Korean public and hospital data for estimating LDL-cholesterol.
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ABSTRACT:
SUBMITTER: Lee T
PROVIDER: S-EPMC6301972 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Objective:Data on the intensity of statin therapy for patients with acute myocardial infarction (MI) and very low baseline low-density lipoprotein (LDL) cholesterol level are lacking. We sought to assess the impact of statin intensity in patients with acute MI and LDL cholesterol <70 mg/dL. Methods:A total of 1,086 patients with acute MI and baseline LDL cholesterol <70 mg/dL from the Korea Acute Myocardial Infarction Registry-National Institute of Health database were divided into less intensive statin (expected LDL reduction <40%, n=302) and more intensive statin (expected LDL reduction ?40%, n=784) groups. The primary endpoint was major adverse cardiac and cerebrovascular events (MACCEs), a composite of cardiac death, MI, revascularization occurring at least 30 days after admission, and stroke, at 12 months. Results:After 1:2 propensity matching, differences were not observed between less intensive (n=302) and more intensive statin (n=604) groups in incidence of cardiac death (0.3% vs. 0.3%) and hemorrhagic stroke (0.3% vs. 0.5%, p=0.727) at 12 months. Compared with the less intensive statin group, the more intensive statin group showed lower target-vessel revascularization (4.6% vs. 1.8%, p=0.027) and MACCE (11.6% vs. 7.0%, p=0.021). Major bleeding was not different between less intensive and more intensive statin groups (1.0% vs. 2.6%, p=0.118). Conclusion:More intensive statin therapy was associated with significantly lower major adverse cardiovascular events in patients with acute MI and very low LDL cholesterol compared with less intensive statin therapy.
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Project description:BackgroundLimited data are available for validation of low-density lipoprotein cholesterol (LDL) calculation (LDLcal) in the adult Korean population. The aim of this study was to develop and validate a new equation for LDLcal and to compare it with previous such equations in a Korean population.MethodsA new equation for LDLcal was developed (LDLChoi). LDLChoi and 11 other previously published equations were applied and compared with directly measured LDL concentration (LDLdirect) in a development cohort (population 1), an independent validation cohort in the same laboratory (population 2), and the Korea National Health and Nutrition Examination Survey 2017 cohort (population 3).ResultsAmong the 12 equations, the newly-developed equation (LDLChoi = total cholesterol - 0.87 x high-density lipoprotein cholesterol - 0.13 x triglycerides) had the highest intraclass correlation coefficient (ICC) and the lowest mean systemic difference and median absolute percentage error in populations 1 and 2 but not in population 3. Subgroup analysis showed good agreement between LDLChoi and LDLdirect (ICC > 0.75) in population 2, whose LDLdirect < 70 mg/dL. For samples with high triglycerides (> 400 mg/dL), equation accuracy varied. Categorization concordance according to the National Cholesterol Education Program Adult Treatment Panel III criteria with the other 11 equations were less than 80%; that of LDLChoi was 87.6 and 87.4% in populations 1 and 2, respectively.ConclusionsAccuracy of 12 equations for LDLcal varied by cohort and subgroup based on LDLdirect and triglycerides. A laboratory-specific equation for LDLcal and/or LDLdirect may be needed for accurate evaluation of LDL status.
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Project description:OBJECTIVE: To develop a tool for estimating hospital-specific inpatient prices for major payers. DATA SOURCES: AHRQ Healthcare Cost and Utilization Project State Inpatient Databases and complete hospital financial reporting of revenues mandated in 10 states for 2006. STUDY DESIGN: Hospital discharge records and hospital financial information were merged to estimate revenue per stay by payer. Estimated prices were validated against other data sources. PRINCIPAL FINDINGS: Hospital prices can be reasonably estimated for 10 geographically diverse states. All-payer price-to-charge ratios, an intermediate step in estimating prices, compare favorably to cost-to-charge ratios. Estimated prices also compare well with Medicare, MarketScan private insurance, and the Medical Expenditure Panel Survey prices for major payers, given limitations of each dataset. CONCLUSIONS: Public reporting of prices is a consumer resource in making decisions about health care treatment; for self-pay patients, they can provide leverage in negotiating discounts off of charges. Researchers can also use prices to increase understanding of the level and causes of price differentials among geographic areas. Prices by payer expand investigational tools available to study the interaction of inpatient hospital price setting among public and private payers--an important asset as the payer mix changes with the implementation of the Affordable Care Act.
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Project description:In the past decade, microRNAs (miRNAs) have emerged as key regulators of circulating levels of lipoproteins. Specifically, recent work has uncovered the role of miRNAs in controlling the levels of atherogenic low-density lipoprotein LDL (LDL)-cholesterol by post-transcriptionally regulating genes involved in very low-density lipoprotein (VLDL) secretion, cholesterol biosynthesis, and hepatic LDL receptor (LDLR) expression. Interestingly, several of these miRNAs are located in genomic loci associated with abnormal levels of circulating lipids in humans. These findings reinforce the interest of targeting this subset of non-coding RNAs as potential therapeutic avenues for regulating plasma cholesterol and triglyceride (TAG) levels. In this review, we will discuss how these new miRNAs represent potential pre-disposition factors for cardiovascular disease (CVD), and putative therapeutic targets in patients with cardiometabolic disorders. This article is part of a Special Issue entitled: MicroRNAs and lipid/energy metabolism and related diseases edited by Carlos Fernández-Hernando and Yajaira Suárez.
| S-EPMC5375104 | biostudies-literature
Project description:Although statin therapy is a cornerstone of current low density lipoprotein (LDL)-lowering strategies, there is a need for additional therapies to incrementally lower plasma LDL cholesterol. In this study, we investigated the effect of several methylenedioxyphenol derivatives in regulating LDL cholesterol through induction of LDL receptor (LDLR). INV-403, a modified methylenedioxyphenol derivative, increased LDLR mRNA and protein expression in HepG2 cells in a dose- and time-dependent fashion. These effects were apparent even under conditions of HMG-CoA reductase inhibition. Electrophoresis migration shift assays demonstrated that INV-403 activates SREBP2 but not SREBP1c, with immunoblot analysis showing an increased expression of the mature form of SREBP2. Knockdown of SREBP2 reduced the effect of INV-403 on LDLR expression. The activation of SREBP2 by INV-403 is partly mediated by Akt/GSK3? pathways through inhibition of phosphorylation-dependent degradation by ubiquitin-proteosome pathway. Treatment of C57Bl/6j mice with INV-403 for two weeks increased hepatic SREBP2 levels (mature form) and upregulated LDLR with concomitant lowering of plasma LDL levels. Transient expression of a LDLR promoter-reporter construct, a SRE-mutant LDLR promoter construct, and a SRE-only construct in HepG2 cells revealed an effect predominantly through a SRE-dependent mechanism. INV-403 lowered plasma LDL cholesterol levels through LDLR upregulation. These results indicate a role for small molecule approaches other than statins for lowering LDL cholesterol.
| S-EPMC3329387 | biostudies-literature
Project description:Maintaining optimal low-density lipoprotein (LDL) cholesterol levels is necessary to prevent cardiovascular disease (CVD). Excessive fat mass and decreased muscle mass are both associated with increased risks of developing dyslipidemia. Thus, we investigated the longitudinal relationship between the fat-to-muscle ratio (FMR) and the non-achievement of LDL cholesterol targets. We analyzed a total of 4386 participants aged 40-69 years from the Korean Genome and Epidemiology Study. FMR was defined as the ratio of total fat mass to total muscle mass, measured by bioelectrical impedance. The non-achievement of an LDL cholesterol target was defined as an LDL cholesterol level higher than the established target level according to individual CVD risk. The adjusted hazard ratios and 95% confidence interval for the incidence of non-achievement of LDL cholesterol targets for the sex-specific middle and highest tertiles vs. the referent lowest tertile of FMR were 1.56 (1.29-1.90) and 1.86 (1.47-2.31) in men and 1.40 (1.18-1.66) and 1.31 (1.06-1.62) in women after adjusting confounders. Our findings suggest that FMR, a novel indicator of the combined effects of fat and muscle mass, is useful for predicting non-achievement of LDL cholesterol targets.
| S-EPMC8396939 | biostudies-literature
Project description:This article supports experimental evidence on the time-dependent effect on gene expression related to inflammation and cholesterol deposition in lipid-loaded cells. The cells employed were human monocytes THP1 line transformed into macrophages by treatment with phorbol esters. Macrophages were treated at different times with oxidized low density lipoprotein (Ox-LDL) and then gene expression was measured. We also include data about the different types of oxidized lipoprotein obtained (low, media or high oxidation) for differential exposure with Cu ions. These data include characterization to lipid and protein peroxidative damage and also quantification of cell viability by exposure to native and modified LDL. The present article complements data published in "Decreased OxLDL uptake and cholesterol efflux in THP1 cells elicited by cortisol and by cortisone through 11?-hydroxysteroid dehydrogenase type 1" Ledda et al. (in press) [1].
| S-EPMC4906131 | biostudies-other
Project description:Objectives:To measure correlation and concordance between measured LDL cholesterol (mLDLc) and Friedewald's calculated LDL cholesterol (cLDLc). To compare the mLDLc and cLDLc values for various anthropometric measures and biochemical indices including insulin resistance, nephropathy, glycated hemoglobin and triglycerides. Methods:Two hundred thirty two subjects were included in this cross-sectional analysis from Jan-2016 to July-2017 from a target population visiting PNS HAFEEZ hospital. Mean age of the subjects was 46.56(±11.95) years (n=232). These subjects underwent clinical evaluation including measurement of anthropometric measurements, biochemical testing for fasting plasma glucose (FPG), glycated hemoglobin (HbA1c), lipid profile, urine albumin creatinine ratio (UACR), and insulin. Correlation and concordance between mLDLc and Friedewald's cLDLc were measured. Finally, Comparison of risk evaluation for mLDLc and cLDLc between groups formulated based upon UACR (Based upon a cut off of 2.5 mg/g) and fasting triglycerides (Group-1 :< 1.0 mmol/L, Group-2: 1.0-1.99 mmol/L and Group-3 :> 1.99 mmol/) was carried out. Results:There was significant positive linear correlation between mLDLc and cLDLc [r=0.468, <0.001]. Kendall's Coefficient of concordance between mLDLc and cLDLc was 0.055 (p<0.001). Differences evaluated by one way ANOVA analysis for mLDLc between various triglycerides groups were only significant between group-1 and group-2 [{Group-1:Mean=2.40, (2.19-2.61), n=43}, {Group-2:Mean=2.81, (2.69-2.92), n=136}, [{Group-3:Mean=2.59,(2.37-2.81), n=53}],(p=0.004) in comparison to cLDLc [{Group-1:Mean=2.63, (2.43-2.84), n=43}, {Group-2:Mean=2.85, (2.76-2.93), n=136}, [{Group-3:Mean=2.75, (2.60-2.90), n=53}]. Calculated method for LDLc showed higher UACR than mLDLc. (p=0.021). Conclusion:cLDLc over estimates LDL-cholesterol in comparison to mLDLc. The correlation between cLDLc and mLDLc was only moderate. However, cLDLc provided better degree of risk prediction for nephropathy and glycated hemoglobin than mLDLc.
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