Results show favorable impact of renal denervation on BP in hypertension

Decreases in office BP were reported at several time points in a cohort of patients with hypertension who underwent renal denervation in a recent study.

The researchers suggested that despite evidence showing renal denervation lowers BP, the long-term impact of the strategy on muscle sympathetic nerve activity has not been fully described. The current study was an investigation of whether renal denervation has an impact on muscle sympathetic nerve activity over time in a cohort of 35 patients with resistant hypertension.

Clinicians recorded office BP and muscle sympathetic nerve activity at baseline, 3, 6 and 12 months after renal denervation was performed.

The average BP in the cohort was 166 ± 22/88 ± 19 mm Hg. Patients used an average of 4.8 ± 2.1 antihypertensive medications.

At baseline, muscle sympathetic nerve activity in the patient cohort was 51 ± 11 bursts/min, which the researchers reported was approximately two to three times higher than what was reported in the healthy control group.

At 3 months, the mean office systolic and diastolic BP decreased by –12.6 ± 18.3/–6.5 ± 9.2 mm Hg, which was a significant difference (P<.001). The trend toward decrease continued through 6 months (–16.1 ± 25.6/–8.6 ± 12.9 mm Hg) and 12 months (–21.2 ± 29.1/–11.1 ± 12.9 mm Hg; P<.001).

The 3-month reduction in muscle sympathetic nerve activity was –8 ± 12 bursts per minute (P<.01). This trend also continued through 6 (–6 ± 12 bursts per minute) and 12 (–6 ± 11 bursts per minute) months (P<.01).

Even with the progressive decrease in BP over time, the reduction in muscle sympathetic nerve activity was maintained, according to the findings. The researchers did not report similar changes in seven control patients at the 6-month mark.

“These findings confirm previous reports on the favorable effects of [renal denervation] on elevated BP and demonstrate sustained reduction of central sympathetic outflow ≤1-year follow-up in patients with resistant hypertension and high baseline [muscle sympathetic nerve activity],” the researchers concluded. “These observations are compatible with the hypothesis of a substantial contribution of afferent renal nerve signaling to increased BP in resistant hypertension and argue against a relevant reinnervation at 1 year after [the] procedure.”

In an accompanying editorial, Michael J. Joyner, MD, of the department of anesthesiology at the Mayo Clinic in Rochester, Minn., raised the question of whether it is possible to optimize renal denervation in a subset of patients in whom the strategy is most likely to be beneficial, and how the approach can be employed in an environment where clinical centers are becoming devoid of mechanistic clinical physiology capabilities.

“So, perhaps the real question is how best to target the sympathetic nervous system for therapy,” Joyner wrote. “Hering et al have given us hints about who might benefit from such therapy, and they have also demonstrated that in the right set of patients renal denervation offers real promise. For this promise to be realized, the marriage of human physiology and novel cardiovascular therapies needs to be revivified.”

For more information:

Hering D. Hypertension. 2014;doi:10.1161/hypertensionaha.113.03098.

Joyner MJ. Hypertension. 2014;doi:10.1161/hypertensionaha.114.03201.

Disclosure: The researchers report financial disclosures with Abbott Pharmaceuticals, Allergan, BI, Medtronic, Novartis, Pfizer, Servier Australia and Wyeth Pharmaceuticals. Joyner reports financial disclosures with Boston Scientific, CVRX and Medtronic.