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.
Patients with resistant arterial hypertension have a high prevalence of cardiac pathology. In particular, left ventricular hypertrophy and reduced coronary reserve play independent role in determining the risk of cardiovascular complications. Diagnostic approaches to their detection are currently represented by a wide range of highly informative studies using modern ultrasound equipment, magnetic resonance imaging, computed tomography scanner, and gamma camera. The active study of the involvement of the cascade of pathophysiological mechanisms in the development of cardiac changes in hypertension allows not only to identify the factors associated with the severity of the lesion, but also to find new application points for the cardioprotection and to reduce cardiovascular risk. Along with the pharmacological capabilities, the renal denervation method is currently under active study. Despite high variability of the results and their poor predictability, a number of studies show the efficiency of this method in correcting the structural and functional changes in the heart, which is of important prognostic value for resistant hypertension.
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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