Transforming Growth Factor-β1, Arterial Stiffness and Vascular Age in Patients With Uncontrolled Arterial Hypertension

Lack of blood pressure control leads to a higher incidence of hypertension-mediated target organ damage (HMOD). One of the markers of HMOD is an increased arterial stiffness, an independent predictor of cardiovascular complications. However, abstract numbers showing the level of arterial stiffness do not give patients a clear understanding of the risk of their condition. In order to increase patient compliance, the term "vascular age" (VA) was introduced. Arteriosclerosis plays the main role in increasing VA. The greatest interest, according to the literature, in the study of this issue is in arteriosclerosis caused by transforming growth factor β1 (TGF-β1)-the effect of TGF-β1 on the culture of smooth muscle cells leads to their proliferation and growth; also, TGF-β1 increases the amount of collagen and accelerates the degradation of elastin.We included 140 people in the study: 80 patients with controlled arterial hypertension (CAH), 30 with uncontrolled arterial hypertension (UAH), and 30 patients who formed the control group. All patients underwent a determination of arterial stiffness and VA using the cardio-ankle vascular index (CAVI), a corrected (blood-pressure independent) cardio-ankle vascular index (CAVIThe TGF-β1 value in the UAH group was 22.6 (25th percentile=20.6; 75th percentile=25.6) ng/mL, and in the control group it was 17.4 (25th percentile=11.8; 75th percentile=19.3) ng/mL. In the CAH group, an intermediate value was noted-19.2 (25th percentile=17.2; 75th percentile=24.7) ng/mL. The CAVI in the UAH group was 9.2 (25th percentile=8.5; 75th percentile=9.9), in the control group-7 (25th percentile=6.5; 75th percentile=7.5). In the CAH group, the average CAVI was 7.8 (25th percentile=7.0; 75th percentile=8.5). The CAVI 0 in the UAH group was 14.8 (25th percentile=12.0; 75th percentile=15.6), in the control group - 9.7 (25th percentile=8.8; 75th percentile=9.7). In the CAH group, the average CAVI was 11.1 (25th percentile=10.1; 75th percentile=13.6). Vascular age in the UAH group was 71.5 (25th percentile=64; 75th percentile=74) years, in the CAH group 59 (25th percentile=49; 75th percentile=69) years, and in both groups (UAH, CAH), VA was significantly higher than the chronological age (p0.05). In the control group, the VA did not significantly differ from the chronological age (p0.05) and it was 54 (25th percentile=44; 75th percentile=59) years. A significant relationship was found between the TGF-β1 level and CAVI (CAH r=0.777; UAH r=0.753; p0.05), CAVI 0 (CAH r=0.625; UAH r=0.502; p0.05) and VA in patients with AH (CAH r=0.649; UAH r=0.753; p0.05).In patients in the UAH group, there was an increase in the concentration of TGF-β1, an increase in the arterial stiffness and in VA in comparison with patients in the CAH group and the control group. The relationship between TGF-β1 and the arterial stiffness and VA was revealed in patients with hypertension.