Vascular calcification and fibroblast growth factor in resistant hypertension

Abstract

Background . Pathological vascular calcification in hypertension (HTN) is studied worldwide. The relationship between endothelial dysfunction (ED) and vascular wall calcification in HTN has been demonstrated, and an increase in the level of fibroblast growth factor (FGF23) is considered one of the contributing factors. The aim of the study was to assess the incidence and severity of thoracic aortic calcification, and its relationship with fibroblast growth factor and ED in patients with resistant HTN. Design and methods . Ninety-two patients with resistant HTN were included. All of them underwent: 24-hour blood pressure monitoring (ABPM), the assessment ofendothelial function, the thoracic aortic calcium (TAC) index using multispiral computed tomography, and the level of FGF23. Results . According to the results of ABPM, patients were divided into group 1 with controlled HTN (n = 44) and group 2 with uncontrolled (n = 48) resistant HTN. In the 2nd group, there was an increase in TAC and ED, in both groups, changes in the blood flow velocity were recorded. There were no significant differences in FGF23 levels between the groups. We found a positive relationship between TAC and pulse pressure according to the results of ABPM (r = 0,49, p = 0,007), HTN duration (r = 0,68, p = 0,04) and a negative relationship with the duration of regular antihypertensive therapy (r = –0,33, p = 0,02). In addition, participants with higher FGF23 levels were older (r = 0,663, p = 0,006) and had a longer history of HTN (r = 0,57, p = 0,03). Conclusions . In patients with resistant HTN, ED and calcification of the thoracic aorta are more pronounced when the target blood pressure level is not achieved. The level of FGF23 is associated with an increase in the resistance indices assessed by dopplerography of the brachial artery and the severity of calcification of the thoracic aorta.