MD Conference Express EASD 2012 - (Page 32)
n sElEcTEd UpdATEs On REnAl dEnERvATiOn
EASD/ESC Symposium: Renal Denervation
Written by Maria Vinall
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]. rHT is believed to be caused by over- and chronic activation of the sympathetic nervous system. 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. Michael Böhm, MD, Universitätsklinikum des Saarlandes, Saarbrücken, Germany, discussed the impact of renal denervation as a treatment for hypertension. A better understanding of renal nerve anatomy has enabled the use of a catheter-based radio frequency approach for the ablation of nerves using a standard interventional technique. The Renal Denervation in Patients with Refractory Hypertension [Symplicity HTN-1; NCT00664638] study established the safety and proof-ofprinciple for catheter-based renal sympathetic denervation in patients with rHT. In the study, 95% of patients experienced significant reductions in BP, which were sustained for 24 months without significant adverse events. There was no evidence of the development of tolerance or re-enervation. In the Symplicity HTN-2 [NCT00888433] study, the primary endpoint was change in seated officebased systolic BP (SBP). At 6 months, 41 (84%) of 49 patients who underwent renal denervation had a reduction in SBP of 10 mm Hg or more compared with 18 (35%) of 51 controls (p<0.0001) [Symplicity HTN-2 Investigators. Lancet 2010]. In an extension of the Symplicity HTN-2 study, investigators assessed the effects of renal denervation on cardiorespiratory response to exercise. The results showed that BP during exercise was reduced, heart rate at rest decreased, and heart rate recovery improved (Figure 1) [Ukena C et al. J Am Coll Cardiol 2011]. In addition to its known effect on BP, renal denervation has also been shown to significantly reduce left ventricular mass and improve diastolic function, which might have important prognostic implications in patients with resistant hypertension at high cardiovascular risk [Brandt MC et al. J Am Coll Cardiol 2012]. Luis M. Ruilope, MD, Hospital 12 de Octubre, Madrid, Spain, discussed the prevalence, treatment, and risk factors for rHT.
Figure 1. Heart Rate Change During Exercise.
ns 50
Change of Heaart Rate (bpm)
Baseline 3 months after RD ns
40
30 ns
ns
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0
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RD=renal denervation. Reprinted from Ukena C et al. Cardiorespiratory response to exercise after renal sympathetic denervation in patients with resistant hypertension. J Am Coll Cardiol. 2011 Sep 6;58(11):1176-82 , with permission from Elsevier.
Data from the National Health and Nutrition Examination Survey [NHANES] found that rHT increased from 15.9% (1988 to 2004) to 28.0% (2005 to 2008) of treated patients (p<0.001) [Egan BM et al. Circulation 2011]. However, another study found the percentage to be as low as 12.2%, of which only 7.6% was true rHT (the remaining 4.6% was “white-coat” hypertension) [de la Sierra A et al. Hypertension 2011]. Part of the problem with identifying rHT is how BP is measured. The best method for a correct diagnosis is likely 24-hour ambulatory BP monitoring (ABPM), particularly in diabetic patients [Gorostidi M et al. Hypertens Res 2011]. Twenty-four-hour ABPM can identify variations in BP levels throughout the day and eliminate the white-coat effect. High ABPM values are associated with worse prognosis in rHT patients, as well as higher incidence of cardiovascular events. rHT is almost always multifactorial in etiology. In addition to obesity and diabetes, excessive salt consumption is an important contributor, hence strategies to reduce dietary salt intake should be part of the overall treatment plan [Pimenta E et al. Hypertension 2009]. Secondary causes include obstructive sleep apnea (OSA), renal parenchymal disease, primary aldosteronism, and renal artery stenosis [Calhoun DA et al. Hypertension 2008]. Once it has been determined that the patient has truly resistant hypertension (pseudoresistance has been ruled
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November 2012
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Table of Contents for the Digital Edition of MD Conference Express EASD 2012
MD Conference Express EASD 2012
Contents
Understanding Incretin Hormone Action and the Treatment of Diabetes
New ADA/EASD Guidelines Focus on Patient-Centered Care
ORIGIN Trial: Insulin Glargine and n-3 Fatty Acids Fail to Reduce CV Events in Diabetic Patients
Exenatide Once Weekly Sustained Improvement in Glycemic Control with Weight Loss Through 4 Years
DiaPep277® Shows Promise as a Therapeutic Strategy for T1DM
Linagliptin Proves Safe and Effective as Add-on Therapy to Basal Insulin
12-Week Treatment with LY2409021 Significantly Lowers HbA1C and Is Well Tolerated in Patients with T2DM
Insulin Degludec Is Superior to Sitagliptin in Improving Glycemic Control in Uncontrolled Patients with Type 2 Diabetes on Oral Agents
Dapagliflozin Does Not Impact Renal Function in Patients with T2DM
Population-Based Screening for T2DM:The ADDITION-Cambridge Trial
The Challenges of Pharmaceutical Management of Painful Diabetic Peripheral Neuropathy
Enterovirus Infection
Novel Oral Agents
GLP-1
Genetics
Renal Denervation
Hypertension and Renal Function Are Risk Factors for CAD in T1DM
MD Conference Express EASD 2012
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