Cardiovascular disease remains the leading cause of mortality and healthcare expenditures in the United States. It is also a major contributor to premature mortality, years lived with disability, and rising healthcare costs around the world. Despite the availability of proven therapies and interventions that could vastly decrease the burden of cardiovascular disease and cardiometabolic conditions, their implementation is poor, with generally less than half of patients being treated with the most effective therapies. Implementation science offers promise in bridging this gap and mitigating disparities. However, even though small studies have shown that there are effective methods to improve the implementation of evidence-based therapies, these methods have not been scaled to make an impact at the level of health systems or nationally. A coordinated, multi-stakeholder approach is essential to identify barriers to implementation on a broad scale and, more critically, to develop and deploy practical solutions. The Duke Clinical Research Institute conducted an Implementation Summit entitled "Scalability, Spread, and Sustainability" to explore strategies for advancing the uptake of evidence-based interventions for cardiometabolic diseases in healthcare in the United States. This manuscript presents the participants' multi-stakeholder perspective on the steps necessary to improve the implementation of evidence-based therapies in cardiometabolic disease. Key recommendations include focused efforts on evidence generation around broad implementation strategies, dissemination of the evidence generated, uptake of evidence into usual care settings, and investment in training the current and next generations of leaders in implementation.

Cholesterol sulfate (CS), one of the most abundant cholesterol derivatives, recently emerged as a key regulatory molecule in several physiological processes. Here, we demonstrate multiple mechanisms by which CS reduces intracellular cholesterol levels. CS promotes the proteasomal degradation of 3-hydroxy-3-methylglutaryl-CoA reductase reductase by enhancing insulin-induced gene-mediated ubiquitination, thereby inhibiting cholesterol synthesis. In addition, CS blocks low-density lipoprotein receptor endocytosis, reducing low-density lipoprotein cholesterol uptake. CS further suppresses the proteolytic activation of sterol regulatory element-binding protein 2, a master transcription factor governing cholesterol synthesis and uptake. Using in vitro and in vivo models, we show that CS lowers cholesterol by targeting both the cholesterol synthesis and uptake pathways, while also modulating an important feedback loop via sterol regulatory element-binding protein 2. These findings highlight the potential of CS as a modulator of cholesterol metabolism, offering new therapeutic insights into cholesterol-related disorders.

Gastrodin, a bioactive ingredient extracted from the Chinese herb Gastrodia gastrodia, has shown potential therapeutic effects in cardiovascular diseases, but its specific role in myocardial infarction is unclear. This study investigated the protective effect of gastrodin on myocardial infarction and its potential mechanism. By clamping the left coronary artery, we created a model of myocardial infarction in C57BL/6J mice. For 14 days, mice in the control and myocardial infarction groups received a daily dose of 100 mg/kg gastrodin. Gastrodin significantly improved cardiac dysfunction in mice with myocardial infarction, decreased heart weight/body weight (HW/BW) and heart weight/tibial length (HW/TL) ratios, and inhibited mRNA expression levels of cardiac fibrosis biomarkers (Collagen Type I (Col1), Collagen Type III (Col3), Matrix Metalloproteinase-2 (MMP-2), Matrix Metalloproteinase-9 (MMP-9)). In addition, gastrodin also inhibited the activity of apoptosis marker Caspase 3, decreased the Bax/Bcl2 mRNA ratio, decreased the expression of pro-inflammatory factors (Interleukin-1 beta (IL-1β), Tumor Necrosis Factor-alpha (TNF-α), Interleukin-6 (IL-6)) and pro-inflammatory adhesion molecule Monocyte Chemoattractant Protein-1 (MCP1), and promoted the expression of angiogenesis marker Cluster of Differentiation 31 (CD31). RNA sequencing and Rt-qPCR analysis showed that gastrodin treatment significantly up-regulated the expression of genes related to cell proliferation (Cyclin-Dependent Kinase 1 (CDK1), Threonine Tyrosine Kinase (TTK), Cyclin B2 (CCNB2), Polo-Like Kinase 1 (PLK1)), and promoted the proliferation of human aortic endothelial cells (HAECs). These findings suggest that gastrodin can effectively reduce the pathological changes of myocardial infarction by inhibiting inflammation, reducing apoptosis, and promoting endothelial cell proliferation, thus providing a new strategy for the prevention and treatment of myocardial infarction.

Peripheral artery disease (PAD) is one of the most prevalent forms of cardiovascular (CV) disease, with many progressing to CV morbidity/death. Adherence to guideline-directed optimal medical therapy (OMT) in PAD is vital. This study evaluated provider adherence to OMT patients with PAD.

This is a retrospective cohort study of 3471 patients with PAD who underwent vascular laboratory imaging between 2017 and 2022 at a single large, academic, tertiary referral center. OMT was defined by 2016 American Heart Association guidelines. Adherence to guidelines was denoted by active prescriptions for antiplatelet and statin. The presence of high-intensity OMT (HIOMT) was defined as prescriptions for an antiplatelet and high-intensity statin. Prevalence and incidence (change to OMT/HIOMT within 60 days of index ankle-brachial index [ABI]) were evaluated. Multivariable models were created evaluating predictors of OMT and HIOMT prevalence and incidence.

The OMT prevalence was 45.3%, whereas the HIOMT prevalence was 23.6% at the time of index vascular laboratory. Incident OMT was 24.3%, whereas incident HIOMT was 11.2% within 60 days. Age, minimum/maximum ABI, insurance status, smoking status, and comorbidities were associated with prevalent OMT/HIOMT. Age, gender, minimum/maximum ABI, smoking status, and hemoglobin A1C were associated with incident HIOMT. In multivariable models, incident HIOMT was less common for female patients (odds ratio: 0.7; 95% confidence interval: 0.52-0.91), whereas lower ABIs were predictive of HIOMT (odds ratio: 0.6; 95% confidence interval: 0.51-0.72).

Despite clear guidelines regarding OMT for patients with atherosclerotic CV disease, in this real-world study of guideline-directed management of PAD, adherence to OMT remains low, especially for HIOMT. Predictors of appropriate HIOMT prescription include lower ABI and non-female sex. Given the high prevalence of PAD, the heterogeneity of caregivers, and the widespread availability of screening, this population should be targeted for better adherence to HIOMT to prevent CV morbidity and death.

Cardiovascular disease (CVD) is the leading cause of mortality in the United States and globally. This review describes changes in CVD lipid and lipoprotein biomarker measurements that occurred in line with the evolution of clinical practice guidelines for CVD risk assessment and treatment. It also discusses the level of comparability of these biomarker measurements in clinical practice. Comparable and reliable measurements are achieved through assay standardization, which not only depends on correct test calibration but also on factors such as analytical sensitivity, selectivity, susceptibility to factors that can affect the analytical measurement process, and the stability of the test system over time. The current status of standardization for traditional and newer CVD biomarkers is discussed, as are approaches to setting and achieving standardization goals for low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), triglycerides (TG), lipoprotein(a) (Lp(a)), apolipoproteins (apo) A-I and B, and non-HDL-C. Appropriate levels of standardization for blood lipids are maintained by the Centers for Disease Control and Prevention's (CDC) CVD Biomarkers Standardization Program (CDC CVD BSP) using the analytical performance goals recommended by the National Cholesterol Education Program. The level of measurement agreement that can be achieved is dependent on the characteristics of the analytes and differences in measurement principles between reference measurement procedures and clinical assays. The technical and analytical limitations observed with traditional blood lipids are not observed with apolipoproteins. Additionally, apoB and Lp(a) may more accurately capture CVD risk and residual CVD risk, respectively, than traditional lipids, thus prompting current guidelines to recommend apolipoprotein measurements. This review further discusses CDC's approach to standardization and describes the analytical performance of traditional blood lipids and apoA-I and B observed over the past 11 years. The reference systems for apoA-I and B, previously maintained by a single laboratory, no longer exist, thus requiring the creation of new systems, which is currently underway. This situation emphasizes the importance of a collaborative network of laboratories, such as CDC's Cholesterol Reference Methods Laboratory Network (CRMLN), to ensure standardization sustainability. CDC is supporting the International Federation of Clinical Chemistry and Laboratory Medicine's (IFCC) work to establish such a network for lipoproteins. Ensuring comparability and reliability of CVD biomarker measurements through standardization remains critical for the effective implementation of clinical practice guidelines and for improving patient care. Utilizing experience gained over three decades, CDC CVD BSP will continue to improve the standardization of traditional and emerging CVD biomarkers together with stakeholders.

The comorbid presence of Rheumatologic Diseases (RDs) and Atherosclerotic Cardiovascular Disease (ASCVD) substantially accentuates cardiovascular risk. We aimed to compare rates of secondary prevention statin utilization in patients with established ASCVD both with and without underlying comorbid RDs- and to highlight any potential gender, racial, or ethnic disparities in statin use in a contemporary US cohort.

We queried the electronic medical record (EHR)-linked Houston Methodist Learning Health System Outpatient Registry containing data for approximately 1.2 million patients to identify patients with diagnosed ASCVD and RDs using ICD-10 codes. Statin prescription rates and dosage were evaluated via ATC codes.

Among 113,021 patients with ASCVD, 7286 (6.4 %) had comorbid RDs. The majority (71.1 %) of patients with ASCVD were prescribed statins, with discernibly lower utilization in patients with comorbid RDs compared to the non-RD population (63.2 % vs. 71.7 %, p < 0.005). High-intensity statins were prescribed in 42,636 (37.7 %) of ASCVD patients, with similarly reduced utilization in RD vs non-RD patients (30.4 % vs. 38.2 %). These trends remained consistent across sociodemographic subgroups. Moreover, women were consistently less likely to receive high intensity statins in both RD and non-RD groups. Reduced statin utilization was not accounted for with non-statin lipid lowering therapies in RD vs non RD subgroups.

In this real-world study, co-morbid RDs were associated with significant lower utilization of secondary prevention statin therapy in patients with ASCVD. A multidisciplinary team approach may help to better understand key drivers of statin uptake in this clinically vulnerable population.

Cardiovascular disease (CVD) is one of the largest global disease burdens. Despite guidelines and recommendations and the proven advantages of lipid-lowering therapies (LLTs) in preventing CVD, achieving treatment targets remains disappointing. A key barrier to optimal LLT is therapy discontinuation. To be widely adopted in clinical practice, new lipid-lowering therapies must both prevent major adverse cardiovascular events (MACEs) and exhibit cost effectiveness to ensure widespread utilization by patients, physicians, and insurers. While non-statin LLTs have shown cardiovascular value, their cost effectiveness is controversial. This review highlights the LLTs that are currently widely adopted and summarizes the available evidence on their cost effectiveness.

Cardiovascular disease complications are the leading cause of morbidity and mortality in patients with Type 2 diabetes (T2DM). Left ventricular diastolic dysfunction (LVDD) is one of the earliest myocardial characteristics of diabetic cardiac dysfunction. Therefore, we aimed to develop an LVDD-risk predictive model to diagnose cardiac dysfunction before severe cardiovascular complications arise. We trained an artificial neural network model to predict LVDD risk with patients' clinical information. The model showed better performance than classical machine learning methods such as logistic regression, random forest and support vector machine. We further explored LVDD-risk/protective features with interpretability methods in neural network. Finally, we provided a freely accessible web server called LVDD-risk, where users can submit their clinical information to obtain their LVDD-risk probability and the most noteworthy risk indicators.

Gut microbes are important for the development of atherosclerotic cardiovascular disease (ASCVD), and the dietary index for gut microbiota (DI-GM), a new measure of gut flora-friendly diets, has not been systematically investigated in relation to ASCVD.

This study aimed to evaluate the correlation between DI-GM and the risk of ASCVD in American older adults, also to analyze the mediating role of body mass index (BMI).

Researchers selected 2234 elderly participants ≥ 65 years of age from the National Health and Nutrition Examination Survey (NHANES) from 2015 to 2018 for a cross-sectional cohort study. Stratified analyses were taken based on DI-GM quartile. To achieve our research objectives, we employed logistic regression analysis, smooth curve fitting, interaction effects analysis, and mediation analysis.

After adjusting for confounders, individuals with higher DI-GM had a significantly lower risk of ASCVD (highest quartile vs. lowest quartile OR = 0.73, 95% CI: 0.52-1.01, P < 0.001). DI-GM was linearly negatively associated with ASCVD (P = 0.13) and the association was stable in the diabetes subgroup (interaction P > 0.05), but age, gender and BMI may modify the association between DI-GM and ASCVD (interaction P < 0.05). BMI mediated 11.51% of the association between DI-GM and ASCVD (95% CI: 2.54%-54.1%, P = 0.016).

DI-GM is likely to be a promising indicator for the assessment of the risk of ASCVD, with BMI exhibiting a partial mediating effect in this association. Future studies should prioritize a comprehensive investigation of the underlying mechanisms by which DI-GM contributes to atherogenesis, with the aim of enhancing the efficacy of early prevention strategies for ASCVD.

Findings from RCTs and observational studies indicate a positive association between statin use and risk of type 2 diabetes. Mendelian randomisation studies provide evidence to support that the effect is causal. However, little is known about the long-term effects, and data on different types of statins remain limited.

We analysed participants with hypercholesterolaemia from the Nurses' Health Study (NHS; 30,510 participants), the Nurses' Health Study II (NHSII; 21,547 participants) and the Health Professionals Follow-Up Study (HPFS; 9934 participants) who were free of diabetes, CVD and cancer at baseline. Statin use was assessed every 2 years starting in 2000 in the NHS and the HPFS and in 1999 in the NHSII. Incident cases of type 2 diabetes were confirmed by a validated supplementary questionnaire until the end of follow-up (31 January 2023).

We documented 6762 incident type 2 diabetes cases during up to 23 years of follow-up. Compared with non-users, statin users had a significantly higher risk of type 2 diabetes after adjustment for BMI and other potential confounding variables (pooled HR 1.40; 95% CI 1.33, 1.48). Compared with non-use, durations of statin use of 1-5, 6-10, 11-15 and >15 years were associated with HRs of 1.36 (95% CI 1.27, 1.44), 1.41 (95% CI 1.31, 1.52), 1.60 (95% CI 1.44, 1.78) and 1.76 (95% CI 1.50, 2.06), respectively; significant linear trends were observed when the comparison included non-users and within statin users only (both ptrend<0.001). Compared with non-users, the HRs for type 2 diabetes associated with 10 year use of specific types of statins were 1.99 (95% CI 1.45, 2.73) for rosuvastatin, 1.66 (95% CI 1.12, 2.47) for lovastatin, 1.62 (95% CI 1.39, 1.89) for atorvastatin, 1.44 (95% CI 1.06, 1.97) for pravastatin and 1.37 (95% CI 1.13, 1.66) for simvastatin. Use of a low-potency statin for 10 years was associated with a 34% higher risk of type 2 diabetes (HR 1.34; 95% CI 1.15, 1.56), while use of a high-potency statin for 10 years was associated with a 72% higher risk (HR 1.72; 95% CI 1.46, 2.04). The difference in the 10 year cumulative risk of type 2 diabetes comparing statin users vs non-users was most pronounced in participants with the least healthy lifestyles (4.5% vs 3.1%), while the smallest risk differential was observed among participants who adhered to the healthiest lifestyles (1.0% vs 0.4%).

The positive association between statin use and type 2 diabetes was more pronounced with a longer duration of use, and the association varied across different types of statins. Adopting and maintaining a healthy lifestyle can serve as a viable approach to diabetes prevention during statin treatment.

Coronary artery disease (CAD) is one of the most prevalent cardiovascular diseases where serum lipoprotein oxidation plays a significant role. Polyunsaturated fatty acids (PUFA) n -6 :  n -3 unbalance ratio consumption, affects lipoprotein oxidation, and inflammation processes. This study aimed to analyze the relationship between n -6 :  n -3 PUFA ratio intake with oxidized lipoproteins in individuals with CAD.

A cross-sectional study was performed including 105 subjects (51 diagnosed with CAD and 54 non-CAD) from western Mexico. Dietary information was collected using a habitual day food record. Serum oxidized low-density lipoprotein (oxLDL) and oxidized high-density lipoprotein (oxHDL) concentrations were quantified by enzyme linked immunosorbent assay.

CAD subjects had higher oxHDL/HDL cholesterol (HDL-c) ratio [0.102 (0.092-0.112) vs. 0.080 (0.070-0.090), P  = 0.004] and oxLDL/LDL cholesterol (LDL-c) ratio [129.2 (108-150.4) vs. 59.7 (39.3-80), P  < 0.001] compared to non-CAD subjects. Risk factors associated with CAD were a high n -6 :  n -3 PUFA ratio (odds ratio, OR = 2.3, P  = 0.046), hypoalphalipoproteinemia in men (OR = 3.2, P  = 0.014), moderate/high tobacco index (OR = 6.33, P  = 0.003), elevated waist circumference in women (OR = 7, P  = 0.004), hypertension (OR = 21.14, P  < 0.001), and type 2 diabetes (OR: 25, P  < 0.001). The oxHDL/HDL-c ratio was positively associated with the n -6 :  n -3 PUFA ratio [ r2  = 28.3, B  = 0.002 (0.001-0.003), P  < 0.001] in CAD patients.

This study showed that a higher n -6 :  n -3 PUFA ratio intake correlates with higher serum oxHDL/HDL-c in CAD patients.

Cardiometabolic disease (CMD) status increases the risk of functional disability; however, the reverse relationship remains unclear. This study aimed to examine the impact of different patterns of functional disability on CMD status among Chinese middle-aged and older adults.

We used data from two waves of the China Health and Retirement Longitudinal Study. Functional disability was assessed based on activities of daily living (ADL) and instrumental activities of daily living (IADL), while CMD status was evaluated based on the incidence of diabetes, heart disease, and stroke. Generalized ordinal logistic regression analysis was employed to investigate the impact of functional disability on CMD status.

In the longitudinal study, 509 individuals (20.0 %) developed CMD, and 102 individuals (4.0 %) developed cardiometabolic multimorbidity. After adjusting for confounders, Model 1 showed an odds ratio of 1.64 (95 % CI: 1.17, 2.29) for increased CMD status in individuals with ADL and IADL disability compared to those without functional disability. Model 2 and Model 3 produced similar results.

Functional disability, particularly ADL and IADL disability, increases the risk of CMD status in Chinese middle-aged and older adults. Measures should be implemented to maintain functional status in middle-aged and older adults.

Guidelines recommend target levels of low-density lipoprotein cholesterol (LDL-C) and intensive lipid-lowering therapy (LLT) in high-risk patients. However, the value of escalating LLT when the LDL-C targets are achieved with moderate-intensity statins is unknown. We aimed to evaluate the benefits of LLT escalation in this population.

In this retrospective propensity score-matched study, we screened data from two university hospitals between 2006 and 2021. Of the 54,069 patients with atherosclerotic cardiovascular disease (ASCVD), 3,205 who achieved LDL-C levels <70 mg/dL with moderate-intensity statins were included. After 1:3 matching, 1,315 patients (339 with LLT escalation and 976 without) were ultimately examined. The primary outcomes were major adverse cardiovascular and cerebrovascular events (MACCE)1 (cardiovascular death, nonfatal myocardial infarction, and nonfatal ischemic stroke) and all-cause death.

During a median follow-up of 5.7 years, the MACCE1 rate was not significantly lower in the escalation group than in the non-escalation group (9.8 and 14.3/1,000 person-years, respectively; hazard ratio [HR], 0.68; 95% confidence interval [CI], 0.43-1.09; p=0.11). Kaplan-Meier curves showed similar results (log-rank p=0.11). The risk of all-cause death did not differ between the groups. MACCE2 rate, which additionally includes coronary/peripheral revascularization, was lower in the escalation group (24.5 and 35.4/1,000 person-years, respectively; HR, 0.70; 95% CI, 0.52-0.94; p=0.017).

LLT escalation did not significantly lower hard cardiovascular outcomes and all-cause death in patients with ASCVD achieving LDL-C levels <70 mg/dL with moderate-intensity statins. However, it had benefit in reducing revascularization rates in this population.

Atherosclerotic cardiovascular disease (ASCVD) remains a major cause of global morbidity and mortality. Emerging research suggests that oral hygiene practices, particularly dental floss use, may reduce the risk of ASCVD.

The purpose of this study was to examine the association between dental floss use and ASCVD prevalence.

Data from NHANES participants who completed home interviews and dental evaluations were analyzed. ASCVD was defined as angina, stroke, myocardial infarction, or coronary artery disease. Dental floss use was self-reported over the past seven days. Covariates included demographic, socioeconomic, lifestyle, and clinical factors. Weighted logistic regression was used to assess the relationship between dental floss use and ASCVD prevalence.

This study included a total sample of 7253 participants with a mean age of 53.8±14.6 years. The sample consisted of 47.6 % male participants. The ethnic composition included 64.3 % Non-Hispanic White. Regular dental floss use was correlated with a lower likelihood of developing ASCVD and Stringent Criteria (infarction or stroke), with ORs of 0.76 (95 % CI: 0.60, 0.97) p=0.028 and 0.68 (95 % CI: 0.49, 0.94) p=0.022, respectively. Flossing 3-4 days/week was associated with reduced ASCVD risk, OR = 0.57 (95 % CI: 0.38, 0.84) p=0.006. Similar reductions were seen for stringent criteria: flossing 3-4 days/week: OR = 0.57 (95 % CI: 0.32, 0.99) p=0.047, flossing ≥5 days/week: OR = 0.69 (95 % CI: 0.47, 1.00) p=0.049.

Regular dental floss use may reduce the risk of ASCVD. These results support the inclusion of oral hygiene practices in cardiovascular disease prevention strategies.

Objective: Rapid improvements in glucose control may lead to early worsening of diabetic retinopathy (EWDR). There is a need to demonstrate safety in people commencing automated insulin delivery (AID) due to the known efficacy in rapid glycemic improvement. We aimed to investigate short-term DR outcomes in people (aged ≥13 years) with type 1 diabetes after initiation of AID (use ≥6 months). Research Design and Methods: Retrospective four center observational study with participants drawn from hospital databases (Dunedin and Christchurch, New Zealand) and also from two research studies based out of Auckland, New Zealand, and Perth, Australia. Demographic and clinical characteristics and DR grading data before and after AID initiation were collected, and statistical analysis was performed. Results: DR grading data from 165 people using AID (three different AID systems) were available, and mean improvement in HbA1c for the total sample was 1.0 ± 1.3 percentage points. Improvements in grading were seen in 32/165 (19%), 99/165 (60%) were stable, and 34/165 (21%) worsened in their R- and/or M-grade. Age at AID initiation ≥18 years was the only significant risk factor for any worsening of DR (P = 0.028). Proliferative change and need for photocoagulation were uncommon but did occur in 3% (5/165); all noted to have prior DR, diabetes duration >10 years, and with at least another diabetes complication or prior DR treatment. Conclusions: In this study, stable or improved DR grades were evident in most who had recently commenced AID. Age at AID initiation <18 years appears protective.

The ability of the American Heart Association Predicting Risk of Cardiovascular Disease Events (PREVENT) calculator to accurately assign 10-year atherosclerotic cardiovascular disease (ASCVD) risk in older individuals, including those aged ≥80 years, is unknown. This study compares PREVENT with the 2013 Pooled Cohort Equation (PCE) calculator for predicting 10-year ASCVD risk in a large cohort of older adults.

This was a prospective cohort study of adults without CVD from Australia and the United States aged ≥70 years (≥65 years, if US minorities). They were enrolled from 2010 to 2014 in the ASPREE trial (Aspirin in Reducing Events in the Elderly), a 5-year randomized trial of low-dose aspirin in community-dwelling older adults with posttrial observational follow-up extending to 2022. ASCVD events were adjudicated by expert panels. The discriminative ability of the 2 risk calculators was assessed by Harell C statistic following Cox regression in the 65- to 79-year age group and >80-year age group, separately. For calibration, predicted event numbers were calculated using PREVENT and PCE, scaled for the actual length of follow-up, and compared with the number of observed events in-trial and during extended follow-up.

Among the 15 510 participants aged 65 to 79 years (median age, 73.2 years; 56.1% women), 1084 ASCVD events occurred (median follow-up, 8.3 years); PCE predicted 3102 events while PREVENT predicted 1290 events. For the 2787 participants ≥80 years (median age, 82.6 years; 59.2% women), 355 ASCVD events occurred (median follow-up, 7.4 years); PCE predicted 1067 events while PREVENT predicted 350 events. PREVENT showed superior discriminative performance compared with PCE (PREVENT versus PCE, C statistic, 0.793 versus 0.740; P<0.001 in participants aged 65 -79 years; 0.854 versus 0.799; P<0.001 in those aged ≥80 years).

The PREVENT risk calculator is superior to the PCE calculator in predicting ASCVD events in older adults from the United States and Australia, including those aged ≥80 years.

URL: https://www.clinicaltrials.gov; Unique identifier: NCT01038583. URL: https://www.isrctn.com; Unique identifier: ISRCTN83772183.

Coronary artery calcium (CAC) scoring provides prognostic information, especially in patients at intermediate risk for coronary artery disease (CAD). However, the benefit of combining CAC score with a primary prevention strategy has not been tested in a randomized trial.

To assess whether combining the CAC score with a prevention strategy can be used to limit plaque progression in intermediate-risk patients with a family history of premature CAD.

Prospective, randomized, open-blinded end point clinical trial in 7 hospitals across Australia (between 2013 and 2020; the last date of follow-up was June 5, 2021). Asymptomatic people aged 40 to 70 years with a first-degree relative with CAD onset at younger than 60 years old or second-degree relative with onset at younger than 50 years old were recruited from the community.

Intermediate-risk participants underwent CAC scoring. Those with a CAC score greater than 0 but less than 400 underwent coronary computed tomography angiography (CCTA) and were randomized to CAC score-informed prevention or usual care.

Follow-up CCTA was obtained at 3 years, with plaque volume measured by an independent core laboratory. The primary outcome was total plaque volume, with further analysis for calcified and noncalcified plaque volume.

This study included 365 participants (mean [SD] age, 58 [6] years; 57.5% male); 179 in the CAC score-informed and 186 in the usual care groups. Compared with usual care, the CAC score-informed group showed a sustained reduction in total (mean [SD], -3 [31] mg/dL vs -56 [38] mg/dL; P < .001) and LDL (mean [SD], -2 [31] vs -51 [36] mg/dL; P < .001) cholesterol levels at 3 years, which was associated with a reduction in pooled cohort equation risk calculation (mean [SD], 2.1% [2.9%] vs 0.5% [2.9%]; P < .001). Plaque progression was greater in usual care than CAC score-informed participants for total plaque volume (mean [SD], 24.9 [37.7] mm3 vs 15.4 [30.9] mm3; P = .009), noncalcified plaque volume (mean [SD], 15.7 [32.2] mm3 vs 5.6 [28.5] mm3; P = .002), and fibrofatty and necrotic core plaque volume (mean [SD], 4.5 [25.8] mm3 vs -0.8 [12.6] mm3; P = .02). These plaque volume changes were independent of other risk factors including baseline plaque volume, blood pressure, and lipid profile.

The combination of CAC score with a primary prevention strategy in intermediate-risk patients with a family history of CAD was associated with reduction of atherogenic lipids and slower plaque progression compared with usual care. These data support the use of CAC score to assist intensive preventive strategies in intermediate-risk patients.

anzctr.org.au Identifier: ACTRN12614001294640.

Objective: This research focuses on analyzing the link between the systemic inflammatory response index (SIRI) and all-cause mortality in individuals with atherosclerotic cardiovascular disease (ASCVD) . Methods: This research analyzed data from 4693 patients using nine cycles of the National Health and Nutrition Examination Survey (NHANES). The connection between SIRI and mortality was determined by employing survey-weighted Cox models, with hazard ratios (HRs) and 95% confidence intervals (CIs) being computed. Kaplan-Meier method illustrated survival differences across SIRI levels. Sensitivity analyses involved restricted cubic splines (RCS), stratified analysis, and E-value calculations. Landmark analysis assessed survival differences at multiple follow-up intervals, while time-dependent receiver operating characteristic curves evaluated SIRI's prognostic value. Mediation analysis identified potential intermediaries impacting the SIRI-mortality relationship. Results: Over 406,564 person-months, 1933 deaths occurred. Adjusted Cox models discovered that higher SIRI was connected with elevated overall mortality [HR 1.192, (95% CI 1.131-1.256), p < 0.001]. Higher SIRI consistently showed lower survival probabilities. RCS and stratified analysis confirmed the robustness of these findings. Survival probability at different follow-up periods was considerably lower in those with higher SIRI. Additionally, SIRI demonstrated a prognostic value of 0.66 for all-cause mortality at 1 year and 3 years, and 0.65 at 5 years. Notably, serum uric acid (6.2%) partially mediated the connection between SIRI and mortality from all causes. Conclusion: In ASCVD patients, SIRI was robustly correlated with all-cause mortality, partially mediated by serum uric acid.

Statins, widely used lipid lowering drugs, have been associated with pleiotropic beneficial effects. Notably, studies conducted in vitro and in vivo suggest a link between statins and bone metabolism. Observational data in humans also hint at a decreased fracture rate among statin users. Revision of total hip arthroplasty (THA) is a serious and costly medical event. Whether statins might influence THA failure is not clear. Aim of the current study is to assess how the preoperative use of statins may influence the risk of THA revision in patients with hip osteoarthritis (OA).

We performed a retrospective analysis of patients who underwent THA for OA in the Italian RIPO registry of Emilia-Romagna. Electronic health records were scrutinized to gather information regarding comorbidities and statin prescriptions. We employed propensity score (PS) matching to pair 1:1 statin users (SU) with statin non-users (SNU), considering factors such as age, sex, and the duration of follow-up. Survival of THA was compared between the two groups; secondary analyses were performed to ascertain the role of mortality, sex, indication for statin treatment, and statin potency or lipophilicity.

10,927 patients were classified as SU and PS-matched with SNU. SU showed a reduced risk of THA revision over a 15-year period (adjHR 0.76, 95% CI: 0.67-0.88; p < 0.001). Notably, this observation remained consistent regardless of the indication for statin therapy or the specific characteristics of the statin medications prescribed, and it was more pronounced among male patients (adjHR 0.64, 95% CI: 0.52-0.80, p < 0.001).

Our findings suggest that statin treatment is associated with a decreased risk of long-term THA revision in patients with OA, irrespective of the original indication for statin therapy.

Statins, a kind of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, are first-line cholesterol-lowering drugs that are widely used in the primary and secondary prevention of coronary atherosclerotic heart disease (CAD). However, the safety of statins has been in the spotlight as recent studies have shown that statins may increase the incidence of diabetes. Therefore, we conducted a study of statins use and new-onset diabetes(NODM) in people with hypertension and obstructive sleep apnea (OSA) to better understand the relationship and to provide guidance for future clinical management.

We conducted a retrospective cohort study using data from the Urumchi Hypertension Database (UHDATA), including patients aged ≥ 18 years diagnosed with hypertension and obstructive sleep apnoea treated at our Hypertension Centre between 2015 and 2019. The study was followed until November 2023 and the primary endpoint was new onset diabetes during the follow-up period. The hazard ratio (HR) and 95% confidence interval (CI) were calculated using the Cox proportional hazards model. Sensitivity analyses were performed by excluding those with pre-diabetes at baseline.

8755 patients with hypertension and OSA, and 80.1% were followed up. During median follow-up of 31 months, 740 patients developed NODM. The incidence of NODM per 1000 person-years was 53.1. In Cox regression analysis, the risk of diabetes is significantly higher in patients who continue to take statins (HR = 1.77, 95% CI, 1.34-2.34, P < 0.001), and the results remain significant in sensitive analysis.

In patients with OSA and hypertension, continuous statins use increases the risk of diabetes and physicians should be vigilant about monitoring blood glucose levels when using statins in this patients.

Salivary microbiome alterations are associated with chronic diseases, such as cardiovascular disease, diabetes, and dementia. These chronic diseases often coexist in older adults, leading to polypharmacy. This situation complicates the relationship between systemic diseases and salivary microbiome dysbiosis. Previous studies have demonstrated the association of the human gut microbiome with common prescription drug use, including polypharmacy. However, a comprehensive analysis of the salivary microbiome and prescription drugs is yet to be conducted in older adults. Therefore, in this study, we performed a multivariate analysis to investigate the relationship between salivary microbiomes and host variables, including prescribed drugs, cognitive function, and oral health, in Japanese older adults with different disease backgrounds.

We enrolled non-hospitalised 82 older adults aged ≥70 years from a Japanese village community, and collected metadata, including age, sex, body mass index, cognitive function, oral health, alcohol consumption, smoking, and common prescription drug information. We performed multivariate analyses and functional predictions on the salivary microbiome based on 16S ribosomal RNA gene amplicon sequencing, including the metadata as potential confounders.

We observed a relationship between the human salivary microbiome and prescribed drug use in Japanese older adults with a heterogeneous background of comorbidities. The effects of several prescribed drugs, such as statins, proton pump inhibitors, and transporter/symporter inhibitors, on the salivary microbiome diversity were more prominent than those of host variables, including age, sex, and oral health. Notably, statin use was strongly correlated with a decrease in the Streptococcus abundance. Furthermore, statin intensity and obesity may be associated with altering the salivary microbiome, including functional predictions for vitamin biosynthesis and purine nucleotide degradation pathways in statin users.

Our multivariate analysis, adjusted for prescribed drug use and non-use, revealed the drug-specific alteration of salivary microbiome composition in Japanese older adults with comorbidities. To our knowledge, this study is the first to described the association of common prescription drug use with salivary microbiome alterations in older adults. Our findings indicated that prescribed drug use is a key factor in understanding the link between salivary microbiome changes and systemic diseases in older adults.

No reliable serum diagnostic test currently exists for peripheral arterial disease (PAD). We previously observed that serum circulating Fatty Acid Synthase (cFAS) is elevated in individuals with chronic limb threatening ischemia (CLTI).

We hypothesized that cFAS can be an independent diagnostic biomarker for PAD and CLTI.

Patients with/without PAD and CLTI were retrospectively reviewed. Total serum cFAS content was evaluated using ELISA and normalized to total protein. Patient demographics and PAD incidence were collected via chart review. Serum cFAS and demographics were compared, and regression analysis was used to determine the correlation between cFAS and PAD incidence, and the impact of co-morbidities on cFAS content.

A total 347 patients met inclusion criteria. Of these, 34 were healthy controls without PAD (Group 1), 164 had PAD (Group 2), and 149 had CLTI (Group 3). Compared to Group 1, the remaining groups were significantly older, had more males, and had higher incidence of cardiovascular co-morbidities (p<0.001). Compared to Group 1, Groups 2 and 3 had significantly higher serum cFAS content (p=0.007). ROC analysis revealed an optimal cutoff of 340pg/mg protein for cFAS in distinguishing between individuals with or without PAD (p<0.001), and 490pg/mg protein in distinguishing between those with PAD and those with CLTI (p=0.015).

Our study demonstrates that cFAS is an independent serum-based diagnostic biomarker for PAD, can distinguish between patients with PAD versus CLTI, and may serve as a predictive variable for identifying patients with highest risk of disease progression.

There are currently no reliable serum biomarkers to aid in the diagnosis of peripheral arterial disease (PAD). We hypothesized that circulating Fatty Acid Synthase (cFAS) can be an independent diagnostic biomarker for PAD. Serum cFAS and demographics were compared for patients with and without PAD or CLTI. Patients with PAD or CLTI had significantly higher serum cFAS content. We observed optimal cutoffs for cFAS in distinguishing between individuals with and without PAD or CLTI. Our study demonstrates that cFAS is an independent serum-based diagnostic biomarker for PAD, can distinguish between patients with PAD versus CLTI, and may predict disease severity.

Nut consumption is attributed to improvements in risk factors for cardiovascular disease (CVD), including high blood pressure (BP) and dyslipidemia. However, it is unclear whether these effects are altered with concurrent treatment with BP and lipid-lowering medication.

We sought to investigate the effects of the consumption of whole tree nuts and peanuts (collectively termed nuts) on BP and lipids, and whether BP and lipid-lowering medication use alters these effects.

The MEDLINE, EMBASE, Scopus, and Web of Science databases were systematically searched through June 21, 2023, for randomized controlled trials (RCTs) assessing the effects of nut consumption on BP and/or lipids.

Random effects meta-analyses (mean difference, 95% confidence interval [CI]) were conducted, with subgroup analyses based on reported participant use of BP or lipid-lowering medication, including medicated, unmedicated, unreported (ie, use not specified), and mixed (ie, included combined data from medicated and unmedicated participants). A total of 115 studies were included in the review, of which 109 were meta-analysed.

Nut consumption significantly reduced triglycerides (TG), total cholesterol, low-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B, with no effect on high-density lipoprotein cholesterol or blood pressure. Few studies were conducted in medicated participants only (n = 1 for lipid outcomes only), and for the studies including both medicated and unmedicated participants (ie, mixed), outcomes by medication use were not reported. Significant differences in TG and apolipoprotein B were observed between medication use groups, with nut consumption resulting in the largest reductions in unmedicated participants. Strong heterogeneity was observed with no evidence of publication bias.

Lipid-lowering, but not BP-lowering benefits of nut consumption were observed; however, few studies reported the effect based on participants' medication status. Future studies are required to determine if there are additional benefits of including nuts in the diet of medicated patients with cardiovascular disease.

PROSPERO registration code CRD42022296849.

Evolocumab is a PCSK9 inhibitor designed to significantly reduce low-density lipoprotein cholesterol (LDL-C) levels. Unlike statins, which work by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase to reduce cholesterol synthesis in the liver, evolocumab enhances LDL receptor recycling, leading to more efficient clearance of LDL-C from the bloodstream. Compared to placebo, evolocumab shows a profound LDL-C lowering effect while also offering incremental benefit over statins, especially in high-risk patients or those with statin intolerance. In this meta-analysis, the primary focus was on lipid-lowering efficacy and cardiovascular outcomes, making direct comparisons among evolocumab, statins, and placebo essential. Evolocumab consistently demonstrated a statistically significant reduction in LDL-C and, in several large-scale trials (such as Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk (FOURIER)), also showed a reduction in cardiovascular events, including myocardial infarction and stroke. It is important to specify that the most significant outcomes were both the substantial LDL-C reduction and the associated reduction in major adverse cardiovascular events (MACE). For our meta-analysis, we generated three graphical models using Review Manager (RevMan) version 5.4 (Cochrane Collaboration, Copenhagen, Denmark) based on the selected studies. To conduct our systematic review, we extensively examined a total of 10 articles. The subgroup analyses in these studies looked at how well evolocumab worked on its own, with statins, and as an extra treatment for people who were already taking low or high doses of statins. Additionally, we compared the effectiveness of evolocumab vs. placebo in both individuals with and without cardiovascular conditions. Our findings indicated that evolocumab, whether used as monotherapy or alongside statins, demonstrated statistical significance (p = 0.01). Moreover, all reviewed studies reported statistically significant results (p < 0.05). According to our analysis, there is an urgent need for more research to build on this body of evidence and carry out larger randomized controlled trials (RCTs) to find the best timing and dose for each patient and avoid any possible long-term side effects.

Remnant cholesterol (RC), an emerging cardiovascular risk factor, has garnered increasing attention in atherosclerotic cardiovascular disease (ASCVD) research, though its relationship with arterial stiffness remains incompletely understood. This study investigated the association between RC and estimated pulse wave velocity (ePWV), a reliable marker of arterial stiffness, with the goal of enhancing our understanding of RC's role in cardiovascular risk assessment.

This study utilized the National Health and Nutrition Examination Survey (NHANES) data from 1999 to 2018, including 12,505 participants aged 20 years and above. Weighted linear regression, restricted cubic splines (RCS), and subgroup analyses were used to explore the association between RC levels and ePWV. Analysis revealed a significant positive association between RC levels and ePWV, with participants in the highest RC quintile (Q5) exhibiting substantially elevated ePWV compared to those in the lowest quintile (Q1). Notably, RCS analysis demonstrated a non-linear relationship characterized by a saturation effect (p-nonlinear <0.05). Subgroup analyses indicated stronger associations among specific demographic groups, including individuals under 40 years, females, non-Hispanic whites, and those above the poverty level (all interaction p < 0.05). Furthermore, mediation analysis found that various inflammatory markers such as neutrophil count (NEU), neutrophil-to-lymphocyte ratio (NLR), and monocyte-to-lymphocyte ratio (MLR) played a mediating role in this association.

Increased arterial stiffness is associated with higher RC levels, demonstrating a saturation effect at elevated concentrations. This association is partially mediated by NLR, MLR, and NEU, and was stronger among younger, females, non-Hispanic whites, and non-impoverished individuals.

Lewy body dementia (LBD) is the second common dementia, with unclear mechanisms and limited treatment options. Dyslipidemia has been implicated in LBD, but the role of lipid-lowering drugs remains underexplored. This study aims to investigate the association between lipid traits, drug targets, and LBD risk using Mendelian Randomization (MR) analysis.

We performed univariable and multivariable MR analyses to evaluate the causal effects of lipid traits on the risk of LBD. Then, drug-target MR analysis and subtype analysis were conducted to evaluate the effects of lipid-lowering therapies on LBD.

In univariable MR, genetically predicted low-density lipoprotein cholesterol (LDL-C) and remnant cholesterol (RC) levels were associated with an increased risk of LBD. Mediation analysis suggested a potential interaction between LDL-C and RC in influencing LBD risk. Drug-target MR analysis identified significant associations between genetically proxied inhibition of ANGPTL3, CETP, and HMGCR and LBD risk.

This MR analysis provided evidence that elevated LDL-C and RC may increase the risk of LBD. Additionally, targeting ANGPTL3, CETP, and HMGCR may represent potential therapeutic strategies for the prevention or treatment of LBD.

Noncommunicable diseases (NCDs), particularly cardiovascular disease (CVD), are the leading cause of death worldwide, with hypercholesterolemia being a major risk factor for CVD. This study evaluated the hypercholesterolemia care cascade in Iran-including prevalence, diagnosis, treatment coverage, and effectiveness-using the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) guidelines.

This cross-sectional study drew on data from the 2021 Iran STEPS survey, which employed a systematic cluster sampling of adults aged ≥ 18 years across all provinces in Iran. Hypercholesterolemia was defined per NCEP-ATP III thresholds (LDL ≥ 160 mg/dL, total cholesterol ≥ 240 mg/dL, HDL ≤ 40 mg/dL, or ongoing lipid-lowering therapy). Weighted descriptive statistics were calculated, and Poisson regression with robust variance estimated crude and adjusted prevalence ratios for optimal lipid control among those treated. The 10-year CVD risk was determined using the Framingham Risk Score, stratifying participants into low (< 10%), intermediate (10-20%), and high (> 20%) risk categories.

Out of 18,074 participants, 10,582 (55.32%, 95% CI: 54.29-56.35) met NCEP-ATP III criteria for hypercholesterolemia. Among these, only 20.61% (19.55-21.72) were receiving pharmacological treatment. Treatment coverage was notably lower in males (13.15%, 11.98-14.40) than females (29.12%, 27.35-30.96). Statins were the most commonly used medication (11.43% of males, 25.87% of females). Of those receiving treatment, 52.85% (females) and 53.93% (males) achieved optimal LDL, while 76.98% (females) and 81.06% (males) attained total cholesterol < 200 mg/dL. However, only 19.89% (females) and 3.97% (males) met the HDL > 60 mg/dL goal. The 10-year CVD risk was < 10% in 57.79% of participants, 10-20% in 33.27%, and > 20% in 8.94%.

Despite a high prevalence of hypercholesterolemia in Iran, treatment coverage remains suboptimal, particularly among males and working-age adults. Although most treated individuals achieve favorable LDL and total cholesterol levels, gaps persist in achieving optimal HDL targets. These findings underscore the need for strengthened screening, treatment, and adherence strategies-alongside broader preventive measures-to reduce the burden of hypercholesterolemia and CVD in Iran.

This is a protocol for a Cochrane Review (intervention). The objectives are as follows: To evaluate the relative benefits and harms of statins for preeclampsia prevention in pregnant women.

Systolic blood pressure (BP) is a key factor in the outcomes of patients with acute ischemic stroke (AIS) receiving endovascular thrombectomy (EVT). However, the factors that mediate the association between BP and clinical outcome are unclear.

Consecutive patients with AIS in the anterior circulation underwent continuous BP monitoring for 24 hours. The 3-month modified Rankin scale (mRS) score was defined as the clinical functional outcome. The systolic BPI indices (BPIs) were successive variation, standard deviation, variability independent of mean BP (VIM), and 24-hour mean BP. Regression analysis was used to assess the correlation between different BPIs and functional outcomes, whereas mediation analysis was employed to assess the potential mediating effects of baseline risk factors through BP on functional outcomes.

A total of 140 of 292 patients (47.9%) achieved functional independence, and 87 (29.8%) experienced hemorrhagic transformation (HT). A history of stroke or hypertension and NIHSS score at onset were associated with SD and VIM (P < 0.05). BP variation (BPV) was still strongly associated with functional outcomes after adjustment for different risk factors. Mediation analysis revealed that stroke affected functional outcomes by affecting BPV, while the hypertension history affected functional prognosis by impacting the 24-hour mean BP and BPV. In addition, higher National Institute of Health stroke scale (NIHSS) scores were associated with increased BPV, whereas increased BPV was correlated with a greater proportion of unfavorable outcomes.

To our knowledge, this study is the first to explore the mediating effects of different BPIs on the relationships between risk factors and functional outcomes and may provide new insights and potential mechanisms for improving AIS prognosis.

The cardiometabolic index (CMI) serves as a significant marker of diabetes mellitus (DM) and may predict the potential for cardiovascular disease development. Nevertheless, the correlation between CMI and atherosclerotic cardiovascular disease (ASCVD) among individuals exhibiting varying glucose metabolism statuses (GMS) continues to be unclear.

Overall, 24,006 individuals aged 20 and above were enrolled in the research, drawn from the National Health and Nutrition Examination Survey (NHANES) database. Individuals in the study was classified into three distinct categories according to the level of fasting plasma glucose or glycated haemoglobin: normal glucose regulation, prediabetes, and DM. Multivariate logistic regression models and smoothed curve-fitting techniques were applied to investigate the correlation between CMI and ASCVD risk across varying GMS. Additionally, subgroup analyses stratified by relevant factors were performed to identify potential effect modifiers in this relationship.

Overall, 2352 participants (9.8%) with ASCVD were included. An increasing trend in ASCVD risk was observed for each successive CMI tertile. After adjusting for all related covariates, a significantly positive association was observed between CMI and ASCVD (P = 0.0004). Participants with DM in the highest CMI tertile had a 114% higher ASCVD risk compared to those in the lowest tertile (OR = 2.14; 95% CI = 1.30-3.53). Smoothed curve-fitting consistently confirmed the correlation between CMI and ASCVD across diverse GMS. Subgroup analyses and interaction tests highlighted statistically significant differences within the drinking status subgroup (P-interaction = 0.0479) and GMS subgroups (P-interaction = 0.0397).

This research suggests a positive association between ASCVD and CMI in adults in the United States, particularly among individuals with DM.

Exercise stress testing (EST) remains effective in assessing coronary artery disease (CAD), especially in developing countries, while coronary computed tomography angiography (CCTA) is being increasingly utilized. However, limited data exist on whether CCTA following EST can affect diagnosis or treatment. This study aimed to characterize patients who underwent CCTA following EST and evaluate its clinical impact. Consecutive patients who underwent CCTA after EST for CAD assessment between 2014 and 2021 were included in the study. CCTA results were categorized as obstructive CAD, nonobstructive CAD, and normal. Clinical and EST characteristics were compared among groups. Multivariable logistic regression analysis was used to identify independent predictors of obstructive CAD. The diagnostic impact and therapeutic consequences of CCTA were assessed at the subsequent clinic visits. A total of 209 patients (64% male, age 60 ± 10 years) with 26% known CAD were included. The most common indication for CCTA was an inconclusive EST (31%). CCTA revealed obstructive CAD in 53 patients, nonobstructive CAD in 111 patients, and normal results in 45 patients. Multivariable analysis identified hyperlipidemia (odds ratio 3.60, 95% confidence interval 1.27-10.22, P = .01) and the Duke Treadmill Score (odds ratio 0.86, 95% confidence interval 0.80-0.92, P < .001) as independent predictors of obstructive CAD. CCTA had a diagnostic impact on 69% of all patients (76% for patients with no known CAD and 50% for patients with known CAD), including the exclusion of obstructive CAD in patients with a positive EST; the diagnosis of obstructive CAD, nonobstructive CAD, or normal CCTA in patients with an inconclusive EST; and the diagnosis of both obstructive and nonobstructive CAD in patients with a negative EST. Therapeutically, CCTA led to medication changes in 38% of patients, while 24% underwent invasive procedures. In conclusion, among patients undergoing CCTA following EST for CAD assessment, hyperlipidemia and the Duke Treadmill Score were identified as independent predictors of obstructive CAD. CCTA also had significant diagnostic and therapeutic impacts in this population.

Most studies found that apolipoprotein B (apo B)-100 is a superior marker for coronary risk to non-high-density lipoprotein (HDL) cholesterol (C). Usually, studies use multivariant analysis with single-point odds/risk ratios. In multivariant analysis, when variables are highly correlated they are difficult to interpret. Effects cannot be well discriminated.

Brief review and examination of diagnostic sensitivity and specificity by receiver operator characteristic (ROC) curves at decision levels so that discrimination can be well compared. Since apo B has additional expense, clinical value should be compared in an appropriate format. Apo B and cholesterols were measured in 382 angiographically defined patients.

Non-HDLC and apo B were stronger markers than low-density lipoprotein (LDL)C, when examined by logistic regression, but as a result of strong collinearity, non-HDLC appeared weaker than LDLC in the presence of apo B, based on P values. This was true when analyzed with and without nonlipid risk factors. On ROC analysis, apo B and non-HDLC showed stronger C statistics than LDLC and total C. When analyzed alone apo B showed about 6.1% greater sensitivity than non-HDLC. After adjustment for nonlipid risk factors, the C statistics for apo B and non-HDLC were 0.74 and 0.73, and there was little difference in diagnostic specificity.

Risk is calculated from an algorithm that includes nonlipid risk factors similar to those examined here along with cholesterols. When assessed by the 10-year screening algorithm, these data support the view that non-HDLC would be less expensive than apo B with similar clinical efficacy.

Current research on the association between demographic variables and dietary patterns with atherosclerotic cardiovascular disease (ASCVD) is limited in breadth and depth. This study aimed to construct a machine learning (ML) algorithm that can accurately and transparently establish correlations between demographic variables, dietary habits, and ASCVD. The dataset used in this research originates from the United States National Health and Nutrition Examination Survey (U.S. NHANES) spanning 1999-2018. Five ML models were developed to predict ASCVD, and the best-performing model was selected for further analysis. The study included 40,298 participants. Using 20 population characteristics, the eXtreme Gradient Boosting (XGBoost) model demonstrated high performance, achieving an area under the curve value of 0.8143 and an accuracy of 88.4%. The model showed a positive correlation between male sex and ASCVD risk, while age and smoking also exhibited positive associations with ASCVD risk. Dairy product intake exhibited a negative correlation, while a lower intake of refined grains did not reduce the risk of ASCVD. Additionally, the poverty income ratio and calorie intake exhibited non-linear associations with the disease. The XGBoost model demonstrated significant efficacy, and precision in determining the relationship between the demographic characteristics and dietary intake of participants in the U.S. NHANES 1999-2018 dataset and ASCVD.

Mendelian randomization was employed to investigate the impact of circulating lipids, specifically residual lipids, on the risk of susceptibility to cerebral hemorrhage and ischemic stroke.

According to the previous studies, we chose 19 circulating lipids, comprising 6 regular lipids and 13 residual lipids, to investigate their potential causal relationship with intracranial hemorrhage and ischemic stroke. The effect estimates were computed utilizing the random-effects inverse-variance-weighted methodology.

The findings revealed negative correlations between high-density lipoprotein cholesterol (HDL-C) and cerebral hemorrhage and large artery stroke. HDL-C, apolipoprotein A1 (Apo A1), TG in very small VLDL, and TG in IDL were found to be negatively correlated with any ischemic stroke. apolipoprotein B (Apo B), triglycerides (TG), low-density lipoprotein cholestrol (LDL-C), L.VLDL-TG, TG in medium VLDL, and TG in small VLDL exhibited positive correlations with large artery stroke. TG in very large HDL and TG in IDL were positively correlated with cardioembolic stroke. No significant causal relationship was observed between circulating lipids, with the exception of HDL-C and cerebral hemorrhage. No causal relationship was identified between any circulating lipids and small vessel stroke. Furthermore, the causal relationships were only found between residual lipids and ischemic stroke.

This study provides evidence for the beneficial impact of Apo A1 and HDL-C in reducing the risk of ischemic stroke, as well as the protective effect of HDL-C against cerebral hemorrhage. It highlights the detrimental effects of Apo B, TG, and LDL-C in increasing the risk of ischemic stroke, particularly in cases of large artery stroke. Furthermore, the study underscores the heterogeneity and 2-sided effects of the causal relationship between triglyceride-rich lipoproteins and ischemic stroke, offering a promising avenue for the treatment of ischemic stroke.

Atherosclerosis (AS) is a chronic vascular disease primarily affecting large and medium-sized arteries, involving complex pathological mechanisms such as inflammatory responses, lipid metabolism disorders and vascular plaque formation. In recent years, several emerging research hotspots have appeared in the field of atherosclerosis, including gut microbiota, pyroptosis, ferroptosis, autophagy, cuproptosis, exosomes and non-coding RNA. Traditional lipid-lowering drugs play a crucial role in the treatment of AS but are not able to significantly reverse the pathological changes. This article aims to summarize the latest research progress in the pathogenesis of AS and the diagnosis and treatment of the disease by comprehensively analyzing relevant literature mainly from the past five years. Additionally, the mechanisms of action and research advances of statins, cholesterol absorption inhibitors, fibrates and novel lipid-lowering drugs are reviewed to provide new insights into the diagnosis and treatment of AS.

Current guidelines advocate achieving a fixed low-density lipoprotein cholesterol (LDL-C) target and ≥50% reduction in LDL-C levels. However, sufficient LDL-C reduction is often not achieved even in patients achieving a fixed LDL-C target.

This study investigated the clinical impact of insufficient LDL-C reduction following lipid lowering therapy on cardiovascular outcomes in acute coronary syndrome (ACS) patients.

A total of 561 consecutive ACS patients who had undergone percutaneous coronary intervention (PCI) and LDL-C level measurement at index PCI and 12 months afterwards were evaluated retrospectively. We investigated a relationship between ≥50% LDL-C reduction and cardiovascular events including the composite of cardiac death, myocardial infarction, target vessel revascularization and stent thrombosis.

Of the patients, 145 (25.8%) achieved ≥50% LDL-C reduction within 12 months. There were no significant differences in cardiovascular events between patients achieving the LDL-C target of 55 mg/dL and those not achieving it (23.6% vs 19.3%, P = .77), whereas the incidence of cardiovascular events was higher in the <50% LDL-C reduction group than the ≥50% LDL-C reduction group (26.0% vs 12.4%, P = .009). Even in patients with LDL-C < 55 mg/dL, cardiovascular events were more frequently in the <50% LDL-C reduction group than the ≥50% LDL-C reduction group (28.8% vs 13.2%, P = .04). Cox proportional hazard models revealed that <50% LDL-C reduction was an independent predictor of cardiovascular outcomes (hazard ratio: 2.03, 95% CI: 1.23-3.36).

The current study underscores the significance of achieving ≥50% LDL-C reduction in addition to a target of 55 mg/dL in preventing additional cardiovascular events in ACS patients.

Performing lipid testing after statin initiation is recommended to monitor response. Inadequate response may indicate non-adherence, which is associated with an increased risk of cardiovascular events and increased costs. Group-based trajectory modeling is an approach to establish probabilistic developmental trajectories of adherence, differentiating individuals by their distinct longitudinal medication-taking behaviors. We examined whether lipid testing is associated with distinct trajectories of statin adherence among individuals enrolled in a Medicare fee-for-service plan in the USA.

A retrospective cohort study was conducted using the Centers for Medicare & Medicaid Chronic Condition Warehouse 5% sample of Medicare fee-for-service data between 2006 and 2015. Statin use and lipid testing were identified using claims data. The proportion of days covered was calculated for each 30 days after the index date, which was used to estimate the probability of belonging to each potential adherence trajectory.

In a cohort of 138,101 statin initiators, four statin adherence trajectory groups were identified. The four groups were differentiated as "rapid decline" (21.53%), "gradual decline" (10.25%), "decline first then improve later" (26.47%), and "high adherence" (41.75%). Compared with "high adherence," initiators who had lipid tests within 360 days after statin initiation were less likely to fall into "rapid decline" (adjusted odds ratio: 0.661; 95% confidence interval 0.641-0.683), "gradual decline" (adjusted odds ratio: 0.834; 95% confidence interval 0.801-0.868), and "decline first then improve later" groups (adjusted odds ratio: 0.936; 95% confidence interval 0.910-0.962).

Lipid testing is positively associated with greater use of statin medication across different adherence trajectories in the present study.