AbstractBackground: Renal denervation (RDN) is an endovascular ablation technique for the treatment of resistant hypertension through disruption of the afferent and efferent renal nerves, thereby abolishing the feedback loop which drives increased sympathetic nerve activity and hypertension. This study aimed to develop measures of technical efficacy for RDN and to identify parameters to guide patient selection for this invasive therapy.
Methods: Autonomic profiling, including measurement of office and ambulatory BP, muscle sympathetic nerve activity (MSNA), heart rate variability, sympathovascular transduction, baroreflex sensitivity (BRS), chemoreflex sensitivity, and markers of inflammation, was carried out at 0,1,3,6 and 12 months, with quantification of aortic distensibility, left ventricular mass and function and cerebral blood flow at baseline and 6 months post-RDN. Procedural success was assessed through abolition of the reflex systemic BP response to intra-renal adenosine infusion (afferent nerves) and of the reflex reduction in renal blood flow in response to a handgrip stressor (efferent nerves).
Results: 18 participants (office BP 192 ± 21/105 ± 23 mmHg, 5.2 ± 1.8 antihypertensive medications) underwent RDN. Office SBP (oSBP) reduced by 16 ± 9mmHg (n=18, p=0.10) and 26 ± 8 mmHg (n=17, p=0.005) at 6 and 12 months post-RDN, respectively. MSNA incidence did not change following RDN (n=11, 61 ± 7 bursts/100heartbeats versus 66 ± 5 bursts/100heartbeats, p=0.47). Baseline oSBP (n=18, R=-0.61, p=0.01) and spontaneous sympathetic BRS (n=13, R=0.56, p=0.045) correlated with the change in oSBP post-RDN. Post-RDN non-responders had an increase in renal vascular resistance not seen in responders (n=7 arteries; 17 ± 5%, p=0.01, n=6 arteries; -9 ± 12%, p=0.49, respectively).
Conclusions: These preliminary studies suggest that patients with a higher office SBP and greater spontaneous sympathetic BRS may respond to RDN, and that an inability to increase renal vascular resistance with handgrip stress after denervation is indicative of disruption of the renal sympathetic nerves.
|Date of Award||23 Jan 2019|
|Supervisor||Julian Paton (Supervisor) & Andreas Baumbach (Supervisor)|