Open AccessPositive effects of renal denervation on markers of cardiovascular inflammation and left ventricular mass. 24-months follow-up
Author(s) -
E. Sitkova,
V. Mordovin,
S. Pekarskiy,
T. Ripp,
Tamara Ryabova,
A. Falkovskaya,
V. Lichikaki,
I. Zyubanova,
A. Baev,
А. М. Гусакова
Publication year - 2021
Publication title -
kardiovaskulârnaâ terapiâ i profilaktika
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.158
H-Index - 16
eISSN - 2619-0125
pISSN - 1728-8800
DOI - 10.15829/1728-8800-2021-2678
Subject(s) - medicine , interventricular septum , left ventricular hypertrophy , cardiology , blood pressure , interleukin 6 , inflammation , denervation , muscle hypertrophy , c reactive protein , systemic inflammation , body mass index , gastroenterology , ventricle
Aim. To study the long-term effect of renal denervation (RDN) on left ventricular mass (LVM) and inflammatory markers in resistant hypertensive patients. Material and methods. Forty-one patients with resistant hypertension and 24-h blood pressure (BP) 158,7±15,8/87,3+14,6 mmHg, aged 56,6+10,2 years, were enrolled in the study and undergone RDN. Mean 24-h BP, left ventricular mass (transthoracic echocardiography), high sensitivity C-reactive protein (hsCRP), interleukin- 1β (IL1β), IL-6, IL-10) and tumor necrosis factor alpha (TNF- α) were assessed at baseline and 2 years after the RDN. Results. A baseline prevalence of left ventricular hypertrophy (LVH) was 90,2%. Two years after RDN LVM and interventricular septum (IVS) decreased significantly (p 0 g) was documented in 24 patients. The regression of LVM was accompanied by a significant decrease in levels of inflammatory markers — hsCRP by 38,3% (p=0,031), TNF-α by 60,7% (p=0,009), IL- 1β — by 71,1% (p=0,001), and IL-10 by 58,2% (p=0,001). In patients in the absence of LVM regression only TNF-α decreased significantly (-68,8%, p=0,001). There was no correlation between changes of LVM and the inflammatory markers at 24 months after RDN. Conclusion. The RDN in RH patients may have long-term cardioprotective effect in terms of significant regress of LVH, which may be partly attributed to the regress in systemic or myocardial inflammation.