Levesquebryant3837
Most of the laboratories make use of the Friedewald formula to assess low-density lipoprotein cholesterol (LDL-C). The accuracy of this approach, however, crucially depends on triglyceride concentrations. Since hypertriglyceridaemia is a characteristic trait of the lipid profile in chronic kidney disease (CKD), the present study examines the accuracy of the Friedewald formula in this population. It aims to derive and validate a more accurate equation for CKD.
Cross-sectional study on two cohorts of subjects (overall n = 3.514) with estimated glomerular filtration rate (eGFR) <60 mL/min comparing directly measured LDL-C (LDL-Cmeas) as assessed by an enzymatic assay (Roche, Switzerland) to concentrations estimated by the Friedewald (LDL-CF) and the Martin's formula (LDL-CM). Accuracy was analysed by Bland-Altman and linear regression analyses. In the first cohort, a novel formula was derived to assess LDL-C in CKD. Bardoxolone The formula was validated in Cohort 2.
Cohort 1 comprised 1738 subjects, and Cohort 2 comprised 1776 subjects. The mean eGFR was 29.4 ± 14.4 mL/min. In Cohort 1, LDL-CF was highly correlated with LDL-Cmeas (R2 = 0.92) but significantly underestimated LDLmeas by 11 mg/dL. LDL-C = cholesterol - HDL - triglycerides/7.98 was derived as the optimal equation for the calculation of LDL-C in Cohort 1 and was successfully validated in Cohort 2 (bias of 1.6 mg/dL). The novel formula had a higher accuracy than both the Friedewald (bias -12.2 mg/dL) and the Martin's formula (bias -4.8 mg/dL).
The Friedewald formula yields lower LDL-C concentrations in CKD than direct enzymatic measurements, which may lead to undersupply of this cardiovascular high-risk population in a treat-to-target approach.
The Friedewald formula yields lower LDL-C concentrations in CKD than direct enzymatic measurements, which may lead to undersupply of this cardiovascular high-risk population in a treat-to-target approach.
Declining prevalence of abdominal aortic aneurysm (AAA) might force a more targeted screening approach (high-risk populations only) in order to maintain (cost-)effectiveness. We aimed to determine temporal changes in the prevalence of screening-detected AAA, to assess AAA-related surgery, and evaluate all-cause mortality in patients with manifest vascular disease.
We included patients with manifest vascular disease but without a history of AAA enrolled in the ongoing single-centre prospective UCC-SMART cohort study. Patients were screened at baseline for AAA by abdominal ultrasonography. We calculated sex- and age-specific prevalence of AAA, probability of survival in relation to the presence of AAA, and the proportion of patients undergoing AAA-related surgery. Prevalence of screening-detected AAA in 5440 screened men was 2.5% [95% confidence interval (CI) 2.1-2.9%] and in 1983 screened women 0.7% (95% CI 0.4-1.1%). Prevalence declined from 1997 until 2017 in men aged 70-79 years from 8.1% to 3.2% and inthis remains to be determined.
To investigate relationships between takeaway food and sugar-sweetened beverage (SSB) consumption with cardiometabolic phenotypes during childhood and mid-adulthood.
Design Cross-sectional Child Health CheckPoint within the national population-representative Longitudinal Study of Australian Children. Participants 1838 children (mean age 11.5 years; 49.1% female) and 1846 adults (mean age 43.7 years; 87.6% female). Exposures Self-reported takeaway food and SSB consumption ('frequent' ≥ weekly). Outcomes Functional (pulse wave velocity (PWV), blood pressure (BP)) and structural (carotid intima-media thickness, retinal microvascular calibre) preclinical cardiovascular phenotypes; lipids (total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglycerides). Analysis Linear regression (exposure takeaway or SSB consumption, individually or together) adjusted for age, sex and socio-economic position; and mediation analysis for body mass index (BMI).
Associations were small among chiof strong associations in children highlights opportunities for prevention.
The aim of this study was to analyse the role of inflammation and established clinical scores in predicting acute kidney injury (AKI) after acute coronary syndromes (ACS).
In a prospective multicentre cohort including 2034 patients with ACS undergoing percutaneous coronary intervention, high-sensitivity C-reactive protein (hsCRP), neutrophil count, neutrophil-to-lymphocyte ratio (NL-ratio), and creatinine were measured at the index procedure. AKI (n = 39, defined according to RIFLE criteria) and major cardiovascular and cerebrovascular events were adjudicated after 1 year. Associations between inflammation, AKI, and cardiac death (CD) were assessed by C-statistics and Cox proportional hazard models with log-rank test to compare survival. Patients with ACS with elevated neutrophil count >7.8 × 109/L, NL-ratio >5, combined neutrophil-count/creatinine, or NL-ratio/creatinine at baseline showed a higher incidence of AKI (all P < 0.05) and CD (all P < 0.001). The risk of AKI, CD, and their combinatalTrials.gov, NCT01000701.The acquired immunodeficiency syndrome (AIDS), caused by the human immunodeficiency virus (HIV), has been a global public health challenge for several decades. The majority of HIV infection is caused by the human immunodeficiency virus type 1 (HIV-1), which enters and infects a host cell via the cell surface proteins of CD4 as the primary receptor, and chemokine receptors CXCR4 or CCR5 as the coreceptor-then undergoing replication using the cell's intracellular machinery. Whereas many drugs targeting CCR5-mediated entry or HIV-1 replication via reverse transcriptase or proteases have long been used clinically, agents targeting CXCR4 are yet to be advanced to clinical application. Here in this review we highlight some of the strategies for and progress made in the discovery of novel small molecules, peptides, and larger molecules that target CXCR4, and their future prospects for translation into the clinic as a new class of anti-HIV therapeutics.
Animal models repeatedly show fasting increases longevity. Human data, though, are limited to anecdotal claims. This study evaluated the association of routine fasting with survival and, secondarily, with incident major adverse cardiovascular events.
Cardiac catheterization patients enrolled in the Intermountain INSPIRE longitudinal cohort (n = 2785) during 2013-2015 were followed through March 2019. A fasting survey was completed in n = 2025 (73%) of this cohort and 1957 were included in the final data analysis after 68 participants were removed (24 for data issues and 44 for fasting less than 5 years). Self-reported routine fasting behaviour, years of participation in fasting, and other fasting characteristics were surveyed. Mortality was the primary outcome and incident myocardial infarction (MI), stroke, and heart failure (HF) were secondary. Routine fasters (n = 389, mean age 64 ± 14 years, 34% female) averaged 42 ± 18 years of routine fasting (minimum 5 years). Non-fasters (n = 1568, aged 63 ± 14 years, 36% female) included never fasters (n = 1120 with 0 years of fasting) and previous fasters (n = 448 who averaged 32 ± 21 years of prior fasting but had stopped prior to enrolment).
