UNASSIGNED: No studies have reported simultaneous evaluation of the two coronary risk markers of testosterone and skin autofluorescence (SAF) as a marker of advanced glycation end products in patients with type 2 diabetes mellitus (T2DM) at present. This study aimed to clarify the clinical significance of both indicators as risk markers of coronary artery disease (CAD), including the association and background factors between testosterone and SAF in male patients with T2DM.
UNASSIGNED: This study enrolled 162 male patients with T2DM (CAD: n = 35). Testosterone was evaluated by serum total testosterone concentration (T-T). Various analyses related to T-T and SAF as coronary risk markers were performed.
UNASSIGNED: T-T was significantly lower, and SAF was significantly higher in patients with CAD than in patients with non-CAD. A significant negative correlation was found between T-T and SAF (r = -0.45, P < 0.001), and the correlation was stronger in patients with CAD than in patients with non-CAD (non-CAD, r = -0.27, P = 0.003; CAD, r = -0.51, P < 0.001). However, both T-T and SAF had significant associations with triglyceride-glucose index as an insulin resistance marker and cardio-ankle vascular index as an arterial function marker. Multiple regression analysis revealed that both T-T and SAF were selected as independent variables to the presence of CAD as a dependent variable. However, the odds ratio increased due to the merger of two coronary risk markers, low T-T and high SAF (odds ratio: one risk marker: 3.24, 95% confidence interval: 1.01 - 10.50, P = 0.045; two risk markers: 13.22, 95% confidence interval: 3.41 - 39.92, P < 0.001).
UNASSIGNED: The results of this cross-sectional study indicate that T-T and SAF are closely related in CAD patients with T2DM. It also shows that insulin resistance and arterial dysfunction are in the background of both indicators. Additionally, not only are both indicators independent coronary risk markers, but the overlap of both indicators increases their weight as coronary risk markers.

暂无摘要。

UNASSIGNED: Arterial stiffness causes cardiovascular disease and target-organ damage. Carotid-femoral pulse wave velocity is regarded as a standard arterial stiffness metric. However, the prognostic value of cardio-ankle vascular index (CAVI), which is mathematically corrected for blood pressure, remains understudied.
UNASSIGNED: The purpose of this study was to determine the association of CAVI with cardiovascular and kidney outcomes.
UNASSIGNED: PubMed, Scopus, and Web of Science were searched until May 6, 2023, for longitudinal studies reporting the association of CAVI with mortality, cardiovascular events (CVEs) (including death, acute coronary syndromes, stroke, coronary revascularization, heart failure hospitalization), and kidney function decline (incidence/progression of chronic kidney disease, glomerular filtration rate decline). Random-effects meta-analysis was performed. Studies were assessed with the \"Quality in Prognostic Studies\" tool.
UNASSIGNED: Systematic review identified 32 studies (105,845 participants; follow-up range: 12-148 months). Variable cutoffs were reported for CAVI. The risk of CVEs was higher for high vs normal CAVI (HR: 1.46 [95% CI: 1.22-1.75]; P < 0.001; I2 = 41%), and per SD/unit CAVI increase (HR: 1.30 [95% CI: 1.20-1.41]; P < 0.001; I2 = 0%). Among studies including participants without baseline cardiovascular disease (primary prevention), higher CAVI was associated with first-time CVEs (high vs normal: HR: 1.60 [95% CI: 1.15-2.21]; P = 0.005; I2 = 65%; HR per SD/unit increase: 1.28 [95% CI: 1.12-1.47]; P < 0.001; I2 = 18%). There was no association between CAVI and mortality (HR = 1.31 [0.92-1.87]; P = 0.130; I2 = 53%). CAVI was associated with kidney function decline (high vs normal: HR = 1.30 [1.18-1.43]; P < 0.001; I2 = 38%; HR per SD/unit increase: 1.12 [95% CI: 1.07-1.18]; P < 0.001; I2 = 0%).
UNASSIGNED: Higher CAVI is associated with incident CVEs, and this association is present in the primary prevention setting. Elevated CAVI is associated with kidney function decline.

UNASSIGNED: Arterial stiffness (AS) can be used to predict future cardiovascular diseases. High lipoprotein(a) (Lp(a)) levels were independently correlated with cardiovascular (CV) morbidity and death in patients with chronic renal insufficiency. The cardio-ankle vascular index (CAVI) is a useful biomarker of arteriosclerotic disorders and has a close relationship with a variety of CV events. This study aimed to investigate the correlation between serum Lp(a) levels and AS in patients on peritoneal dialysis (PD) using the CAVI.
UNASSIGNED: A total of 86 adult patients who were on regular PD for at least 3 months were recruited in this study. The CAVI values were determined using the waveform device (VaSera VS-1000). A CAVI value of ≥ 9.0 on either side was defined as high. Serum Lp(a) levels were measured by an enzyme-linked immunosorbent assay.
UNASSIGNED: Among these participants, 35 of 86 (40.7%) belonged to the high CAVI group. In contrast to those with a normal CAVI, PD recipients in the high CAVI group had higher serum levels of total cholesterol (p = 0.003), triglycerides (p = 0.044), C-reactive protein (p < 0.001), and Lp(a) (p < 0.001), whereas their albumin levels were significantly lower (p = 0.026). Based on multivariable logistic regression analysis, serum Lp(a) (odds ratio [OR] 1.025, 95% confidence interval [CI] 1.010-1.040, p = 0.001), total cholesterol (OR 1.042, 95% CI 1.005-1.081, p = 0.027), and C-reactive protein (each increase 0.1 mg/dL, OR 1.217, 95% CI 1.008-1.469, p = 0.041) levels were found as the parameters that could independently predict AS in patients on PD. Further, using Spearman\'s correlation analysis, both the left and right CAVIs revealed a significantly positive correlation with log-transformed Lp(a) levels (r = 0.588, p < 0.001; r = 0.639, p < 0.001, respectively).
UNASSIGNED: Serum Lp(a) levels were postulated to participate in the pathogenic processes of AS in adult patients undergoing PD.

UNASSIGNED: High soluble urokinase plasminogen activator receptor (suPAR) levels are correlated with cardiovascular (CV) disease. Arterial stiffness is associated with aging-related vascular diseases and is an independent risk factor for CV morbidity and mortality. It can be measured by the cardio-ankle vascular index (CAVI). We evaluated the association between serum suPAR levels and arterial stiffness according to the CAVI in kidney transplantation (KT) recipients.
UNASSIGNED: In this study, 82 patients undergoing KT were enrolled. Serum suPAR levels were analyzed using an enzyme immunoassay. The CAVI was measured using a plethysmograph waveform device, and patients with a CAVI of ≥ 9.0 were assigned to the peripheral arterial stiffness (PAS) group.
UNASSIGNED: Twenty KT patients (24.4%) had PAS, were of older age (p = 0.042), and had higher serum triglyceride (p = 0.023) and suPAR levels (p < 0.001) than the normal group. After adjusting for factors significantly associated with PAS by multivariate logistic regression analysis, serum suPAR levels (odds ratio [OR] 1.072, 95% confidence interval (CI) 1.023-1.123; p = 0.004) were independently associated with PAS in KT patients. The logarithmically transformed suPAR level (log-suPAR) was also positively correlated with the left or right CAVI values (all p < 0.001) from the results of the Spearman correlation analysis in KT patients.
UNASSIGNED: Serum suPAR levels are positively associated with left or right CAVI values and are independently associated with PAS in KT patients.

UNASSIGNED: Cross sectionally measured, elevated arterial stiffness is associated with unfavorable left ventricular (LV) remodeling, suggesting its important role in the pathophysiology of heart failure. However, data linking the degree of arterial stiffness progression with LV remodeling are scarce.
UNASSIGNED: The purpose of this study was to investigate the association between longitudinal change in arterial stiffness and changes in LV remodeling.
UNASSIGNED: Serial measurements of arterial stiffness by cardio-ankle vascular index (CAVI) were performed in 317 participants without cardiovascular disease and with normal arterial stiffness. LV size, mass, and function were assessed by transthoracic echocardiography and including LV global longitudinal strain (LVGLS) by speckle-tracking and tissue Doppler velocity (e\') of the mitral annulus (diastolic function).
UNASSIGNED: During a median follow-up of 26.8 mo, there was a significant increase in CAVI (P < 0.001). Generalized estimating equation analyses showed that longitudinal increase in CAVI was associated with impaired LVGLS (estimate 0.46, 95% CI: 0.11-0.82; P = 0.010) after adjustment for demographics and baseline cardiovascular factors, but not with changes of LV mass index and e\' velocity. When controlling for longitudinal change of covariates, CAVI progression remained associated with change in LVGLS (estimate 0.50, 95% CI: 0.16-0.85; P = 0.004). In sex stratified analysis, progression of CAVI was significantly associated with LVGLS deterioration only in women (estimate 0.92, 95% CI: 0.27-1.58; P = 0.006).
UNASSIGNED: Longitudinal increase in arterial stiffness is associated with deterioration in LVGLS. Vascular-ventricular coupling plays an important role in the progressive decline in ventricular function even at an early, subclinical stage.

The aim of this study was to examine the long-term prognostic value of changes in the cardio-ankle vascular index (CAVI) within a year after coronary artery bypass grafting (CABG).
METHODS: Patients with coronary artery disease (n = 251) in whom CAVI was assessed using the VaSera VS-1000 device before and one year after CABG. Groups with improved CAVI or worsened CAVI were identified. We assessed the following events at follow-up: all-causes death, myocardial infarction, and stroke/transient ischemic attack.
RESULTS: All-causes death was significantly more common in the group with worsened CAVI (27.6%) than in the group with CAVI improvement (14.8%; p = 0.029). Patients with worsened CAVI were more likely to have MACE, accounting for 42.2% cases, compared with patients with CAVI improvement, who accounted for 24.5%; p = 0.008. Worsened CAVI (p = 0.024), number of shunts (p = 0.006), and the presence of carotid stenosis (p = 0.051) were independent predictors of death from all causes at 10-year follow-up after CABG. The presence of carotid stenosis (p = 0.002) and the group with worsened CAVI after a year (p = 0.008) were independent predictors of the development of the combined endpoint during long-term follow-up.
CONCLUSIONS: Patients with worsening CAVI one year after CABG have a poorer prognosis at long-term follow-up than patients with improved CAVI. Future research would be useful to identify the most effective interventions to improve CAVI and correspondingly improve prognosis.

BACKGROUND: The cardio-ankle vascular index (CAVI) measure of arterial stiffness is associated with prevalent cardiovascular risk factors, while its predictive value for cardiovascular events remains to be established. The aim was to determine associations of CAVI with cardiovascular morbimortality (primary outcome) and all-cause mortality (secondary outcome), and to establish the determinants of CAVI progression.
METHODS: TRIPLE-A-Stiffness, an international multicentre prospective longitudinal study, enrolled >2000 subjects ≥40 years old at 32 centres from 18 European countries. Of these, 1250 subjects (55% women) were followed for a median of 3.82 (2.81-4.69) years.
RESULTS: Unadjusted cumulative incidence rates of outcomes according to CAVI stratification were higher in highest stratum (CAVI > 9). Cox regression with adjustment for age, sex, and cardiovascular risk factors revealed that CAVI was associated with increased cardiovascular morbimortality (HR 1.25 per 1 increase; 95% confidence interval, CI: 1.03-1.51) and all-cause mortality (HR 1.37 per 1 increase; 95% CI: 1.10-1.70) risk in subjects ≥60 years. In ROC analyses, CAVI optimal threshold was 9.25 (c-index 0.598; 0.542-0.654) and 8.30 (c-index 0.565; 0.512-0.618) in subjects ≥ or <60 years, respectively, to predict increased CV morbimortality. Finally, age, mean arterial blood pressure, anti-diabetic and lipid-lowering treatment were independent predictors of yearly CAVI progression adjusted for baseline CAVI.
CONCLUSIONS: The present study identified additional value for CAVI to predict outcomes after adjustment for CV risk factors, in particular for subjects ≥60 years. CAVI progression may represent a modifiable risk factor by treatments.
BACKGROUND: International Society of Vascular Health (ISVH) and Fukuda Denshi, Japan.

UNASSIGNED: Aging is associated with a higher prevalence of sarcopenia, sarcopenic obesity (SO), and increased arterial stiffening, with possible detrimental effects on morbidity and mortality. The aim of this study was to assess the relationships between sarcopenia, SO, and different indexes of arterial stiffness in older adults.
UNASSIGNED: A total of 77 hospitalized patients (mean age 78.68 ± 9.65 years) were evaluated, obtaining anthropometric variables, biochemical samples, handgrip test, and body composition assessment. Arterial stiffness was evaluated by measuring both carotid-femoral pulse wave velocity (cfPWV), a proxy for central stiffness, and cardio-ankle vascular index (CAVI), as well as considering peripheral arteries. The population was sorted into four subgroups: obese, sarcopenic, SO, and controls.
UNASSIGNED: The highest CAVI (11.31 ± 2.58) was found in sarcopenic patients. SO had the highest value of cfPWV (15.18 ± 8.44 m/s), even after adjustment for significant covariates. In multiple regressions, SO diagnosis resulted as a significant predictor of cfPWV (p = 0.03, R2 = 0.20), and sarcopenia diagnosis resulted as a predictor of CAVI (p = 0.042, R2 = 0.12).
UNASSIGNED: In conclusion, a positive correlation is found between sarcopenia, SO, and arterial stiffness among older subjects. In particular, greater central arterial stiffness is associated with SO, outlining a remarkable effect on the cardiovascular risk profile.

It has been documented that large-artery stiffness is independently associated with increased cardiovascular risk and may potentially lead to heart and kidney failure and cerebrovascular disease. A systematic review of studies investigating changes in arterial stiffness in patients undergoing endovascular repair of aortic disease was conducted. In addition, a review of the available literature was performed, analyzing findings from studies using the cardio-ankle vascular index (CAVI) as a marker of arterial stiffness. Overall, 26 studies were included in the present analysis. Our research revealed a high heterogeneity of included studies regarding the techniques used to assess the aortic stiffness. Aortic stiffness was assessed by pulse wave velocity (PWV), elastic modulus (Ep), and augmentation index (AI). Currently a few studies exist investigating the role of CAVI in patients having an aortic aneurysm or undergoing endovascular aortic repair. The majority of studies showed that the treatment of an abdominal aortic aneurysm (AAA) either with open repair (OR) or endovascular aortic repair (EVAR) reduces aortic compliance significantly. Whether EVAR reconstruction might contribute a higher effect on arterial stiffness compared to OR needs further focused research. An increase of arterial stiffness was uniformly observed in studies investigating patients following thoracic endovascular aortic repair (TEVAR), and the effect was more pronounced in young patients. The effects of increased arterial stiffness after EVAR and TEVAR on the heart and the central hemodynamic, and an eventual effect on cardiac systolic function, need to be further investigated and evaluated in large studies and special groups of patients.