Excess sodium consumption contributes to arterial dysfunction in humans. The C57BL/6 strain of mice have been used to identify mechanisms by which arterial dysfunction occurs after excess sodium consumption. However, there are concerns that C57BL/6 mice have strain-specific resistance to high-sodium (HS) diet-induced hypertension. To address this concern, we performed a meta-analysis to determine if excess sodium consumption in C57BL/6 mice induces arterial dysfunction. Databases were searched for HS vs. standard diet studies that measured arterial function (i.e., systolic blood pressure [BP], endothelium-dependent dilation [EDD], and central arterial stiffness) in C57BL/6 mice. A total of 39 studies were included, demonstrating that HS condition resulted in higher systolic BP than control mice with a mean difference of 9.8 mmHg (95% CI [5.6, 14], P<0.001). Subgroup analysis indicated that the systolic BP was higher in HS compared to the control condition when measured during night compared to daytime with telemetry (P<0.001). We also identified that the difference in systolic BP between HS and control was ~2.5-fold higher when administered through drinking water than through food (P<0.001). A total of 12 studies were included, demonstrating that HS condition resulted in lower EDD than control with a weighted mean difference of -12.0% (95% CI [-20.0, -4.1], P=0.003). It should be noted that there was considerable variability across studies with more than half of the studies showing no effect of HS condition on systolic BP and EDD. In summary, excess sodium consumption elevates systolic BP and impairs EDD in C57BL/6 mice.

The intima, comprising the endothelium and the subendothelial matrix, plays a crucial role in atherosclerosis pathogenesis. The mechanical stress arising from disturbed blood flow (d-flow) and the stiffening of the arterial wall contributes to endothelial dysfunction. However, the specific impacts of these physical forces on the mechanical environment of the intima remain undetermined. Here, we investigated whether inhibiting collagen crosslinking could ameliorate the detrimental effects of persistent d-flow on the mechanical properties of the intima. Partial ligation of the left carotid artery (LCA) was performed in C57BL/6J mice, inducing d-flow. The right carotid artery (RCA) served as an internal control. Carotids were collected 2 days and 2 weeks after surgery to study acute and chronic effects of d-flow on the mechanical phenotype of the intima. The chronic effects of d-flow were decoupled from the ensuing arterial wall stiffening by administration of β-aminopropionitrile (BAPN), an inhibitor of collagen crosslinking by lysyl oxidase (LOX) enzymes. Atomic force microscopy (AFM) was used to determine stiffness of the endothelium and the denuded subendothelial matrix in en face carotid preparations. The stiffness of human aortic endothelial cells (HAEC) cultured on soft and stiff hydrogels was also determined. Acute exposure to d-flow caused a slight decrease in endothelial stiffness in male mice but had no effect on the stiffness of the subendothelial matrix in either sex. Regardless of sex, the intact endothelium was softer than the subendothelial matrix. In contrast, exposure to chronic d-flow led to a substantial increase in the endothelial and subendothelial stiffness in both sexes. The effects of chronic d-flow were largely prevented by concurrent BAPN administration. In addition, HAEC displayed reduced stiffness when cultured on soft vs. stiff hydrogels. We conclude that chronic d-flow results in marked stiffening of the arterial intima, which can be effectively prevented by inhibition of collagen crosslinking.

BACKGROUND: The Chinese visceral adiposity index (CVAI) is a new index to evaluate visceral adipose tissue in the Chinese population. Arterial stiffness (AS) is a kind of degeneration of the large arteries, and obesity is an essential contributing factor to AS. Our study aimed to explore the longitudinal association between CVAI and the risk of AS and to compare the predictive power of CVAI, body mass index (BMI), and waist circumference (WC) for AS.
METHODS: Between 2010 and 2020, a total of 14,877 participants participating in at least two brachial-ankle pulse wave velocity (baPWV) measurements from the Kailuan study were included. The Cox proportional hazard regression models were performed to evaluate the longitudinal association between CVAI and the risk of AS. The area under the receiver operating characteristic (ROC) curve was calculated to compare the predictive power of CVAI, BMI, and WC for AS.
RESULTS: After adjusting for potential confounding factors, CVAI was significantly associated with the risk of AS. Compared with the first CVAI quartile, the hazard ratios (HR) and 95% CI of the second, third, and fourth quartiles were 1.30 (1.09-1.56), 1.37 (1.15-1.63), and 1.49 (1.24-1.78), respectively. The area under ROC curve of CVAI was 0.661, significantly higher than BMI (AUC: 0.582) and WC (AUC: 0.606).
CONCLUSIONS: CVAI may be a reliable indicator to identify high-risk groups of AS in the Chinese general population, and the predictive power of CVAI for AS was better than BMI and WC.

UNASSIGNED: While observational studies have demonstrated connections between cigarette smoking, alcohol consumption, and arterial stiffness, establishing a causal relationship has proven challenging because of potential confounding factors. To address this problem, we employed a two-sample Mendelian randomization approach.
UNASSIGNED: We selected genetic instruments for these risk factors from genome-wide association studies encompassing 3,383,199 individuals at the genome-wide significance level (p < 5 × 10 - 9 ). Arterial stiffness data were acquired from the UK Biobank, which included 127,121 participants. Our primary analysis utilized the inverse variance-weighted method to explore causality. To confirm our results\' robustness, we conducted sensitivity analyses using Egger regression, the weighted median method, and Mendelian Randomization Pleiotropy RESidual Sum and Outlier (MR-PRESSO).
UNASSIGNED: Our analysis revealed a significant association between genetic inclination to smoking initiation and an increase in the arterial stiffness index ( β = 0.11; 95% confidence interval [CI], 0.06 to 0.16; p = 1.95 × 10 - 5 ). Additionally, there was a suggestive connection between genetically predicted number of cigarettes per day and the arterial stiffness index ( β = 0.05; 95% CI, 5.25 × 10 - 4 to 0.10; p = 4.75 × 10 - 2 ). No causal relationships were observed between the genetically predicted age of smoking initiation, smoking cessation, or alcohol consumption and the risk of arterial stiffness index.
UNASSIGNED: This Mendelian randomization study indicates that smoking initiation is likely a causative risk factor for arterial stiffness. However, further research is needed to determine if the quantity of daily cigarettes directly contributes to arterial stiffness development. Regarding alcohol consumption, age of smoking initiation, and smoking cessation, there was insufficient evidence to establish causality.

BACKGROUND: Aerobic exercises like running and cycling may lower cardiovascular disease (CVD) risk through favorable effects on central blood pressure and vascular function. Arm ergometry is a popular exercise modality used in rehabilitation settings, but little is known regarding the central hemodynamic and vascular effects of this form of exercise.
OBJECTIVE: To compare the acute effects of leg versus arm exercise on central blood pressure and vascular function.
METHODS: Twenty-one participants (n = 11 female, Age 21 ± 3, BMI 24.5 ± 3.2 kg/m2) completed two visits to the Human Performance Laboratory. Central systolic blood pressure (cSBP), central diastolic blood pressure (cDBP), and peripheral augmentation index (pAIx) were measured using a brachial oscillometric blood pressure cuff with measures being taken before and after 20 min of acute moderate-intensity (submaximal) arm or leg cycling exercise.
RESULTS: There was a condition-by-time interaction for pAIx (p = 0.011). pAIx slightly increased following arm exercise but significantly decreased following leg exercise. There was a condition-by-time interaction for cDBP (p = 0.011). cDBP significantly decreased following arm exercise but increased immediately following leg exercise. There was no condition-by-time interaction for cSBP (p = 0.721). There were similar acute increases in cSBP immediately post-exercise for both conditions.
CONCLUSIONS: Arm exercise increased pAlx and decreased cDBP compared to leg exercise. As an increase in pAIx may increase left ventricular work and a reduction in cDBP may reduce coronary perfusion pressure, these findings suggest that a single bout of arm exercise may not have the same favorable acute effect on central hemodynamic load as a single bout of leg exercise.

UNASSIGNED: Arterial stiffness measured by total pulse wave velocity (T-PWV) is associated with increased risk of multiple age-related diseases. T-PWV can be described by structural (S-PWV) and load-dependent (LD-PWV) arterial stiffening. T-cells have been associated with arterial remodeling, blood pressure, and arterial stiffness in humans and animals; however, it is unknown whether T-cells are related to S-PWV or LD-PWV. Therefore, we evaluated the cross-sectional associations of peripheral T-cell subpopulations with T-PWV, S-PWV, and LD-PWV stiffness.
UNASSIGNED: Peripheral blood T-cells were characterized using flow cytometry and the carotid artery was measured using B-mode ultrasound to calculate T-PWV at the baseline examination in a subset of the Multi-Ethnic Study of Atherosclerosis (MESA, n=1,984). A participant-specific exponential model was used to calculate S-PWV and LD-PWV based on elastic modulus and blood pressure gradients. The associations between five primary (p-significance<0.01) and twenty-five exploratory (p-significance<0.05) immune cell subpopulations, per 1-SD increment, and arterial stiffness measures were assessed using adjusted, linear regressions.
UNASSIGNED: For the primary analysis, higher CD4+CD28-CD57+ T-cells were associated with higher LD-PWV (β=0.04 m/s, p<0.01) after adjusting for co-variates. For the exploratory analysis, T-cell subpopulations that commonly shift with aging towards memory and differentiated/immunosenescent phenotypes were associated with greater T-PWV, S-PWV, and LD-PWV after adjusting for co-variates.
UNASSIGNED: In this cross-sectional study, several T-cell subpopulations commonly associated with aging were related with measures of arterial stiffness. Longitudinal studies that examine changes in T-cell subpopulations and measures of arterial stiffness are warranted.

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Psoriasis predisposes to cardiovascular dysfunction. We investigated whether glycocalyx dietary supplement (GDS), which contains glycosaminoglycans and fucoidan, improves endothelial glycocalyx and arterial stiffness in psoriatic patients. Fifty participants with psoriasis under biological agents were randomly assigned to GDS (n = 25) or placebo (n = 25) for 4 months. We measured at baseline and at follow-up: (a) perfused boundary region (PBR) of the sublingual microvessels (range 4 to 25 μm), a marker of endothelium glycocalyx integrity; (b) carotid-femoral pulse wave velocity (PWV-Complior SP-ALAM) and augmentation index (AIx), markers of arterial stiffness and (c) psoriasis area and severity index (PASI) score. Both groups displayed a similar decrease in PASI at four months (p < 0.05), and no significant differences were found between groups (p > 0.05). Compared to the placebo, participants in the GDS showed a greater percentage reduction in PBR4-25 μm (-9.95% vs. -0.87%), PBR 4-9 μm (-6.50% vs. -0.82%), PBR10-19 μm (-5.12% vs. -1.60%), PBR 20-25 μm (-14.9% vs. -0.31%), PWV (-15.27% vs. -4.04%) and AIx (-35.57% vs. -21.85%) (p < 0.05). In the GDS group, the percentage reduction in PBR 4-25 μm was associated with the corresponding decrease in PWV (r = 0.411, p = 0.015) and AΙx (r = 0.481, p = 0.010) at follow-up. Four-month treatment with GDS improves glycocalyx integrity and arterial stiffness in patients with psoriasis. Clinical trial Identifier: NCT05184699.

Atrial myopathy-defined as abnormal left atrial (LA) size and function-is associated with an increased risk of atrial fibrillation, heart failure, and dementia. Central arterial stiffness is associated with increased atrial afterload and fibrosis and may be a risk factor for atrial myopathy. We examined the association of carotid-femoral pulse wave velocity (cfPWV) with LA function and assessed potential causal relationships. We included 2825 Atherosclerosis Risk in Communities (ARIC) study participants from Visit 5 (2011-2013). cfPWV was related to echocardiographic LA function continuously per 1-SD and categorically in quartiles. Mendelian randomization (MR) analysis was performed using U.K. Biobank-derived genetic variants associated with arterial stiffness index and cardiac magnetic resonance measures of LA function. When analyzed per SD increment (297.6 cm/s), higher cfPWV was significantly associated with lower LA reservoir and conduit strain (β = -0.53%, 95% CI [-0.81, -0.25] and β = -0.46%, 95% CI [-0.68, -0.25], respectively) after adjusting for demographics, clinical characteristics, systolic blood pressure, and left ventricular (LV) morphology and function. In MR analyses there was a non-significant inverse association of arterial stiffness index with LA total, passive, and active emptying fractions. Higher cfPWV is associated with lower LA reservoir and conduit strain, independent of systolic blood pressure and LV morphology and function. No evidence for a causal relationship between arterial stiffness index and alterations in LA function was found. Future studies should examine the prospective association of central arterial stiffness with LA function alterations.

BACKGROUND: Evidence on the association of arterial stiffness and left ventricular (LV) concentric remodelling/ LVH assessed by echocardiography, with abnormal blood pressure (BP) phenotypes, defined by office and ambulatory BP monitoring (ABPM) in the community is scanty. We investigated this issue in the participants to the Pressioni Monitorate E Loro Associazioni (PAMELA) study.
METHODS: The study included 491 participants who attended the second and third survey of the PAMELA study performed after 10 and 25 years from the initial evaluation. Data collection included medical history, anthropometric parameters, blood examinations, office, ABPM, echocardiographic and Cardio-Ankle Vascular Index (CAVI) measurements.
RESULTS: In the whole study sample (age 66 + 10 years, 50% males), the prevalence rates of sustained normotension (NT), white coat hypertension (WCH), masked hypertension (MH), sustained hypertension (SH) and non-dipping (ND) were 31.2, 10.0, 24.2, 34.6, and 35.8% and respectively. The likelihood of having SH, the BP phenotype carrying the greatest CV risk, was four times higher (OR= 4.31, CI:2.39-7.76, p<0.0001) in participants with increased CAVI and LV remodelling/LVH compared to their counterparts without organ damage. This association showed an incremental value in discriminating SH compared to both isolated markers of organ damage (OR=1.92,p=0.03 for increased CAVI and OR= 2.02, p=0.02 for LV remodelling/LVH). The presence of isolated but also combined organ damage was unrelated to ND.
CONCLUSIONS: Our study provides new evidence of the incremental value of looking for both vascular and cardiac organ damage to optimize the identification and clinical management of SH in the general population.