ABSTRACT
Objective: To explore the association of blood pressure variability (BPV), especially diurnal blood pressure rhythm with brachial ankle pulse wave velocity (baPWV) and left ventricular mass index (LVMI). Methods: A total of 184 hypertensive patients participated this cross sectional study. Patients were divided into dippers, non-dippers, inverted dippers and extreme dippers groups according to nocturnal systolic blood pressure (SBP) decline. baPWV and LVMI in different groups were compared. Correlation of baPWV and LVMI with blood pressure and BPV variables were analyzed by univariate and multivariate regression analysis. Results: After adjusted by age, BMI, hypertension duration, blood pressure in consulting room, SBP and diastolic blood pressure (DBP) in 24 h, total cholesterol, low density lipoprotein cholesterin, brain natriuretic peptide and ejection fraction, baPWV in non-dippers group and inverted-dippers group were significantly higher than that in dippers group and extreme dippers group (P=0.000), and LVMI was significantly higher in non-dippers group than in dippers group (P=0.001) and extreme-dippers group (P=0.022). baPWV and LVMI were both significantly correlated to age, 24 h SBP and 24 h DBP, SD value of 24 h SBP and 24 h DBP, daytime SBP and DBP, nocturnal SBP and DBP, SD values of daytime SBP and DBP, SD values of nocturnal SBP and DBP in univariate linear regression models (P<0.05). In multivariate linear regression model, baPWV was independently associated to SD value of nocturnal SBP (β=0.289, P=0.000), nocturnal SBP decline (β=-0.398, P=0.000), daytime SBP (β=0.214, P=0.001) and SD value of daytime DBP (β=0.207, P=0.002), while LVMI was independently associated to 24 h SBP (β=0.348, P=0.000) and SD value of nocturnal SBP (β=0.196, P=0.026). Conclusion: baPWV was independently correlated to SD value of nocturnal SBP, nocturnal SBP decline, daytime SBP and SD value of daytime DBP, while LVMI was independently correlated to 24 h SBP and SD value of nocturnal SBP.
ABSTRACT
Objective·To explore the association of blood pressure variability (BPV),especially diurnal blood pressure rhythm with brachial ankle pulse wave velocity (baPWV) and left ventricular mass index (LVMI).Methods· A total of 184 hypertensive patients participated this cross sectional study.Patients were divided into dippers,non-dippers,inverted dippers and extreme dippers groups according to nocturnal systolic blood pressure (SBP) decline.baPWV and LVMI in different groups were compared.Correlation of baPWV and LVMI with blood pressure and BPV variables were analyzed by univariate and multivariate regression analysis.Results· After adjusted by age,BMI,hypertension duration,blood pressure in consulting room,SBP and diastolic blood pressure (DBP) in 24 h,total cholesterol,low density lipoprotein cholesterin,brain natriuretic peptide and ejection fraction,baPWV in non-dippers group and inverted-dippers group were significantly higher than that in dippers group and extreme dippers group (P=0.000),and LVMI was significantly higher in non-dippers group than in dippers group (P=0.001) and extreme-dippers group (P=0.022).baPWV and LVMI were both significantly correlated to age,24 h SBP and 24 h DBP,SD value of 24 h SBP and 24 h DBP,daytime SBP and DBP,nocturnal SBP and DBP,SD values of daytime SBP and DBP,SD values of nocturnal SBP and DBP in univariate linear regression models (P＜0.05).In multivariate linear regression model,baPWV was independently associated to SD value of nocturnal SBP (β=0.289,P=0.000),nocturnal SBP decline (β=0.398,P=0.000),daytime SBP (β=0.214,P=0.001) and SD value of daytime DBP (β=0.207,P=0.002),while LVMI was independently associated to 24 h SBP (β=0.348,P=0.000) and SD value of nocturnal SBP (β=0.196,P=0.026).Conclusion· baPWV was independently correlated to SD value of nocturnal SBP,nocturnal SBP decline,daytime SBP and SD value of daytime DBP,while LVMI was independently correlated to 24 h SBP and SD value of nocturnal SBP.
ABSTRACT
Accumulating studies have proved that systemic inflammation is one of the important pathophysiologic mechanisms of heart failure. This article focuses on the sources of inflammation mediators and the causes of inflammation activation in heart failure including hemodynamic changes and oxidative stress, Toll-like receptors, microbial antigens and microorganisms, endotoxin hypothesis and neurohormonal activation. Furthermore, the effects of inflammation mediators such as cytokines and chemokines on heart failure are introduced. All lead to the conclusion that heart failure is a process with complex inflammation.