Meeting Highlights


Effects of Renal Denervation on Endothelial Function, and Inflammatory and Metabolic Markers

Presented by Nina Eikelis, Australia

It has been shown that renal denervation (RDN; also called renal nerve ablation) can lower blood pressure (BP) in patients with resistant hypertension and that this effect can be maintained to more than 24 months [Symplicity HTN-1 Investigators. Hypertens 2011]. However, there are few data about the effect of RDN on organs and the sympathetic nervous system. There is an independent association between hypertension and inflammatory markers, but it is unknown whether treatment of one of these conditions impacts the other and whether lowering BP can also reduce vascular inflammation.

Nina Eikelis, MD, Baker IDI Heart & Diabetes Institute, Melbourne, Australia, presented data from a study to determine whether RDN has an effect on inflammation and endothelial function in patients with resistant hypertension.

Assessments were conducted at baseline and at 3 months after RDN in 63 patients with resistant hypertension (male, 64%; mean age, 61 years). At baseline, patients had a high body mass index (BMI; 32.3 kg/m2), and were taking an average of 4.6 antihypertensive medications.

BP was significantly reduced from baseline (169/90 mmHg) to 3 months (156/84 mmHg; p<0.001), but there was no significant change in HR.

There were no significant changes from baseline to 3 months in the reactive hyperemia index, which is a measure of endothelial function, and the augmentation index, which is an indirect measure of arterial stiffness.

There were also no significant differences from baseline to 3 months in plasma renin activity, which is an indirect measure of angiotensin I production, and the level of the inflammatory markers (Figure 1).

Leptin levels did not significantly change from baseline to 3 months. The levels of nonesterified fatty acid (NEFA), a metabolic biomarker, were significantly reduced (from 1 mEq/L to 0.4 mEq/L; p<0.001), but there were no significant reductions in body weight, BMI, or waist-to-hip ratio.

In explaining the high baseline NEFA levels in this patient population that has resistant hypertension and high BMI, it should be noted that NEFA has been implicated in elevated BP, particularly in animal studies [Sarafidis PA, Bakris GL. J Hum Hypertens 2007]. Furthermore, the levels of NEFA tend to be higher in overweight and obese persons as it is primarily released from adipose tissue [Heptulla R et al. J Clin Endiocrinol Metab 2001; Koutsari C, Jensen MD. J Lipid Res 2006].

NEFA and insulin levels seem to have an inverse relationship, said Prof. Eikelis. Therefore, it is no perhaps surprise that in the present study, NEFA levels significantly decreased while insulin levels significant increased from baseline (21 uU/mL) to 3 months (28 uU/mL; p<0.01).

Whole body noradrenaline spillover, a measure of whole body sympathetic activity, did not change significantly over the 3 months. However, Prof. Eikelis noted that sympathetic responses are regionalized and global measures lack precision. When looking at regional sympathetic activity, there were significant reductions from baseline to 3 months and to 6 weeks in muscle and kidney sympathetic activity, respectively (Figures 2 and Figure 3; p<0.05 for both).

Study findings show that while RDN led to significant reductions in office BP, and muscle and renal sympathetic activity, there were no significant changes in endothelial function and inflammatory markers. There was a significant reduction in NEFA, without changes in body weight, and this may be an indirect measure showing reduction or withdrawal of nervous activity from adipose tissue.