Denervation of the renal arteries in metabolic syndrome : The DREAMS-study

Chronic elevation of sympathetic nervous system is a key factor in metabolic syndrome. Because renal denervation (RDN) is thought to modulate sympathetic activity, we performed the Denervation of the Renal Arteries in Metabolic Syndrome (DREAMS)-study to investigate the effects of RDN on insulin sensitivity and blood pressure (BP) in patients with metabolic syndrome. Twenty-nine patients fulfilling the criteria for metabolic syndrome and who used a maximum of 1 antihypertensive or 1 antidiabetic drug or 1 of both gave informed consent and were treated by RDN. Glucose tolerance tests and 24-hour ambulatory BP measurements were performed at baseline, at 6 and 12 months of follow-up. Moreover, we performed self-monitored BP measurements at home every month. To assess sympathetic activity, we performed muscle sympathetic nerve activity and heart rate variability measurements at baseline and follow-up. The majority of the included patients was men (57%), mean body mass index was 31±5 kg/m2. Median insulin sensitivity as assessed by the Simple Index assessing Insulin Sensitivity oral glucose tolerance test did not change at 6- and 12-month follow-up (P=0.60 and P=0.77, respectively). Mean 24-hour BP decreased by 6±12/5±7 mm Hg 12 months after RDN (P=0.04/0.01). However, self-monitored BP measurements data showed no reduction over time. Measurements of sympathetic activity showed no reduction in systemic sympathetic activity. In conclusion, RDN did not lead to a significant improvement of insulin sensitivity ≤12 months after treatment. Although a significant reduction in ambulatory BP was observed in this nearly drug-naïve population, the self-monitored BP measurements data suggest that this may be explained by regression to the mean. Moreover, no effect in systemic sympathetic activity was observed

Denervation of the renal arteries in metabolic syndrome : The DREAMS-study

Chronic elevation of sympathetic nervous system is a key factor in metabolic syndrome. Because renal denervation (RDN) is thought to modulate sympathetic activity, we performed the Denervation of the Renal Arteries in Metabolic Syndrome (DREAMS)-study to investigate the effects of RDN on insulin sensitivity and blood pressure (BP) in patients with metabolic syndrome. Twenty-nine patients fulfilling the criteria for metabolic syndrome and who used a maximum of 1 antihypertensive or 1 antidiabetic drug or 1 of both gave informed consent and were treated by RDN. Glucose tolerance tests and 24-hour ambulatory BP measurements were performed at baseline, at 6 and 12 months of follow-up. Moreover, we performed self-monitored BP measurements at home every month. To assess sympathetic activity, we performed muscle sympathetic nerve activity and heart rate variability measurements at baseline and follow-up. The majority of the included patients was men (57%), mean body mass index was 31±5 kg/m2. Median insulin sensitivity as assessed by the Simple Index assessing Insulin Sensitivity oral glucose tolerance test did not change at 6- and 12-month follow-up (P=0.60 and P=0.77, respectively). Mean 24-hour BP decreased by 6±12/5±7 mm Hg 12 months after RDN (P=0.04/0.01). However, self-monitored BP measurements data showed no reduction over time. Measurements of sympathetic activity showed no reduction in systemic sympathetic activity. In conclusion, RDN did not lead to a significant improvement of insulin sensitivity ≤12 months after treatment. Although a significant reduction in ambulatory BP was observed in this nearly drug-naïve population, the self-monitored BP measurements data suggest that this may be explained by regression to the mean. Moreover, no effect in systemic sympathetic activity was observed

Effects of renal denervation on end organ damage in hypertensive patients

Background: Renal denervation (RDN) is believed to reduce sympathetic nerve activity and is a potential treatment for resistant hypertension. The present study investigated the effects of RDN on end organ damage (EOD). Design: The present study was a prospective cohort study (registered as NCT01427049). Methods: Uncontrolled hypertensive patients underwent a work-up prior to and one year after RDN. Cardiac magnetic resonance (CMR) imaging was used to determine left ventricular (LV)-mass; pulse wave analysis and pulse wave velocity (PWV) were used for evaluation of central blood pressure (BP) and arterial stiffness and 24-hour urine was collected for assessment of urinary albumin excretion. The 24-hour ambulatory BP measurement (ABPM) was used to evaluate the effect of RDN on BP. Results: Fifty-four patients gave informed consent for study participation. Mean age was 58±10 years, 50% were male. One year after RDN, mean ABPM decreased by 7±18/5±11mm Hg (p=0.01/p&0.01). In the patients followed-up in a standardised fashion ABPM decreased by 5±18/4±12mm Hg (n=34; p=0.11/p=0.09). Mean body surface area indexed LV-mass decreased by 3.3±11.5 g/m2 (corresponding to a 3±11% reduction; p=0.09). PWV increased by 2.9 (-2.2 to 6.1) m/s (p=0.04). Augmentation index corrected for 75 beats per min did not change (median increase 3.0 (-7 to 17) mm Hg; p=0.89). Urinary albumin excretion did not change during follow-up (mean decrease 10±117 mg/ 24 hour; p=0.61). Conclusion: In the current study, we observed a modest effect from renal denervation. Moreover, RDN did not result in a statistical significant effect on end organ damage 12 months after treatment