PS 14-66 RENAL DENERVATION IN PATIENTS WITH RESISTANT HYPERTENSION AND DIABETES MELLITUS TYPE 2 LEADS TO DECREASE IN INFLAMMATORY MARKERS: A 12- MONTH FOLLOW-UP

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Abstract

Objective:

Chronic activation of the sympathetic nervous system (SNS) is causative in the pathophysiology of hypertension. Besides this, SNS activates immune system. Inflammation, and hypertension may interact and treatment of one of the two conditions could have some impact on the other. Renal denervation (RDN) is a promising treatment for hypertension. Beforehand, we hypothesized that a reduction of SNS following RDN may lead to a decreased inflammatory cytokines. The aim of this study was to evaluate the dynamics of TNF-α and interleukin-1β after catheter-based RDN in patients with resistant hypertension and diabetes mellitus type 2.

Design and Method:

Thirty two patients with true resistant hypertension and type 2 diabetes mellitus were included in single-arm prospective interventional study (detailed protocol was published on ClinicalTrial.gov, number NCT01499810). Office blood pressure (BP) measurement, ambulatory 24-h BP, assessments levels of inflammatory cytokines (TNF-α, IL-1β) were performed at baseline and 12 months after RDN. On average, patients were taking 4 (3–6) antihypertensive drugs. None of the patients changed the antihypertensive treatments during follow-up. A 12 months follow-up was completed by 26 patients (43–75 years old, mean aged 59.3 ± 7.9 years, 14 male).

Results:

RDN reduced both systolic/diastolic office and 24-hour BP by −31.7/-12.8 mmHg, P > 0.01 for office BP and −13.4/-10.0 mmHg, P < 0.01, for 24-h BP. After RDN there was a decrease both TNF- α levels (from 2.21 (1.54–3.65) to 1.4 (1.11–1.47 pg/mL), p = 0.007) and IL-1β level (from 1.27 ± 0.60 to 1.00 ± 0.51, P = 0.02). There were no direct relationships between decrease in these cytokines and BP reduction.

Conclusions:

Renal denervation may reduce activity of chronic inflammatory process and therefore may have potential benefit of inflammation inhibition in patients with resistant hypertension and diabetes mellitus type 2.

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