Catheter-based Renal Nerve Ablation Research Articles

Function of Renal Nerves in Kidney Physiology and Pathophysiology.

Renal sympathetic (efferent) nerves play an important role in the regulation of renal function, including glomerular filtration, sodium reabsorption, and renin release. The kidney is also innervated by sensory (afferent) nerves that relay information to the brain to modulate sympathetic outflow. Hypertension and other cardiometabolic diseases are linked to overactivity of renal sympathetic and sensory nerves, but our mechanistic understanding of these relationships is limited. Clinical trials of catheter-based renal nerve ablation to treat hypertension have yielded promising results. Therefore, a greater understanding of how renal nerves control the kidney under physiological and pathophysiological conditions is needed. In this review, we provide an overview of the current knowledge of the anatomy of efferent and afferent renal nerves and their functions in normal and pathophysiological conditions. We also suggest further avenues of research for development of novel therapies targeting the renal nerves.

Catheter-Based Renal Nerve Ablation as a Novel Hypertension Therapy: Lost, and Then Found, in Translation.

The hypothesis that renal nerves mediate, at least in part, the pathogenesis and maintenance of hypertension is based on decades of preclinical studies and, to a certain extent, recent clinical trials of catheter-based renal nerve ablation (CBRNA) in humans. The first 2 clinical trials for CBRNA, Symplicity HTN-1 and Symplicity HTN-2, reported sustained reductions in arterial pressure in patients with drug-resistant hypertension and set the stage for the first blinded US trial, Symplicity HTN-3. However, Symplicity HTN-3 failed to reach its 6-month efficacy end point, thus jeopardizing the clinical application of CBRNA in the United States. The goal of this article is to reexamine the feasibility of CBRNA to treat hypertension. Preclinical studies on the role of renal nerves in hypertension have been extensively reviewed,1,2 as have the Symplicity HTN-1, 2, and 3 trials.3–7 Therefore, we will review these topics only briefly to provide context for the primary purpose of this article which is to answer the following question: is the outcome of Symplicity HTN-3 because of the failure to translate preclinical knowledge to the clinic, or is our basic understanding of the mechanisms by which renal nerves contribute to hypertension flawed? The kidney is innervated by sympathetic efferent fibers that modulate 3 pharmacological targets for the treatment of hypertension: renin release, tubular sodium reabsorption, and renal vascular resistance.1,2 Although conventional pharmacological treatments of these targets lower arterial pressure, patients often present with negative side effects which may lead to drug incompliance. One rationale for CBRNA is that this treatment would suppress renin release, tubular sodium reabsorption, and renal vasoconstriction, while avoiding the side effects associated with more globally acting pharmacotherapies. The kidney is also innervated by renal afferent fibers that provide the central nervous system sensory information related to the …

Device-Based Approaches for the Treatment of Arterial Hypertension.

Device-based antihypertensive treatments have primarily been developed and clinically tested for patients with hypertension refractory to pharmacological treatment. Most but not all device-based treatments target the sympathetic nervous system and provided important new insight in the mechanisms of human hypertension. This review provides an overview on the scientific rational and clinical data on recent device-based antihypertensive treatment approaches. Device-based treatments targeting the sympathetic nervous system include catheter-based renal nerve ablation, electrical carotid sinus stimulation, modulation of baroreflex transduction through a dedicated carotid stent, carotid body denervation, and deep brain stimulation. Creation of a defined arteriovenous stent with a coupler device and removal of stimulatory antibodies against alpha adrenoreceptors have also been tested. The clinical evidence differs from therapy to therapy with the largest dataset for renal nerve ablation followed by electrical carotid sinus stimulation. Yet, none has been proven efficacious in sham-controlled clinical trials, and none has been shown to reduce cardiovascular morbidity or mortality. Before efficacy is proven, these treatments should not be part of routine medical care and only be applied in the setting of clinical studies.

Sub-acute Safety and Efficacy Evaluation of Single versus Double Treatment Cycles of a Monopolar Radiofrequency Catheter-Based Renal Nerve Ablation and its Chronic Evolution in a Large Animal Model

<p><strong>Aims:</strong>We aimed to evaluate the transcatheter renal denervation(RDN) effects delivered by a mono-electrode catheter in a large animal model including safety implications of delivery of one cycle versus two cycles of ablations.</p><p><strong>Methods and Results:</strong>18 animals underwent bilateral RDN; 4 untreated naïve swine were enrolled as controls for norepinephrine levels(NE) only. Animals recieved 120-second (follow up-7,30 and 90 days) or 240-second cycles ablations (follow up-7 days). Norepinephrine evaluation, histology and immunohistochemistry evaluation was performed. No luminal obstruction was observed at follow up. A 70% decrease in NE levels (76.68±57.87ng/g) was observed at 7 days, 81% at 30 days(49.05±45.81ng/g), and 51% at 90 days(12.7±73.2 ng/g) compared to naïve controls(254.1±54.1ng/g;p<0.05). Histologically, the thermal effect extended to a complete circumferential involvement with a depth ~8mm. The primary histological feature at 7 days was nerve necrosis and distal atrophy; at 30 days, necrosis was replaced by healing changes of fibrosis. Neuromatous regeneration was apparent at 30 days at RF treated levels. At 90 days these features progressed to become more conspicuous. There were no appreciable differences in depth and circumferential extent of RF injury between one and two cycle treatment groups.<strong></strong></p><p><strong>Conclusion:</strong>RDN performed with a mono-electrode catheter (Iberis) appears to be safe following single or double-cycle RF ablation.NE decrease following RDN was demonstrated at 7, 30, and 90 days compared to naïve controls, suggesting efficient nerve ablation with the device as intended for human use.</p>

TCT-766 Sub-acute Safety and Efficacy Evaluation of a Single versus Double Treatment Cycles of a Monopolar Radiofrequency Catheter-Based Renal Nerve Ablation and its Chronic Evolution in a Large Animal Model

TCT-766 Sub-acute Safety and Efficacy Evaluation of a Single versus Double Treatment Cycles of a Monopolar Radiofrequency Catheter-Based Renal Nerve Ablation and its Chronic Evolution in a Large Animal Model

Spike rate of multi-unit muscle sympathetic nerve fibers after catheter-based renal nerve ablation

Patients with treatment-resistant arterial hypertension exhibited profound reductions in single sympathetic vasoconstrictor fiber firing rates after renal nerve ablation. In contrast, integrated multi-unit muscle sympathetic nerve activity (MSNA) changed little or not at all. We hypothesized that conventional MSNA analysis may have missed single fiber discharges, thus, obscuring sympathetic inhibition after renal denervation. We studied patients with difficult-to-control arterial hypertension (age 45–74 years) before, 6 (n = 11), and 12 months (n = 8) after renal nerve ablation. Electrocardiogram, respiration, brachial, and finger arterial blood pressure (BP), as well as the MSNA and raw MSNA signals were analyzed. We detected MSNA action-potential spikes using 2 stage kurtosis wavelet denoising techniques to assess mean, median, and maximum spike rates for each beat-to-beat interval. Supine heart rate and systolic BP did not change at 6 (ΔHR: −2 ± 3 bpm; ΔSBP: 2 ± 9 mm Hg) or at 12 months (ΔHR: −1 ± 3 mm Hg, ΔSBP: −1 ± 9 mm Hg) after renal nerve ablation. Mean burst frequency and mean spike frequency at baseline were 34 ± 3 bursts per minute and 8 ± 1 spikes per second. Both measurements did not change at 6 months (−1.4 ± 3.6 bursts/minute; −0.6 ± 1.4 spikes/second) or at 12 months (−2.5 ± 4.0 bursts/minute; −2.0 ± 1.6 spikes/second) after renal nerve ablation. After renal nerve ablation, BP decreased in 3 of 11 patients. BP and MSNA spike frequency changes were not correlated (slope = −0.06; P = .369). Spike rate analysis of multi-unit MSNA neurograms further suggests that profound sympathetic inhibition is not a consistent finding after renal nerve ablation.

Blood pressure decrease in spontaneously hypertensive rats folowing renal denervation or dopamine β-hydroxylase inhibition with etamicastat.

Overactivity of the sympathetic nervous system has an important role in the development and progression of arterial hypertension. Catheter-based renal nerve ablation for the treatment of drug-resistant hypertension has recently been developed. An alternative strategy for the modulation of sympathetic nerve function is to reduce the biosynthesis of noradrenaline (NA) by inhibiting dopamine β-hydroxylase (DβH), the enzyme that catalyzes the conversion of dopamine (DA) to NA in the sympathetic nerves. Renal denervation (RDN) surgery was performed in spontaneously hypertensive rats (SHR) to evaluate the effect of RDN on the DA and NA levels and on blood pressure over a 28-day period. The selective peripheral DβH inhibitor etamicastat (30 mg kg (-1)day(-1)) was administered to another cohort of SHR. RDN and etamicastat treatment had no effect on the renal function, as assessed by measuring the water balance response, renal function and urinary electrolyte levels. RDN significantly decreased the systolic blood pressure (SBP) and the diastolic blood pressure (DBP). A gradual return of the SBP and the DBP to the high baseline levels was observed over time. Conversely, treatment with etamicastat resulted in a significant decrease in the SBP and the DBP at all time points. On the last day of the assessment, NA levels in renal tissue were significantly decreased in both RDN and etamicastat-treated groups. In contrast, the NA levels in the left ventricle were decreased only in the etamicastat-treated group. Thus, RDN produces transitory decreases in blood pressure, whereas prolonged downregulation of sympathetic drive with the DβH inhibitor etamicastat results in a sustained decrease in the SBP and the DBP.

CRT-314 Preclinical Evaluation Of Lesion Coverage Using A Multi-electrode Catheter System For Sympathetic Renal Nerve Ablation

Radio frequency (RF) catheter-based renal artery nerve ablation is under investigation for the treatment of patients with drug- resistant hypertension. Recent clinical results suggest that a four quadrant coverage is necessary to achieve optimal denervation. These results also suggest that

The sympathetic nervous system in hypertension: back to the future?

The seventeenth century London neuroanatomical school headed by Thomas Willis published the first images of the sympathetic nervous system. Nineteenth century European physiologists characterised these as the "pressor nerves". Von Euler's demonstration that the sympathetic transmitter was norepinephrine brought the field into the modern era. Sympathetic nervous system responses are regionally differentiated; human regional sympathetic activity is best studied by recording from postganglionic sympathetic efferents directed to the skeletal muscle vasculature (clinical microneurography) and by measurement of organ-specific norepinephrine release to plasma from sympathetic nerves (regional "norepinephrine spillover"). With these techniques, the sympathetic nervous system became accessible to clinical scientists, allowing the demonstration that sympathetic nervous system activation is crucial in the development and outcomes of cardiovascular disorders, most notably heart failure and essential hypertension. Activation of the renal sympathetic outflow is pivotal in the pathogenesis of essential hypertension. An important goal for clinical scientists is translation of knowledge of pathophysiology, such as this, into better treatment for patients. Although disputed, the case is strong that in hypertension, we are now on the cusp of effective "mechanisms to management" transition, with the use of catheter-based renal sympathetic nerve ablation for treating drug-resistant hypertension.

TCT-410 Evaluation of the Acute and Long Term Renal Artery Re-Innervation Attempt Response Following Radiofrequency Catheter-Based Renal Nerve Ablation in a Swine Model: A Immunohistochemical Characterization

TCT-410 Evaluation of the Acute and Long Term Renal Artery Re-Innervation Attempt Response Following Radiofrequency Catheter-Based Renal Nerve Ablation in a Swine Model: A Immunohistochemical Characterization

Abstract 526: Blood Pressure in the SHR Following Renal Denervation or Etamicastat, a Novel Dopamine-β-Hydroxylase Inhibitor

Overactivity of the sympathetic nervous system plays an important role in the development and progression of hypertension. Catheter-based renal nerve ablation for treatment of drug-resistant hypertension has been recently developed. An alternative strategy for modulation of sympathetic nerve function is to reduce the biosynthesis of norepinephrine (NE) via inhibition of dopamine β-hydroxylase (DβH), the enzyme that catalysis the conversion of dopamine to NE in sympathetic nerves. Renal denervation (RDN) was performed in spontaneously hypertensive rats (SHR) to evaluate the effect of RDN on NE levels and blood pressure throughout a 28-day period. Chronic oral treatment with the peripheral selective DβH inhibitor etamicastat (30 mg/kg/day) was performed in another cohort of SHR. RDN and chronic oral treatment with etamicastat did not affect renal function, as assessed by urinary protein, creatinine and urea levels. RDN significantly decreased mean arterial blood pressure (MAP, in mm Hg) 7 days post-surgery (139±6, P<0.01) versus baseline values (158±6). A gradual MAP return to high baseline levels was observed overtime; 139±7 at day 14, 151±12, at day 21 and 155±12 at day 28 after RDN. Treatment with etamicastat decreased baseline MAP (150±5) in a sustained and significant (P<0.01) manner at all-time points: 141±5 at day 7, 139±5 at day 14, 138±5 at day 21 and 143±5 at day 28. At day 28, NE levels (in pmol/mg tissue) in renal tissue were significantly decreased in both RDN (0.12±0.08, P=0.001) and etamicastat-treated group (0.48±0.04, P=0.01) as compared to vehicle group (0.88±0.13). On the other hand, left ventricle NE levels were decreased only after treatment with etamicastat (1.24±0.12, P=0.04) but not in the RDN group (2.53±0.24, P=0.9) when compared to controls (2.59±0.58). It is concluded that RDN produces transitory decreases in MAP, whereas prolonged down regulation of sympathetic drive with the DβH inhibitor etamicastat results in sustained decreases in MAP.

Renal nerves: time for reassessment of their role in hypertension?

Renal nerves: time for reassessment of their role in hypertension?

Targeting the Sympathetic Nervous System

Evidence has accumulated during the past several decades, strongly suggesting that abnormalities of the sympathetic nervous system contribute to the development and maintenance of multiple disease states, including hypertension, heart failure, diabetes mellitus, sleep apnea, kidney disease, and atrial fibrillation.1 The renal nerves have been identified as important contributors to the development of hypertension in both experimental animals and humans.2 Patients with essential hypertension and other disease states often have increased efferent sympathetic drive to the kidneys as demonstrated by elevated rates of renal norepinephrine spillover.1,2 In addition to increased renal efferent nerve activity, there is indirect evidence for increased renal afferent activity in patients with essential hypertension.3 Nonselective surgical sympathectomy has been effectively used as a treatment for severe hypertension,4 with a remarkable difference in outcomes at 5 years of follow-up. Recently developed endovascular catheter technology has allowed selective denervation of the human kidney using radiofrequency (RF) energy delivered via the renal artery lumen.5 Although the initial clinical trials with this minimally invasive technique have documented the safety and efficacy of such an approach, critical questions have been raised pertaining to long-term safety, mechanisms of action, appropriate patient selection, reductions in ambulatory blood pressure (BP), definition and level of responder rates, need for identification of characteristics that predict nonresponse, phenomenon of a delayed response, and several others.6 Here, we address several of these key questions. Catheter-based renal nerve ablation interrupts both efferent and afferent nerves (Figure 1). It is well established that activation of renal sympathetic efferents can decrease renal blood flow, increase tubular sodium and water reabsorption, and increase renin release.2 However, there is emerging evidence that renal afferent signaling may be as important as renal efferent activity in elevating BP. Activation of renal afferents can cause a …

Sympathetic Nervous System Moves Toward Center Stage in Cardiovascular Medicine

In 1664, the first anatomically correct depiction of the sympathetic nervous system came from Thomas Willis and his circle of London anatomists,1 included in The Anatomy of the Brain and Nerves , 1664 (Figure 1). This, the first work dedicated completely to the nervous system, also described the arterial loops at the base of the brain, which we now know as the Circle of Willis.1 Christopher Wren, an anatomist member of the group, was the principal illustrator1 before being asked by the City Fathers to turn his talents to town planning, architecture, and cathedral building after the 1666 Great Fire of London. Figure 1. An illustration of the human sympathetic nerves of the neck and thorax, from The Anatomy of the Brain and Sympathetic Nerves , published in 1664 by Thomas Willis and reproduced in Soul Made Flesh .1 Almost 2 centuries later, subsequent microscopic examination demonstrated that blood vessel walls were densely innervated, leading Stelling in 18402 to correctly conclude that these vasomotor fibers were in fact sympathetic nerves that were carried from the central nervous system to the blood vessels. In the mid-19th century, celebrated European physiologists, including Brown-Sequard, Waller, and Bernard,2 built on these observations, demonstrating vasoconstriction with electrical stimulation of the cut nerves and vasodilatation on nerve section, which indicated that the sympathetic fibers exerted a tonic, vasoconstrictor influence. The pressor nerves had gained recognition. Identification of the sympathetic neurotransmitter proved to be difficult. Claims for epinephrine3,4 and the hypothetical sympathins I and E confused the picture. Ulf von Euler compared bioassay responses of epinephrine, norepinephrine, and dihydroxy norephedrine with those of cattle splenic nerve extract, by testing blood pressure (BP) responses in the anesthetized cat and contractile responses in the isolated pregnant rabbit uterus, to definitively demonstrate the …

Blood pressure and neurohormonal responses to renal nerve ablation in treatment-resistant hypertension

Catheter-based renal nerve ablation is a novel therapy for treatment-resistant hypertension. Although the precise mechanism is unknown, a reduction in global sympathetic tone and renal sympathetic tone, potentially resulting in a decrease in renin, may account for the antihypertensive effect. In 17 patients (mean age 51.2 ± 9.4 years) with treatment-resistant hypertension (antihypertensive drugs 4.7 ± 1.3), office and ambulatory blood pressure (BP) measurements and circulating concentrations of catecholamines, renin, aldosterone and endothelin-1 were measured at baseline and 6 and 12 months after ablation. Office BP was measured for 1 h at 5-min intervals using an automatic device. Office BP (164.7 ± 27.7/102.3 ± 19.3 mmHg) decreased by 5.7 ± 18.8 mmHg (P = 0.11) systolic and by 2.6 ± 10.7 (P = 0.33) mmHg diastolic after 6 months, whereas after 12 months decreases were 12.7 ± 16.0 mmHg (P = 0.007) and 7.3 ± 11.9 mmHg (P = 0.02). Heart rate, 24-h (151.8 ± 12.6/94.2 ± 10.3 mmHg) and day and night ambulatory BP did not change, after either 6 or 12 months. Of the neurohormones, only plasma noradrenaline (397 pg/ml, interquartile range 268-461 pg/ml) decreased by 128 ± 167 pg/ml (P = 0.008) after 6 months, whereas other neurohormones remained unchanged. Forty-seven percent of patients had at least 10 mmHg decrease in 24-h ambulatory SBP. In these responders, office and ambulatory BP tended to be higher than in nonresponders, but neurohormones or changes after ablation between responders and nonresponders did not differ. Renal nerve ablation in treatment-resistant hypertensive patients had a moderate effect on office BP and is associated with a decrease in plasma noradrenaline but not in renin. The absent decrease in renin may imply that the intensity of efferent renal denervation achieved with the number of ablations applied was insufficient.

Abstract 454: Hypertension Control by Decrease of Sympathetic Hyperactivity in SHR Rats: Comparison Between Renal Denervation and Dopamine ß-hydroxylase Inhibition

Activation of the sympathetic nervous system has been described in the development and progression of systemic hypertension. Recently, catheter-based renal nerve ablation for treatment of drug-resistant hypertension has been developed. An alternative strategy for modulation of sympathetic nerve function is to reduce the biosynthesis of norepinephrine (NE) via inhibition of dopamine β-hydroxylase (DβH), the enzyme that catalysis the conversion of dopamine (DA) to NE in sympathetic nerves. Renal denervation was assessed in the rat by transient (90 sec) ischemia of renal tissues. Bilateral renal artery occlusion (RAO) was assessed in spontaneously hypertensive rats (SHR) to evaluate the effect of renal denervation on NE levels and blood pressure throughout a 28-day period. Oral treatment with the selective peripheral DβH inhibitor etamicastat (30 mg/Kg body weight) was performed in a second cohort of SHR and NE levels and blood pressure was assessed. Renal denervation resulted in marked depletion of NE levels, selective for the renal sympathetic innervations, 5 days after RAO in renal cortex (16.5±7.7% of control values, P<0.0001). Decreased NE levels persisted up to 28 days after RAO (40.8±19.4% of control values, P<0.0001). No differences in left ventricle NE levels were observed. Renal denervation significantly decreased systolic blood pressure (SBP) 5 days (165±6 vs. 187±2 mmHg, P<0.05) and 14 days post-surgery (194±3 vs. 204±2 mmHg, P<0.05), but had no effect on heart rate. Systolic blood pressure recovered to basal values 28 days post-surgery. Likewise, etamicastat treatment resulted in a depletion of NE levels in both renal cortex (70.9±9.1% of control values, P<0.05) and left ventricle (55.8±3.9% of control values, P<0.01). Etamicastat treatment decreased SBP (228±7 vs. 174±9 mmHg, P<0.001) without effects on heart rate. In conclusion, these results suggest that renal denervation and DβH inhibition similarly decreases sympathetic hyperactivity and high blood pressure in the SHR. Downregulation of sympathetic drive with DβH inhibitors may be useful in the treatment of hypertension.

Optical coherence tomography to reveal vascular lesions after catheter-based renal nerve ablation with a novel multi-electrode EnligHTNTM system

A 72-year-old female with a history of sleep apnoea syndrome was referred to the Andreas Gruentzig Catheterisation Laboratories for catheter-based renal nerve ablation (RNA) due to drug-resistant, uncontrolled hypertension. After intravenously loading with aspirin, the RNA was obtained using the first generation multi-electrode EnligHTNTM system (St. Jude Medical, Westford, MA, USA) delivering 8 ablation runs on both the left and the right renal artery. Before and after the RNA procedure, optical coherence tomography (OCT) was performed using the C7-XR imaging system (LightLab Imaging, Inc., Westford, MA, USA) with a non-occlusive technique and a single-mode optical fibre catheter (frequency domain-OCT-catheter, DragonFlyTM, St. Jude Medical, Westford, MA, USA). The OCT catheter was advanced over a standard 0.014’’ angioplasty guidewire using a monorail lumen at the tip. To optimise pullback recordings, renal arteries were flashed of blood with Ultravist 300 (Bayer House, Berkshire, United Kingdom) at a flow rate of 8.0 mL/s and the application of an automated pullback speed of 20 mm/s. The post-procedural pullback visualised local oedemas (Fig. 1A, B) concomitant with significant thrombi formations (Fig. 1A, C) and small disruptions (Fig. 1D, arrow). The clinical course was uneventful and the patient was discharged home on the second day of hospitalisation. Catheter-based RNA has been recently approved for the treatment of resistant hypertension. During the RNA procedure, transmural lesions are delivered along the walls of the renal arteries to disrupt the sympathetic nerve network located within the arterial adventitia. Here, we report a case in which OCT was performed to reveal potential periprocedural vascular side effects. The RNA was obtained using a novel EnligHTNTM catheter delivering a basket with 4 radiopaque electrodes (Fig. 1E, inset). The design of the EnligHTNTM system enabled simultaneous ablation runs, minimising catheter manipulation (Fig. 1E, arrows). However, the performance of OCT revealed several local lesions including post-ablation oedemas, thrombi formations and tissue disruptions. OCT provides novel insights on vascular effects of RNA, suggesting the potential need for double antiplatelet therapy before the procedure. However, the safety and efficacy of the new catheter-based RNA devices require soon to be evaluated in greater detail.

Peri-Procedural Care of Renal Nerve Ablation Candidates

Percutaneous catheter-based transluminal renal nerve ablation (RNA) by delivery of radiofrequency energy constitutes a novel therapeutic strategy for the treatment of resistant hypertension. The sympathetic nervous activation to the kidney and the sensory afferent signals to the central nervous system represent the targets of RNA. In this review we summarize current recommendations for appropriate patient selection for RNA and multimodal strategies in order to optimize pharmacological treatment for resistant hypertension. The safety and efficacy of the RNA based on published trials are also presented. Furthermore, a detailed description of the periprocedural management, the methodology of the RNA procedure and appropriate follow-up are provided. In conclusion, in order to improve the overall clinical outcome and achieve optimal management of resistant hypertensive patients before and after the RNA, experienced and certified centers are of major importance.

Correction

HomeHypertensionVol. 61, No. 5Correction Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection Originally published1 May 2013https://doi.org/10.1161/HYP.0b013e31828f158cHypertension. 2013;61:e52This article corrects the followingResponse to Catheter-Based Renal Nerve Ablation and Centrally Generated Sympathetic Activity in Difficult-to-Control Hypertensive PatientsIn the Hypertension article by Heusser et al (Heusser K, Tank J, Jordan J. Response to Catheter-Based Renal Nerve Ablation and Centrally Generated Sympathetic Activity in Difficult-to-Control Hypertensive Patients. Hypertension. 2013;61:e9), a correction was needed.Not all of the authors were listed in this Letter to the Editor response. The complete author listing is as follows:Karsten HeusserJens TankJulia BrinkmannInstitute of Clinical PharmacologyHannover Medical SchoolHannover, GermanyBernhard SchmidtJan MenneDepartment of Nephrology and HypertensionHannover Medical SchoolHannover, GermanyGunnar KleinJohann BauersachsDepartment of Cardiology and AngiologyHannover Medical SchoolHannover, GermanyHermann HallerDepartment of Nephrology and HypertensionHannover Medical SchoolHannover, GermanyFred C. SweepDepartment of Chemical EndocrinologyRadboud University Nijmegen Medical CentreNijmegen, the NetherlandsAndre DiedrichDivision of Clinical PharmacologyDepartment of MedicineVanderbilt UniversityNashville, TNJens JordanInstitute of Clinical PharmacologyHannover Medical SchoolHannover, GermanyThis correction has been made to the current online version of the article, which is available at http://hyper.ahajournals.org/content/61/2/e9.full. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesResponse to Catheter-Based Renal Nerve Ablation and Centrally Generated Sympathetic Activity in Difficult-to-Control Hypertensive PatientsKarsten Heusser, et al. Hypertension. 2013;61:e9-e10 May 2013Vol 61, Issue 5 Advertisement Article InformationMetrics © 2013 American Heart Association, Inc.https://doi.org/10.1161/HYP.0b013e31828f158c Originally publishedMay 1, 2013 PDF download Advertisement

Correction

HomeHypertensionVol. 61, No. 5Correction Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection Originally published1 May 2013https://doi.org/10.1161/HYP.0b013e31828f183eHypertension. 2013;61:e54This article corrects the followingResponse to Catheter-Based Renal Nerve Ablation and Centrally Generated Sympathetic Activity in Difficult-to-Control Hypertensive Patients: Prospective Case SeriesIn the Hypertension article by Jordan et al (Jordan J, Heusser K, Tank J. Response to Catheter-Based Renal Nerve Ablation and Centrally Generated Sympathetic Activity in Difficult-to-Control Hypertensive Patients: Prospective Case Series. Hypertension. 2013;61:e18), a correction was needed.Not all of the authors were listed in this Letter to the Editor response. The complete author listing is as follows:Jens JordanKarsten HeusserJulia BrinkmannInstitute of Clinical PharmacologyHannover Medical SchoolHannover, GermanyBernhard SchmidtJan MenneDepartment of Nephrology and HypertensionHannover Medical SchoolHannover, GermanyGunnar KleinJohann BauersachsDepartment of Cardiology and AngiologyHannover Medical SchoolHannover, GermanyHermann HallerDepartment of Nephrology and HypertensionHannover Medical SchoolHannover, GermanyFred C. SweepDepartment of Chemical EndocrinologyRadboud University Nijmegen Medical CentreNijmegen, the NetherlandsAndre DiedrichDivision of ClinicalPharmacology Department of MedicineVanderbilt UniversityNashville, TNJens TankInstitute of Clinical PharmacologyHannover Medical SchoolHannover, GermanyThis correction has been made to the current online version of the article, which is available at http://hyper.ahajournals.org/content/61/2/e18.full. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesResponse to Catheter-Based Renal Nerve Ablation and Centrally Generated Sympathetic Activity in Difficult-to-Control Hypertensive Patients: Prospective Case SeriesJens Jordan, et al. Hypertension. 2013;61:e18-e18 May 2013Vol 61, Issue 5 Advertisement Article InformationMetrics © 2013 American Heart Association, Inc.https://doi.org/10.1161/HYP.0b013e31828f183e Originally publishedMay 1, 2013 PDF download Advertisement