Abstract

Abstract Background and Aims Leptin is mainly produced by adipose tissue and has hypertensinogenic properties. In patients with arterial hypertension, plasma concentration of leptin is higher than in healthy subjects. Percutaneous ablation of the sympathetic nervous system fibers located in the wall of the renal arteries by radio frequency waves (renal denervation - RDN), was introduced as a method of invasive treatment of resistant arterial hypertension. The aim of this single center, interventional, clinical study was to assess the effect of RDN on the plasma leptin concentration in patients with resistant arterial hypertension. Method Eighteen patients (9 women, 9 men) aged 53.2±6.5 years with resistant hypertension who underwent RDN using Simplicity catheters (Medtronic, Inc., Northridge, CA) were enrolled in the study. Plasma leptin concentration was determined using the Human Leptin RIA HL-81K (Linco Research, Inc., Missouri, USA) before RDN denervation and 6 months after RDN. Additionally, patients were divided into two subgroups: responders (systolic and diastolic blood pressure - BP reduction 6 months after RDN >25 mmHg and >12 mmHg, respectively; n=9) and low responders (systolic and diastolic BP reduction 6 months after RDN ≤25 mmHg and ≤12 mmHg, respectively; n=9). Results Systolic and diastolic BP was significantly reduced after RDN (196.6±28.2 and 162.9±15.6; p<0.001 and 117.9±26.4 and 90.7±8.6 mmHg; p<0.001, respectively). Body mass index (BMI) before RDN and 6 months after RDN was similar (31.0±4.4 and 31.3±4.4 kg/m2; P = .8, respectively). Mean plasma leptin concentration before RDN and 6 months after RDN did not change significantly in the entire studied group (27.2±14.3 and 24.6±13.1 [ng/mL], NS), as well as both in responders (29.9±14.4 and 28.2±12.9 [ng/mL, NS) and low-responders subgroups (24.4±14.7 and 21.0±12.9 [ng/mL], NS), respectively. Conclusion Renal denervation is effective in the treatment of patients with resistant hypertension, however this effect is not mediated by the influence on plasma leptin concentration.

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