Renal Denervation in the Management of Heart Failure: History
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Contributor:
Kameel Kassab
,
Ronak Soni
,
Adnan Kassier
,
Tim A. Fischell

Norepinephrine (NE) spillover in the kidneys is associated with a worse prognosis. Since the kidneys constitute an integral part of the sympathetic activation feedback loop between the brain, the heart, the vasculature, and the kidneys, the therapies targeting this afferent loop may provide a novel and promising target in the management of patients with heart failure. Renal denervation has evolved from surgical denervation to transcatheter-based technology. This latter technique is a minimally invasive, catheter-based procedure that ablates both the afferent and efferent renal sympathetic nerves. Various catheter-based technologies exist today, including radiofrequency ablation, ultrasound thermal ablation, and chemical ablation utilizing alcohol. Renal denervation has been predominantly studied as a tool for the management of resistant hypertension. 

  • renal denervation
  • heart failure
  • therapies

1. Renal Denervation in Heart Failure with Reduced Ejection Fraction

The ACC/AHA define heart failure with reduced ejection fraction (HFrEF) as systolic dysfunction with left ventricular ejection fraction (LVEF) <40%, with or without symptoms of congestion [1]. As previously discussed, patients with heart failure have a substantial increase in renal norepinephrine spillover, significantly higher than the patients with essential hypertension, due to increased SNS activity. Pharmacotherapies targeting sympathetic over activation have been a cornerstone of heart failure management. Indeed, the current guideline-directed management of HFrEF, with proven morbidity and mortality benefits, revolves around neurohormonal modulators, including beta-blockers, ACEi, ARBs, aldosterone antagonists, diuretics, and neprilysin inhibition [1][2]. However, pharmacotherapy has limitations, including a low patient adherence rate, inability to tolerate the therapeutic doses of medications, polypharmacy with various drug–drug interactions, and side effects. Poor medication adherence (average of 40–60%) is associated with worse heart failure outcomes [3][4]. Hence, non-pharmacological-based therapies targeting these neurohormonal pathways, including RDN, may play an important complementary role in heart failure management. Proof of concept studies were predominantly conducted in animal models of heart failure, including rodent and swine models. Initially, Zheng et al. produced rat heart failure models by inducing MI in Sprague–Dawley rats by coronary ligation [5]. Four weeks later, RDN was performed. The authors demonstrated that RDN lowered norepinephrine and brain natriuretic peptide levels in the hearts of rats with HF. The RDN also decreased the left ventricular end diastolic pressure (LVEDP) and blunted the loss of β1-adrenoceptor β2-adrenoceptor protein expression. The authors concluded that RDN can potentially improve cardiac function mediated by adrenergic agonists and the blunting of β-adrenoceptor expression loss [5]. Polhemus et al. evaluated the cardio-protective effect of RDN on ischemia-reperfusion injury in a rodent model [6]. The hypertensive rats received either bilateral radio frequency (RF) RDN or sham-RDN. At 4 weeks after RF-RDN, the spontaneously hypertensive rats were subjected to 30 min of transient coronary artery occlusion, followed by reperfusion. The authors demonstrated a significant reduction in myocardial infarct size, and preservation of cardiac function 7 days post reperfusion following RDN pretreatment, as compared to a sham control, with reduction in oxidative stress and increased nitric oxide bioavailability [6]. The same group later studied the effects of RDN on LV function and remodeling in a similar ischemia-reperfusion injury rat model [7]. Kyoto rats underwent a myocardial ischemia reperfusion protocol. After 4 weeks, the rats were randomized to sham or radiofrequency RDN. The rats treated with RDN therapy demonstrated a significant improvement in the left ventricular function, vascular reactivity, and reduced cardiac fibrosis [7]. Subsequently, a swine heart failure model was studied to reproduce the rodent findings. Sharp et al. investigated the therapeutic benefits of RF-RDN in normotensive Yucatan swine who underwent the myocardial ischemia reperfusion protocol. The swine with LVEF < 40% underwent blinded randomization to receive sham RDN or RF-RDN treatment, with 12 weeks of follow-up. The authors demonstrated that the RF-RDN therapy resulted in significant reductions in the renal norepinephrine content and circulating angiotensin I and II and an increase in natriuretic peptide levels [8]. Additionally, the LV end-systolic volume was significantly reduced, leading to a marked and sustained improvement in the LV ejection fraction. Additionally, RF-RDN reduced LV fibrosis and improved coronary artery responses to vasodilators. The authors concluded that RDN, via the inhibition of the renal sympathetic activity, leads to attenuation of the renin-angiotensin system activation and improved coronary artery vasorelaxation [8]. Wang et al. redemonstrated similar benefits of RDN in improving heart failure hemodynamics in a dog-heart failure model [9].
It is important to note that, while most of the prior studies demonstrated a favorable RDN effect via the downregulation of SNS, hence the modulation of renal Norepinephrine (NE), adrenoceptor expression, and RAAS pathway, a novel finding was the effect of RDN on neprilysin levels. Neprilysin is a metallopeptidase responsible for the degradation of several peptides, including ANP, BNP, bradykinin, and Angiotensin 2. Recently neprilysin inhibition, with a concomitant increase in the circulating plasma natriuretic peptides, has become of great interest in the management of HFrEF. Large scale clinical trials, such as PARADIGM-HF, demonstrated that combining a neprilysin inhibitor (Sacubitril) with valsartan was superior to the standard guideline-directed therapy with a RAAS inhibitor alone (enalapril) [10]. Polhemus et al. demonstrated in their rat model that RF-RDN leads to reduced renal nerprilysin levels and increased levels of circulating natriuretic peptides [7]. Later, Sharp et al. demonstrated in swine model that not only did RF-RDN reduce the renal neprilysin levels and increase natriuretic peptide levels, it did so without increasing the angiotensin 2 levels. In fact, the angiotensin 2 levels are decreased after RF-RDN [8]. This combination of downregulation of RAAS and neprilysin pathways potentially have very favorable hemodynamic effects in heart failure.
Apart from the animal models of heart failure, there has been limited clinical data with RDN as a therapy for heart failure (Table 1).
Table 1. Use of Renal Denervation in Patients with Heart Failure with Reduced Ejection Fraction.
Study N, Population Clinical Findings
Gao et al. (2019) [11] 60, Single-center RCT, EF < 40% 30 patients in RDN group. At 6 months, compared to control group, RDN was associated with significant increase in LVEF, decrease in NT-ProBNP, BP, and NYHA class. No significant changes in glomerular filtration between two groups.
Drożdż et al. (2019) [12] 20, Single-center RCT, EF < 35% There were no significant differences in LVEF, BP, 6MWT and NT-proBNP concentration at 6 and 12 months after RD or control.
Chen et al. (2017) [13] 60, Single-center RCT, EF < 40% 30 patients RDN group. At 6 months, compared to control group, RDN was associated with significant improvement in symptoms, BP, quality of life, LVEF, NT-ProBNP, and NYHA class. No significant changes in glomerular filtration nor complication of renal artery stenosis were observed.
Gao et al. (2017) [14] 14, Single-arm, EF < 45% There was a significant decrease in symptoms and improvement in 6-min walk test with increase in LVEF at 6 months follow up. No RDN-related complications were observed during the follow-up period. Additionally, there was significant improvement in BP and GFR remained stable.
Hopper et al. (2017) [15] 39, Multi-center, Single-arm, EF < 40% RDN was associated with reductions in NT-proBNP and 120-min glucose tolerance test in HF patients 12 months after RDN treatment. No significant change in LVEF, 6 min walk test of GFR.
Dai et al. (2015) [16] 20, Single-center, Single-arm, EF < 40% No obvious change in heart rate or blood pressure was recorded. Symptoms of heart failure were improved in patients after RDN. No complications were recorded in the study.
Davis et al. (2013) [17] 7, Single-center, Single-arm, EF < 40% Over 6 months there was a non-significant trend in blood pressure reduction. No hypotensive or syncopal episodes were reported. Renal function remained stable. There was a significant improvement in symptoms and a 6-min walk test.
Xia et al. (2022) [18] 220, meta-analysis of the above studies Bilateral RDN increased the LVEF, decreased the LVESD, and decreased the LVEDD. In addition, RDN significantly decreased systolic and diastolic BP and decreased HR. RDN did not significantly change GFR or serum creatinine levels. The mean 6-min walk test was increased and NT-pro BNP was decreased.

2. Renal denervation in Heart Failure with Preserved Ejection Fraction

Heart failure with preserved ejection fraction (HFpEF) is a systemic disorder characterized by normal left ventricular ejection fraction, elevated filling pressures, and increased ventricular and arterial stiffness [19]. It is highly prevalent, but generally an under-diagnosed condition with significant morbidity and mortality, and accounts for around half of all heart failure patients. The patients with HFpEF typically have a high prevalence of other conditions, such as hypertension, obesity, sleep apnea, diabetes, chronic kidney disease, and metabolic syndrome [19]. It is important to note the strong association between arterial hypertension, vascular stiffness, left ventricular hypertrophy, and increased sympathetic tone in patients with HFpEF [20]. This increase in ventricular afterload can lead to increased ventricular contractility, myocardial demand, and cardiac remodeling. Unlike HFrEF, the therapies targeting neurohormonal pathways have been less beneficial in HFpEF, most likely secondary to the heterogeneous nature of the disease with various phenotypic manifestations. The pharmacotherapies targeting beta adrenergic receptors, RAAS, or neprilysin pathways have not yielded any major improvement in the outcomes in randomized controlled trials in patients with HFpEF [21][22][23]. It has been noted that the sympathetic nervous system mediates hypertension-induced hypertrophy via the direct stimulation of cardiomyocyte beta-adrenergic receptors. On the other hand, cardiac fibrosis and inflammation is a more heterogeneous process, involving mast cell activation, stimulation of the afferent sympathetic nerves, RAAS activation, and norepinephrine release [24]. Hence, targeting of the afferent signals from the kidney may reduce the sympathetic input to the heart, hence may prove to have a favorable effect on the hemodynamic profile, and prevent cardiac remodeling in those patients. The major evidence for the use of renal denervation in patients with HFpEF comes from the studies of renal denervation used for the treatment of resistant hypertension, due to the high prevalence of HFpEF in the patients enrolled in those studies (Table 2).
Table 2. Use of Renal Denervation in Patients with Heart Failure with Preserved Ejection Fraction.
Study N, Population Clinical Findings
Brandt et al. (2012) [25] 64, Single-center non-randomized study, EF > 55% 46 patients and 18 controls. RDN significantly reduced BP, and LV mass and improved diastolic function at 1 and 6 months.
Mahfoud et al. (2014) [26] 16, Multi-center non-randomized study, EF > 55% Significant improvement in global longitudinal strain at 6 months. Reduction in left ventricular mass index suggesting an improved diastolic function.
Kresoja et al. (2021) [20] 66, Single center, single-arm, EF > 55% Patients with HFpEF undergoing RDN showed reduced BP, and increased stroke volume index. LV diastolic stiffness and LV filling pressures as well as NT-proBNP decreased.

3. Renal Denervation and Cardiac Dysrhythmias in Heart Failure

The patients with chronic heart failure are predisposed to various types of atrial or ventricular tachyarrhythmias, including atrial fibrillation (afib) and ventricular tachycardia. In the patients who suffer myocardial infarction or develop heart failure, autonomic dysregulation leads to an excessive sympathetic drive, and compensatory mechanisms, as previously discussed, become a nidus for cardiac pathology [27]. This sympathetic overstimulation and cardiac remodeling is one of the main drivers of tachyarrhythmias in heart failure. There has been increasing interest in using RDN for the treatment and prevention of arrhythmias and arrhythmia-related morbidity, both atrial and ventricular [28]. The support for this concept was initially demonstrated in animal models, although not necessarily that of heart failure. In a canine model of tachycardia-mediated cardiomyopathy, ventricular remodeling was attenuated by RDN in dogs that were chronically paced at elevated heart rates [29]. In a pig model of myocardial infarction, RDN significantly reduced the occurrence of ventricular fibrillation during ischemia induction, as compared to animals in the sham control group [30]. Similarly, Zhang et al. demonstrated, in a canine model, that surgical and chemical renal denervation decreased whole-body and local tissue sympathetic activity and reversed neural remodeling in the heart and stellate ganglion. RDN was associated with the beneficial remodeling of the infarction zone, translating to a decrease in ventricular arrhythmia after myocardial infarction [31]. Although limited, there are small scale human studies on the effects of RDN on cardiac tachyarrhythmias. Pokushalov et al. randomized a small cohort of 27 patients with afib and hypertension to undergo afib ablation alone, or afib ablation with RDN. The group demonstrated that significantly more patients who underwent concomitant RDN were free of atrial fibrillation at 12 months, compared to those who did not (69% vs. 29%, p = 0.033) [32]. ERADICATE-AF was a larger randomized control trial of 302 patients which demonstrated that, among patients with paroxysmal atrial fibrillation and hypertension, renal denervation added to catheter ablation, compared with catheter ablation alone, significantly increased the likelihood of freedom from atrial fibrillation at 12 months (hazard ratio, 0.57; 95% CI, 0.38 to 0.85; p  = 0 .006) [33]. More than 75% of the randomized patients had HFpEF with NYHA class 2 symptoms. Hence, the findings of the trials may not apply to lone atrial fibrillation patients. Remo et al. presented four patients with refractory ventricular tachyarrhythmias, despite antiarrhythmic therapy and prior VT ablations (two with ischemic and two with non-ischemic cardiomyopathy). The number of VT episodes decreased from 11.0 ± 4.2 (5.0–14.0) during the month before ablation to 0.3 ± 0.1 (0.2–0.4) per month after ablation. The responses to RDN were similar for ischemic and non-ischemic patients [34]. More recently, in a pooled analysis of 121 patients, Howson and colleagues demonstrated a significant effect of RDN in reducing implantable cardiac defibrillator therapies, reducing the number of VA episodes, antitachycardia pacing and defibrillator shocks [35]. The aforementioned studies represent heterogeneous groups of patients. There is an important need for randomized controlled trials specifically evaluating the antiarrhythmic role of RDN in heart failure patients, with both preserved and reduced EF, for both prevention and as a therapy.

This entry is adapted from the peer-reviewed paper 10.3390/jcm11144147

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