Percutaneous renal denervation treatment was significantly less effective at lowering 24-h blood pressure in treatment-resistant hypertensive patients when therapy was applied conventionally in the trunk of renal artery as compared with when applied to distal segmental branches. This observation is in accordance with previous surgical and anatomical findings showing that most renal nerve fibers are distant from the lumen proximally and become available for endovascular treatment mainly in the distal portion of the vessel.
The overall estimate of baseline SBP and β-AR of EM in patients with RH could determine the expediency of the RSD procedure in order to lower BP. The proposed procedure can optimize the selection of patients and enhance the efficiency of RSD in the treatment of RH.
Hypertension remains the main risk factor of cardiovascular diseases despite the improvement of pharmacotherapy methods. This provides rationale for an in-depth study of pathogenetic mechanisms and development of new methods for the treatment of hypertension. There is increasingly more evidence for the essential role of immune-inflammatory disorders in the pathogenesis of hypertension. The article reviews the current state of knowledge on this problem. The authors provide a detailed analysis of the studies focusing on the role of abnormal factors of cellular immunity essentially associated with cell abilities to produce pro-inflammatory cytokines. Particular attention is paid to the effects of state-of-the-art methods of endovascular treatment on the changes in degree of severity of immune-inflammatory processes in patients with pharmacotherapy resistant form of hypertension. Possible mechanisms of the therapeutic action of renal denervation and the prospects for further clinical use of this method are discussed.
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.
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