Impaired cardiac baroreflex sensitivity predicts response to renal sympathetic denervation

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By Axel Bauer

Christine S Zuern, Abteilung Innere Medizin III, Department of Cardiology, Eberhard-Karls-Universität Tübingen, Tübingen, Germany, and others report in a study published ahead of print in the Journal of the American College of Cardiology that impaired cardiac baroreflex sensitivity could be used to identify patients who will respond to renal denervation. Study author Axel Bauer describes the main findings of the study.


Renal denervation effectively reduces efferent and central sympathetic tone, which is a key factor in the pathophysiology of arterial hypertension. However, genesis of arterial hypertension is multifactorial, making it unlikely that every patient benefits equally from the intervention. At the same time, it is a new invasive procedure with the inherent risk of side-effects—little is known about the safety of the procedure in the long term. Therefore, identification of patients who benefit the most from renal denervation and, equally importantly, identification of patients who do not is of great clinical importance. Previous studies only identified increased pre-procedural baseline arterial blood pressure as predictor of response to renal denervation.


It is plausible to assume that renal denervation is most effective in patients with increased baseline sympathetic activity. In our study, we therefore used baroreflex sensitivity as a surrogate measure of sympathetic activity and hypothesised that patients with impaired baroreflex sensitivity would benefit the most from renal denervation. We studied 50 consecutive patients (age 60±2 years) with treatment-resistant arterial hypertension (mean 24-hour systolic blood pressure: 157±22mmHg despite treatment with 5.4±0.2 antihypertensive drugs) who underwent renal denervation at our institution.

Baroreflex sensitivity was assessed at baseline from non-invasive 30-minute recordings of continuous arterial blood pressure (Finapres Medical Systems) and high-resolution ECGs. We defined response to renal denervation as reduction of mean systolic blood pressure 10mmHg or more on ambulatory blood pressure monitoring six months after renal denervation. In contrast to office-based blood pressure measurements, which have been used in most studies on renal denervation, ambulatory blood pressure monitoring reduces the “white coat” effect, has a greater reproducibility and yields more accurate prognostic information.


Six months after renal denervation, we noted a significant reduction of mean systolic blood pressure on ambulatory blood pressure monitoring from 157±22mmHg to 149±20mmHg (p=0.003). Baroreflex sensitivity was highly significantly correlated with reduction of mean systolic blood pressure (p<0.001). Patients with impaired baroreflex sensitivity showed the most pronounced reductions of systolic blood pressure. Twenty-six of the 50 patients were classified as responders (ie. ≥10mmHg reduction of systolic blood pressure on ambulatory blood pressure monitoring). Also, baroreflex sensitivity was lower to a highly significant extent in patients who responded to renal denervation compared with those who did not (0.16±0.75ms/mmHg vs. 1.54±1.73ms/mmHg in responders and non-responders, respectively; p<0.001). Elevated baseline systolic blood pressure and increased body mass index, which is known to be associated with increased sympathetic activity, were the only other factors that were associated with response to renal denervation in our patients. Multivariable analysis, however, identified impaired baroreflex sensitivity as the strongest independent predictor of response to renal denervation.


The findings of the study indicate that assessment of baroreflex sensitivity might help to identify patients with treatment-resistant arterial hypertension who benefit from renal denervation. Assessment of baroreflex sensitivity is non-invasive and inexpensive but requires certain technical equipment. However, these findings need to be validated in independent and larger patient cohorts.


Axel Bauer is at Abteilung für Kardiologie und Herzkreislauferkrankungen, Eberhard-Karls-Universität, Tübingen, Germany

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