Key result
Endovascular baroreflex amplification did not significantly decrease muscle sympathetic nerve activity burst frequency (mean change -4.1 bursts/min) at 3 months in patients with resistant hypertension.
Why the study?
First-in-human studies suggest endovascular baroreflex amplification lowers blood pressure, but the effects on muscle sympathetic nerve activity and baroreceptor sensitivity required exploration to understand potential mechanisms.
Does endovascular baroreflex amplification reduce muscle sympathetic nerve activity in patients with resistant hypertension?
Observational (n=14)
Open-label
No
Does endovascular baroreflex amplification reduce muscle sympathetic nerve activity in patients with resistant hypertension?
Mean Difference: -4.1 (95% CI -12.2–4)
Absolute Event Rate: 34.2% vs 38.3%
p-value: p=0.284
Endovascular baroreflex amplification did not significantly reduce muscle sympathetic nerve activity or impair baroreflex function at 3 months in patients with resistant hypertension.
EVBA did not lower MSNA in resistant hypertension; leaves open alternative mechanisms for observed BP reduction.
BACKGROUND: First in human studies suggest that endovascular baroreflex amplification (EVBA) lowers blood pressure (BP). To explore potential mechanisms for BP reduction, this study examines the effects of EVBA on muscle sympathetic nerve activity (MSNA) and baroreceptor sensitivity (BRS). METHODS: In a single-center sub-study of the CALM-DIEM study (Controlling And Lowering blood pressure with the MobiusHD-Defining Efficacy Markers), 14 patients with resistant hypertension were treated with EVBA. Microneurography and non-invasive continuous BP measurements were performed at baseline and three months after MobiusHD implantation. The primary outcome was change in MSNA. Secondary outcomes were change in baroreflex sensitivity (BRS), cardiovascular responses to a sympathetic stimulus, BP, heart rate (HR) and heart rate variability (HRV). RESULTS: The primary endpoint was obtained in 10 of 14 patients enrolled in the sub-study. MSNA burst frequency and burst incidence decreased in 6 of 10 patients: mean change -4.1 bursts/min (95% confidence interval -12.2 to 4.0) and -3.8 bursts/100 heartbeats (-15.2 to 7.7). MSNA spike frequency and spike count decreased in 8 of 10 patients: mean change -2.8 spikes/sec (-7.3 to 1.8) and -3.0 spikes/heartbeat (-6.1 to 0.1). Change in MSNA and BP were not correlated. Office BP decreased by -14/-6 mmHg (-27 to -2/-15 to 3). We observed a trend towards decreased HR (-5 bpm, -10 to 1) and increased total power HRV (623 msec2, 78 to 1168). In contrast, BRS and cardiovascular responses remained unchanged after EVBA. CONCLUSIONS: In this proof-of-principle study, EVBA did not significantly decrease MSNA in patients with resistant hypertension. EVBA did not impair baroreflex function. TRIAL REGISTRATION: Clinical trial registration at NCT02827032.
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Kleef et al. (2021) conducted an observational in Resistant hypertension (n=14). Endovascular baroreflex amplification (MobiusHD) vs. Baseline was evaluated on Change in muscle sympathetic nerve activity (burst frequency) (MD -4.1 bursts/min, 95% CI -12.2 to 4.0, p=0.284). Endovascular baroreflex amplification did not significantly decrease muscle sympathetic nerve activity burst frequency (mean change -4.1 bursts/min) at 3 months in patients with resistant hypertension.
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