The quality of phantom images was previously shown to be higher on digital (Vereos Philips®) compared to analog PET (Ingenuity Philips®) cameras. This study aimed to determine the extent to which this difference still remains significant on normal brain 18F-FDG PET images. Relative noise and contrast as well as border sharpness (a spatial resolution index) of central (striata) and peripheral (occiput) gray-matter structures were compared between 10 sets of normal brain 18F-FDG PET images recorded and reconstructed on digital and analog last-generation PET cameras, together with a subjective visual analysis of image quality provided by experienced physicians. Compared with analog PET, digital PET provided marked improvements in image quality parameters. The median relative noise was decreased (− 22%), while gray/white-matter contrast was increased (+ 27%/+ 41% for central/peripheral gray-matter structures), with these results being consistent with visual analysis. In addition, a clear enhancement in image sharpness was further documented for digital PET owing to the possible use of a 1-mm3 voxel size (+ 24%/+ 21%). On normal brain 18F-FDG images and compared with a last-generation analog PET, the fully digital PET camera offers marked improvements in image noise and contrast, as well as significant potential for further enhancing spatial resolution.

Objective:: Determining the factors associated with new-onset pre-diabetes and type 2 diabetes mellitus (T2D) is important for improving the current prevention strategies and for a better understanding of the disease. Design:: To study the factors (clinical, circulating protein and genetic) associated with new onset pre-diabetes and T2D in an initially healthy (without diabetes) populational familial cohort with a long follow-up (STANISLAS cohort). Methods:: A total of 1506 participants attended both the visit 1 and visit 4, separated by ≈20 years. Over 400 proteins, GWAS and genetic associations were studied using models adjusted for potential confounders. Both prospective (V1 to V4) and cross-sectional (V4) analyses were performed. Results:: People who developed pre-diabetes (n = 555) and/or T2D (n = 73) were older, had higher BMI, blood pressure, glucose, LDL cholesterol, and lower eGFR. After multivariable selection, PAPP-A (pappalysin-1) was the only circulating protein associated with the onset of both pre-diabetes and T2D with associations persisting at visit 4 (i.e. ≈20 years later). FGF-21 (fibroblast growth factor 21) was a strong prognosticator for incident T2D in the longitudinal analysis, but not in the cross-sectional analysis. The heritability of the circulating PAPP-A was estimated at 44%. In GWAS analysis, the SNP rs634737 was associated with PAPP-A both at V1 and V4. External replication also showed lower levels of PAPP-A in patients with T2D. Conclusions:: The risk of developing pre-diabetes and T2D increases with age and with features of the metabolic syndrome. Circulating PAPP-A, which has an important genetic component, was associated with both the development and presence of pre-diabetes and T2D.

Assessing VAC is especially useful in heart failure and valvular heart disease, but less is known about VAC in the pathophysiology of CV disease risk in younger individuals. In young individuals without overt CV disease, we showed descriptive data regarding VAC, determined by PWV/GLS ratio, and explored the associations of VAC with clinical CV disease risk factors. Worse VAC, reflected by higher values of PWV/GLS, associated with high blood pressure and smoking in young adults.

Background: Heart failure with preserved ejection fraction (HFpEF) is a multifaceted syndrome, likely stemming from comorbidity‐induced inflammation resulting in endothelial dysfunction. Endothelial glycocalyx degradation's role in the development and prognosis of HFpEF remains largely unexplored. Our study aimed at exploring the association between glycocalyx degradation and diastolic dysfunction and determining whether glycocalyx degradation can predict clinical outcomes in patients with HFpEF. Methods: Perlecan and thrombomodulin concentrations were assessed in individuals deemed healthy (STANISLAS [Suivi Temporaire Annuel Non‐Invasif de la Santé des Lorrains Assurés Sociaux (Annual Noninvasive Temporary Monitoring of the Health of Insured Lorrainers)] cohort, n=1705) and patients with HFpEF (MEDIA‐DHF [Metabolic Road to Diastolic Heart Failure], n=460 and BIOSTAT‐CHF [Biology Study to Tailored Treatment in Chronic Heart Failure], n=556) to evaluate endothelial glycocalyx degradation. Results: In patients with HFpEF, perlecan but not thrombomodulin was increased compared with controls ( P <0.0001 versus P =0.73). In adjusted analysis, perlecan was associated with peak early mitral inflow velocity/peak early diastolic mitral annular velocity ratio and thrombomodulin with peak early diastolic mitral annular velocity in control individuals, whereas perlecan and thrombomodulin were associated with peak early mitral inflow velocity/peak early diastolic mitral annular velocity and left atrial volume index in patients with HFpEF (all P <0.03). Perlecan was significantly associated with cardiovascular hospitalization and death in the MEDIA‐DHF (adjusted hazard ratio [HR] for highest tertile versus first tertile, 2.44 [95% CI, 1.11–5.34]; P =0.026) and BIOSTAT‐CHF cohorts (adjusted HR, 2.12 [95% CI, 1.49–3.03]; P <0.0001). Thrombomodulin was associated with a worse outcome in BIOSTAT‐CHF ( P =0.004) but not in MEDIA‐DHF. Conclusions: Higher circulating levels of the endothelial glycocalyx degradation biomarkers like perlecan and, to a lesser extent, thrombomodulin are associated with features of diastolic dysfunction in population and HFpEF settings and predict poor outcome in patients with HFpEF. These results suggest that glycocalyx degradation may be an early step in the pathological processes leading to HFpEF and gain further prognostic value in later stages (ie, overt HFpEF). Registration: URL: https://clinicaltrials.gov/ ; Unique identifiers: NCT01391442, https://clinicaltrials.gov/study/NCT01391442?cond=stanislas&rank=1 ; NCT02446327; URL: https://cordis.europa.eu ; BIOSTAT‐CHF ID: 242209.