Macdonalddaugherty0079

Objective Chronic kidney disease (CKD) and cardiovascular disease (CVD) have a high morbidity and mortality among the elderly. Low levels of high-density lipoprotein cholesterol (HDL-C), a traditional risk marker for CVD, are common in CKD patients. Little is known about the association of low HDL-C with renal dysfunction in the community dwelling population. Methods This was a population-based cross-sectional study included 4,753 participants enrolled in a prospective study, the Shanghai Elderly Cardiovascular Health (SHECH) study. GSK2334470 Estimated glomerular filtration rate (eGFR), calculated by the Chinese Modification of Diet in Renal Disease (C-MDRD equation), was used to assess renal dysfunction. Associations between renal dysfunction and low HDL-C were evaluated using multiple logistic regression models and restricted cubic splines. Results Of 4,649 individuals who met inclusion criteria, 620 (13.34%) had low HDL-C at less then 40 mg/dl. In the fully adjusted model, lower eGFR of less then 60 ml/min/1.73 m2 (OR, 2.03; 95% CI, 1.21-3.43) and marginal eGFR of 60 to 90 ml/min/1.73 m2 (OR, 1.26; 95% CI, 1.01-1.58) were significantly associated with low HDL-C, compared with normal eGFR of ≥90 ml/min/1.73 m2. Moreover, consistent findings were obtained in subsidiary analyses using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. Fully adjusted cubic spline models indicated a significant dose-response relationship between eGFR and low HDL-C (P for non-linearity, 0.356). Conclusion In this general elderly population, renal dysfunction was independently and significantly associated with low HDL-C, and the prevalence of low HDL-C increased with decreasing eGFR, such that even slight changes in renal function may be associated with altered lipid levels.Background The etiology of cerebral small vessel disease (SVD) remains elusive, though evidence is accumulating that inflammation contributes to its pathophysiology. We recently showed retrospectively that pro-inflammatory monocytes are associated with the long-term progression of white matter hyperintensities (WMHs). In this prospective high-frequency imaging study, we hypothesize that the incidence of SVD progression coincides with a pro-inflammatory monocyte phenotype. Methods Individuals with SVD underwent monthly magnetic resonance imaging (MRI) for 10 consecutive months to detect SVD progression, defined as acute diffusion-weighted imaging-positive (DWI+) lesions, incident microbleeds, incident lacunes, and WMH progression. Circulating inflammatory markers were measured, cytokine production capacity of monocytes was assessed after ex vivo stimulation, and RNA sequencing was performed on isolated monocytes in a subset of participants. Results 13 out of 35 individuals developed SVD progression (70 ± 6 years, 54% men) based on incident lesions (n = 7) and/or upper quartile WMH progression (n = 9). Circulating E-selectin concentration (p less then 0.05) and the cytokine production capacity of interleukin (IL)-1β and IL-6 (p less then 0.01) were higher in individuals with SVD progression. Moreover, RNA sequencing revealed a pro-inflammatory monocyte signature including genes involved in myelination, blood-brain barrier, and endothelial-leukocyte interaction. Conclusions Circulating monocytes of individuals with progressive SVD have an inflammatory phenotype, characterized by an increased cytokine production capacity and a pro-inflammatory transcriptional signature.Myocardial ischemia/reperfusion (IR) injury represents a critical problem associated with interventional approaches for coronary reperfusion. Pharmacological cardioprotective interventions are advocated to ameliorate IR injury. Melatonin is an anti-inflammatory and antioxidant agent with a wide range of therapeutic properties that may contribute to its cardioprotective effects. No systematic review or meta-analysis has compared melatonin vs. placebo as a cardioprotective agent in humans. The present study, based on a systematic review and meta-analysis, was carried out to assess melatonin's efficacy as a cardioprotective treatment. We performed a systematic review of the available literature. Randomized controlled trials (RCTs) were identified and information was extracted using predefined data extraction forms. The primary outcomes were (a) left ventricular ejection fraction (LVEF) and (b) blood troponin levels in patients who underwent myocardial revascularization and were randomized to melatonin or placebo. The inverse-variance random-effects method was used to pool the estimates. Heterogeneity and publication bias were assessed. Weighted mean differences or standardized mean differences were calculated. A total of 283 records were screened and seven RCTs met all the inclusion criteria. After the pooled analysis, the results on LVEF were consistent across all studies, and a significant heterogeneity was found in the results on troponin levels. The melatonin-treated patients had on average higher LVEF than the placebo-treated individuals with a weighted mean difference = 3.1% (95% CI 0.6-5.5, p = 0.01). Five works compared the levels of troponin after melatonin or placebo treatment. The melatonin-treated patients had lower levels of troponin with a standardized mean difference = -1.76 (95% CI -2.85 to -0.67, p = 0.002). The findings of this meta-analysis revealed that melatonin administration in humans as a cardioprotective agent attenuated heart dysfunction with a favorable effect on the LVEF.Objective Altered coagulation parameters in COVID-19 patients is associated with a poor prognosis. We tested whether COVID-19 patients on chronic oral anticoagulants (cOACs) for thromboembolism prophylaxis could receive protection from developing more severe phenotypes of the disease. Approach and Results We searched the database of the SARS-RAS study (Clinicaltrials.gov NCT04331574), a cross-sectional observational multicenter nationwide survey in Italy designed by the Italian Society of Hypertension. The database counts 2,377 charts of Italian COVID-19 patients in 26 hospitals. We calculated the Charlson comorbidity index (CCI), which is associated with death in COVID-19 patients. In our population (n = 2,377, age 68.2 ± 0.4 years, CCI 3.04 ± 0.04), we confirm that CCI is associated with increased mortality [OR 1.756 (1.628-1.894)], admission to intensive care units [ICU; OR 1.074 (1.017-1.134)], and combined hard events [CHE; OR 1.277 (1.215-1.342)]. One hundred twenty-five patients were on cOACs (age 79.3 ± 0.9 years, CCI 4.35 ± 0.13); despite the higher CCI, cOACs patients presented with a lower risk of admissions to the ICU [OR 0.469 (0.250-0.880)] but not of death [OR 1.306 (0.78-2.188)] or CHE [OR 0.843 (0.541-1.312)]. In multivariable logistic regression, cOACs confirmed their protective effect on ICU admission and CHE. The CCI remains the most important risk factor for ICU admission, death, and CHE. Conclusions Our data support a mechanism for the continuation of cOAC therapy after hospital admission for those patients who are on chronic treatment. Our preliminary results suggest the prophylactic use of direct cOACs in patients with elevated CCI score at the time of the COVID-19 pandemic even in absence of other risks of thromboembolism.Background Anemia is a commonly occurring comorbidity in patients with heart failure (HF). Although there are a few reports of a higher prevalence of mortality and hospitalization-related outcomes due to accompanying anemia, other studies suggest that anemia does not have an adverse impact on the prognostic outcomes of HF. Two meta-analyses in the past decade had reported the adverse impact of anemia on both mortality and hospitalization- related outcomes. However, only one of these studies had evaluated the outcome while using multivariable adjusted hazard ratios. Moreover, several studies since then reported the prognostic influence of anemia in HF. In this present study, we evaluate the prognostic impact of anemia on mortality and hospitalization outcomes in patients with HF. Methods We carried out a systematic search of the academic literature in the scientific databases EMBASE, CENTRAL, Scopus, PubMed, Cochrane, ISI Web of Science, clinicaltrial.gov, and MEDLINE based on the PRISMA guidelines. Meta-analy prognostic outcome of chronic HF.Background To explore the association of DNA methylation and gene expression in the pathology of obesity. Methods (1) Genomic DNA methylation and mRNA expression profile of visceral adipose tissue (VAT) were performed in a comprehensive database of gene expression in obese and normal subjects. (2) Functional enrichment analysis and construction of differential methylation gene regulatory networks were performed. (3) Validation of the two different methylation sites and corresponding gene expression was done in a separate microarray dataset. (4) Correlation analysis was performed on DNA methylation and mRNA expression data. Results A total of 77 differentially expressed mRNAs matched with differentially methylated genes. Analysis revealed two different methylation sites corresponding to two unique genes-s100a8-cg09174555 and s100a9-cg03165378. Through the verification test of two interesting different expression positions [differentially methylated positions (DMPs)] and their corresponding gene expression, we found that methylation in these genes was negatively correlated to gene expression in the obesity group. Higher S100A8 and S100A9 expressions in obese subjects were validated in a separate microarray dataset. Conclusion This study confirmed the relationship between DNA methylation and gene expression and emphasized the important role of S100A8 and S100A9 in the pathogenesis of obesity.Anomalous aortic origin of a coronary artery (AAOCA) is reported as the second leading cause of sudden cardiac death in otherwise healthy young individuals. Several surgical studies have reported a shallow operative risk, describing repair as safe and effective with short or medium-term follow-up. However, surgical repair can also be associated with a high risk of complications. Numerous repair techniques have been described in the literature, but each technique's indications and limitations are often not well-understood or understated. Since explicit technical knowledge of the most appropriate surgical technique is highly desirable, we sought to thoroughly and clearly outline the safeguards and pitfalls of the most common surgical techniques used to repair AAOCA.Background Liver dysfunction is prevalent in patients with heart failure (HF), but the prognostic significance of liver function tests (LFTs) remains controversial. Heart failure with preserved ejection fraction (HFpEF) had been introduced for some time, but no previous study had focused on LFTs in HFpEF. Thus, we aim to evaluate the prognostic significance of LFTs in well-defined HFpEF patients. Methods and Results We conveyed a post-hoc analysis of the Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist Trial (TOPCAT). The primary outcome was the composite of cardiovascular mortality, HF hospitalization, and aborted cardiac arrest, and the secondary outcomes were cardiovascular mortality and HF hospitalization. In Cox proportional hazards models, aspartate transaminase (AST) and alanine transaminase (ALT) were not associated with any of the outcomes. On the contrary, increases in total bilirubin (TBIL) and alkaline phosphatase (ALP) were associated with increased risks of the primary outcome [TBIL adjusted hazard ratio (HR), 1.