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A dose-response meta-analysis to evaluate the relationship between high-density lipoprotein cholesterol and all-cause and cardiovascular disease mortality.
Liu, L, Han, M, Qie, R, Li, Q, Zhang, X, Zhang, J, Zhan, S, Zhang, L, Xu, Z, Zhang, C, et al
Journal of endocrinological investigation. 2022;(3):551-562
Abstract
PURPOSE Previous studies have not fully described the relationship between high-density lipoprotein cholesterol (HDL-C) and death risks from all cause and cardiovascular disease (CVD). This study quantitatively evaluates HDL-C-mortality associations. METHODS Embase and PubMed databases were searched for relevant articles published up to 1 June 2019. Random-effects models were used to pool relative risks (RRs) and 95% confidence intervals (CIs). We used restricted cubic splines to model the dose-response association. RESULTS We identified 32 prospective cohort studies including 369,904 participants and 33,473 total deaths (9426 CVD deaths). Compared to the lowest HDL-C levels, all cause and CVD mortality risks were reduced by 18% (RR 0.82; 95% CI, 0.73-0.93) and 36% (0.64, 0.46-0.89), respectively, for the highest HDL-C levels. All cause and CVD mortality risks were reduced by 15% (0.85, 0.79-0.92) and 23% (0.77, 0.69-0.87), respectively, with each 1 mmol/L increment of HDL-C. We found evidence of nonlinear and negative dose-response associations of HDL-C with all cause and CVD mortality (Pnonlinearity < 0.001), and the lowest death risks from all cause and CVD were observed at approximately 1.34 and 1.55 mmol/L, respectively. CONCLUSION HDL-C is inversely associated with all cause and CVD mortality risks under approximately 2.05 and 2.33 mmol/L, respectively. Optimal doses require investigation via clinical practice or high-quality research.
2.
Impact of triglyceride playing on stroke severity correlated to bilirubin.
Li, Z, Zhang, J, Luo, Y
Medicine. 2020;(36):e21792
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Abstract
Major lipids making effects on the occurrence of acute ischemic stroke (AIS) is well recognized, but their roles on stroke severity remain uncertain. To explore the exact roles of lipids playing on stroke severity and the possible mechanism, we conduct this observational study.Data was collected from patients with AIS from February 2008 to May 2012. The level of major lipids was compared among AIS groups with different severity and investigated the correlation. Also, the relationship existed between major lipids and bilirubin. Mechanism of major lipids playing on stroke severity was researched to determine if oxidative stress reflected by bilirubin.Lower triglyceride (TG) and higher high density lipoprotein cholesterol (HDL-C) were observed in severe stroke, and obvious correlation existed between TG and stroke severity or HDL-C and stroke severity. TG was associated negatively with direct bilirubin (DBIL) and total bilirubin (TBIL), and lower level of DBIL and TBIL were related to higher quartiles of TG. There was no obvious difference of DBIL and TBIL among the groups of quartiles of HDL-C. TG was the influence factor of stroke severity in severe stroke through multiple univariable logistic regression. But it was not the independent influence factor after multivariable logistic regression adjusted by DBIL or TBIL. However, HDL-C was the influence factor of stroke severity through both univariable and multivariable logistic regression.Lower TG or higher HDL-C predicted severer stroke. The effect of TG on stroke severity was mediated by bilirubin, not HDL-C.
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The association between peroxisome proliferator-activated receptor Δ rs3777744, rs3798343, and rs6922548 and coronary artery disease.
Zhang, J, Liu, XL, Jia, QW, Zhao, CH, Liu, JY, An, FH, Li, LH, Chen, ZH, Wang, LS, Ma, WZ, et al
Bioscience reports. 2019;(1)
Abstract
Objective: The aim of the present study is to investigate the association between the single nucleotide polymorphism (SNP) sites of peroxisome proliferator-activated receptor Δ (PPARD) and the risk of coronary artery disease (CAD). To this end, a prospective observational single-center study of the clinical data from 880 subjects in a Chinese population was conducted. Methods: A total of 880 subjects, including 609 CAD patients and 271 control subjects, were selected for the present study. All inpatients had 4 ml of venous blood drawn after 12 h of fasting, and then clinical tests were conducted to obtain the biochemical parameters. CAD patients and Controls were distinguished by coronary angiography. Statistical analysis was conducted with SPSS software (ver 16.0). Results: A significant association between the G-alleles of PPARD rs3777744 and rs3798343 and a decreased risk for CAD was found. Moreover, we found an interaction between high fasting high-density lipoprotein cholesterol (HDL-C) serum levels, low serum glucose levels and their genotypes, ultimately decreasing the risk of CAD. Haplotype analysis was conducted on the three SNP sites, rs3777744 and rs3798343 to form a block [r2 = 0.79, D' = 0.99). The A-C haplotypes were associated with an increased risk of CAD (odds ratio (OR), 95% confidence interval (CI): 1.321 (1.060-1.647), P=0.013], and the G-G haplotypes were associated with a decreased risk [OR, 95% CI: 0.714 (0.567-0.849), P=0.004]. Conclusions: Our study indicates a significant association between the G-alleles of PPARD rs3777744 and rs3798343 and a decreased CAD risk. In addition, genotypes interact with high serum HDL-C levels and low serum glucose levels, resulting in decreased prevalence of CAD.