Abstract:
Objective To analyze risk factors of impairment of carotid vascular elastic function pulse wave conduction velocity at onset of systole (PWV-BS) and pulse wave conduction velocity at end of systole (PWV-ES) based on ultrafast pulse wave velocity (ufPWV) quantitative evaluation technique, providing objective evidence for prevention and treatment of vascular elasticity function injury of hypertension.
Methods The desensitization physical examination data of 189 hypertensive patients were retrospectively collected. According to whether the arterial vascular elastic function was damaged, the patients were divided into vascular elastic function injury group (125 cases) and vascular elastic function normal group (64 cases). The clinical indicators of the two groups were compared. The relations of left common carotid artery (LCCA) PWV-BS (LCCA-BS), right common carotid artery (RCCA) PWV-BS (RCCA-BS), LCCA PWV-ES (LCCA-ES) and RCCA PWV-ES(RCCA-ES) in hypertensive patients with age, gender, history of smoking/drinking, systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure difference (PP), heart rate (HR), history of diabetes, history of hyperlipidemia, use of antiplatelet drugs/antilipidemia drugs, blood routine indexes, blood biochemical indexes, electrocardiogram (ECG) were analyzed, and binary Logistic regression analysis and multiple linear stepwise regression analysis were performed to analyze the factors with differences in univariate analysis of vascular elastic function injury, PWV-BS (average value of LCCA-BS and RCCA-BS) and PWV-ES (average value of LCCA-ES and RCCA-ES).
Results There were statistically significant differences in age, platelet (PLT), total bilirubin (TBIL), alkaline phosphatase (ALP) and fasting blood glucose (FBG) between the vascular elasticity function injury group and the normal vascular elasticity function group (P < 0.05). Stratified comparison results showed that there were statistically significant differences in LCCA-ES and RCCA-ES among the four age subgroups (F=6.721, P < 0.001; F=8.251, P < 0.001); there was significant difference in LCCA-ES among the four subgroups (F=4.493, P=0.005). The RCCA-ES of PP≥60 mmHg group showed a significant difference compared with that of PP < 60 mmHg group (P < 0.05). Compared with males of the non-smoking and drinking history group, RCCA-ES in males of the smoking/drinking history group showed a significant difference (P < 0.05). Compared with normal ECG group, RCCA-ES in abnormal ECG group showed a significant difference (P < 0.05). Binary Logistic regression analysis showed that age (OR=1.134, 95%CI, 1.069 to 1.202, P < 0.001), DBP (OR=1.101, 95%CI, 1.034 to 1.174, P=0.003), TBIL (OR=0.879, 95%CI, 0.805 to 0.959, P < 0.001), TBIL(OR=0.879, 95%CI, 0.805 to 0.959, P=0.004) were the influencing factors of vascular elastic function injury. Multiple linear stepwise regression analysis results showed that age (β=0.045, 95%CI, 0.013 to 0.058, P < 0.001), TBIL (β=-0.063, 95%CI, -0.099 to -0.016, P=0.003), red blood cells (β=0.622, 95%CI, 0.110 to 1.043, P=0.008) were the influencing factors of PWV-BS. Age (β=0.071, 95%CI, 0.042 to 0.100, P < 0.001), ECG (β=0.709, 95%CI, 0.160 to 1.259, P=0.012), DBP (β=0.043, 95%CI, 0.008 to 0.078, P < 0.001) were the influencing factor of PWV-ES.
Conclusion Injury of carotid vascular elastic function in hypertensive patients may be correlated with age, course of disease, DBP, PP, HR, ECG, PLT, TBIL and FBG. Anti-plate and lipid-lowering therapy can improve arterial function to a certain extent, while alcohol consumption may have a bidirectional regulatory effect on vascular elasticity function. Clinical diagnosis and treatment of hypertension should not only actively reduce blood pressure, but also perform early assessment and intervention of arterial vascular elastic function, fully identify and pay attention to the risk factors related to arterial vascular elastic function injury, so as to prevent and delay the injury of arterial vascular elastic function in hypertension.