Lipid Parameters In Patients Research Articles

PON1 rs662, rs854560 and TRIB1 rs17321515, rs2954029 Gene Polymorphisms Are Associated with Lipid Parameters in Patients with Unstable Angina.

Acute coronary heart disease (CHD) is mainly caused by the rupture of an unstable atherosclerotic plaque. Many different factors can cause stenosis or even occlusion of the coronary artery lumen, such as vasculitis and platelet aggregation. Our study was performed to assess the association between PON1 rs662, rs854560 and TRIB1 rs17321515, rs2954029 polymorphisms and the risk of CHD, as well as the association between studied polymorphisms and selected clinical parameters affecting the risk of developing ischemic heart disease. A total of 232 patients with unstable angina were enrolled in this study. There were no statistically significant differences in the PON1 rs662, rs854560 and TRIB1 rs17321515, rs2954029 polymorphism distributions between the total study and control groups. Total cholesterol plasma levels were significantly higher in patients with the PON1 rs662 TT genotype compared to those with the CC+TC genotypes, as well as in patients with the PON1 rs854560 TT genotype compared to those with the AA+AT genotypes. LDL plasma levels were significantly increased in patients with the PON1 rs854560 TT genotype compared to those with the AA+AT genotypes. Plasma levels of HDL were significantly decreased in patients with the TRIB1 rs17321515 AA+AG genotypes compared to those with the GG genotype, as well as in patients with the TRIB1 rs2954029 AA+AT genotypes compared to those with the TT genotype. Our results suggest that the analysed polymorphisms are not risk factors for unstable angina in the Polish population. However, the results of this study indicate an association between the PON1 rs662, rs854560 and TRIB1 rs17321515, rs2954029 polymorphisms with lipid parameters in patients with coronary artery disease.

#707 Effectiveness of a personalized approach to the treatment of patients with chronic coronary syndrome with type 2 diabetes and renal dysfunction

Abstract Background and Aims To evaluate the effectiveness of complex personalized treatment of patients with chronic coronary syndrome (CCS) with type 2 diabetes mellitus (T2DM). Method We observed patients with chronic stable angina pectoris III (FC) (Group I, 16) and CV IV FC (Group II, 18) with T2DM who underwent planned stenting of the coronary arteries (SCA). At baseline and after 3 and 6 months, we studied cholesterol, LDL cholesterol and HDL cholesterol, triglycerides (TG), ALT and AST, total bilirubin (TB), polymorphism of the CYP2C19 and 9p21 genes (rs 2383206 and rs 10757272), assessed myocardial viability (ECHOCG, MSCT), an ultrasound of the liver was performed. Against the background of basic therapy (antiplatelet agents, statins, beta blockers, ACE inhibitors), patients received a herbal hepatoprotector. Results Initial lipid parameters in patients with CCS and T2DM: cholesterol—6.9 mmol/l; LDL cholesterol –3.6; HDL cholesterol –1.1; TG –2.5 mmol/l. Parameters of global and regional systolic function were reduced. At the end of observation, lipid content: cholesterol—5.0; LDL cholesterol—2.3; HDL cholesterol –1.18; TG—1.61 mmol/l. Statins and antiplatelet agents were well tolerated, and there were no cases of withdrawal. Enzyme activity (ALT, AST), OB content were within normal values. The genetic studies carried out helped to select the most effective and safe doses of antiplatelet drugs and statins and significantly reduced the risk of complications and drug resistance. The hepatoprotector had a beneficial effect on the condition and function of the liver and improved the tolerability of medications. A personalized approach to the treatment of CCS was carried out taking into account the results of genetic testing with the selection of optimal doses of drugs. When the genotypes of CYP2C19*17 (rs 12248560) CC, ST and TT were distributed, the dose of antiplatelet agents was increased, and when the genotypes of the CYP2C19 gene (rs 4244285) GG, AG and AA were distributed, they were reduced. Assessment of myocardial viability, selection of doses of statins and antiplatelet agents according to individual characteristics, as well as a hepatoprotector increased the effectiveness and safety of treatment. SCA and basic treatment had an impact on the pathogenetic links of CCS, which is especially important in the treatment of patients with concomitant T2DM. Conclusion A personalized approach to the treatment of patients with CCS with T2DM who require SCA, taking into account the functional state and viability of the myocardium, the pharmacogenetic characteristics of the drugs, increases the effectiveness of revascularization, prevents the development of resistance, side effects and complications.

Effects of Multi-species Synbiotic Supplementation on Circulating miR-27a, miR-33a Levels, and Lipid Parameters in Adult Men with Dyslipidemia; A Randomized, Double-Blind, Placebo-Controlled Clinical Trial.

MicroRNAs (miRNAs) have emerged as important regulators of lipid metabolism. Recent studies have suggested synbiotics may modulate miRNA expression and lipid metabolism. This study aimed to investigate the effects of synbiotic supplementation on circulating miR-27a, miR-33a, and lipid parameters in patients with dyslipidemia. Fifty-six eligible participants were randomly allocated to receive either synbiotic or placebo sachets twice a day for 12 weeks. Each synbiotic sachet contained 3×1010 CFU six species of probiotic microorganisms and 5 grams of inulin and fructooligosaccharide (FOS) as prebiotics. Serum miR-27a and miR-33a expression levels, serum lipids, and apolipoproteins, the fecal concentration of short-chain fatty acids (SCFAs), and Firmicutes and Bacteroidetes phyla were assessed before and after the study. Real-time PCR was used to determine the relative expression levels of miRNAs. The results showed synbiotic supplementation significantly downregulated the expression levels of miR-27a and miR-33a compared to the placebo group (p = 0.008 and p = 0.001, respectively). Furthermore, the intervention group exhibited significant improvements in serum high-density lipoprotein (HDL-C), small dense low-density lipoprotein (sdLDL-C), apoA-I, and apoB-100 (p = 0.008, p = 0.006, p = 0.003, p = 0.001, respectively). The results showed a significant negative correlation between miR-33a expression levels with HDL-C, butyrate, propionate, and a significant positive correlation with total cholesterol (TC), low-density lipoprotein (LDL-C), and sdLDL-C in the intervention group. Fecal bacteria and SCFAs were significantly increased in the intervention group. This study provides evidence that synbiotic supplementation can modulate miR-27a and miR-33a expression and improve lipid metabolism in patients with dyslipidemia.

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.

Effect of ABCA1-R219K Polymorphism in Serum Lipid Parameters in Patients under Statin Therapy Visiting Tertiary Cardiac Center of Nepal.

Introduction ATP-binding cassette transporter A1 (ABCA1) encoded by ABCA1 gene is one of the important protein involved in lipid metabolism. The effect of statin therapy on dyslipidemia varies among individuals and it may be due to different genetic polymorphism. The R219K polymorphism of ABCA1 gene is found to have a significant role in the response of statin. Objective This study was designed to evaluate the effect of R219K polymorphism in lipid-lowering action of statin in patients with dyslipidemia. Material and Methods This study was conducted in 88 patients. Blood samples were taken from patients before and at the end of 3 months of statin use and were analyzed for lipid profile. Whole blood was analyzed for R219K Polymorphism using polymerase chain reaction-restriction fragment length polymorphism. Results R219K polymorphism was associated with significant percentage reduction of serum triglyceride/high-density lipoprotein (TG/HDL) ratio and total cholesterol/high-density lipoprotein (TC/HDL) ratio in atorvastatin users. However, there was no significant association of polymorphism with change in serum TC, HDL-C, LDL-C, TG, and very low-density lipoprotein (VLDL). Among KK genotype individuals, value of TG, VLDL, TG/HDL, and TC/HDL were significantly lower than in RR genotypes. Also, TG/HDL and TC/HDL were significantly lower in RK genotype than in RR. Treatment of dyslipidemia with statin was found to be comparatively better in patients having the genotypes KK and RK. Conclusion Our study demonstrated association of R219K polymorphism with the significant reduction of TG/HDL and TC/HDL and particularly the KK genotype was associated with significant improvement of lipid parameters following atorvastatin treatment.

Investigations on fibroblast growth factor 21 and lipid parameters in patients with Hashimoto thyroiditis

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Determinants of Lipid Parameters in Patients without Diagnosed Cardiovascular Disease-Results of the Polish Arm of the EUROASPIRE V Survey.

To assess the determinants of lipid parameters in primary care patients without diagnosed cardiovascular disease (CVD), a cross-sectional study was conducted during 2018-2019 with a total of 200 patients. The following lipid parameters were measured: total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), small, dense LDL (sdLDL-C), and lipoprotein (a) (Lp(a)). Predictors of elevated and adequately controlled lipid parameters were assessed with logistic regression analysis. Older age was related to higher risk of TC ≥ 6.2 mmol/L [OR 1.03 (95% CI 1.0-1.05)], sdLDL-C ≥ 1.0 mmol/L [OR 1.05 (95% CI 1.0-1.1)], and decreased risk of Lp(a) ≥ 50 mg/dL [OR 0.97 (95% CI 0.94-0.99)]. Patients with diabetes mellitus (DM) had increased probability of TG ≥ 2.25 mmol/L [OR 3.77 (95% CI 1.34-10.6)] and Lp(a) ≥ 50 mg/dL [OR 2.97 (1.34-6.10)] as well as adequate control of TG and Lp(a). Higher material status was related to lower risk of TC ≥ 6.2 mmol/L [OR 0.19 (95% CI 0.04-0.82)] and LDL-C ≥ 3.6 mmol/L [OR 0.33 (95% CI 0.12-0.92)]. High BMI was related to increased [OR 1.14 (95% CI 1.02-1.29)], and female gender [OR 0.33 (95% CI 0.12-0.96)] and hypertension [OR 0.29 (95% CI 0.1-0.87)] to decreased risk of TG ≥ 2.25 mmol/L [OR 1.14 (95% CI 1.02-1.29)]. Taking lipid-lowering drugs (LLD) was associated with LDL-C < 2.6 mmol/L [OR 2.1 (95% CI 1.05-4.19)] and Lp(a) < 30 mg/dL [OR 0.48 (95% CI 0.25-0.93)]. Physical activity was related to LDL-C < 2.6 mmol/L [OR 2.02 (95% CI 1.02-3.98)]. Higher abdominal circumference was associated with decreased risk of TG < 1.7 mmol/L [OR 0.96 (95% CI 0.93-0.99)]. Elevated lipid parameters were related to age, gender, material status, BMI, history of DM, and hypertension. Adequate control was associated with age, education, physical activity, LLD, history of DM, and abdominal circumference.

Interplay between microRNAs, Serum Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9), and Lipid Parameters in Patients with Very High Lipoprotein(a) Treated with PCSK9 Inhibitors

Proprotein convertase subtilisin/kexin type 9 (PCSK9) has an important function in the regulation of lipid metabolism. PCSK9 reduces hepatic low-density lipoprotein receptors, thereby increasing low-density lipoprotein cholesterol levels. However, its regulation remains to be elucidated, including post-transcriptional regulation by microRNAs (miRNAs). We aimed to explore the interplay between miRNAs, total serum PCSK9, and lipids during treatment with PCSK9 inhibitors. A total of 64 patients with stable coronary artery disease and very high lipoprotein(a) levels and 16 sex- and age-matched control subjects were enrolled. Patients received a PCSK9 inhibitor (evolocumab or alirocumab). Total serum PCSK9 levels were measured by immunoassay. RNA was isolated from plasma using magnetic beads, and expression of selected miRNAs was analyzed by quantitative PCR. Total serum PCSK9 levels were significantly higher in control subjects compared with patients. After 6 months of treatment with PCSK9 inhibitors, total serum PCSK9 levels increased significantly. The expression of miR-191-5p was significantly lower, and the expression of miR-224-5p and miR-483-5p was significantly higher in patients compared with control subjects. Using linear regression, the expression of miR-483-5p significantly predicted the serum PCSK9 level at baseline. After the 6-month period of therapy, the expression of miR-191-5p and miR-483-5p significantly increased. Our results support a role for miR-483-5p in regulating circulating PCSK9 in vivo. The difference in expression of miR-191-5p, miR-224-5p, and miR-337-3p between patients and control subjects suggests their possible role in the pathogenesis of coronary artery disease.

TGF-β1 and TGFβR2 Gene Polymorphisms in Patients with Unstable Angina.

Acute coronary syndromes result from a sudden reduction in the lumen of a coronary artery as a result of atherosclerotic plaque rupture, its swelling or the formation of thrombotic lesions. Many mediators with inflammatory, prothrombotic and proatherogenic effects have been shown to be involved, including numerous cytokines, chemokines, adhesion molecules and growth factors. TGF-β1 is a pleiotropic cytokine found in various cells that regulates cell growth, differentiation and matrix production. The aim of our study was to assess the association between polymorphisms in the TGF-β1 gene (rs1800469, rs1800470) and polymorphisms in the TGFBR2 receptor gene (rs6785358, rs9838682) and the risk of unstable angina, as well as selected clinical parameters affecting the risk of ischemic heart disease. The study included 232 patients with unstable angina. The diagnosis of unstable angina was made by typical clinical presentation and confirmation of significant coronary artery lumen stenosis (&gt;70%) during coronary angiography. There were no statistically significant differences in the distribution of TGFBR2 rs6785358 and rs9838682 genotypes and haplotypes between patients with unstable angina and control subjects. We observed increased values of plasma total and LDL cholesterol levels, as well as triglycerides, in patients with the TGFBR2 rs9838682 AA genotype. In patients with the TGFBR2 rs6785358 AA genotype, we noted increased BMI values. There were no statistically significant associations between other studied polymorphisms and clinical parameters. Polymorphisms in the TGF-β1 gene (rs1800469, rs1800470) and polymorphisms in the TGFBR2 receptor gene (rs6785358, rs9838682) are not significant risk factors for unstable angina in our population. The TGFBR2 gene rs9838682 polymorphism may influence the lipid parameters in patients with coronary artery disease.

Correlation of the Dutch Lipid Clinic Network score as a diagnostic tool and lipid parameters in patients with familial hypercholesterolemia

Introduction. Familial hypercholesterolemia is a congenital disorder of lipid metabolism. The Dutch Lipid Clinic Network score is used for early diagnosis of familial hypercholesterolemia. The aim of the study was to examine correlation between the above score and the first measured lipid values in patients who had not used lipid-lowering therapy. Material and Methods. 390 patients identified as familial hypercholesterolemia+ (n=247) and familial hypercholesterolemia-(n=143) according to the Dutch Lipid Clinic Network score. Family and personal history, physical examination, demographic and anthropometric characteristics and lipid status were analyzed. Results. The familial hypercholesterolemia+group had all Dutch Lipid Clinic Network score components significantly higher than the familial hyper?cholesterolemia-group. The highest average number of points in familial hypercholesterolemia+ group carries low-density lipoprotein level and family history data. Significantly higher levels of total cholesterol, low-density lipoprotein and apolipoprotein B were found in the familial hypercholesterolemia+ group, while high-density lipo?protein was lower in the familial hypercholesterolemia-group. The Dutch Lipid Clinic Network score correlates best with level of low-density lipoprotein and apolipoprotein B (p&lt;0.001). The cut-off point for low-density lipoprotein is 4.9 mmol/L (sensitivity 56%; specificity 8%), while the cut-off point for apolipoprotein B is 1.52 g/L (sensitivity 42%; specificity 12.5%) for diagnosis of familial hypercholesterolemia. Conclusion. Low-density lipoprotein and apolipoprotein B values significantly correlate with Dutch Lipid Clinic Network score values. Elevated values of low-density lipoprotein (&gt;4.9 mmol/L) significantly affect the total value of the Dutch Lipid Clinic Network score and are considered components that carry large number of points for the diagnosis of familial hypercholesterolemia.

Management of Familial Hypercholesterolemia with Special Emphasis on Evinacumab.

Familial hypercholesterolemia (FH) is an underdiagnosed disease that contributes to a significant number of cardiovascular incidents through high serum Low-Density Lipoprotein Cholesterol (LDL-C) values. Its treatment primarily requires healthy lifestyle and therapy based on statins, ezetimibe and Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9); however, there are also new treatment options that can be used in patients who do not respond to therapy, among which we highlight evinacumab. Elevated LDL-C values, together with clinical manifestations associated with cholesterol deposition (e.g., tendon xanthomas, xanthelasma and arcus cornealis) and family history are the main elements in the diagnosis of FH. Pathognomonic signs of FH include extensor tendon xanthomas; however, their absence does not exclude the diagnosis. Elevated LDL-C levels lead to premature Atherosclerotic Cardiovascular Disease (ASCVD), which is why early diagnosis and treatment of FH is essential. Evinacumab, a novelty in pharmacological practice, having a complex mechanism of action, causes desirable changes in lipid parameters in patients with homozygous form of familial hypercholesterolemia (HoFH). This review collects and summarizes the most important aspects of the new drug, especially being a discovery in the treatment of HoFH, giving these patients hope for a longer and more comfortable life.

Long Term Safety and Efficacy of Saroglitazar in Indian Patients with Diabetic Dyslipidemia and Very High Triglyceride Levels: Real World Evidence

Objective: Diabetes and diabetic dyslipidemia with high triglycerides (TGs) are commonly associated. Saroglitazar is the first dual PPAR α/γ agonist approved in India for the management of diabetic dyslipidemia. The objective of this observational study was to assess the long-term safety and efficacy of saroglitazar in patients with diabetic dyslipidemia with very high triglycerides (&gt; 500 mg/dL). Materials and methods: This was a single-center, retrospective observational study which was conducted among 150 patients with type 2 diabetes who had diabetic dyslipidemia with hypertriglyceridemia (&gt; 500 mg/dL at baseline). All patients were on saroglitazar 4 mg once daily and all had complete follow-up data. At baseline, all patients were on stable doses of antidiabetic and statin therapy. Results: Significant reduction of TG and LDL-cholesterol was observed from baseline to 12th week: from 669.93 ± 81.22 to 268.72 ± 82.32 mg/dL and from 167.68 ± 10.881 to 118.88 ± 12.16 mg/dL (p &lt; 0.0001 and &lt; 0.001), respectively. The mean HbA1c was reduced from 8.02 ± 0.3 to 7.71 ± 0.5% (&lt; 0.001). This reduction in lipid and glycemic parameters continued till 52th week. At 52 weeks mean TG, LDL-cholesterol and HbA1c were reduced to 221.51 ± 61.81 mg/dL, 118.88 ± 12.16 mg/dL and 7.12 ± 0.2 % (p &lt;0.001 for all). No major adverse event was reported during the study period. Creatine phosphokinase (CPK), liver enzymes and creatinine did not alter significantly. Conclusions: Long term use of saroglitazar leads to significant improvement in both glycemic and lipid parameters in patients with diabetic dyslipidemia with very high triglycerides (&gt;500 mg/dl) and initially not controlled by statins alone. Therefore, to fulfil the unmet need, long-term use of saroglitazar could be an effective, well tolerated and safe option.

Does low glycemic index diet superior than routine diet to control blood inflammation state and lipid parameters in patients with coronary artery disease?

Abstract Background and aims Low glycemic index diet has been shown several benefits in terms of reduction in atherosclerotic biomarkers in patients with coronary artery disease (CAD). Objective of the study To demonstrate superiority of the low glycemic index diet in patients with CAD in terms of blood inflammation state and lipid parameters. Methods One hundred and sixty patients aged 38–76 years established with CAD entered as 12 week dietary intervention either with low glycemic index (n=80) or routine diet (n=80) together with standard therapy from 2016 to 2019 (male=48%; 58.2±12.0 years). Laboratory (including hs-CRP, pro-inflammatory interleukins, IL-1β, IL-6, TNF-α, lipid parameters TC, TG, LDL-Cholesterol, HDL-Cholesterol) and instrumental data were obtained at baseline and in 12 weeks of the intervention. Results There were no statistically differences in biochemical data between two groups at their baseline characteristics. Low glycemic index diet positively influenced on hs-CRP (from 252.4±40.6 mg/dL to 161.9±28.5 mg/dL vs. from 237.8±35.6 mg/dL to 202.4±23.8 mg/dL; P&amp;lt;0.05), HbA1c (from 6.95±1.95% to 4.78±1.18% vs. 6.80±1.65% to 6.25±1.45%; P&amp;lt;0.05), TG (from 5.2±2.2 to 3.1±1.8 vs. from 5.8±2.8 to 4.9±2.0, P&amp;lt;0.05), TNF-α (from 1.48±0.91 to 0.88±0.19 vs. from 1.55±1.35 to 1.12±0.35, P&amp;lt;0.05), IL-6 (from 8.2 pg/mL to 4.9 pg/mL vs. from 8.2 pg/mL to 4.9 pg/mL, P&amp;lt;0.005) than routine diet. Although reduction in IL-1β were observed in both groups (from 32.5±17.2 pg/ml to 28.9±16.8 pg/ml, P&amp;gt;0.05; vs. 33.6±21.6 pg/ml to 29.8±20.4, P&amp;gt;0.05;), however there were no statistically significant from baseline and between groups (P&amp;gt;0.05). Conclusions Low glycemic index diet demonstrated superiority to routine diet to improve inflammatory state and lipid parameters in patients with CAD. Funding Acknowledgement Type of funding sources: None.

Does low glycemic index diet superior than routine diet to control blood inflammation state and lipid parameters in patients with coronary artery disease?

Does low glycemic index diet superior than routine diet to control blood inflammation state and lipid parameters in patients with coronary artery disease?

Real-life impact of tenofovir disoproxil fumarate and entecavir therapy on lipid profile, glucose, and uric acid in chronic hepatitis B patients.

The impact of long-term nucleos(t)ide analogs treatment on host metabolism is a concern. Hence, we conducted this study to compare the effect of entecavir (ETV) and tenofovir disoproxil fumarate (TDF) on metabolic parameters among chronic hepatitis B(CHB) patients.In this real-life retrospective study, 2030 CHB outpatients treated with ETV or TDF at Nanfang Hospital, China, were included. For treatment-naïve patients, pretreatment and semiannual metabolic parameters were collected. For treatment-experienced patients, metabolic parameters were collected at the first visit. Propensity score matching (PSM) was used to balance the effects of potential confounding factors.Among 122 treatment-naïve patients and 1908 treatment-experienced patients, ETV-treated patients were older with a higher percentage of metabolic syndrome. After PSM, the characteristics were comparable between the two groups. For treatment-naïve patients, four lipid parameters, including total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein, and triglyceride levels showed a decreasing trend during the 42-month TDF treatment, while they remained relatively stable or increased during ETV treatment. At Month 30, the levels of TC and LDL among TDF-treated patients were significantly lower than those among ETV-treated patients (TC: 4.7 mmol/L vs. 3.9 mmol/L, p = 0.004; LDL: 3.0 mmol/L vs. 2.4 mmol/L, p = 0.009). For treatment-experienced patients, we also observed lower levels of lipid parameters in patients with different durations of TDF treatment. The levels of glucose and uric acid were similar among ETV- and TDF-treated patients.TDF has a lipid-lowering effect in CHB patients, which provides a basis for the selection of antiviral drugs for aging CHB patients.

Obicetrapib Lowers LDL-C in Patients Taking High Intensity Statins - Results from the ROSE Clinical Trial

Lead Author's Financial Disclosures New Amsterdam Pharma. Study Funding NewAmsterdam Pharma. Background/Synopsis Mendelian randomization studies have predicted that cholesteryl ester transfer protein (CETP) inhibition would reduce the risk of cardiovascular events. This was confirmed in REVEAL; by lowering LDL-C, anacetrapib was associated with a reduction in cardiovascular events. Early studies of the selective CETP inhibitor obicetrapib demonstrated LDL-C lowering up to 45% as monotherapy and 68% in combination with moderate intensity statin therapy. Objective/Purpose To assess the effects of obicetrapib on LDL-C and lipid parameters in patients treated with high intensity statins. Methods Patients (n=120) with an LDL-C ≥70 mg/dL, despite treatment with high intensity statins, were randomized to treatment with obicetrapib 5 or 10 mg or matching placebo for 8 weeks. The primary endpoint was the difference between groups in percent change in LDL-C from baseline to week 8. Secondary endpoints included changes in ApoB, non-HDL-C and HDL-C. Exploratory analyses evaluated differences in Friedewald and preparative ultracentrifugation measurement (PUC) of LDL-C. Safety assessment included biochemistry, vital signs, physical examinations, and adverse events. Results Patients had a median LDL-C of 88 mg/dL at baseline. Compared with placebo, obicetrapib produced greater dose-dependent lowering of LDL-C (up to 50.8%, P<0.0001), which was comparable between PUC and Friedewald measures. Obicetrapib also produced greater lowering of apoB (up to 29.8%, P<0.0001), non-HDL-C (up to 44.4%, P<0.0001), Lp(a) (up to 56.5%, P<0.0001) and raising of HDL-C (up to 165%, P<0.0001) in a dose-dependent fashion compared with placebo. Fewer patients in the obicetrapib arms (26%) experienced treatment-emergent adverse events than in the placebo arm (48%). No patients in either obicetrapib arm experienced a treatment-emergent SAE. There were no clinically significant changes in laboratory parameters, vital signs, or physical examinations in any study group. Conclusions Obicetrapib at doses of 5 and 10 mg produced robust decreases in LDL-C, ApoB, Lp(a) and Non-HDL-C and increases in HDL-C compared to placebo in patients treated with high intensity statins and was safe and well tolerated. New Amsterdam Pharma.

Obicetrapib Lowers LDL-C in Patients Taking High Intensity Statins - Results from the ROSE Clinical Trial

<h3>Lead Author's Financial Disclosures</h3> Nothing to disclose. <h3>Study Funding</h3> NewAmsterdam Pharma. <h3>Background/Synopsis</h3> Mendelian randomization studies have predicted that cholesteryl ester transfer protein (CETP) inhibition would reduce the risk of cardiovascular events. This was confirmed in REVEAL; by lowering LDL-C, anacetrapib was associated with a reduction in cardiovascular events. Early studies of the selective CETP inhibitor obicetrapib demonstrated LDL-C lowering up to 45% as monotherapy and 68% in combination with moderate intensity statin therapy. <h3>Objective/Purpose</h3> To assess the effects of obicetrapib on LDL-C and other lipid parameters in patients treated with high intensity statins. <h3>Methods</h3> Patients (n=120) with an LDL-C ≥70 mg/dL, despite treatment with high intensity statins, were randomized to treatment with obicetrapib 5 or 10mg or matching placebo for 8 weeks. The primary endpoint was the difference between groups in percent change in LDL-C from baseline to week 8. Secondary endpoints included changes in ApoB, non-HDL-C and HDL-C. Exploratory analyses evaluated differences in Friedewald and preparative ultracentrifugation measurement (PUC) of LDL-C. Safety assessment included biochemistry, vital signs, physical examinations, and adverse events. <h3>Results</h3> Patients had a median LDL-C of 88mg/dL at baseline. Compared with placebo, obicetrapib produced greater dose-dependent lowering of LDL-C (up to 50.8%, P<0.0001), which was comparable between PUC and Friedewald measures. Obicetrapib also produced greater lowering of apoB (up to 29.8%, P<0.0001) and non-HDL-C (up to 44.4%, P<0.0001) and raising of HDL-C (up to 165%, P<0.0001) in a dose-dependent fashion compared with placebo. (Table) Fewer patients in the obicetrapib arms (26%) experienced treatment emergent adverse events than in the placebo arm (48%). No patients in either obicetrapib arm experienced a treatment emergent SAE. There were no clinically significant changes in laboratory parameters, vital signs, or physical examinations in any study group. <h3>Conclusions</h3> Obicetrapib at doses of 5 and 10mg produced robust decreases in LDL-C, ApoB and Non-HDL-C and increases in HDL-C compared to placebo in patients treated with high intensity statins and was safe and well tolerated.

The Effect of Curcumin on Lipid Profile and Glycemic Status of Patients with Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis

Type 2 diabetes mellitus (T2DM) is a progressive metabolic disorder, some natural compounds are thought to be beneficial in improving the metabolic status of patients with T2DM. Curcumin is the main bioactive agent of turmeric, the impact of curcumin on T2DM is still controversial. This meta-analysis aimed to evaluate the effects of curcumin on lipids profile and glucose status in patients with T2DM. Randomized controlled trials (RCTs) examining the effects of curcumin on lipids profile and glycemic control of T2DM patients were searched in PubMed, Embase, Web of Science and Cochrane Library. Pooled estimates of weighted mean difference (WMD) were calculated between intervention and control groups using random-effects or fixed-effects model. Subgroup and sensitivity analyses were conducted to assess the effects. Nine eligible RCT with 604 subjects were included. The estimated pooled mean changes with curcumin were −18.97 mg/dL (95% CI: −36.47 to −1.47; P=0.03) for triglyceride (TG), −8.91 mg/dL (95% CI: −14.18 to −3.63, P=0.001) for total cholesterol (TC), -4.01 mg/dL (95% CI: -10.96 to 2.95, P=0.259) for low density lipoprotein cholesterol (LDL-c), 0.32 mg/dL (95% CI: −0.74 to 1.37, P=0.557) for high density lipoprotein cholesterol (HDL-c), −8.85 mg/dL (95% CI: −14.4 to −3.29, P=0.002) for fasting blood glucose (FBG), -0.54 (95% CI: −0.81 to −0.27, P ≤ 0.001) for glycated hemoglobin (HbA1c) (%) compared with controls. There was a significant heterogeneity for the influence of curcumin on TG, LDL-c, FBG and HbA1c. Subgroup analysis revealed that the heterogeneity mainly attributed to trial period, curcumin dosage and other therapy. The results of this study showed that curcumin supplementation had beneficial effects on glycemic status and some lipid parameters in patients with T2DM. Further studies with large-scale are still needed to confirm the results.

Impact of Sacubitril/Valsartan on Lipid Parameters in Patients with Heart Failure with Reduced Ejection Fraction.

Sacubitril/valsartan, an angiotensin receptor-neprilysin inhibitor, has been shown to significantly reduce cardiovascular mortality, heart failure hospitalizations, and all-cause mortality in patients with heart failure with reduced ejection fraction. This study aims to investigate the long-term impact of the sacubitril/valsartan combination on lipid parameters in patients with heart failure with reduced ejection fraction. For this single-center retrospective cross-sectional study, data of patients using sacubitril/valsartan because of heart failure with reduced ejection fraction were collected. In addition to routine controls, the patients' lipid levels were measured at 3-month intervals. The parameters that were obtained over 3 years included total cholesterol, high-density lipoprotein cholesterol, triglyceride, and N-terminal pro-B-type natriuretic peptide levels. A total of 192 patients with a functional capacity New York Heart Association II-V, and who were using sacubitril/valsartan because of heart failure with reduced ejection fraction, were included in this study. Independent of statin use, there was a decrease in total cholesterol levels (196.1 ± 44.8 mg/dL vs 161.5 ± 41.7 mg/dL, p < 0.001) and triglyceride levels (159.1 ± 10.4 mg/dL vs 121.4 ± 6.9 mg/dL, p < 0.001), and there was an improvement in high-density lipoprotein cholesterol levels (44.9 ± 1.9 mg/dL vs 48.2 ± 2.4 mg/dL, p < 0.001) when comparing baseline levels with third-year levels. Sacubitril/valsartan in patients with heart failure with reduced ejection fraction, independent of statin use, may cause a decrease in total cholesterol and triglyceride levels and an improvement in high-density lipoprotein cholesterol levels.

Do patients with psoriasis are at higher risk for atherogenity? Acase-control study.

Psoriasis is a chronic, inflammatory skin disease that is common in both adult and childhood. Patients with psoriasis are at significant risk for the development of many comorbid conditions, including cardiovascular diseases. We aimed to investigate the cardiovascular risk status and serum lipid parameters in patients with psoriasis and to determine the risk of cardiovascular disease by atherogenic indices obtained accordingly. This retrospective case-control study was conducted with a total of 142 individuals, 72 patients with psoriasis vulgaris and 70healthy volunteers over the age of 18 who were admitted to the dermatology outpatient clinic. Demographic information and laboratory values were retrieved from the hospital database. Afterward, atherogenic indexes such as Atherogenic index of plasma (AIP), Castelli Risk Index I and II (CRI-I and II), and Atherogenic coefficient (AC) were calculated. There was a significant difference in lipid profile between the psoriasis patients and the control group. In patients with psoriasis, triglyceride level (140.09±71.20mg/dl vs. 116.10±63.95, p=0.037) was higher, while HDL level (44.34±11.77mg/dl vs. 50.31±11.62, p=0.003) was lower. Regarding atherogenic indices; AIP (0.10±0.24 vs. -0.04±0.27, p=0.001), CRI-I (4.63±1.40 vs. 3.94±1.02, p=0.001), CRI-II (2.98±1.01 vs. 2.61±0.82, p=0.019) and AC (3.63±1.40 vs.. 2.94±1.02, p=0.001) were significantly higher in patients with psoriasis. Our study shows that patients with psoriasis have higher pro-atherogenic lipid profile and atherogenic indexes at a high risk level. Patients with psoriasis have an increased risk of cardiovascular diseases.