Possible mechanisms of renal denervation long-term cardiac effects

Abstract

Background.The renin-angiotensin-aldosterone system (RAAS) plays a key role in target organ damage in arterial hypertension (HTN), initiating the development of left ventricular hypertrophy (LVH), as well as the heart and vascular wall fibrosis and remodeling. In addition, one of the mechanisms of the cardiovascular disease progression is the angiotensin II-induced inflammation.Objective.To study the changes in renin, aldosterone and high-sensitive C‑reactive protein (CRP) levels two years after sympathetic renal denervation (RDN), to compare these changes with antihypertensive efficacy of the intervention and LVH regression.Design and methods.We included 77 patients with drug-resistant hypertension in the absence of contraindications to renal denervation. All patients underwent renal radiofrequency ablation. The active renin, aldosterone and a high-sensitive CRP concentrations assessment, 24‑hour blood pressure (BP) measurement and echocardiography were performed before, at 6 months, one and two years after the intervention.Results.There was a gradual decrease in CRP levels (the difference was significant after 6 months), aldosterone (significant two years after surgical treatment), and active renin (the difference was the most pronounced after one year). At all follow-up assessments, plasma renin activity correlated with left ventricular mass. At the same time, there were no significant differences between responders and non-responders.Conclusions.RDN leads to a RAAS activity attenuation, manifested by the decrease in both renin and aldosterone and CRP, probably due to angiotensin II proinflammatory effects reduction. Given these effects are long-term, correlate with LVH degree and unrelated to the BP lowering, a direct cardioprotective effect of renal denervation should be considered.