Lipids in Health and Disease最新文献

Background: Previous observations have reported inconsistent results on the association between low-density lipoprotein cholesterol (LDL-C) at presentation and long-term outcomes after acute myocardial infarction (AMI). We aimed to clarify the potential impact of baseline characteristics on the inverse association between LDL-C and all-cause mortality, known as the lipid paradox.

Methods: A total of 1,305 critically ill patients with AMI from the Medical Information Mart for Intensive Care IV database were included in the analysis. Patients were stratified according to LDL-C quartiles. The primary outcome was 180-day and 360-day all-cause mortality. Baseline characteristics were included in stepwise Cox regression models. Restricted cubic spline analyses across multiple models and subgroups were performed to assess the influence of baseline characteristics on the association between LDL-C and long-term outcomes.

Results: A total of 244 (18.7%) and 291 (22.3%) mortality events occurred at 180 and 360 days of follow-up, respectively. Patients in the lowest LDL-C quartile had the highest all-cause mortality at both 180 and 360 days (28.7% and 35.2%, respectively). After stepwise adjustment for baseline covariates, the J-shaped relationship observed in the unadjusted model was gradually attenuated and disappeared. The inverse association between LDL-C and mortality was more pronounced in subgroups characterized by elevated mortality risk, including patients with low albumin levels, elevated neutrophil-to-lymphocyte ratio, and higher SOFA scores. Nevertheless, in-hospital statin use was consistently associated with reduced all-cause mortality across nearly all subgroups.

Conclusions: The lipid paradox observed in critically ill patients with AMI is attributed to differences in baseline characteristics across LDL-C strata. After adjusting for potential confounders, baseline LDL-C was not an independent predictor of long-term mortality in AMI. Lipid-lowering therapy was associated with favorable long-term outcomes irrespective of baseline LDL-C levels.

Background: Inflammation and metabolic disorders significantly contribute to frailty development. The C-reactive protein-triglyceride-glucose index (CTI) indicates both inflammation and insulin resistance (IR). This study delves into the connection between various dimensions of CTI-baseline CTI, cumulative CTI (cumCTI), and CTI change-and the incidence of frailty among the Chinese middle-aged and elderly demographic. Inflammation and metabolic disorders significantly contribute to frailty development.

Methods: This research employed the China Health and Retirement Longitudinal Study (CHARLS). K-means clustering was utilized to categorize the dynamic variations in CTI. The connection between various CTI dimensions and the frailty risk was evaluated through the Cox proportional hazards model and restricted cubic spline (RCS) regression model. Subgroup analyses, interaction tests, and sensitivity analyses were performed to ensure result robustness.

Results: The research involved a total of 5,366 participants. Through the application of K-means clustering, 3 classifications of changes in CTI trajectories were identified.Baseline characteristics from the K-means clustering analysis showed that the median age of individuals was 58 years (52, 64). Within the studied group, there were 2,899 males, constituting 54.0% of the total sample. During follow-up, there were 964 newly identified instances of frailty, accounting for 18.0% of the total cases documented. A notable positive linear correlation between increased CTI levels and the likelihood of experiencing frailty. In Model 3, each unit increment in the baseline CTI was associated with a 35% escalation in the likelihood of frailty (HR, 1.35; 95% CI, 1.21-1.50). Furthermore, each additional unit of cumCTI was linked to a 14% escalation in frailty risk (HR, 1.14; 95% CI, 1.09-1.19).The RCS analysis revealed a positive linear correlation between the initial CTI, cumCTI, and the likelihood of developing frailty. Subgroup and interaction analyses did not demonstrate any significant variations among the different subgroups (P>0.05). Sensitivity analyses further validated the consistency and reliability of these findings.

Conclusion: Elevated CTI are linked to an increased likelihood of frailty. Ongoing longitudinal assessment of CTI levels across multiple dimensions can facilitate the timely detection of patients who are at a significant risk of developing frailty.

Background: Residual cardiovascular risk persists in type 2 diabetes mellitus (T2DM) despite intensive risk-factor management. Apolipoprotein B (apoB) and excess apoB are potentially promising biomarkers for identifying residual cardiovascular risk. We assessed apoB and excess apoB in T2DM for incremental prediction of atherosclerotic cardiovascular disease (ASCVD) risk.

Methods: This prospective cohort included 11,918 UK Biobank participants (mean age 59.7 ± 6.6 years; 61% male) with T2DM and no ASCVD at baseline. Excess apoB was defined as the observed minus predicted apoB, where the predicted value was derived using a linear regression model of apoB on low-density lipoprotein cholesterol (LDL-C) fitted in a statin-naïve reference subset with triglycerides ≤ 1.0 mmol/L. The primary endpoint was incident ASCVD. Secondary endpoints included major adverse cardiovascular events (MACE) and all-cause mortality. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using multivariable Cox models. Nonlinearity was assessed using restricted cubic splines. Incremental improvements were quantified using the C-index, net reclassification improvement (NRI).

Results: During a median 185.3-month follow-up, 2,548 ASCVD and 1,205 MACE events occurred. ApoB was linearly related to ASCVD and MACE, while excess apoB showed J-shaped associations with a nadir near - 7.5 mg/dL for ASCVD. Both apoB and excess apoB showed positive associations with ASCVD across ascending percentile categories. Versus < 50th percentile, HRs (95% CIs) for ASCVD in higher apoB categories (50-<75th, 75-<90th, ≥ 90th) were 1.31 (1.16-1.49), 1.51 (1.25-1.81), and 1.47 (1.10-1.95); corresponding HRs (95% CIs) for excess apoB were 1.50 (1.36-1.66), 1.45 (1.29-1.63), and 1.53 (1.33-1.76), respectively. Similar but weaker risk gradients were observed for MACE. Neither apoB nor excess apoB was associated with all-cause mortality. Excess apoB yielded greater prediction improvement than apoB (ΔC-index: 0.009 vs. 0.002; NRI: 0.270 vs. 0.101) and better stratified risk in statin users and those with LDL-C ≤ 100 mg/dL (P for interaction < 0.05).

Conclusions: In T2DM, apoB is independently associated with ASCVD but adds limited discrimination over conventional lipids. Excess apoB yielded improved discrimination and reclassification, and may serve as a complementary ASCVD risk marker, particularly in statin-treated settings. However, its clinical application requires external validation and standardization.

Background: Previous studies suggest that HDLs may protect against the effects of acute injury. Given their multiple beneficial properties, this study aimed to investigate whether exogenous HDLs administration reduces acute tissue damage in a HgCl₂-induced renal injury model, potentially contributing to health improvement and disease prevention.

Methods: Acute tubular injury was induced in male Wistar rats with a single intraperitoneal dose of 3.5 mg/kg HgCl₂ (ATI group). Two additional groups received either HDLs (ATI + HDL group) or apolipoprotein B-containing lipoproteins (ATI + Lp-B) isolated from human plasma, at a dose equivalent to 0.9 mg of cholesterol per 100 g of body weight, administered twice on consecutive days. The study follow-up lasted four days. Urine and blood samples were collected to evaluate renal function markers. Histological analysis was also performed. In vitro, the ability of these lipoproteins to maintain cell viability under mercury exposure was assessed using the HEK-293 cell line.

Results: During the follow-up, plasma creatinine decreased, creatinine clearance improved, and proteinuria levels recovered more rapidly in the ATI + HDL group than in the ATI group. Glucosuria remained similar across both groups throughout the study. Histological analysis revealed increased cellularity and reduced necrosis in the kidneys of the ATI + HDL group compared to ATI rats. Rats in the ATI + Lp-B group died 48 h after HgCl₂ administration and tubular lesions were more severe. In vitro, HDLs effectively preserved cell viability under mercury exposure, while Lp-B did not provide similar protection.

Conclusion: Exogenous HDLs supplementation improves biochemical markers of renal function in vivo and promotes cell survival in vitro in a HgCl₂ toxicity model. These findings reveal a new beneficial property of HDLs, unlike apo B-containing lipoproteins, and underline the importance of such interventions for health support and disease management.

Background: Nutritional status, recognized as a modifiable determinant of oral health, has recently gained increasing attention in the context of edentulism. The triglyceride-total cholesterol-body weight index (TCBI) is a novel nutritional indicator derived from routine clinical measures. However, its association with edentulism remains unclear. This study was designed to assess the association between TCBI and edentulism risk.

Methods: This study utilized survey data provided by the China Health and Retirement Longitudinal Study (CHARLS). Three analyses were performed: cross-sectional (n = 9,686), prospective (participants without baseline edentulism, n = 8,568), and trajectory analyses (TCBI trajectories and incident edentulism, n = 4,921). Logistic regression, Cox proportional hazards models, group-based trajectory modeling, and restricted cubic spline analyses were applied. Sensitivity analyses using cumulative TCBI during follow-up were also conducted.

Results: In the cross-sectional analysis, individuals in the highest TCBI tertile demonstrated a significantly lower risk of prevalent edentulism (adjusted OR = 0.80, 95% CI: 0.65-0.97). In the prospective analysis, higher TCBI levels were independently associated with a reduced risk of incident edentulism (adjusted HR = 0.85, 95% CI: 0.77-0.92). Trajectory modeling demonstrated that individuals with persistently high TCBI had the lowest risk of incident edentulism (adjusted HR = 0.59, 95% CI: 0.40-0.89). These associations remained robust in sensitivity analyses.

Conclusion: TCBI was consistently and inversely associated with edentulism across cross-sectional, prospective, and trajectory analyses. As a readily obtainable nutritional index, TCBI may have clinical utility for the early identification and risk prediction of edentulism.

Background: The connection between low-density lipoprotein cholesterol (LDL-C) levels and postoperative outcomes following cardiac valve surgery (CVS) remains controversial. Therefore, this research aimed to study the connection of LDL-C levels with the incidence of adverse clinical outcomes in patients undergoing CVS.

Methods: 1,304 patients undergoing first-time CVS were identified from the MIMIC-IV database. Participants were split into two groups based on admission LDL-C levels: a low LDL-C group (< 1.4 mmol/L, n = 215) as well as a high LDL-C one (≥ 1.4 mmol/L, n = 1,089). The main endpoint was 30-day all-cause mortality (ACM), with secondary endpoints including in-hospital, 90-, 180- and 365-day ACM rates. The connection between preoperative LDL-C levels and clinical outcomes was evaluated via survival analysis, mediation analysis, and subgroup analyses.

Results: Multivariable Cox regression analysis demonstrated preoperative LDL-C level served as an independent protective factor against 30-day ACM following cardiac valve surgery (adjusted HR: 0.594; 95% CI: 0.368-0.960). In stratified analysis, patients in the higher LDL-C tertile exhibited a remarkably lower mortality risk (HR: 0.285; 95% CI: 0.134-0.604). Consistent subgroup analyses validated these findings' robustness across all clinically relevant subgroups. Notably, mediation analysis provided mechanistic evidence that the mortality-increasing effect of lower LDL-C levels may be partially mediated through activation of systemic inflammation.

Conclusion: Lower preoperative LDL-C levels are independently related with higher 30-day mortality following cardiac valve surgery, potentially mediated by the activation of inflammatory pathways.