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The nocturnal blood pressure (BP) has been identified as a prognostic factor for cardiovascular events. This study aimed to investigate the association between different patterns of nocturnal masked hypertension (MH) and the echocardiographic parameters in the untreated nocturnal MH patients. A total of 721 untreated MH patients (309 females and 412 males, mean age = 56.59 ± 15.20 years) from June 2006 and June 2016 were included and divided into nocturnal systolic MH (n = 77), nocturnal diastolic MH (n = 232), and nocturnal systolic/diastolic MH (n = 412) groups according to the ambulatory blood pressure monitoring. Baseline characteristics, office BP values, ambulatory BP monitoring parameters, and echocardiographic parameters were compared among the three groups. The independent factors associated with echocardiographic parameters were analyzed by multivariate linear regression. The nocturnal systolic group had the highest ratio of males, mean age, and office systolic BP (SBP), and the lowest office, 24‐hour, daytime, nocturnal diastolic BP and heart rate among the three groups. The nocturnal diastolic group had the lowest interventricular septum (IVS) thickness, left atrium (LA) dimension, and left ventricular (LV) mass among the three groups. Multivariate linear regression analysis revealed that 24‐hour, daytime, and nocturnal SBPs were all positively associated with LA dimension, IVS thickness, and LV mass (all B were positive and P

Objectives To investigate sex differences associated with changes in brachial artery flow-mediated dilatation and carotid intima-media thickness by Framingham Risk Score. Methods The study included 1083 patients aged 30 to 80 years. According to the Framingham Risk Score, patients were divided into 3 groups: low, mid, and high risk. Traditional cardiovascular risk factors such as age, sex, smoking, diabetes, hypertension, and cholesterol were assessed by Framingham Risk Score, as well as laboratory and vascular parameters, including flow-mediated dilatation and intima-media thickness. Correlations between flow-mediated dilatation, intima-media thickness, and the Framingham Risk Score were analyzed by sex. Results Compared with women, flow-mediated dilatation in men was significantly lower in the low-risk group (mean ± SD, 8.31% ± 2.89% versus 9.76% ± 3.62%; P< .001) but significantly higher in the mid- and high-risk groups (mid-risk, 7.43% ± 2.65% versus 6.67% ± 2.42%; high-risk, 6.41% ± 2.27% versus 5.78% ± 2.39%; P< .001). Flow-mediated dilatation decreased with an increasing Framingham Risk Score in both sexes but especially in women. Although intima-media thickness increased with the Framingham Risk Score in both sexes, there was no significant sex difference between the groups. Univariate analysis showed significant negative correlations between flow-mediated dilatation and the Framingham Risk Score in both sexes (Rmen = −0.308; P < .001; Rwomen = −0.572; P < .001) and flow-mediated dilatation and intima-media thickness (Rmen = −0.295; P < .001; Rwomen = −0.474; P< .001). There was a significant positive correlation between intima-media thickness and the Framingham Risk Score (Rmen = 0.571; P< .001; Rwomen = 0.633; P < .001). Conclusions A sex difference existed only for flow-mediated dilatation at the same Framingham risk level. Flow-mediated dilatation might be more sensitive than intima-media thickness for detecting sex differences in vascular dysfunction, according to Framingham risk stratification in a Chinese population.

Summary The purpose of this study is to investigate the possible underlying pathogenesis of erectile dysfunction(ED) in young men with low risk of coronary heart disease and no well-known aetiology. To conduct this study, 122 patients with ED under the age of 40 were enrolled, along with 33 age-matched normal control subjects. The patients with ED had significantly higher levels of systolic blood pressure (SBP), total cholesterol and triglyceride, high sensitivity C-reactive protein (hs-CRP), greater carotid intima-media thickness (CIMT) and Framingham risk score (FRS) than the control group, though all of these values were within the respective normal range. Further, the brachial artery flow- mediated vasodilation (FMD) values were significantly lower in ED patients and correlated positively with the severity of ED (r = 0.714, p

1. Metformin is an activator of AMP-activated protein kinase (AMPK). Recent studies suggest that pharmacological activation of AMPK inhibits cardiac hypertrophy. In the present study, we examined whether long-term treatment with metformin could attenuate ventricular hypertrophy in a rat model. The potential involvement of nitric oxide (NO) in the effects of metformin was also investigated. 2. Ventricular hypertrophy was established in rats by transaortic constriction (TAC). Starting 1 week after the TAC procedure, rats were treated with metformin (300 mg/kg per day, p.o.), N(G)-nitro-L-arginine methyl ester (L-NAME; 50 mg/kg per day, p.o.) or both for 8 weeks prior to the assessment of haemodynamic function and cardiac hypertrophy. 3. Cultured cardiomyocytes were used to examine the effects of metformin on the AMPK-endothelial NO synthase (eNOS) pathway. Cells were exposed to angiotensin (Ang) II (10⁻⁶ mol/L) for 24 h under serum-free conditions in the presence or absence of metformin (10⁻³ mol/L), compound C (10⁻⁶ mol/L), L-NAME (10⁻⁶ mol/L) or their combination. The rate of incorporation of [³H]-leucine was determined, western blotting analyses of AMPK-eNOS, neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) were undertaken and the concentration of NO in culture media was determined. 4. Transaortic constriction resulted in significant haemodynamic dysfunction and ventricular hypertrophy. Myocardial fibrosis was also evident. Treatment with metformin improved haemodynamic function and significantly attenuated ventricular hypertrophy. Most of the effects of metformin were abolished by concomitant L-NAME treatment. L-NAME on its own had no effect on haemodynamic function and ventricular hypertrophy in TAC rats. 5. In cardiomyocytes, metformin inhibited AngII-induced protein synthesis, an effect that was suppressed by the AMPK inhibitor compound C or the eNOS inhibitor L-NAME. The improvement in cardiac structure and function following metformin treatment was associated with enhanced phosphorylation of AMPK and eNOS and increased NO production. 6. The findings of the present study indicate that long-term treatment with metformin could attenuate ventricular hypertrophy induced by pressure overload via activation of AMPK and a downstream signalling pathway involving eNOS-NO.