Renal Sympathetic Hyperactivity Research Articles

Catheter-Based Ultrasound Renal Denervation in Patients with Resistant Hypertension: A Systematic Review

Background: The maintenance and development of hypertension are fundamentally dependent on renal sympathetic hyperactivity. Through regulation of the renal sympathetic nerves, catheter-based renal sympathetic denervation has been demonstrated to dramatically lower blood pressure (BP) in patients with resistant hypertension (systolic blood pressure 160 mm Hg on three or more antihypertensive medicines, including a diuretic). This study assessed a catheter-based ultrasound device of the next generation intended to maximize nerve coverage using circumferential ultrasound energy. This study's objective is to describe the results of renal denervation (RDN) in patients with resistant hypertension using a catheter-based ultrasonography device to measure blood pressure and safety. A potential new non-pharmacological therapy for resistant hypertension is renal denervation. Method: PubMed, Web of Science, Science Direct, Cochrane Library, and Google Scholar were thoroughly searched for relevant material. Throughout this meticulous process, the Rayyan QRCI was used. Results: our review included 10 studies with parameters including the period of study, age range of patients, office blood pressure, ambulatory blood pressure and the used approach. Clinical studies are required to determine whether this method is effective in treating this resistant hypertension. Conclusion: In individuals with resistant hypertension, catheter-based ultrasound renal denervation significantly and persistently lowers blood pressure and has no negative effects on renal function or renal artery anatomy.

Renal Sympathetic Hyperactivity in Diabetes Is Modulated by 5-HT1D Receptor Activation via NO Pathway.

Renal vasculature, which is highly innervated by sympathetic fibers, contributes to cardiovascular homeostasis. This renal sympathetic outflow is inhibited by 5-HT in normoglycaemic rats. Considering that diabetes induces cardiovascular complications, we aimed to determine whether diabetic state modifies noradrenergic input at renal level and its serotonergic modulation in rats. Alloxan diabetic rats were anaesthetized (pentobarbital; 60 mg/kg i.p.) and prepared for in situ autoperfusion of the left kidney to continuously measure systemic blood pressure (SBP), heart rate (HR), and renal perfusion pressure (RPP). Electrical stimulation of renal sympathetic outflow induces frequency-dependent increases (Δ) in RPP (23.9 ± 2.1, 59.5 ± 1.9, and 80.5 ± 3.5 mm Hg at 2, 4, and 6 Hz, respectively), which were higher than in normoglycaemic rats, without modifying HR or SBP. Intraarterial bolus of 5-HT and 5-CT (5-HT1/5/7 agonist) reduced electrically induced ΔRPP. Only L-694,247 (5-HT1D agonist) reproduced 5-CT inhibition on sympathetic-induced vasoconstrictions, whereas it did not modify exogenous noradrenaline-induced ΔRPP. 5-CT inhibition was exclusively abolished by i.v. bolus of LY310762 (5-HT1D antagonist). An inhibitor of guanylyl cyclase, ODQ (i.v.), completely reversed the L-694,247 inhibitory effect. In conclusion, diabetes induces an enhancement in sympathetic-induced vasopressor responses at the renal level. Prejunctional 5-HT1D receptors, via the nitric oxide pathway, inhibit noradrenergic-induced vasoconstrictions in diabetic rats.

Rezistentna arterijska hipertenzija i modaliteti lečenja

Hypertension is one of the most common diseases in the general population. Despite the new generation of antihypertensive drugs and improved guidelines, there is still a poor number of patients with well-controlled hypertension. The particular group is patients with resistant hypertension. It is highly prevalent in the general hypertensive population and good control of those patients remains a great challenge. Renal sympathetic hyperactivity is a response mechanism of resistant hypertension. One of the options for those patients is transcatheter renal sympathetic denervation. Recent studies show promising results and it has become a possible therapeutic alternative to treat this group of patients.

Effects of renal denervation on cardiovascular, metabolic and renal functions in streptozotocin-induced diabetic rats

Diabetes promotes renal sympathetic hyperactivity, autonomic imbalance, and cardiovascular and renal dysfunction. Bilateral renal denervation (BRD) has emerged as a treatment for diabetes; however, the mechanisms that underlie the beneficial effects of BRD are unknown. AimsThe present study evaluated the effects of BRD on autonomic, cardiovascular, metabolic, and renal function in streptozotocin-diabetic rats. Main methodsWistar rats were separated into three experimental groups: control (CTR), diabetic (DM), and diabetic that underwent BRD (DM BRD). BRD was performed two weeks after STZ-diabetes induction, the experiments were performed four weeks after DM induction. This study evaluated sympathetic vasomotor nerve activity in different territories (renal, lumbar and splanchnic), arterial baroreceptor reflex, metabolic and renal function. Key findingsBRD significantly reduced glycemia, glycosuria, albuminuria, and SGLT2 gene expression in the kidney in DM rats. Renal sympathetic nerve activity (rSNA) was significantly increased and splanchnic sympathetic nerve activity (sSNA) was significantly decreased in DM rats, without changes in lumbar sympathetic nerve activity (lSNA). BRD was able to normalize sSNA and significantly increase lSNA in DM rats compared to control rats. Additionally, cardiac baroreceptor sensitivity was impaired in DM rats, and BRD significantly improved baroreflex sensitivity. SignificanceOur data suggest that renal nerves play an important role in autonomic, cardiovascular, and renal dysfunction in STZ-DM rats. Thus, sympathetic renal hyperactivity should be considered a possible therapeutic target in diabetic patients.

Renal Deafferentation Improves Renal Function and Blood Pressure, but not Cardiac Parameters in an experimental model chronic kidney disease.

Chronic kidney disease is highly prevalent and its mortality is associated with cardiovascular disease. Experimental evidence shows that the renal nerves contribute to arterial hypertension and renal sympathetic hyperactivity worsening the disease; renal denervation has shown renoprotective and cardioprotective effects. However, renal sympathetic innervation plays a fundamental role in renal homeostasis and its removal is associated with impaired compensatory mechanisms during hemodynamic changes. Thus, the aim of this work was to investigate the effects of selective renal denervation of afferent fibers on renal and cardiovascular repercussions in chronic kidney disease (CKD) induced by 5/6 nephrectomy in Wistar rats. The use of animals was approved by the Federal University of São Paulo Animal Care and Use Committee and performed according to the National Institutes of Health guidelines for the conduct of experiments in animals. After five weeks of nephrectomy, denervation of renal afferent fibers with a periaxonal application of 33 mM capsaicin was performed. Cardiovascular and renal function parameters were evaluated three weeks after deafferentation.ResultsCKD induced increase in blood pressure (CTL 113±7.2 × CKD 185±14 mmHg), creatinine plasma levels (CTL 0.5±0.1 × CKD 1.2±0.5 mg/dl) and proteinuria (CTL 14±10 × 300±129 mg/24h). It was also observed an increase in cardiac hypertrophy, reduction in baroreflex sensitivity and in parasympathetic tone after autonomic double blockade. Afferent renal denervation reduced blood pressure (165±21 mmHg), improved creatinine plasma levels (0.8 ±0.2 mg/dl) and proteinuria (178±102 mg/24h). No alterations were observed after deafferentation over baroreflex sensitivity, cardiac hypertrophy and autonomic control to the heart. Together these results suggest that renal deafferentation improves blood pressure and renal function, without, however, improving the cardiac changes found in this CKD model. It is possible that the time expected after deafferentation or the stage of the disease in which it was performed was not sufficient to induce cardiac improvements. Further studies are necessary to elucidate this question.Support or Funding InformationCoordenação de Aperfeiçoamento de Pessoal de Nível Superior – Brasil (CAPES) – Finance Code 001; by the São Paulo Research Foundation (FAPESP 18/02671‐3) and by the Brazilian National Research Council (CNPq)

Acute changes in morphology and renal vascular relaxation function after renal denervation using temperature-controlled radiofrequency catheter

BackgroundResistant hypertension and renal sympathetic hyperactivity are closely linked, and catheter-based renal denervation (RDN) is regarded as a new treatment strategy. However, the acute changes in vascular morphology and relaxation function have yet to be evaluated, and these may be important for the efficacy and safety of the procedure. In this study, we explored these questions by conventional temperature-controlled cardiac radiofrequency catheter-based RDN in a pig model.MethodsSix mini-pigs were randomly divided into the renal denervation (RDN) group (n = 3) and the Sham-RDN group (n = 3). Animals in the RDN group underwent unilateral radiofrequency ablation, and those in the Sham-RDN group underwent the same procedure except for the ablation. The pigs were examined by angiography pre- and post-RDN and were euthanized immediately thereafter. Renal arteries were processed for histological and molecular biology analyses as well as for in vitro vascular tension testing.ResultsCompared with the Sham-RDN group, the RDN caused vascular intima and media injury, renal nerve vacuolization, mild collagen fiber hyperplasia and elastic fiber cleavage (all p < 0.05). The RDN group also significantly exhibited nitric oxide synthase pathway inhibition and decreased endothelium-independent vascular relaxation function Compared to the Sham-RDN group (all p < 0.05).ConclusionsIn this porcine model, renal artery denervation led to vascular wall injury and endothelial dysfunction in the acute phase, which negatively affected vascular relaxation function. Thus, this process may be detrimental to the prognosis and progress of hypertension patients.

Is Renal Denervation Back

Renal sympathetic hyperactivity is a contributor to hypertension, and renal denervation (RDN) by percutaneous ablation was for a time considered a very

Early morphologic alterations in renal artery wall and renal nerves in response to catheter-based renal denervation procedure in sheep: difference between single-point and multiple-point ablation catheters.

Renal sympathetic hyperactivity is critically involved in hypertension pathophysiology; renal denervation (RDN) presents a novel strategy for treatment of resistant hypertension cases. This study assessed effects of two RDN systems to detect acute intravascular, vascular and peri-vascular changes in the renal artery, and renal nerve alterations, in the sheep. The procedures using a single-point or multi-point ablation catheters, Symplicity Flex(TM), Medtronic versus EnligHTN(TM), St. Jude Medical were compared; the intact contralateral kidneys served as controls. Histopathological and immunohistochemical assessments were performed 48 h after RDN procedures; the kidney and suprarenal gland morphology was also evaluated. Special staining methods were applied for histologic analysis, to adequately score the injury of renal artery and adjacent renal nerves. These were more pronounced in the animals treated with the multi-point compared with the single-point catheter. However, neither RDN procedure led to complete renal nerve ablation. Forty-eight hours after the procedure no significant changes in plasma and renal tissue catecholamines were detected. The morphologic changes elicited by application of both RDN systems appeared to be dependent on individual anatomical variability of renal nerves in the sheep. Similar variability in humans may limit the therapeutic effectiveness of RDN procedures used in patients with resistant hypertension.

Renal Denervation for Resistant Hypertension

Background Resistant hypertension is highly prevalent among the general hypertensive population and the clinical management of this condition remains problematic. Different approaches, including a more intensified antihypertensive therapy, lifestyle modifications, or both, have largely failed to improve patients' outcomes and to reduce cardiovascular and renal risk. As renal sympathetic hyperactivity is a major driver of resistant hypertension, renal sympathetic ablation (renal denervation) has been recently proposed as a possible therapeutic alternative to treat this condition. Objectives We sought to evaluate the short- and long-term effects of renal denervation in individuals with resistant hypertension on clinical end points, including fatal and non-fatal cardiovascular events, all-cause mortality, hospital admissions, quality of life, blood pressure control, left ventricular hypertrophy, cardiovascular and metabolic profile, and kidney function, as well as the potential adverse events related to the procedure. Search methods We searched the following databases to 17 February 2016 using relevant search terms: the Cochrane Hypertension Group Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE and ClinicalTrials.gov Selection criteria We considered randomised controlled trials (RCTs) that compared renal denervation to standard therapy or sham procedure to treat resistant hypertension, without language restriction. Data collection and analysis Two authors independently extracted data and assessed study risks of bias. We summarised treatment effects on available clinical outcomes and adverse events using random-effects meta-analyses. We assessed heterogeneity in estimated treatment effects using Chi² and I² statistics. We calculated summary treatment estimates as a mean difference (MD) or standardised mean difference (SMD) for continuous outcomes, and a risk ratio (RR) for dichotomous outcomes, together with their 95% confidence intervals (CI). Main results We found 12 eligible studies (1149 participants). In four studies, renal denervation was compared to sham procedure; one study compared a proximal ablation to a complete renal artery denervation; in the remaining, renal denervation was tested against standard or intensified antihypertensive therapy. None of the included trials was designed to look at hard clinical end points as primary outcomes. When compared to control, there was low quality evidence that renal denervation did not reduce the risk of myocardial infarction (4 studies, 742 participants; RR 1.31, 95% CI 0.45 to 3.84), ischaemic stroke (4 studies, 823 participants; RR 1.15, 95% CI 0.36 to 3.72), or unstable angina (2 studies, 201 participants; RR 0.63, 95% CI 0.08 to 5.06), and moderate quality evidence that it had no effect on 24-hour ambulatory blood pressure monitoring (ABPM) systolic BP (5 studies, 797 participants; MD 0.28 mmHg, 95% CI -3.74 to 4.29), diastolic BP (4 studies, 756 participants; MD 0.93 mmHg, 95% CI -4.50 to 6.36), office measured systolic BP (6 studies, 886 participants; MD -4.08 mmHg, 95% CI -15.26 to 7.11), or diastolic BP (5 studies, 845 participants; MD -1.30 mmHg, 95% CI -7.30 to 4.69). Furthermore, low quality evidence suggested that this procedure produced no effect on either serum creatinine (3 studies, 736 participants, MD 0.01 mg/dL; 95% CI -0.12 to 0.14), estimated glomerular filtration rate (eGFR), or creatinine clearance (4 studies, 837 participants; MD -2.09 mL/min, 95% CI -8.12 to 3.95). Based on low-quality evidence, renal denervation significantly increased bradycardia episodes compared to control (3 studies, 220 participants; RR 6.63, 95% CI 1.19 to 36.84), while the risk of other adverse events was comparable or not assessable. Data were sparse or absent for all cause mortality, hospitalisation, fatal cardiovascular events, quality of life, atrial fibrillation episodes, left ventricular hypertrophy, sleep apnoea severity, need for renal replacement therapy, and metabolic profile. The quality of the evidence was low for cardiovascular outcomes and adverse events and moderate for lack of effect on blood pressure and renal function. Authors' conclusions In patients with resistant hypertension, there is low quality evidence that renal denervation does not change major cardiovascular events, and renal function. There was moderate quality evidence that it does not change blood pressure and and low quality evidence that it caused an increaseof bradycardia episodes. Future trials measuring patient-centred instead of surrogate outcomes, with longer follow-up periods, larger sample size and more standardized procedural methods are necessary to clarify the utility of this procedure in this population.

Renal Sympathetic Hyperactivity in Hypertension: True or False?

Increased renal norepinephrine spillover, observed by using isotope-dilution method, is thought to indicate renal sympathetic hyperactivity and to play a crucial role in hypertension. However, SYMPLICITY HTN-3 (Renal Denervation in Patients With Uncontrolled Hypertension), the first randomized sham-controlled trial, failed to show a benefit of renal denervation for resistant hypertension.1 This raises the issue of whether the sympathetic hyperactivity hypothesis is true. In a recent issue of Circulation Research , Grassi et al2 have emphasized the presence and importance of sympathetic hyperactivity in hypertension, primarily based on the results of isotope-dilution studies. However, the isotope-dilution method cannot exclude the involvement of intraorgan platelet release of norepinephrine. We would argue that platelet norepinephrine release, rather than sympathetic nervous system alterations, may be the cause of increased norepinephrine spillover in hypertension for …

Effect of renal ablation on blood pressure and muscle sympathetic nerve activity in chronic kidney disease patients (LB722)

Chronic kidney disease (CKD) is associated with renal sympathetic hyperactivity and uncontrolled hypertension. Catheter‐based renal ablation may reduce arterial blood pressure and muscle sympathetic nerve activity (MSNA) in patients with drug resistant hypertension. A cohort of 4 dialysis patients are reported who had uncontrolled hypertension despite two agents and clinical normovolemia, and in whom successful MSNA and BP recordings were obtained in both pre and post ablation tests. These patients were tested to determine whether renal ablation would reduce blood pressure and whether changes in blood pressure would be associated with changes in MSNA. This was achieved by comparing burst activity (incidence and frequency) and action potential (AP) composition (APs/burst, APs/min and APs/100 heart beats) pre‐ and one month post‐ablation. Analyses were conducted using software that detected AP content of the multi‐unit recording in human neural signals. Compared to the pre session, these patients had reductions in average ambulatory blood pressure (Systolic 178 ± 18 to 158 ± 25 mmHg p=0.04 and diastolic 95 ± 13 to 82 ± 7 mmHg p=0.046) post‐ablation. Average burst frequency (64 ± 15 to 61 ± 18 p=0.58) and burst incidence (84 ± 12 to 82 ±19 p=0.6) were unaffected by ablation. However, ablation increased average APs/burst (4.5 ± 1.3 to 7 ± 2.3 p= 0.03), APs/min (223 ± 103 to 423 ± 202 p=0.039) and APs/100 heart beats (297 ± 117 to 582 ± 280 p=0.04). These data suggest that the observed decrease in blood pressure was not associated with changes in burst activity (frequency and incidence): However, the observed increases in sympathetic AP content/burst and per minute suggest an affect of ablation on AP recruitment and synchronization.Grant Funding Source: Supported by The Kidney and Health and Disease reserach theme Univeristy of Otago

Renal Denervation Therapy for Hypertension

An overweight 78-year-old man with hypertension treated with spironolactone (50 mg daily), amlodipine (10 mg daily), lisinopril (40 mg daily), and extended-release metoprolol (200 mg daily), intolerant of multiple antihypertensives including clonidine (dry mouth) and hydralazine (diarrhea), is referred for renal sympathetic denervation (RSDN). He reports dietary and medication compliance. Secondary causes of hypertension have been excluded. Blood pressure (BP) is 184/93 mm Hg. Hypertension remains a major modifiable risk factor associated with cardiovascular morbidity and mortality.1 Resistant hypertension is defined as BP≥160/100 mm Hg, despite maximally tolerated doses of ≥3 classes of antihypertensives, including a diuretic, without secondary hypertension (eg, renovascular hypertension, chronic kidney disease, mineralocorticoid excess, or obstructive sleep apnea).2 Recently, the prevalence of resistant hypertension in patients with atherosclerosis was reported to be 12.7%.3 It is associated with a high risk for future adverse cardiovascular events.4 Sympathetic hyperactivity promotes hypertension (Figure 1). In hypertensive rats demonstrating renal sympathetic hyperactivity, renal efferent denervation delays the onset and lessens the severity of hypertension.5 Renal afferent denervation through dorsal rhizotomy mitigates hypertension.6 Following renal transplantation, sympathetic hyperactivity continues until the diseased kidneys are excised; BP improvement typically follows.7 The BP reduction following renal excision provides evidence that detrimental sympathetic signals originate from diseased kidneys.8 Figure 1. Systemic effects of sympathetic nervous system hyperactivity. Before modern pharmacotherapy, malignant hypertension had a ≈100% mortality at 5 years.9 Radical sympathectomy was used and RSDN was achieved, albeit nonselectively. In an observational study of 1266 patients undergoing sympathectomy in comparison with 467 treated conventionally, improved survival rates and BP control were demonstrated with surgery. …

EASD/ESC Symposium: Renal Denervation

Hypertensive individuals, who cannot achieve target blood pressure (BP) levels despite being treated with triple-drug regimens, including a diuretic, are diagnosed as having resistant hypertension (rHT) [Calhoun DA et al. Circulation 2008], which is an increasingly common clinical problem [Egan BM et al. Circulation 2011]. Renal sympathetic hyperactivity is influential in the maintenance and progression of hypertension, while the interruption of sympathetic nerves in the kidney has a strong impact on BP and survival. This article discusses the impact of renal denervation as a treatment for hypertension.

Renal Denervation: A New Approach to an Old Problem.

Renal sympathetic hyperactivity is associated with hypertension. Renal denervation is an interventional approach to selectively denervate the renal sympathetic fibers. The reduction of systolic and diastolic blood pressure in patients with resistant hypertension has been demonstrated in the Symplicity HTN-1 and HTN-2 trials. Before the patient undergoes an interventional procedure, causes of secondary hypertension or pseudoresistance must be excluded.

PERCUTANEOUS RENAL DENERVATION FOR RESISTANT HYPERTENSION: REAL WORLD OUTCOMES

Background: Arterial hypertension is the largest single contributor to global mortality, and is poorly controlled in approximately 50% of patients despite lifestyle and pharmacologic interventions. Renal sympathetic hyperactivity is a key factor in the maintenance and progression of hypertension and randomized clinical trials have shown that catheter-based renal sympathetic denervation reduces blood pressure (BP) in patients with resistant hypertension. “Real world” data regarding the eficacy of this novel therapy are not available.

Abstract 9590: Early Blood Lowering Effects of Renal Sympathetic Denervation

Introduction and Hypothesis Hypertension is a major global health problem. Renal sympathetic hyperactivity has been identified as a major contributor to the complex pathophysiology of hypertension. Catheter-based renal sympathetic denervation (RDN) has been shown to significantly reduce blood pressure (BP) in patients with severe hypertension. According to Symplicity HTN-1 and -2 trials it is known that the BP lowering effect will take about 1 to 6 month to develop. However, there is little information available on the immediate BP lowering effects of RDN. Our study carefully investigated early BP response to RDN in a cohort of patients with resistant hypertension (systolic BP &gt;150 mm Hg on &gt;3 antihypertensive drugs). Methods and Results Our study enrolled 28 consecutive patients (mean age 65 years, 48% women, 47% diabetic). Baseline values included a mean of 5.7 antihypertensive medications. A 24h Holter BP monitoring was recorded in every patient 24h before and after RDN. BP readings were then averaged according to daytime (7:00am-22:00pm), night (22:00pm-7:00am) and 24 hours intervals (figure 1). In treated patients mean averaged systolic BP was reduced by 15.3±3.34 mmHg (p&lt;0.001) during the first 24 hours. Systolic BP reduction appeared to be much higher at daytime (17.5±3.59 mmHG; p&lt;0.001) compared to night (9.6±3.88 mmHg; p&lt;0.021) which might indicate the role of sympathetic activity at daytime. A concordant effect on diastolic BP was observed: 6.9±1.72 mmHg (p&lt;0.001). Heart rate was not affected at the early time points (1.64±1.62; p=0.319). The missing changes in heart rate may indicate the absence of inpatient stress factors that could have influenced BP. Conclusion In patients with resistant hypertension, catheter-based renal sympathetic denervation results in an immediate substantial reduction of systolic and diastolic BP. The relationship between the immediate and long-term BP lowering effect of RDN-therapy remains to be investigated.

Catheter-based renal sympathetic denervation: chronic preclinical evidence for renal artery safety

Renal sympathetic hyperactivity is associated with hypertension, a leading cause of mortality worldwide. Renal sympathetic denervation via the Symplicity Catheter System has been shown to decrease blood pressure by 33/11mmHg by 6months, with no radiofrequency (RF)-related adverse sequelae visible by CT/MR angiography or renal duplex ultrasound 6months after the procedure. Here, we present preclinical work predating those clinical results. We performed therapeutic renal sympathetic denervation in a swine animal model to characterize the vascular safety and healing response 6months after renal denervation therapy. In December 2007, seven domestic swine received a total of 32 radiofrequency ablations via the Symplicity Catheter System and were euthanatized 6months later. Renal angiography was done before, immediately after, and 6months after procedure. The renal vessels were examined histologically with H&E and Movat pentachrome stains to identify evidence of vascular and neural injury. The kidneys and urinary system were also examined for evidence of gross and microscopic abnormalities. Renal nerve injury involved primarily nerve fibrosis, replacement of nerve fascicles with fibrous connective tissue, and thickening of the epineurium and perineurium. Renal arterial findings included fibrosis of 10-25% of the total media and underlying adventitia, with mild disruption of the external elastic lamina. No significant smooth muscle hyperplasia or inflammatory components were observed. There was no renal arterial stenosis or thrombosis observed by angiography or histology. No gross or microscopic device-related abnormalities were noted in the kidney, surrounding stroma, or urinary bladder. In a swine model, renal denervation via the Symplicity Catheter System resulted in no clinically significant adverse renal artery or renal findings 6months after the procedure. This is corroborated by the vascular safety profile demonstrated in subsequent human clinical studies.

Something New to Offer: Renal Denervation

Renal sympathetic hyperactivity is seminal in the maintenance and progression of hypertension. Catheter-based renal sympathetic denervation has been shown to significantly reduce blood pressure (BP) in patients with hypertension. Durability of effect beyond 1 year using this novel technique has never been reported. A cohort of 45 patients with resistant hypertension (systolic BP ≥160 mm Hg on ≥3 antihypertension drugs, including a diuretic) has been originally published. Herein, we report longer-term follow-up data on these and a larger group of similar patients subsequently treated with catheter-based renal denervation in a nonrandomized manner. We treated 153 patients with catheter-based renal sympathetic denervation at 19 centers in Australia, Europe, and the United States. Mean age was 57±11 years, 39% were women, 31% were diabetic, and 22% had coronary artery disease. Baseline values included mean office BP of 176/98±17/15 mm Hg, mean of 5 antihypertension medications, and an estimated glomerular filtration rate of 83±20 mL/min per 1.73 m. The median time from first to last radiofrequency energy ablation was 38 minutes. The procedure was without complication in 97% of patients (149 of 153). The 4 acute procedural complications included 3 groin pseudoaneurysms and 1 renal artery dissection, all managed without further sequelae. Postprocedure office BPs were reduced by 20/10, 24/11, 25/11, 23/11, 26/14, and 32/14 mm Hg at 1, 3, 6, 12, 18, and 24 months, respectively. In conclusion, in patients with resistant hypertension, catheter-based renal sympathetic denervation results in a substantial reduction in BP sustained out to ≥2 years of follow-up, without significant adverse events.

Catheter-Based Renal Sympathetic Denervation for Resistant Hypertension

Renal sympathetic hyperactivity is seminal in the maintenance and progression of hypertension. Catheter-based renal sympathetic denervation has been shown to significantly reduce blood pressure (BP) in patients with hypertension. Durability of effect beyond 1 year using this novel technique has never been reported. A cohort of 45 patients with resistant hypertension (systolic BP ≥160 mm Hg on ≥3 antihypertension drugs, including a diuretic) has been originally published. Herein, we report longer-term follow-up data on these and a larger group of similar patients subsequently treated with catheter-based renal denervation in a nonrandomized manner. We treated 153 patients with catheter-based renal sympathetic denervation at 19 centers in Australia, Europe, and the United States. Mean age was 57±11 years, 39% were women, 31% were diabetic, and 22% had coronary artery disease. Baseline values included mean office BP of 176/98±17/15 mm Hg, mean of 5 antihypertension medications, and an estimated glomerular filtration rate of 83±20 mL/min per 1.73 m(2). The median time from first to last radiofrequency energy ablation was 38 minutes. The procedure was without complication in 97% of patients (149 of 153). The 4 acute procedural complications included 3 groin pseudoaneurysms and 1 renal artery dissection, all managed without further sequelae. Postprocedure office BPs were reduced by 20/10, 24/11, 25/11, 23/11, 26/14, and 32/14 mm Hg at 1, 3, 6, 12, 18, and 24 months, respectively. In conclusion, in patients with resistant hypertension, catheter-based renal sympathetic denervation results in a substantial reduction in BP sustained out to ≥2 years of follow-up, without significant adverse events.

TWO-YEAR DURABILITY OF BLOOD PRESSURE REDUCTION WITH CATHETER-BASED RENAL SYMPATHETIC DENERVATION: HT.3.04

Background: Renal sympathetic hyperactivity is seminal in the progression of hypertension (HTN). Catheter-based renal sympathetic denervation (RDN) has been shown to significantly reduce blood pressure in patients with hypertension (HTN). Durability of effect at 2-years using this novel technique has never been reported. Methods: A cohort of 45 patients with resistant HTN (SBP ≥160 mmHg on ≥3 anti-HTN drugs, including a diuretic) was originally reported in the Lancet. We report longer term data on these patients and similar patients subsequently treated with the catheter-based renal denervation in non-randomized studies. Office blood pressure (BP) data and safety data were available at 1, 3, 6, 12, 18 and 24 months post-procedure. eGFR at 3 and 12 months were available. Results: 117 pts were treated with catheter-based RDN at 17 centers in Australia, Europe, and the US. Mean age was 57±11 yrs, 40% were female, 33% diabetic, 22% with CAD. Baseline values include mean office BP 176/98 ± 17/14 mmHg, mean of 5.0 anti-HTN medications, and eGFR 82 ± 19 mL/min. The procedure lasted a median of 38 minutes. Four acute procedural complications occurred: three groin pseudoaneurysms and one renal artery dissection, all managed without further sequelae. Post-procedure office BPs were reduced by 20/11, 24/10, 24/12, 25/12, 29/17, and 33/14 mmHg at 1, 3, 6, 12, 18, and 24 months respectively. At 3-months the eGFR had changed by -1.4 mL/min (95% CI: -4.6 to 1.7), and at 12-months the eGFR had changed by -2.8 mL/min (95% CI: -6.4 to 0.8). One patient required stenting of a renal artery ostial stenosis that was present at baseline but grew by 6 months; no radiofrequency energy had been delivered in this location. Otherwise, there were no late adverse events associated with the therapy. Conclusions: Catheter-based RDN results in a substantial reduction in BP sustained to at least 2 years, without significant adverse events, in patients with resistant HTN. The changes in eGFR are better than the natural history reported in similar patients.