Key result
In patients with metabolic syndrome, renal denervation reduced resting muscle sympathetic nerve activity from 55 to 46 bursts per minute (P=0.0008) at 3 months, with no significant change in HOMA-IR.
Why the study?
Does multielectrode renal denervation reduce sympathetic nerve activity and insulin resistance in patients with metabolic syndrome and hypertension?
RCT (n=17)
3:1 ratio
Does multielectrode renal denervation reduce sympathetic nerve activity and insulin resistance in patients with metabolic syndrome and hypertension?
In a small pilot study, renal denervation reduced sympathetic nerve activity and blood pressure in patients with metabolic syndrome, but did not improve insulin resistance at 3 months.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for renal denervation in metabolic syndrome; leaves open effects on insulin resistance and clinical outcomes.
OBJECTIVE: This study aimed to investigate the effects of renal denervation (RDN) on sympathetic nerve activity and insulin resistance in patients with metabolic syndrome. METHODS: Seventeen patients fulfilled at least four of five criteria for metabolic syndrome and under stable use of at least two antihypertensive drugs were randomized in 3 : 1 ratio to RDN (n = 13, 12 men, age: 58 ± 7 years) and control groups (n = 4, three men, age: 60 ± 5 years) and followed up for 3 months. Muscle sympathetic nerve activity (MSNA) at rest and during standard 75 g oral glucose tolerance test (OGTT) was assessed. RESULTS: In the RDN group, office and average 24-h blood pressures reduced by 16 ± 21/10 ± 11 mmHg (P = 0.01/0.007) and 14 ± 16/5 ± 8 mmHg (P = 0.008/0.03) respectively; waist circumference reduced by 3.1 ± 3.6 cm (P = 0.008); and resting MSNA reduced from 55 ± 9 bursts per minute to 46 ± 8 bursts per minute (P = 0.0008) at month 3 post-RDN. During OGTT, although blunted MSNA responses were noted at baseline throughout the 120-min test, improved MSNA responses with burst frequency increased to 52 ± 8 bursts per minute (P < 0.001 vs. the resting MSNA, n = 13) at 30 min and to 54 ± 8 bursts per minute (P = 0.004 vs. the resting MSNA, n = 10) at 120 min and were observed at month 3 post-RDN. No such improvements were observed in the controls. No significant change was observed in the HOMA-IR in both groups at month 3. CONCLUSION: In this pilot study of patients with metabolic syndrome and associated hypertension, RDN reduced elevated sympathetic nerve activity and restored the normal neural response to oral glucose loading.
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Tsioufis et al. (2017) conducted an RCT in Metabolic syndrome (n=17). Multielectrode renal denervation vs. Control was evaluated on Resting muscle sympathetic nerve activity (MSNA) (p=0.0008). In patients with metabolic syndrome, renal denervation reduced resting muscle sympathetic nerve activity from 55 to 46 bursts per minute (P=0.0008) at 3 months, with no significant change in HOMA-IR.
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