Renal Nerve Ablation
A sympathetic overdrive is central to the development and clinical course of heart failure. As the kidneys are significant modulators of sympathetic activity, renal nerve ablation (RNA) stands as an intriguing therapeutic option to control the progression
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Konstantinos Tsioufis, Panagiotis Iliakis, and Alexandros Kasiakogias
Abbreviations AT1R AT2R BP HF HFpEF HFrEF LV LVEF MSNA NT-pro-BNP NYHA OMT RNA
Angiotensin II type 1 receptor Angiotensin II type 2 receptor Blood pressure Heart failure Heart failure with preserved ejection fraction Heart failure with reduced ejection fraction Left ventricle Left ventricular ejection fraction Muscle sympathetic nerve activity N-terminal pro-B-type natriuretic peptide New York Heart Association Optimal medical therapy Renal nerve ablation
K. Tsioufis (*) First Cardiology Clinic, National and Kapodistrian University of Athens, Hippokration Hospital, Athens, Greece P. Iliakis · A. Kasiakogias First Cardiology Clinic, Medical School, National and Kapodistrian University of Athens, Hippokration Hospital, Athens, Greece e-mail: [email protected] © Springer Nature Switzerland AG 2019 M. Dorobantu et al. (eds.), Hypertension and Heart Failure, Updates in Hypertension and Cardiovascular Protection, https://doi.org/10.1007/978-3-319-93320-7_24
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24.1 R enal Nerve Ablation: From Pathophysiology to the Patient Autonomic imbalance stands out as a principal pathophysiological pathway that promotes the natural history of the failing heart, and sympathetic activation assessed by circulating norepinephrine levels is associated with worse cardiovascular outcomes [1]. It is clear that sympathetic activity is strongly modulated by the kidney. Specifically, renal afferent arterioles branch from the renal artery and supply the nephrons, playing an important role in the regulation of blood pressure (BP) as a part of the tubuloglomerular feedback mechanism. Renal nerves provide efferent fibers from the brain that decrease renal blood flow and increase sodium retention. When stimulated, renal afferents promote sympathetic efferent activation to the kidney [2]. In heart failure (HF), renal dysfunction associated with a sympathetic overdrive, an increase in the release of renin and vasoconstrictive substances, renal sodium and water retention, and a decrease in renal blood flow is associated with poor prognosis [3]. Well before medical therapy that confronts sympathetic overactivity, such as b-blockers, was even introduced to our pharmacological arsenal, nonselective surgical nerve sympathectomy was performed in the 1950s to treat severe hypertension [4]. Debilitating side effects and the advent of effective drugs led to the practical abandonment of this rather radical procedure. But as there was clear evidence of persistently high rates of cardiovascular disease attributed to uncontrolled and resistant hypertension, as well as limitations of pharmacological therapy such as the lack of patient adherence, side effects, and multidrug interactions, an interventional approach to hypertension based on a solid pathophysiological background was an intriguing idea [5]. Technology played an important role, as well as the knowledge and experience from coronary angiographies that would help develop endovascular catheter
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