Increase In Low-density Lipoprotein Cholesterol Levels Research Articles

Impact of Chronic Psychological Stress on Cardiovascular Disease Risk: A Narrative Review

Cardiovascular disease (CVD) remains a leading cause of death worldwide, and identification of its risk factors is pivotal in ensuring a lower socioeconomic burden on society. Psychological stress shows a strong causal link with CVD through the interaction of physiological and behavioral risk factors. Importantly, there is an association between the duration and level of stress and propensity for CVD. Chronic stress exerts its physiological effects through the release of glucocorticoids (GCs) such as cortisol, which subsequently promote proinflammatory effects, exacerbating atherosclerotic plaque development. Stress also exacerbates the secretion of cardiokines such as tumor necrosis factor-alpha (TNF-α). Elevated TNF-α is associated with endothelial dysfunction and angiogenesis-mediated atherosclerotic plaque progression, with increased secretion as the duration of stress is extended. Stress-induced GC secretion also inhibits glucose uptake leading to hyperglycemia and consequent hyperinsulinemia. This increases an individual’s susceptibility to another CVD risk factor, type 2 diabetes mellitus (T2DM). These risk factors are further exacerbated by the impact of chronic stress on behavior such as eating habits. Increased consumption of comfort foods, typically containing high fat and sugar contents, is directly associated with increased body mass index and increased low-density lipoprotein (LDL) cholesterol, both of which are well-known drivers of atherosclerosis. Moreover, chronic stress often results in reductions in physical activity, particularly in individuals at low baseline levels of activity. This further increases an individual’s susceptibility to obesity, T2DM, and increased LDL-cholesterol levels, all of which promote the development of CVD. This review outlines key research findings relating to the role chronic psychological stress plays in altering physiological and behavioral risk factors for CVD.

Cholesterol 7 alpha-hydroxylase (CYP7A1) gene polymorphisms are associated with increased LDL-cholesterol levels and the incidence of subclinical atherosclerosis.

The cholesterol 7 alpha-hydroxylase (CYP7A1) enzyme plays an important role in the conversion of cholesterol to bile acid, contributing to the reduction of cholesterol plasma levels in normal conditions. Nonetheless, recent studies have shown that some genetic variants in the enhancer and promoter regions of the CYP7A1 gene reduce the expression of the CYP7A1 enzyme, increasing plasma lipid levels, as well as the risk of developing coronary heart disease. The aim of this work was to explore whether the genetic variants (rs2081687, rs9297994, rs10107182, rs10504255, rs1457043, rs8192870, and rs3808607) of the CYP7A1 gene are involved in subclinical atherosclerosis and plasma lipid levels. We included 416 patients with subclinical atherosclerosis (SA) with coronary artery calcium (CAC) greater than zero, and 1046 controls with CAC = 0. According to the inheritance models (co-dominant, dominant, recessive, over-dominant and additive), the homozygosity of the minor allele frequencies of 7 analyzed polymorphisms showed a high incidence of SA (P < 0.05). In a sub-analysis performed including only the patients with SA, the same SNPs were associated with increased low-density lipoprotein cholesterol (LDL-C) levels. On the other hand, our findings showed that the haplotype (TGCGCTG) increases the risk of developing SA (P < 0.05). In conclusion, the rs2081687, rs9297994, rs10107182, rs10504255, rs1457043, rs8192870, and rs3808607 polymorphisms of CYP7A1 confer a risk of developing SA and elevated LDL-C levels. Our results suggest that the CYP7A1 is involved in the incidence of SA through the increase in the plasma lipid profile.

Cellular and functional evaluation of LDLR missense variants reported in hypercholesterolemic patients demonstrates their hypomorphic impacts on trafficking and LDL internalization.

Familial hypercholesterolemia (FH) is an autosomal dominant disorder characterized by increased LDL-cholesterol levels. About 85% of FH cases are caused by LDLR mutations encoding the low-density lipoprotein receptor (LDLR). LDLR is synthesized in the endoplasmic reticulum (ER) where it undergoes post-translational modifications and then transported through Golgi apparatus to the plasma membrane. Over 2900 LDLR variants have been reported in FH patients with limited information on the pathogenicity and functionality of many of them. This study aims to elucidate the cellular trafficking and functional implications of LDLR missense variants identified in suspected FH patients using biochemical and functional methods. We used HeLa, HEK293T, and LDLR-deficient-CHO-ldlA7 cells to evaluate the subcellular localization and LDL internalization of ten LDLR missense variants (p.C167F, p.D178N, p.C243Y, p.E277K, p.G314R, p.H327Y, p.D477N, p.D622G, p.R744Q, and p.R814Q) reported in multiethnic suspected FH patients. We also analyzed the functional impact of three variants (p.D445E, p.D482H, and p.C677F), two of which previously shown to be retained in the ER. We show that p.D622G, p.D482H, and p.C667F are largely retained in the ER whereas p.R744Q is partially retained. The other variants were predominantly localized to the plasma membrane. LDL internalization assays in CHO-ldlA7 cells indicate that p.D482H, p.C243Y, p.D622G, and p.C667F have quantitatively lost their ability to internalize Dil-LDL with the others (p.C167F, p.D178N, p.G314R, p.H327Y, p.D445E, p.D477N, p.R744Q and p.R814Q) showing significant losses except for p.E277K which retained full activity. However, the LDL internalization assay is only to able evaluate the impact of the variants on LDL internalization and not the exact functional defects such as failure to bind LDL. The data represented illustrate the hypomorphism nature of variants causing FH which may explain some of the variable expressivity of FH. Our combinatorial approach of in silico, cellular, and functional analysis is a powerful strategy to determine pathogenicity and FH disease mechanisms which may provide opportunitites for novel therapeutic strategies.

Association of LDLR Gene Polymorphism with the Risk of Cardiovascular Disease in End-Stage Kidney Disease Patients on Maintenance Hemodialysis

Background The low-density lipoprotein receptor (LDLR) is essential for regulating intracellular cholesterol levels. Mutations in the LDLR gene can cause a increase in LDL cholesterol levels in the blood, elevating the vulnerability to cardiovascular disease (CVD). This study evaluated the correlation between the LDLR rs688 polymorphism and CVD risk in chronic kidney disease (CKD). Materials and Methods Polymorphism in this case-control study was genotyped using the TaqMan real-time polymerase chain reaction in a cohort of 100 CKD patients (Group I) and 100 healthy controls (Group II). We examined the LDLR rs688 allele and genotype distribution in 50 CKD cases with CVD and 50 cases without CVD. Results There was a significantly greater frequency of CT variant of LDL SNP rs688 in Group I than in Group II (p = 0.006). CT and TT genotypes were significantly higher in CKD patients with CVD, with odds ratios (ORs) (95% CI) of 4.3 (1.6–11.8, p = 0.004) and 7.6 (2.3–24.8, p = 0.001), respectively. Conclusion SNP rs688 C&gt;T detection in the LDLR gene showed that CT and TT genotypes are associated with elevated CVD risk in CKD.

Development of a PCSK9-targeted nanoparticle vaccine to effectively decrease the hypercholesterolemia

Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to the low-density lipoprotein receptor (LDLR) and mediates its internalization and degradation, resulting in an increase in LDL cholesterol levels. Recently, PCSK9 emerged as a therapeutic target for hypercholesterolemia and atherosclerosis. In this study, we develop a PCSK9 nanoparticle (NP) vaccine by covalently conjugating the catalytic domain (aa 153-aa 454, D374Y) of PCSK9 to self-assembled 24-mer ferritin NPs. We demonstrate that the PCSK9 NP vaccine effectively induces interfering antibodies against PCSK9 and reduces serum lipids levels in both a high-fat diet-induced hypercholesterolemia model and an adeno-associated virus-hPCSK9D374Y-induced hypercholesterolemia model. Additionally, the vaccine significantly reduces plaque lesion areas in the aorta and macrophages infiltration in an atherosclerosis mouse model. Furthermore, we discover that the vaccine's efficacy relied on T follicular help cells and LDLR. Overall, these findings suggest that the PCSK9 NP vaccine holds promise as an effective treatment for hypercholesterolemia and atherosclerosis.

Plozasiran (ARO-APOC3) for Severe Hypertriglyceridemia

Severe hypertriglyceridemia (sHTG) confers increased risk of atherosclerotic cardiovascular disease (ASCVD), nonalcoholic steatohepatitis, and acute pancreatitis. Despite available treatments, persistent ASCVD and acute pancreatitis-associated morbidity from sHTG remains. To determine the tolerability, efficacy, and dose of plozasiran, an APOC3-targeted small interfering-RNA (siRNA) drug, for lowering triglyceride and apolipoprotein C3 (APOC3, regulator of triglyceride metabolism) levels and evaluate its effects on other lipid parameters in patients with sHTG. The Study to Evaluate ARO-APOC3 in Adults With Severe Hypertriglyceridemia (SHASTA-2) was a placebo-controlled, double-blind, dose-ranging, phase 2b randomized clinical trial enrolling adults with sHTG at 74 centers across the US, Europe, New Zealand, Australia, and Canada from May 31, 2021, to August 31, 2023. Eligible patients had fasting triglyceride levels in the range of 500 to 4000 mg/dL (to convert to millimoles per liter, multiply by 0.0113) while receiving stable lipid-lowering treatment. Participants received 2 subcutaneous doses of plozasiran (10, 25, or 50 mg) or matched placebo on day 1 and at week 12 and were followed up through week 48. The primary end point evaluated the placebo-subtracted difference in means of percentage triglyceride change at week 24. Mixed-model repeated measures were used for statistical modeling. Of 229 patients, 226 (mean [SD] age, 55 [11] years; 176 male [78%]) were included in the primary analysis. Baseline mean (SD) triglyceride level was 897 (625) mg/dL and plasma APOC3 level was 32 (16) mg/dL. Plozasiran induced significant dose-dependent placebo-adjusted least squares (LS)-mean reductions in triglyceride levels (primary end point) of -57% (95% CI, -71.9% to -42.1%; P < .001), driven by placebo-adjusted reductions in APOC3 of -77% (95% CI, -89.1% to -65.8%; P < .001) at week 24 with the highest dose. Among plozasiran-treated patients, 144 of 159 (90.6%) achieved a triglyceride level of less than 500 mg/dL. Plozasiran was associated with dose-dependent increases in low-density lipoprotein cholesterol (LDL-C) level, which was significant in patients receiving the highest dose (placebo-adjusted LS-mean increase 60% (95% CI, 31%-89%; P < .001). However, apolipoprotein B (ApoB) levels did not increase, and non-high-density lipoprotein cholesterol (HDL-C) levels decreased significantly at all doses, with a placebo-adjusted change of -20% at the highest dose. There were also significant durable reductions in remnant cholesterol and ApoB48 as well as increases in HDL-C level through week 48. Adverse event rates were similar in plozasiran-treated patients vs placebo. Serious adverse events were mild to moderate, not considered treatment related, and none led to discontinuation or death. In this randomized clinical trial of patients with sHTG, plozasiran decreased triglyceride levels, which fell below the 500 mg/dL threshold of acute pancreatitis risk in most participants. Other triglyceride-related lipoprotein parameters improved. An increase in LDL-C level was observed but with no change in ApoB level and a decrease in non-HDL-C level. The safety profile was generally favorable at all doses. Additional studies will be required to determine whether plozasiran favorably modulates the risk of sHTG-associated complications. ClinicalTrials.gov Identifier: NCT04720534.

Lipoprotein Ratios: Correlations With Glycated Hemoglobin Among Type 2 Diabetes Mellitus Patients.

Introduction Diabetes mellitus (DM) has become a common disorder in India, and can be even considered as an epidemic in most developing countries. It usually adds a big burden on the economy through its macro and microvascular complications which often require hospitalisation. Glycated hemoglobin (HbA1c) is considered a well-established test to track long-term glycemic control, and hence can be used for both diagnosis and prognosis of disease. On the other hand, lipid profile is a significant marker of cardiovascular risks. Objective To investigate the clinical relevance of lipid profile and correlate with glycemic control in type 2 DM patients. Methodology This observational study used laboratory results (HbA1c and lipid profile) of 140 patients who attended various out-patient departments (OPD) of All India Institute of Medical Sciences (AIIMS), Gorakhpur. On the advice of clinicians, for routine follow-up, blood samples were collected from the patients (aged 20-50 years, 84 males, and 56 females, with a history of more than three years of type 2 DM). The sera were analyzed for HbA1c and lipid profile [which included triglycerides (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C)]. Based on HbA1c levels the study subjects were divided into three groups, namely group I (HbA1c <7%, n=14), group II (HbA1c7%-8.5%, n=91), and group III (HbA1c >8.5%, n=35). Correlation studies between HbA1c and parameters of lipid profile were explored in the study. Data generated were checked for normality and correlation studies were accordingly done. Results Elevated levels of HbA1c were associated with a notable parallel increase in LDL-C levels (P<0.05), TG, and TC. There was no notable correlation observed between HbA1c and HDL-C levels. However, as HbA1c levels increased, the TG/HDL-C and LDL-C/HDL-C ratios displayed a gradual rise (P<0.05). Conclusion LDL-C and the LDL-C/HDL-C ratio serve as valuable tools for evaluating and mitigating cardiovascular disease risk and are correlated to glycemic control among individuals with type 2 DM.

An Assessment of Glutathione-S-Transferase and Lipid Profile in Obese Iraqi Patients

An Assessment of Glutathione-S-Transferase and Lipid Profile in Obese Iraqi Patients

Low-density lipoprotein cholesterol and the risk of hyperemesis gravidarum: a Mendelian randomization study

Objective The inconsistency in conclusions from early observational studies has sparked our interest in elucidating the relationship between lipid levels and susceptibility to hyperemesis gravidarum (HG). This study wishes to employed Mendelian randomization analysis to investigate the causal relationship between low-density lipoprotein cholesterol (LDL-C) and HG. Methods We employed Tow-Sample MR analysis to investigate the causal associations between LDL-C and HG. Specific variables were selected from GWAS database for MR analysis, using single nucleotide polymorphisms (SNPs) as our instruments. The threshold for significant SNPs as genetic instruments has been set at 5 × 10−8. F-statistic was employed to validate the strength of exposure instruments. The causality was mainly evaluated by Inverse Variance Weighted method (IVW). To address potential bias from the selection of genetic variants with pleiotropic effects, sensitivity analysis was performed by Cochrane Q-test, MR Egger, weighted median, MR-PRESSO and Leave-one-out methods. To validate the directionality of causal relationships, we employed Steiger test to filter SNPs. At last, we conducted reverse MR to exclude the causal impact of HG on LDL-C levels. Results Our MR results identified the effect of genetically predicted increased LDL-C levels on increased genetic susceptibility to HG (OR:1.30; 95%CI:1.03-1.65; p = 0.028). In reverse MR analyses, no evidence was found for causal effect of HG on LDL-C levels (OR:1.00; 95%CI:1.00-1.01; p = 0.163). Sensitivity analyses were used to confirm reliability. Conclusion This study may have provided evidence of genetically predicted increased LDL-C levels on increased genetic susceptibility to HG. Appropriate lowering LDL-C levels may serve as a preventive and treatment measure for HG.

Causal relationships between plasma lipids and sepsis: A Mendelian randomization study.

Although observational studies have indicated that plasma lipids are associated with an increased risk of sepsis, due to confounders and reverse causality, the causal relationship remains unclear. This study was designed to assess the causal effects of plasma lipid levels on sepsis. We used a 2-sample Mendelian randomization (MR) method to evaluate the causal effect of plasma lipids on sepsis. MR analysis employs methods such as inverse variance weighted, MR-Egger regression, weighted median regression (WME), simple mode and weighted mode. The inverse variance weighted (IVW) method was predominantly utilized to assess causality. Heterogeneity was affirmed by Cochran Q test, while pleiotropy was corroborated by MR-Egger regression analysis. The robustness and reliability of the results were demonstrated through "leave-one-out" sensitivity analysis. Instrumental variables included 226 single-nucleotide polymorphisms (SNPs), comprising of 7 for triglyceride (TG), 169 for high-density lipoprotein cholesterol (HDL-C), and 50 for low-density lipoprotein cholesterol (LDL-C). The risk of sepsis appeared to increase with rising LDL-C levels, as indicated by the inverse variance weighted analysis (OR 1.11, 95% CI from0.99 to1.24, P = 0.068). However, no causality existed between LDL-C, HDL-C, TG and sepsis. Two-sample MR analysis indicated that increased LDL-C level is a risk factor for sepsis, while TG and HDL-C levels have protective effects against sepsis. However, no significant causal relationship was found between TG, HDL-C, and LDL-C levels and sepsis.

Efektivitas Ekstrak Daun Salam (Syzygium polyanthum) Dalam Mencegah Kenaikan Kadar Kolesterol LDL Tikus Putih (Rattus norvegicus) Diinduksi Kuning Telur Puyuh

Quail egg yolk contains high cholesterol which can trigger dyslipidemia. If Cholesterol is consumed in excess, will increase lipid profile, which can increase LDL cholesterol levels. Bay leaf extract contains several active compounds, like quercetin, a class of flavonoids with antioxidants that can prevent LDL oxidation. The aim of this study is to ensure the effectiveness of bay leaf extract on LDL cholesterol levels in white rats induced by quail egg yolk. The animal tested in this study were male white rats (Rattus norvegicus) with the Sprague Dawley strain. Samples were randomly selected and divided into five groups: three groups given quail egg yolk and bay leaf extract in various doses of 0.18 g/day, 0.36 g/day and 0.72 g/day, positive control given quail egg yolk, and negative control without treatment. The ANOVA test showed that there were significant results between the treatment groups, positive control and negative control (p&lt;0.05). Next, the BNJ test showed that giving bay leaf extract (0.18 g/day, 0.36 g/day) had a significant effect on LDL cholesterol levels (p&lt;0.05), while a dose of 0.72 g/day showed that not significant (p&gt;0.05), so we can conclude that the dose of 0.72 g/day was the most effective in preventing an increase in LDL cholesterol levels.

LDL Cholesterol Variability Impacts the Prognosis of Patients with Chronic Ischemic Heart Disease: A Real-World Italian Experience.

Epidemiologic, genetic, and clinical intervention studies have indisputably shown that low-density lipoprotein cholesterol (LDL-C) is causal in the development of atherosclerotic cardiovascular disease (ASCVD). However, LDL-C variability could be related to increased ASCVD risk in patients already treated with statins. The aim of the present retrospective real-life study was to assess the prognostic impact of LDL-C variability on all-cause mortality and cardiovascular hospitalizations in patients with stable cardiovascular artery disease. A total of 3398 patients were enrolled and followed up for a median of 56 months. Considering LDL-C < 70 mg/dL as the therapeutical target, during follow-up, the percentage of patients who achieved this goal raised from 20.7% to 31.9%. In total, 1988 events were recorded, of which 428 were all-cause deaths and 1560 were cardiovascular hospitalizations. At the last medical examination, each increase in LDL-C levels of 20 mg/dL corresponded to a 6% raise in the risk of any event (HR 1.06; 95%CI, 1.03 to 1.09). In conclusion, our real-world study supports the hypothesis that a continuous and progressive downward trend in LDL-C levels is needed to achieve and maintain a cardiovascular benefit, at least in secondary prevention.

A Retrospective Study on the Adoption of Lipid Management Guidelines in Post-Myocardial Infarction Patients in a Tertiary Care Centre.

Lipid management after acute myocardial infarction (AMI) is one of the important aspects of secondary prevention in the high cardiovascular (CV) risk group, and targeted reduction of low-density lipoprotein cholesterol (LDL-C) remains the primary target for lipid therapy after myocardial infarction (MI). To conduct a retrospective study of the adequacy of lipid management in post-MI patients admitted to a tertiary care centre as compared to the 2019 European Society of Cardiology (ESC) guidelines for the management of dyslipidaemia. The study was a retrospective review of medical records of patients admitted with MI under the Ubora Heart Service, Nairobi Hospital, from January 2020 to June 2022. The study population included 79 patients, with a mean age of 59.3 (SD ±12), predominantly male (61 patients, 77.2%), and of African descent (60 patients, 75.9%). The majority of the study population presented with an ST-segment elevation myocardial infarction (STEMI) (62%), and the six most prevalent cardiovascular risk factors recorded amongst the patients were: systemic arterial hypertension in 50 (63.3%) patients; dyslipidaemia in 34 (43.0%); type II diabetes mellitus (T2DM) in 25 (31.6); history of smoking in 12 (15.2%); obesity or being overweight in 12 (15.1%); and family history of premature coronary artery disease or sudden cardiac death in four (5.1%) patients. Moreover, 88.6% of the patients had their lipid profile assessment done within 48 hours of admission, with a mean LDL-C level of 3.18 mmol/L (SD ±.18). All the patients recruited in the study were started on high-intensity statins with either 40 mg or 80 mg of atorvastatin or 20 mg or 40 mg of rosuvastatin. Thirty-nine (44%) patients recruited had repeat lipid profiles on follow-up, with a median lipid analysis time of five months (interquartile range (IQR): 2.0-10.0). Of those, only six (17.1%) achieved the LDL-C goal of <1.4 mmo/L while only 16 (45.7%) achieved a greater than 50% reduction from their baseline LDL-C level, with three (8.6%) patients having an increased LDL-C level from baseline. Overall, 14.7% of the patients studied achieved the guideline-recommended LDL-C goal of an LDL-C target of <1.4 mmo/L and a ≥ 50% reduction from baseline LDL-C. After five months of follow-up, 75 (94.9%) patients were on statin monotherapy, with 4 (5.1%) on high-intensity statin and ezetimibe combination therapy. This retrospective study highlights the need for early sensitisation and the adoption of secondary prevention strategies in acute coronary syndrome (ACS), as recommended by the 2019 ESC guidelines.

Association between serum lipid levels and lower-extremity functions in older adults with and without Alzheimer's dementia in South Korea: A cross-sectional analysis

PurposeOlder adults with Alzheimer's dementia (AD) experience lower-extremity dysfunction. High serum lipid levels are a risk factor for AD. We investigated the association between serum lipid levels and lower-extremity function in older individuals with and without AD. MethodsIn this cross-sectional study, we enrolled 33,185 senior citizens (aged 66 years) who participated in the National Geriatric Screening Program, sampled from the Korean National Health Insurance Service-National Health Screening Cohort Database, between 2009 and 2015. Participants were dichotomized into 1) an AD group comprising individuals with the International Classification of Diseases, Tenth Revision, diagnostic codes F00, F00.0–F00.9, and G30, G30.0–G30.9; and 2) a control group comprising individuals without AD.Differences in the Timed Up and Go and One-Leg Standing results among the three levels (low, moderate, and high) of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol were evaluated between the groups. Logistic regression analysis was performed to estimate the odds of gait disorder considering clinical and lifestyle variables. ResultsIn participants with low LDL-C levels, increased LDL-C levels correlated with higher gait speed. In the AD group, balancing time with eyes open (BT-EO) was inversely correlated with TG levels in participants with low TG levels. In the control group, BT-EO was negatively correlated with TC levels in participants with low TC levels. ConclusionSerum lipid levels were significantly correlated with lower-extremity function in participants with and without AD but not with gait disorder in participants with AD.

Triglycerides Revisited: is Hypertriglyceridaemia a Necessary Therapeutic Target in Cardiovascular Disease?

Despite the atherosclerotic cardiovascular disease (ASCVD) risk reduction achieved by low-density lipoprotein-cholesterol (LDL-C) lowering therapy, residual ASCVD risk still exists. Previous epidemiological studies have suggested high plasma triglycerides (TG) levels as a risk factor or risk marker for ASCVD independent of LDL-C levels. In this review, we highlighted the underlying pathophysiology of hypertriglyceridaemia, the mechanistic action of therapeutic agents, the interpretation of conflicting results on recent clinical trials, and the present options for primary and secondary prevention. The benefits of fibrates-induced reduction in TG and increase in high-density lipoprotein-cholesterol might outweigh the disadvantages of increasing LDL-C levels in primary prevention. In the secondary CVD prevention, using eicosapentaenoic acid without docosahexaenoic acid, in addition to statins, will be beneficial. This comprehensive review may prove useful for the development of novel approaches that target hypertriglyceridaemia in future.

The Difference of Low Density Lipoprotein Cholesterol Levels on Different Severity of Coronary Artery Disease Patients in Siloam Hospital Lippo Village

&lt;p&gt;&lt;strong&gt;Background:&lt;/strong&gt; Coronary artery disease (CAD) is one of the highest causes of death in the world. Hypercholesterolemia, especially low-density lipoprotein (LDL) levels, is a major risk factor, because it is the main precursor of atherosclerosis. Previous studies showed the relationship between LDL level and the number of vessel disease is still inconsistent, therefore it needs to be observed further. The objective of this study was to know the effect of LDL levels on the number of vessel disease in CAD patients who underwent coronary angiography.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods:&lt;/strong&gt; It was a cross-sectional and retrospective study, where data were taken from medical records of CAD patients who underwent coronary angiography at Siloam Hospital Lippo Village between January to June 2018. Patients with at least one vessel disease were included. The number of vessel disease was categorized into 3 groups: one-vessel, two-vessels, and multi-vessel. The relationship between LDL levels and the number of vessel disease was analyzed using one way ANOVA.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Result:&lt;/strong&gt; The data includes 90 patients; 70 (77.8%) were male with average age of 56±9 years. There were 32 (35.6%) patients in one-vessel group; 27 (30%) in two-vessel group; and 31 (34.4%) in multi-vessel group with an average LDL levels of 106.43±40.51 mg/dl; 111.15±39.43 mg/dl; and 114.52±32.55 mg/dl respectively. Although it seemed that the increase in LDL cholesterol levels was in line with the number of vessel disease, there was no statistically significant relationship between the two variables (&lt;em&gt;p&lt;/em&gt;=0.694).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions:&lt;/strong&gt; LDL cholesterol level does not affect the number of vessel disease in CAD patients.&lt;/p&gt;

Dose-response relationship of elements with blood lipids and the potential interaction: A cross-sectional study from four areas with different pollution levels in China

BackgroundA growing number of researches indicated the association between plasma trace elements and blood lipids. However, the potential interaction and dose-response relationship were less frequently reported. MethodsIn this study, a total of 3548 participants were recruited from four counties in Hunan Province, South China. Demographic characteristics were collected by face-to-face interviews and inductively coupled plasma mass spectrometry (ICPMS) was used to determine the levels of 23 trace elements in plasma. We applied a fully adjusted generalized linear regression model (GLM) and a multivariate restricted cubic spline (RCS) to estimate the correlation, dose-response relationship and possible interaction between 23 trace elements and four blood lipid markers. ResultsThe results indicated positive dose-response relationships of plasma 66zinc with triglycerides (TG) and low density lipoprotein cholesterol (LDL-C), plasma 78selenium with LDL-C and total cholesterol (TCH), and plasma 59cobalt with high-density lipoprotein cholesterol (HDL-C). There was a negative dose-response relationship between 59cobalt and LDL-C. Further analysis found that 66zinc and 59cobalt had an antagonistic effect on the risk of increased LDL-C level. ConclusionsThis study added new evidence for the potential adverse effects of 66Zn and 78Se on blood lipids, and provided new insight into the threshold value setting for metals as well as the intervention strategy for dyslipidemia.

Lipid lowering effects and safety of evolocumab in Chinese patients at very high cardiovascular risk: a single-center study.

Lipid lowering effects and safety of evolocumab in Chinese patients at very high cardiovascular risk: a single-center study.

OA01 No difference in risk of myocardial infarction among patients receiving either IL6 or TNF inhibitors for rheumatoid arthritis

Abstract Background/Aims Interleukin 6 inhibitors (IL-6i) can increase LDL cholesterol levels, which raises concerns about the risk of myocardial infarction (MI) in patients with rheumatoid arthritis (RA) receiving this therapy. This study aims to compare the risk of MI between people with RA in the UK clinical setting receiving IL-6i or tumour necrosis factor inhibitors (TNFi) overall or by line of therapy (LoT). Methods Patients with RA registered between 01/10/2001 and 27/05/2022 with BSRBR-RA starting IL-6i or TNFi treatments were included. Occurrence of MI was identified from clinical follow-up forms and through cause of death reported by the national UK death register. Only those MIs occurring whilst the patient was actively receiving drug were included. The risk of MI in patients receiving IL6i compared to TNFi was compared using Cox regression, adjusted for baseline co-variates using propensity scores (PS, see Table 1). Follow-up commenced at the start of the drug of interest and patients were censored at occurrence of MI, death, discontinuation of therapy or last follow-up visit, whichever came first. Multiple imputation was used for missing data. To account for known differences in LoT use of TNFi and IL6i (with IL6i more likely as a later line bDMARD), overall analyses adjusted for LoT in PS and secondary analyses by LoT were conducted. Direct switches between originator to biosimilars were considered the same treatment. Results A total of 29,596 IL6i or TNFi treatments in 20,725 patients were included (3,098 IL-6i; 26,498 TNFi), representing 153,913 person-years of exposure. Compared to patients receiving TNFi, patients starting IL-6i treatment were older, had longer disease duration, less likely to use methotrexate and steroids, and had more comorbidities. During follow-up, 372 MIs occurred, 27 on IL-6i and 345 on TNFi, with an overall lower crude rate of MI in patients receiving IL6i compared to TNFi. After PS adjustment, the risk of MI was not significantly different between the two treatment overall (HR 0.77, 95% CI 0.48-1.24) or when stratified by LoT (Table 1). Conclusion This study could not identify any difference in risk of MI between IL-6i and TNFi treatment after patient characteristics and LoT were considered. Disclosure Z. Tian: None. L. Kearsley-Fleet: None. K. Lauper: Honoraria; Celltrion, Pfizer, Viatris, Galapagos. S. Haughton: None. K. Watson: None. M. Lunt: None. J. Mclaughlin: None. A. Verma: None. K.L. Hyrich: Honoraria; Abbvie. Grants/research support; Pfizer, BMS.

RELATIONSHIPS BETWEEN LIPID PROFILE AND COMPLETE BLOOD CELL COUNT PARAMETERS

Aim. Given that blood cells play an important role in both atherogenesis and lipid metabolism, the research aimed to assess the specifics of the relationship between the parameters of the blood lipid spectrum and the complete blood count (CBC).&#x0D; Materials and Methods. A total of 475 individuals (245 female and 230 male) were included in the study, who simultaneously underwent CBC and determination of lipid profile, namely: total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG). Statistical processing of the obtained data was carried out using the "Statistica for Windows 6.0" software package (Statsoft, USA).&#x0D; Results. An increase in levels of TC and LDL-C was associated with an increase in the count of lymphocytes and erythrocytes. A rise in VLDL-C and, accordingly, TG levels, as well as a decrease in the level of HDL-C, were associated with an increase in the total leukocyte count in the blood without a significant change in the ratio of their different types, and an increase in erythrocyte sedimentation rate. The count of platelets was directly related to the level of LDL-C and increased in the case of a combination of elevated levels of LDL-C and TG.&#x0D; Discussion. The obtained results indicate that the disposal of excess lipoproteins is based on various types of immune reactions. An increase in the levels of VLDL-C and TG is associated with the development of a nonspecific leukocyte reaction, and an increase in LDL-C levels is associated with a more specific platelet-lymphocytic response. A simultaneous increase in LDL-C and TG levels can be associated with the development of both specific and non-specific immune reactions. An increase in the level of HDL-C leads to a decrease in the intensity of innate and adaptive immune responses. Therefore, the lipid profile of patients should be evaluated by taking into account the blood cell counts, especially in the process of hypolipidemic treatment.&#x0D; Conclusions. An atherogenic lipid profile is associated with increased counts of all blood cells, reflecting specific and nonspecific immune reactions in response to elevated levels of various lipid groups. Platelets play an important role in lipid metabolism.&#x0D; Connection of the research with scientific programs, plans, and topics. The study is a fragment of the planned scientific research of the Department of Internal Medicine No. 2 of the Danylo Halytsky Lviv National Medical University: "Peculiarities and markers of the course of internal diseases under conditions of combination with metabolic syndrome and metabolically associated fatty liver disease", state registration number: 0122U000165.