Risk Factor For Atherosclerotic Disease Research Articles

Abstract P125: Association of Cardiology Encounters for Underrepresented Racial and Ethnic Groups With Human Immunodeficiency Virus With Subsequent Lipid and Blood Pressure Control

Background: People with HIV (PWH) are at elevated atherosclerotic cardiovascular disease (ASCVD) risk. Underrepresented racial and ethnic groups (UREGs) with HIV in the Southern U.S. are disproportionately affected, yet whether cardiology specialist care for this at-risk group improves blood pressure and lipid control is unknown. Methods: We evaluated a cohort of UREGs with HIV at elevated ASCVD risk without known cardiovascular disease. Participants received HIV-related care from 2015-2018 at four academic medical centers in the Southern United States with follow up through 2020. To create the cardiology and non-cardiology comparator groups, we divided the study into 6-month intervals, creating 8 cohorts and identified eligible patients with a new cardiology encounter during the interval. We included those without a cardiology encounter in that interval or any prior as controls. Primary outcomes were blood pressure control (<140/90 mmHg) and lipid control (LDL-C ≤ 100 mg/dl) assessed during 2 years of follow-up. Statistical analyses were adjusted for cohort, patient factors, HIV measures, and comorbidities, and used random effects to account for repeated use of patients across cohorts. Results: Among 4096 included individuals, 411 (10%) had a cardiology encounter (Table 1). Cardiology encounters were associated with subsequent lipid control (OR 2.55, 95% CI 1.17-5.55, p=0.02), but not blood pressure control (OR 0.94, 95% CI 0.46-1.92, p=0.86). Compared to those without a cardiology encounter, those with a cardiology encounter did not subsequently have lower LDL-C (0.46 mg/dl higher per month, p=0.03) or systolic blood pressure (0.05 mm Hg higher per month, p=0.07). Conclusions: Cardiology encounters are associated with lipid control for UREGs with HIV. The lack of a decrease in LDL or systolic blood pressure suggests cardiology encounters may not be adequate to improve blood pressure and lipid control, two major modifiable risk factors for atherosclerotic cardiovascular disease among PWH.

Reductions in remnant cholesterol and VLDL cholesterol through inhibition of ANGPTL3 protein synthesis: an analysis from the TRANSLATE-TIMI 70 trial.

Remnant cholesterol and very low-density lipoprotein cholesterol (VLDL-C) are increasingly recognized risk factors for atherosclerotic disease with few therapeutic options. Angiopoietin-like 3 (ANGPTL3), a key protein in the metabolism of triglyceride-rich lipoproteins, is a promising target. TRANSLATE-TIMI 70 was a double-blind, placebo-controlled randomized trial testing seven dose regimens of vupanorsen, an antisense oligonucleotide against ANGPTL3, in adults with non-HDL-C ≥ 100 mg/dL and triglycerides 150-500 mg/dL. The primary endpoint of this analysis was percentage change in remnant cholesterol (total cholesterol minus directly measured LDL-C minus HDL-C) and VLDL-C (directly measured) over 24 weeks. Two hundred eighty-six patients were enrolled, with a median age of 64 years and 44% female. Median baseline remnant cholesterol and VLDL-C were 42 and 31 mg/dL, respectively (reference: <30 mg/dL). Vupanorsen lowered remnant cholesterol by 42-59% at 24 weeks over placebo (P < 0.001), achieving a median level of 18 mg/dL at the highest dose. Over the same period, VLDL-C was reduced by 52-67% over placebo (P < 0.001), with a median achieved level of 2.5 mg/dL at the highest dose. The effect of vupanorsen on remnant cholesterol and VLDL-C reduction was dose-dependent and directly associated with the degree of ANGPTL3 inhibition: at 90% ANGPTL3 reduction, there was a 61% and 81% decrease in remnant cholesterol and VLDL-C, respectively. Inhibition of ANGPTL3 protein synthesis significantly lowered remnant cholesterol and VLDL-C in patients with hypertriglyceridaemia. The magnitude of reduction was associated with the degree of ANGPTL3 inhibition. These findings support ANGPTL3 inhibition as a promising target for lowering cholesterol on triglyceride-rich lipoproteins.

Clonal hematopoiesis is associated with cardiovascular events in patients with stable coronary artery disease

Clonal hematopoiesis (CH) is a risk factor for atherosclerotic cardiovascular disease, but the impact of smaller clones and the effect on inflammatory parameters is largely unknown. Using ultrasensitive single-molecule molecular inversion probe sequencing, we evaluated the association between CH and a first major adverse cardiovascular event (MACE) in patients with angiographically documented stable coronary artery disease (CAD) and no history of acute ischemic events. CH was associated with an increased rate of MACE at four years follow-up. The size of the clone predicted MACE at an optimal cut-off value of 1.07% variant allele frequency (VAF). Mutation carriers had no change in monocytes subsets or cytokine production capacity but had higher levels of circulating tissue factor, matrilysin, and proteinase-activated receptor-1. Our study identified CH driver mutations with a VAF as small as 1.07% as a residual cardiovascular risk factor and identified potential biomarkers and therapeutic targets for patients with stable CAD.

Lipoprotein(a) as a risk factor for atherosclerotic cardiovascular disease in patients in non-metropolitan areas of Brandenburg, Germany.

In the non-metropolitan region of Brandenburg (Germany), which is characterized by high rates of cardiovascular diseases and underserved medical care, there is a lack of awareness regarding lipoprotein(a) [Lp(a)] as a risk factor. In addition, data from patients with atherosclerotic cardiovascular disease (ASCVD) in diverse regional backgrounds, including the understudied Brandenburg cohort, and various healthcare statuses remain insufficient. In this WalkByLab study, Lp(a) levels were monitored in a non-metropolitan cohort (n = 850) in Brandenburg, Germany, comprising 533 patients at high cardiovascular risk and 317 healthy controls. Patients underwent a comprehensive angiological screening, which included blood serum analysis, assessment of medical and family history, cardiovascular risk, and disease status, and evaluation of lifestyle and quality of life. All parameters were evaluated with regard to two groups based on Lp(a) levels: low (<50 mg/dl) and high (≥50 mg/dl). Brandenburg patients with cardiovascular diseases showed higher Lp(a) levels than healthy controls (24.2% vs. 14.8%, p = 0.001). Logistic regression analysis with different characteristics revealed that Lp(a) was an independent risk factor significantly associated with ASCVD (OR 2.26, 95% CI 1.32-3.95, p = 0.003). The high-Lp(a) group showed a higher proportion of patients with coronary artery disease, peripheral artery disease, or cerebrovascular disease compared to the low-Lp(a) group (50% vs. 36.8%; 57.7% vs. 45.8%; 17.6% vs. 9.2%; p = 0.004); also, a higher percentage of patients in the high-Lp(a) group had heart failure (72.8% vs. 53.2%, p = 0.014) and myocardial infarction (24.7% vs. 13.9%, p = 0.001). The high-Lp(a) group exhibited higher rates of statins (63.1% vs. 50.4%, p = 0.003), ezetimibe (14.8% vs. 5.5.%, p = 0.001), and beta-blockers (55.7% vs. 40.7%, p = 0.001) use. Lp(a) levels were found to be independent of physical activity or smoking behavior and did not change over time (12 months). Our study highlights the significance of elevated Lp(a) levels in Brandenburg cardiovascular patients and identifies them as an independent risk factor for ASCVD, which has implications for addressing cardiovascular health of non-metropolitan populations.

Lipoprotein(a) serum concentrations in children in relation to body mass index, age and sex

BackgroundLipoprotein(a) (Lp(a)) is an inherited risk factor for atherosclerotic cardiovascular disease (ASCVD). Limited data exist on Lp(a) values in children. We aimed to evaluate whether Lp(a) concentrations in youth are influenced by BMI.Methods756 blood samples of 248 children with obesity and 264 matched healthy children aged 5 and 18 years, enrolled in the population-based LIFE Child (German civilization diseases cohort) study, were analyzed. Repeat measurements were available in 154 children (1–4 follow ups, ~1 year apart).ResultsThe median Lp(a) concentration in the total cohort (n = 512) at first visit was 9.7 mg/dL (IQR 4.0–28.3). Lp(a) concentrations between 30–50 mg/dL were observed in 11.5%, while 12.5% exhibited Lp(a) ≧50 mg/dL. There was no association of Lp(a) with body mass index (BMI) (ß = 0.004, P = 0.49). Lp(a) levels did not correlate with age or sex, while Lp(a) was associated positively with low-density lipoprotein cholesterol (ß = 0.05, P < 0.0001). The Lp(a) risk category remained stable in 94% of all children in repeated measurements.ConclusionsThe data showed no association of Lp(a) levels in children with BMI, age or sex. Measurement of Lp(a) in youth may be useful to identify children at increased lifetime risk for ASCVD.ImpactIn youth, Lp(a) levels are not affected by age, sex and BMI.Lp(a) risk categories remain stable over time in repeated measurements in children.Measurement of Lp(a) in children may be useful as an additional factor to identify children at increased lifetime risk for ASCVD and for reverse family screening.

Lipoprotein(a): A Review of Risk Factors, Measurements, and Novel Treatment Modalities.

The study of lipoprotein(a) [Lp(a)] has long been a source of interest as a possible independent risk factor for atherosclerotic cardiovascular disease (ASCVD). The results of large sample observational studies, genome-wide association studies, and Mendelian randomization studies have been strong indicators supporting the link between ASCVD and Lp(a) despite early studies, with less sensitive assays, failing to show a connection. The recommendations for the indications and frequency of testing Lp(a) levels vary between US, Canadian, and European organizations due to the uncertain role of Lp(a) in ASCVD. The innovation of recent therapies, such as antisense oligonucleotides and small interfering RNA, designed to specifically target and reduce Lp(a) levels by targeting mRNA translation have once more thrust LP(a) into the spotlight of inquiry. These emerging modalities serve the dual purpose of definitively elucidating the connection between elevated Lp(a) levels and atherosclerotic cardiovascular risk, as well as the possibility of providing clinicians with the tools necessary to manage elevated Lp(a) levels in vulnerable populations. This review seeks to examine the mechanisms of atherogenicity of Lp(a) and explore the most current pharmacologic therapies currently in development.

Factores asociados a la presencia de xantomas tendinosos en la hipercolesterolemia familiar

Introduction and objectivesTendon xanthomas (TX) are lipid deposits highly specific to familial hypercholesterolemia (FH). However, there is significant variability in their presentation among FH patients, primarily due to largely unknown causes. Lipoprotein(a) is a well-established independent risk factor for atherosclerotic cardiovascular disease in the general population as well as in FH. Given the wide variability of lipoprotein(a) among FH individuals and the likelihood that TX may result from a proatherogenic and proinflammatory condition, the objective of this study was to analyze the size of TX in the Achilles tendons of FH participants and the variables associated with their presence, including lipoprotein(a) concentration. MethodsA cross-sectional study was conducted on 377 participants with a molecular diagnosis of heterozygous FH. Achilles tendon maximum thickness (ATMT) was measured using ultrasonography with standardized equipment and procedures. Demographic variables and lipid profiles were collected. A multivariate linear regression model using a log-Gaussian approach was used to predict TX size. Classical cardiovascular risk factors and lipoprotein(a) were included as explanatory variables. ResultsThe mean low-density lipoprotein cholesterol level was 277mg/dL without lipid-lowering treatment, and the median ATMT was 5.50mm. We demonstrated that age, sex, low-density lipoprotein cholesterol, and lipoprotein(a) were independently associated with ATMT. However, these 4 variables did not account for most the interindividual variability observed (R2=0.205). ConclusionsTX, a characteristic hallmark of FH, exhibit heterogeneity in their presentation. Interindividual variability can partially be explained by age, male sex, low-density lipoprotein cholesterol, and lipoprotein(a) but these factors account for only 20% of this heterogeneity.Full English text available from:www.revespcardiol.org/en

ANGPTL3 and ApoC-III inhibitors for treating hypertriglyceridemia in context: horses for courses?

Hypertriglyceridemia (HTG) is an independent and casual risk factor for atherosclerotic cardiovascular disease (ASCVD). There is an unmet need for more effective treatments for patients with HTG. Angiopoietin-like protein 3 (ANGPTL3) and apolipoprotein C-III (apoC-III) are key regulators of triglyceride-rich lipoprotein (TRL) metabolism. We review recent clinical trials targeting ANGPTL3 and apoC-III with monoclonal antibody and nucleic acid therapies, including antisense oligonucleotides and small interfering RNA. ANGPTL3 and apoC-III inhibitors are effective in lowering plasma triglycerides and TRLs, with possibly greater efficacy with the inhibition of apoC-III. By contrast to ANGPTL3 inhibition that has the advantage of greater lowering of plasma low-density lipoprotein (LDL)-cholesterol and apoB levels, apoC-III inhibition only has a modest or no effect in lowering plasma LDL-cholesterol and apoB concentrations. Therapeutic inhibition of ANGPTL3 and apoC-III can correct HTG possibly by reducing production and increasing catabolism of TRL particles, but this remains to be formally investigated in patients with HTG. Novel agents targeting ANGPTL3 and apoC-III can correct HTG and potentially lower risk of ASCVD in patients with HTG. The long-term safety and cost-effectiveness of these agents await confirmation in ongoing and future studies.

Synergetic impact of lipoprotein(a) and fibrinogen on stroke in coronary artery disease patients.

Emerging data suggested that lipoprotein(a) [Lp(a)] is an independent risk factor for atherosclerotic cardiovascular disease. Previous studies indicated fibrinogen (Fib) had synergetic effect on Lp(a)-induced events. However, combined impact of Fib and Lp(a) on ischemic stroke has not been elucidated. In this prospective study, we consecutively enrolled 8263 patients with stable coronary artery diseases (CAD) from 2011 to 2017. Patients were categorized into three groups according to tertiles of Lp(a) levels [Lp(a)-low, Lp(a)-medium, and Lp(a)-high] and further divided into nine groups by Lp(a) and Fib levels. All subjects were followed up for the occurrence of ischemic stroke. During a median follow-up of 37.7 months, 157 (1.9%) ischemic strokes occurred. Stroke incidence increased by Lp(a) (1.1 vs. 2.1 vs. 2.5%, Cochran-Armitage p < .001) and Fib (1.1 vs. 2.0 vs. 2.6%, Cochran-Armitage p < .001) categories. When further classified into nine groups by Lp(a) and Fib levels, the incidence of ischemic stroke in group 9 [Lp(a)-high and Fib-high] was significantly higher than that in group 1 [Lp(a)-low and Fib-low] (3.1 vs. 6%, p < .001). The group 9 was associated with a highest risk for ischemic stroke (adjusted HR 4.907, 95% CI: 2.154-11.18, p < .001), compared with individuals in the Lp(a)-high (adjusted HR 2.290, 95% CI: 1.483-3.537, p < .001) or Fib-high (adjusted HR 1.184, 95% CI: 1.399-3.410, p = .001). Furthermore, combining Lp(a) with Fib increased C-statistics by .045 (p = .004). Current study first demonstrated that elevated Lp(a) combining with Fib evaluation enhanced the risk of ischemic stroke in patients with CAD beyond Lp(a) or Fib alone.

Neurotensin accelerates atherosclerosis and increases circulating levels of short-chain and saturated triglycerides

Background and aimsObesity and type 2 diabetes are significant risk factors for atherosclerotic cardiovascular disease (CVD) worldwide, but the underlying pathophysiological links are poorly understood. Neurotensin (NT), a 13-amino-acid hormone peptide, facilitates intestinal fat absorption and contributes to obesity in mice fed a high-fat diet. Elevated levels of pro-NT (a stable NT precursor produced in equimolar amounts relative to NT) are associated with obesity, type 2 diabetes, and CVD in humans. Whether NT is a causative factor in CVD is unknown. MethodsNt+/+ and Nt–/– mice were either injected with adeno-associated virus encoding PCSK9 mutants or crossed with Ldlr–/– mice and fed a Western diet. Atherosclerotic plaques were analyzed by en face analysis, Oil Red O and CD68 staining. In humans, we evaluated the association between baseline pro-NT and growth of carotid bulb thickness after 16.4 years. Lipidomic profiles were analyzed. ResultsAtherosclerotic plaque formation is attenuated in Nt-deficient mice through mechanisms that are independent of reductions in circulating cholesterol and triglycerides but associated with remodeling of the plasma triglyceride pool. An increasing plasma concentration of pro-NT predicts atherosclerotic events in coronary and cerebral arteries independent of all major traditional risk factors, indicating a strong link between NT and atherosclerosis. This plasma lipid profile analysis confirms the association of pro-NT with remodeling of the plasma triglyceride pool in atherosclerotic events. ConclusionsOur findings are the first to directly link NT to increased atherosclerosis and indicate the potential role for NT in preventive and therapeutic strategies for CVD.

Unclosing Premature Mortality Gap Among Patients With Gout in the US General Population, Independent of Serum Urate and Atherosclerotic Cardiovascular Risk Factors.

Gout flares are followed by transient major cardiovascular (CV) risk, implicating the role of inflammation; the aim of this study was to determine whether premature mortality rates in patients with gout and CV risk are independent of serum urate (SU) and atherosclerotic CV disease (ASCVD) risk factors. Using serial US nationwide prospective cohorts, we evaluated the independent association of prevalent gout with all-cause and CV mortality, adjusting for SU, ASCVD risk factors, comorbidities, medications, and kidney function and compared mortality rates between the early (1988-1994 baseline) and late cohorts (2007-2016 baseline). We replicated late cohort findings among patients with gout in a nationwide UK cohort (2006-2010 baseline). Adjusted hazard ratios (HRs) for mortality rates in patients with prevalent gout were similar in early and late US cohorts (1.20 [1.03-1.40] and 1.19 [1.04-1.37], respectively); HRs with further adjustment for SU were 1.19 (1.02-1.38) and 1.19 (1.03-1.37), respectively. Adjusted HR among patients with gout from the UK late cohort was 1.61 (1.47-1.75); these associations were larger among women (P = 0.04) and prominent among Black individuals. Adjusted HR for CV mortality rates in the late US cohort was 1.39 (1.09-1.78); those for circulatory, CV, and coronary heart disease deaths among UK patients with incident gout were 1.48 (1.24-1.76), 1.49 (1.20-1.85), and 1.59 (1.26-1.99), respectively. Patients with gout experience a persistent mortality gap in all-cause and CV deaths, even adjusting for SU and ASCVD risk factors, supporting a role for gout-specific pathways (eg, flare inflammation). These findings suggest gaps in current care, particularly in women and possibly among Black patients.

Factors associated with the presence of tendon xanthomas in familial hypercholesterolemia

Introduction and objectivesTendon xanthomas (TX) are lipid deposits highly specific to familial hypercholesterolemia (FH). However, there is significant variability in their presentation among FH patients, primarily due to largely unknown causes. Lipoprotein(a) is a well-established independent risk factor for atherosclerotic cardiovascular disease in the general population as well as in FH. Given the wide variability of lipoprotein(a) among FH individuals and the likelihood that TX may result from a proatherogenic and proinflammatory condition, the objective of this study was to analyze the size of TX in the Achilles tendons of FH participants and the variables associated with their presence, including lipoprotein(a) concentration. MethodsA cross-sectional study was conducted on 377 participants with a molecular diagnosis of heterozygous FH. Achilles tendon maximum thickness (ATMT) was measured using ultrasonography with standardized equipment and procedures. Demographic variables and lipid profiles were collected. A multivariate linear regression model using a log-Gaussian approach was used to predict TX size. Classical cardiovascular risk factors and lipoprotein(a) were included as explanatory variables. ResultsThe mean low-density lipoprotein cholesterol level was 277mg/dL without lipid-lowering treatment, and the median ATMT was 5.50mm. We demonstrated that age, sex, low-density lipoprotein cholesterol, and lipoprotein(a) were independently associated with ATMT. However, these 4 variables did not account for most the interindividual variability observed (R2=0.205). ConclusionsTX, a characteristic hallmark of FH, exhibit heterogeneity in their presentation. Interindividual variability can partially be explained by age, male sex, low-density lipoprotein cholesterol, and lipoprotein(a) but these factors account for only 20% of this heterogeneity.

Evaluation &amp; Assessment of Chest Pain among Dyslipidemic Out-Door Patients without Prior Clinical Ischemic Heart Disease

Dyslipidemia is a significant risk factor for atherosclerotic cardiovascular diseases, including ischemic heart disease. However, hypercholesterolemia patients without a history of clinical ischemic heart disease (IHD) may experience chest pain that presents diagnostic and management challenges. This review aims to summarize the existing literature and assess the prevalence of chest pain in this specific patient without having previous heart disease. Bangladesh Heart Journal 2024; 39(1): 57-62

Prevalence and associated factors of dyslipidemia among university students in Central Thailand: a cross-sectional study

Background: Dyslipidemia is regarded as a significant risk factor for atherosclerotic cardiovascular diseases (ASCVDs). Currently, there is limited data regarding dyslipidemia among Thai university students. Objective: This study aimed to examine the prevalence of dyslipidemia and its related factors among university students in the central region of Thailand. Materials and methods: In this cross-sectional study, a total of 434 students aged 18-25 years at Thammasat University and Kasetsart University were recruited using simple random sampling. Fasting venous blood samples were obtained, and plasma lipid profiles were assessed by an automated analyzer. Dyslipidemia was formally characterized according to the National Cholesterol Education Program Adult Treatment Panel (NCEP-ATP III) guidelines. Demographic information, dietary behavior, and physical activity were collected using questionnaires. Anthropometric measures were also performed according to a standard protocol. Results: The prevalence of elevated total cholesterol, high-risk HDL-C, elevated LDL-C, and elevated triglycerides was 30.4, 18.2, 20.0, and 11.8%, respectively. The most common adverse lipid parameter was total cholesterol in both genders. Obesity and high fat intake were significantly associated with dyslipidemia (p&lt;0.05). Conclusion: This research revealed a significant occurrence of dyslipidemia, primarily driven by elevated total cholesterol, among university students in Thailand. Obesity and high fat intake are significant risk contributors to dyslipidemia. These findings emphasize the need for awareness, prevention, and management strategies targeting this population.

Role of leptin, Plasminogen activator inhibitor type-1 in the occurrence of atherosclerosis: New insights into the mechanism of obesity-induced atherosclerosis

Background and aim: The most widespread pathological condition of peripherals and coronary artery disorders, as well as of cerebellar problems, is atherosclerosis (AS). Obesity is the most common nutritional disorder world wide and is one of the major risk factors for atherosclerotic cardiovascular disease (ASCVD). Leptin, plasminogen activator inhibitor-1 (PAI-1) are released by adipose tissue, which is a tissue that is found throughout the body and is considered an important endocrine system, these are essential for the control of immunological and energy responses. Methods:A case-control study was used in the design of the current investigation. 100 male participants, comprising 60 atherosclerosis individuals, 30 obese patients, 30 normal weight patients, and 40 healthy people, 20 of whom were obese and 20 of whom were of normal weight. Age between(40-65). This work was done between November/2022 and May/2023. Patient from the Karbala Center for Cardiac Disease and Surgery. A 3 ml sample of venous blood was obtained from patients and was healthy. In addition, some information was taken from each person(age,height,weight). Results:There has been a significant increase in concentrations of each one of the hormones (Leptin, PAI-1) in all groups when compared with non obese control. Conclusion:leptin and PAI-1 plays a role in the development of atherosclerosis in obese individuals. A person's risk of developing atherosclerosis increases with rising body mass index. It was discovered that the hormone Leptin, which regulates metabolism, is rising, which might be an indicator that the metabolic problem in obese people is becoming more common.

Comparison of LDL Levels Obtained by Martin-Hopkins Formula and Friedewald’s Formula with Directly Measured LDL: A Cross-sectional Study

Introduction: Low Density Lipoprotein (LDL) is one of the major modifiable risk factor of atherosclerotic diseases and so a potential therapeutic target. So, Low Density Lipoprotein Cholesterol (LDL-C) is of primary importance to assess cardiac risk. Many formulae are used to calculate LDL-C. Friedewald’s formula, despite its limitations, has been widely used due to its simplicity and convenience. The present research was aimed to compare the accuracy of Friedewald’s formula with the Martin-Hopkins formula, providing valuable insights for clinical practice. Aim: To compare LDL levels obtained by the Martin-Hopkins and Friedewald’s formula with LDL levels obtained by directly measuring LDL in the southern India. Materials and Methods: The present hospital-based cross-sectional study was conducted in the Department of Biochemistry, Hassan Institute of Medical Sciences (HIMS), Hassan, Karnataka, India, from March 2023 to June 2023. Total participants were assessed for their serum lipid profile using standard methods. LDL-C was calculated using the Friedewald and Martin formulae, and these calculated values were then correlated with the directly measured LDL-C. Based on Triglyceride (TG) levels, subjects were divided into five groups to ensure a comprehensive analysis (Group-1: TG &lt;100 mg/dL, Group-2: TG=101-150 mg/dL, Group-3: TG=151-200 mg/dL, Group-4: TG=201-400 mg/dL, Group-5: TG &gt;400 mg/ dL). Groups were compared using a correlation analysis using Pearson’s correlation and paired t-test. Results: The study findings are significant. At TG levels &lt;100 mg/dL, the Martin formula demonstrated a superior correlation (r=0.964, p-value≤0.001). At TG 101-150 mg/dL, 151-200 mg/ dL, and 201-400 mg/dL, Friedewald’s formula showed a slightly better correlation. However, at TG &gt;400 mg/dL, Friedewald’s formula had a higher mean difference. ROC curves further confirmed the superiority of Martin’s formula (AUC=0.948, p-value≤0.001), demonstrating better diagnostic performance than Friedewald’s formula (AUC=0.947, p-value≤0.001) at all TG levels. Conclusion: The Martin-Hopkins formula showed better diagnostic performance among the two equations than the Friedewald’s formula. The mean difference was lesser for Martin’s formula than Friedewald’s formula at all TG levels except at levels &lt;100 mg/dL. Considering the mean difference, Martin’s formula provided better LDL-C values than Friedewald’s formula for estimating LDL-C in the present study’s demographic population.

Impact of genetic background as a risk factor for atherosclerotic cardiovascular disease: A protocol for a nationwide genetic case-control (CV-GENES) study in Brazil.

Atherosclerotic Cardiovascular Disease (ASCVD) represents the leading cause of death worldwide, and individual screening should be based on behavioral, metabolic, and genetic profile derived from data collected in large population-based studies. Due to the polygenic nature of ASCVD, we aimed to assess the association of genomics with ASCVD risk and its impact on the occurrence of acute myocardial infarction, stroke, or peripheral artery thrombotic-ischemic events at population level. CardioVascular Genes (CV-GENES) is a nationwide, multicenter, 1:1 case-control study of 3,734 patients in Brazil. Inclusion criterion for cases is the first occurrence of one of the ASCVD events. Individuals without known ASCVD will be eligible as controls. A core lab will perform the genetic analyses through low-pass whole genome sequencing and whole exome sequencing. In order to estimate the independent association between genetic polymorphisms and ASCVD, a polygenic risk score (PRS) will be built through a hybrid approach including effect size of each Single Nucleotide Polymorphism (SNP), number of effect alleles observed, sample ploidy, total number of SNPs included in the PRS, and number of non-missing SNPs in the sample. In addition, the presence of pathogenic or likely pathogenic variants will be screened in 8 genes (ABCG5, ABCG8, APOB, APOE, LDLR, LDLRAP1, LIPA, PCSK9) associated with atherosclerosis. Multiple logistic regression will be applied to estimate adjusted odds ratios (OR) and 95% confidence intervals (CI), and population attributable risks will be calculated. Clinical trial registration: This study is registered in clinicaltrials.gov (NCT05515653).

The impact of baseline dietary fatty acid intake on the association between lipoprotein(a) and mortality in two US cohorts.

Lipoprotein(a) (Lp(a)) is an established casual risk factor for atherosclerotic cardiovascular disease. It remains unknown whether dietary fat modifies the association of Lp(a) with cardiovascular death. To understand if dietary fat modifies the association between Lp(a) and cardiovascular death. We utilized the Atherosclerotic Risk in Communities (ARIC) study and National Health and Nutrition Examination Survey (NHANES) III cohorts and used multivariate cox proportional hazard modeling to test the association between Lp(a), dietary fats, and cardiovascular death. The sample (n = 22,805) had average age 51.3 years and was mostly female (55.4%). Lp(a) ≥ 30 mg/dL was associated with CV death in both ARIC (1.36, p = 0.001) and NHANES (1.31, p = 0.03). In multivariate analysis, no categorical or individual fatty acids modified the association between Lp(a) and CV death. There was no evidence that baseline dietary fat intake modified the association between Lp(a) and CV death.

Prevalence of Lipoprotein(a) Measurement and its Association with Arteriosclerosis in Asymptomatic Individuals in China.

Lipoprotein(a) [Lp(a)] is an independent risk factor for atherosclerotic cardiovascular disease (ASCVD), and its level is genetically determined. Although guidelines and consensuses in various cardiovascular fields have emphasized the importance of Lp(a), screening for Lp(a) in China has not been well studied. A cross-sectional study was conducted using a random sample of 30,000 medical examiners from each of the five health check-up centres. The distribution of Lp(a) was described for those who completed Lp(a) testing, and logistic regression modelling was used to evaluate the relationship between Lp(a) levels and vascular structure and function in the population who underwent carotid ultrasound and brachial‒ankle pulse wave velocity (baPWV) measurements. Lp(a) was measured in only 4400 (3.02%) of the 150,000 participants. Among those tested for Lp(a), the median concentration was 15.85 mg/dL. The proportion of participants with Lp(a) levels ≥ 30 mg/dL was 15.00%. Multiple logistic regression analysis revealed a significant correlation between Lp(a) and cIMT ≥ 1.0 mm (OR: 1.008, 95% CI: 1.001-1.014, P=0.020) and carotid artery plaques (OR: 1.010, 95% CI: 1.004-1.016, P=0.001) but no correlation with baPWV ≥ 1400 (OR: 0.999, 95% CI: 0.993-1.005, P=0.788) or baPWV ≥ 1800 (OR: 1.002, 95% CI: 0.993-1.011, P=0.634). The detection rate of Lp(a) at health checkups is low, and Lp(a) is positively associated with cervical vascular sclerosis and plaque but not with baPWV. Therefore, the testing rate of Lp(a) and the awareness of the risk of vascular structural changes due to Lp(a) should be further improved.

Blood Monocyte Phenotype Is A Marker of Cardiovascular Risk in Type 2 Diabetes.

Diabetes is a major risk factor for atherosclerotic cardiovascular diseases with a 2-fold higher risk of cardiovascular events in people with diabetes compared with those without. Circulating monocytes are inflammatory effector cells involved in both type 2 diabetes (T2D) and atherogenesis. We investigated the relationship between circulating monocytes and cardiovascular risk progression in people with T2D, using phenotypic, transcriptomic, and metabolomic analyses. cardiovascular risk progression was estimated with coronary artery calcium score in a cohort of 672 people with T2D. Coronary artery calcium score was positively correlated with blood monocyte count and frequency of the classical monocyte subtype. Unsupervised k-means clustering based on monocyte subtype profiles revealed 3 main endotypes of people with T2D at varying risk of cardiovascular events. These observations were confirmed in a validation cohort of 279 T2D participants. The predictive association between monocyte count and major adverse cardiovascular events was validated through an independent prospective cohort of 757 patients with T2D. Integration of monocyte transcriptome analyses and plasma metabolomes showed a disruption of mitochondrial pathways (tricarboxylic acid cycle, oxidative phosphorylation pathway) that underlined a proatherogenic phenotype. In this study, we provide evidence that frequency and monocyte phenotypic profile are closely linked to cardiovascular risk in patients with T2D. The assessment of monocyte frequency and count is a valuable predictive marker for risk of cardiovascular events in patients with T2D. URL: https://www.clinicaltrials.gov; Unique identifier: NCT04353869.