is reported to reduce the burden of ventricular tachyarrhythmias [ventricular tachycardia (VT)/ventricular fibrillation (VF)] in cardiomyopathy patients, but the mechanisms behind this benefit are unknown. In addition, the relative contribution to cardiac innervation of the middle cervical ganglion (MCG), which may contain cardiac neurons and is not removed during this procedure, is unclear. The purpose of this study was to compare sympathetic innervation of the heart via the MCG vs. stellate ganglia, assess effects of bilateral CSD on cardiac function and VT/VF, and determine changes in cardiac sympathetic innervation after CSD to elucidate mechanisms of benefit in 6 normal and 18 infarcted pigs. Electrophysiological and hemodynamic parameters were evaluated at baseline, during bilateral stellate stimulation, and during bilateral MCG stimulation in 6 normal and 12 infarcted animals. Bilateral CSD (removal of bilateral stellates and T2 ganglia) was then performed and MCG stimulation repeated. In addition, in 18 infarcted animals VT/VF inducibility was assessed before and after CSD. In infarcted hearts, MCG stimulation resulted in greater chronotropic and inotropic response than stellate ganglion stimulation. Bilateral CSD acutely reduced VT/VF inducibility by 50% in infarcted hearts and prolonged global activation recovery interval. CSD mitigated effects of MCG stimulation on dispersion of repolarization and T-peak to T-end interval in infarcted hearts, without causing hemodynamic compromise. These data demonstrate that the MCG provides significant cardiac sympathetic innervation before CSD and adequate sympathetic innervation after CSD, maintaining hemodynamic stability. Bilateral CSD reduces VT/VF inducibility by improving electrical stability in infarcted hearts in the setting of sympathetic activation.NEW & NOTEWORTHY Sympathetic activation in myocardial infarction leads to arrhythmias and worsens heart failure. Bilateral cardiac sympathetic denervation reduces ventricular tachycardia/ventricular fibrillation inducibility and mitigates effects of sympathetic activation on dispersion of repolarization and T-peak to T-end interval in infarcted hearts. Hemodynamic stability is maintained, as innervation via the middle cervical ganglion is not interrupted.
Subject(s)
Arrhythmias, Cardiac/physiopathology , Arrhythmias, Cardiac/surgery , Ganglia, Sympathetic/physiopathology , Ganglia, Sympathetic/surgery , Heart/innervation , Stellate Ganglion/physiopathology , Stellate Ganglion/surgery , Sympathectomy , Sympathetic Nervous System/physiopathology , Sympathetic Nervous System/surgery , Animals , Arrhythmias, Cardiac/metabolism , Cardiac Pacing, Artificial , Electric Stimulation , Heart Rate , Myocardial Contraction , Myocardial Infarction/complications , Myocardial Infarction/physiopathology , Norepinephrine/metabolism , Swine , Sympathetic Nervous System/metabolism , Tachycardia, Ventricular/metabolism , Tachycardia, Ventricular/physiopathology , Tachycardia, Ventricular/surgery , Ventricular Fibrillation/metabolism , Ventricular Fibrillation/physiopathology , Ventricular Fibrillation/surgeryABSTRACT
Despite the recent advances in the management of heart failure, the mortality of heart failure patients remains high. It is of urgent need to develop new therapy for heart failure. Heart failure is characterized by increased sympathetic activity, and chronic sympathetic activation is involved in the maintenance of the pathological state. Catheter-based renal denervation (RDN) has emerged as an invasive but safe approach that can reduce sympathetic activation. Studies have reported inconsistent results regarding the effect of RDN in heart failure patients due to limited power with small sample sizes. We aimed to conduct a meta-analysis of the effect of RDN on heart failure patients with reduced left ventricular (LV) ejection fraction (EF). An electronic search for studies examining the effect of RDN on LV function in heart failure patients with reduced EF was conducted. Two controlled (80 patients) and 2 uncontrolled studies (21 patients) were included in this meta-analysis. In the pooled analysis, 6 months after RDN, there was a greater increase in EF (weighted mean difference [95% CI] = 8.63 [6.02, 11.24] %) and a greater decrease in LV end-diastolic diameter (-0.58 [-0.83, -0.34] cm) in RDN group than in control group. No serious adverse events such as acute renal artery stenosis and dissection occurred. Our meta-analysis of feasibility studies suggests that RDN may improve LV function in heart failure patients with reduced EF, providing the rationale to conduct next phase trials to confirm the observed potential benefits of RDN.
Subject(s)
Catheter Ablation/methods , Heart Failure/surgery , Kidney/innervation , Stroke Volume/physiology , Sympathectomy/methods , Sympathetic Nervous System/surgery , Ventricular Function, Left/physiology , Animals , Heart Failure/physiopathology , HumansABSTRACT
PURPOSE OF REVIEW: Hypertension (HTN) is a ubiquitous condition and cause for significant morbidity and mortality. Over 400â000 deaths in the United States are related to HTN every year, more than all the Americans who died through all of World War II. As many as half the patients with HTN in the United States have resistant HTN, a blood pressure greater than 140/90âmmHg despite three medications including a diuretic. It appears that the prevalence of HTN and resistant HTN is increasing over time. There is a dire need for newer therapies that may reduce or eliminate the need for multiple pharmacologic agents, thus helping with compliance and reducing the possibility of their adverse events. RECENT FINDINGS: The current review summarizes the techniques and results reported in recent studies utilizing renal denervation technologies from the original Symplicity Trials to newer multipolar electrodes being used for optimal denervation. We also report the early experience with noninvasive renal denervation. Endovascular carotid body stimulation is also being investigated for resistant HTN. Renovascular HTN remains an underlying cause for resistant HTN, and revascularization may prove to be an effective treatment for many of these patients. SUMMARY: A multipronged approach utilizing lifestyle modification, pharmacologic therapy and tailored endovascular treatments may be the algorithm to treat the growing cohort of resistant HTN. However, most of the endovascular treatments remain to be validated, and renal revascularization for renovascular HTN has been set back by recent studies that did not appear to target the real renovascular cohort.
Subject(s)
Antihypertensive Agents/pharmacology , Blood Pressure/drug effects , Denervation , Hypertension/therapy , Kidney/innervation , Sympathectomy , Sympathetic Nervous System/surgery , Drug Resistance , Humans , Hypertension/diagnosis , Hypertension/drug therapy , Hypertension/surgery , Kidney/physiopathology , Sympathectomy/methods , Treatment OutcomeABSTRACT
Denervation of the extrinsic cardiac sympathetic nervous system is a method of altering the autonomic tone experienced by the heart and vasculature. It has been studied and employed as a therapy for cardiac disease for decades. Currently, there is a high level of interest in using cardiac denervation for treatment of arrhythmias. This review describes the anatomy and physiology of the cardiac autonomic nervous system followed by a discussion of the mechanistic studies which provide a basis for the therapeutic use of sympathetic denervation. The clinical research supporting its use in human arrhythmias is then appraised, covering the standard indications, such as long QT syndrome, as well as future possibilities. Last, a detailed account of the methods for performing surgical cardiac denervation and percutaneous stellate ganglion anesthetic block is provided, including the complications of each procedure. An understanding of the anatomy and physiology of the cardiac autonomic nervous system along with the techniques of surgical denervation and percutaneous anesthetic block will allow the clinician to effectively discuss and implement these therapies.