Valsartan reduces arterial stiffness along with level of soluble ST2 independently of blood pressure changes

Autor: A Tomasik, E Kozielska, D Kawecki, W Jachec, C Wojciechowska
Rok vydání: 2022
Předmět:
Zdroj: European Heart Journal. 43
ISSN: 1522-9645
0195-668X
DOI: 10.1093/eurheartj/ehac544.2205
Popis: Introduction Arterial stiffness is one of end-organ damage signs in patients with arterial hypertension. Carotid femoral pulse wave velocity (cfPWV) is a clinical measure of arterial stiffness and its values above 10 m/sec are associated with increased cardiovascular risk. Soluble ST2 is a cytokine involved in fibrotic processes. There is paucity of data on the association between sST2, arterial stiffness, and effect of valsartan on these parameters. Objectives The aim of the study was to assess the effect of valsartan on arterial stiffness and level of soluble ST2 over a 12-month long treatment. Methods This was a randomized, blinded, placebo controlled single center study. There was a 24-hour-long wash-out period from angiotensin converting enzyme inhibitors (ACEI) and other than valsartan, angiotensin receptor blockers ARB (previous use of valsartan was an exclusion criterion). Drugs other than ACEI and ARB were allowed in follow-up to control blood pressure. CfPWV was assessed at baseline and at 12 months using applanation tonometry. Soluble ST2 was measured with lateral flow cassette-based immunofluorescent assay. We present the data for 28 placebo patients (Plac) and 60 valsartan patients (Vals). Results Patients from both groups have had comparable peripheral and central blood pressures. CfPWV has risen in Plac by 6.2% and has fallen by 6.2% in Vals (P=0.01) over 12 months. Soluble ST2 has risen in Plac by 9.4% and has fallen by 43.3% in Vals (P=0.001) over 12 months. Conclusion Valsartan has positive effect on improvement of arterial stiffness. Decrease in soluble ST2 concentration may help explain the alternative mechanism for protective role of valsartan. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): Medical University of Silesia
Databáze: OpenAIRE