This study aimed to explore whether brachial-ankle pulse wave velocity (baPWV) and brachial artery flow-mediated dilation (FMD) or the interaction of both parameters are associated with subclinical target organ damage (STOD) indices in patients with essential hypertension. A total of 4618 patients registered from January 2015 to October 2020 were included. baPWV and FMD were measured to evaluate arterial stiffness and endothelial dysfunction. Whereas left ventricular hypertrophy (LVH), urine albumin-creatinine ratio (UACR), and carotid intima-media thickness (CIMT) were obtained as STOD indicators. On multivariable logistic regression analysis with potential confounders, higher quartiles of baPWV and FMD were significantly associated with an increased risk of STOD. In patients <65 years of age, the odds ratio (OR) of LVH, UACR, and CIMT ≥.9 mm for the fourth versus the first quartile of baPWV were 1.765 (1.390-2.240), 2.832 (2.014-3.813), and 3.075 (2.315-4.084), respectively. In interaction analysis, an increase in baPWV shows a progressively higher risk of STOD across the quartiles of FMD. Also, the estimated absolute risks of LVH, UACR, and CIMT ≥.9 mm for the first to fourth quartile of baPWV increased from 1.88 to 2.75, 2.35 to 4.44, and 3.10 to 6.10, respectively, in patients grouped by FMD quartiles. The addition of baPWV to FMD slightly improved risk prediction for STOD. BaPWV and FMD were independently associated with an increased risk of STOD in patients with essential hypertension especially among patients <65 years of age. Patients with elevated baPWV and decreased FMD parameters are at increased risk of STOD.

The cleavage of osteopontin (OPN) by thrombin results in an N-terminal fragment (OPN-N), which exposes a cryptic integrin-binding motif that promotes the adherence of cells, and plays a proinflammatory role. However, the effect of OPN-N on abdominal aortic aneurysm (AAA) remains unknown. The aim of this study was to investigate the expression of OPN-N in aortic tissue samples obtained from patients, who underwent acute aortic dissection (AD), and normal aorta, effect of OPN-N on angiotensin (Ang) II-induced AAA in mice, and relationship between OPN-N and pyroptosis-related inflammatory factors in vitro. Hematoxylin and eosin staining was conducted to detect histological changes. Next, we detected the expression of the OPN-N protein. Additionally, ApoE−/− mice were divided into four groups: control, control + M5Ab (to block the OPN-N function in mice), Ang II, and Ang II + M5Ab. All mice were euthanized after a 28-day infusion and whole aortas, including thoracic and abdominal aortas, were collected for morphological and histological analysis of the AAA. The OPN-N protein expression was higher in patients with AD than in normal individuals, while histological changes in the aortas of Ang II mice were suppressed in Ang II + M5Ab mice. The expression of OPN-N, NOD-, LRR-, and pyrin domain-containing protein 3, pro-Caspase-1, ASC, Gasdermin-d, interleukin (IL)-18, IL-1β, matrix metalloproteinase (MMP) 2, and MMP9 was lower in the Ang II + M5Ab group than in the Ang II group. The gene expression of monocyte chemoattractant protein-1, IL-6, and tumor necrosis factor-α was suppressed in the aortic tissues of the Ang II + M5Ab group compared with the Ang II group. Moreover, the expression of α-smooth muscle actin was lower in the Ang II group than in the Ang II + M5Ab group. In vitro results showed that the increase in the expression of pyroptosis-related inflammatory factors induced by OPN was mediated through the nuclear factor (NF)-κB pathway. In conclusion, OPN-N promotes AAA by increasing the expression of pyroptosis-related inflammatory factors through the NF-κB pathway, inflammation, and extracellular matrix degradation. These results highlight the potential of OPN-N as a new therapeutic target to prevent AAA expansion.

The study aims to explore the relationship between plasma insulin secretion and arterial stiffness in nondiabetic essential hypertensive patients. A total of 730 nondiabetic essential hypertensive patients registered between January 2016 and October 2020 were enrolled. A two-hour oral glucose tolerance test (OGTT) was performed to detect the levels of C-peptide and blood glucose at 0 hours and 2 hours, as well as the difference between C-peptide (Δ C-peptide) and blood glucose (Δ blood glucose) over the same period. Patients were divided into two groups: the normal glucose tolerance (NGT) group (n = 322) and the impaired glucose tolerance (IGT) group (n = 408). A multiple linear regression analysis was used to evaluate the association between brachial-ankle pulse wave velocity (baPWV) and the other factors. 0 h C-peptide, 2 h C-peptide, and Δ C-peptide were found to be higher in the IGT group. baPWV was positively linear correlated with 2 h C-peptide (r = 0.086, p = 0.020 ) and Δ C-peptide (r = 0.115, p = 0.002 ). baPWV remained independently associated with 0 h C-peptide, 2 h C-peptide, and Δ C-peptide, after adjusting by age, gender, smoking, body mass index (BMI), high-density lipoprotein (HDL), cholesterol, systolic blood pressure (SBP), and triglycerides (TG). Our data shows that higher endogenous insulin secretion might play an important role in the progression of arterial stiffness in nondiabetic essential hypertensive patients.

AimThe aim of this study was to investigate whether hypertension may be causally linked to left atrial (LA) and left ventricular (LV) structure and function.Methods and resultsWe performed a two-Mendelian randomization (MR) analysis implementing the results from the FinnGen large-scale, genome-wide association study for hypertension (N = 218,754), and LV (N = 16,923) and LA studies (N = 35,648) by the UK Biobank to identify genetic instruments. The MR analysis was implemented using an inverse-variance weighted (IVW) approach. We identified a positive potential causal relationship between hypertension and indices for the LA maximum (LAmax with causal estimates of 0.126 [95% CI, (0.093 to 0.160)]); LA minimum (LAmin with causal estimates of 0.122 [95% CI, (0.089 to 0.156)]); LV function (causal estimates are LV end-diastolic volume (LVEDV), 0.078 [95% CI, (0.003 to 0.153)]; LV end-systolic volume (LVESV), 0.102 [95% CI, (0.030 to 0.173)]; LV mass (LVM), 0.171 [95% CI, (0.108 to 0.233)]; and LV mass to end-diastolic volume ratio (LVMVR at 0.098 [95% CI, (0.048 to 0.149)], respectively), which was directionally concordant with other robust MR methods. Other than this, we observed a significantly negative causal relationship between hypertension and the LA active emptying fraction (LAAEF), the LA passive emptying fraction (LAPEF), and the LA total emptying fraction (LATEF).ConclusionOur genetic analyses demonstrated a potential causal relationship between hypertension and the left atrium and left ventricle’s structures and functions.

Background:The aim was to conduct a comparative assessment of the circadian rhythm (CR) abnormalities and blood pressure (BP) levels between pseudo-and true resistant hypertension (RH) in obesity. Methods:The study included 302 patients with uncontrolled hypertension and obesity. Initial treatment efficacy was assessed 3 months after dual therapy was administered. Those patients who did not reach target BP in dual therapy were transferred to triple therapy. Among patients who received triple therapy, 69 people did not reach target BP. All patients were additionally examined 6 months after the therapy initiation.

Objective:To evaluate left atrial (LA) stiffness using two-dimensional speckle-tracking echocardiography (2DSTE) and investigate the impact and interaction of metabolic elements on LA stiffness index (LASI).Design and method:340 subjects were enrolled and divided into three groups: Group I (n = 38), healthy controls; Group II (n = 138), hypertension without metabolic syndrome (MS); Group III (n = 164), hypertension with MS. All subjects were performed LA phasic strains using 2DSTE, and the following parameters were measured: LA reservoir strain and strain rate (LAS-S, LASR-S), LA conduit strain and strain rate (LAS-E and LASR-E), LA booster strain and strain rate (LAS-A and LASR-A). The LASI was defined as the ratio of early diastolic transmitral flow velocity/lateral mitral annulus myocardial velocity (E/e’) to LAS-S. Binary logistic regression models were performed, and the odds ratios (OR) at 95% confidence interval (CIs) were used to approximate the associated risk of the elements of MS (obesity, diabetes and dyslipidaemia) for LA stiffness, with the lowest binary serving as the reference category.Results:LASI was significantly higher in Group II (0.34 ± 0.21) than Group I (0.19 ± 0.04) (p < 0.001), and further increased in Group III (0.39 ± 0.22) (p < 0.001). LA reservoir and conduit functions gradually and significantly decreased from Group I to Group III (p < 0.001). However, there were no significant differences in LA booster pump function among three groups (p> 0.05). Regarding the elements of MS, body mass index (BMI), hemoglobin A1c (HbA1c) and triglyceride (TG) were positively associated with LASI. Furthermore, we performed the interaction analyses between two of the three elements of MS (BMI, HbA1c and TG). We simultaneously stratified both elements into equal-sized binaries of their individual distribution and then showed that compared with the lowest risk reference group, risk for LA stiffness significantly increased in other groups (Figure).Conclusions:LA phasic function was impaired and LA stiffness was increased in hypertensive patients with MS. Elements of MS (BMI, HbA1c and TG levels) had independent and interaction effect on LA stiffness in hypertension.

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