Cardiovascular disease (CVD) is a leading cause of morbidity and mortality in individuals with diabetes. Individuals with type 1 diabetes have a two- to fourfold higher risk of CVD in comparison with the general population, driven by an earlier onset and increased lifetime incidence of CVD events and mortality. Similarly, type 2 diabetes confers two- to threefold increased CVD risk, usually alongside metabolic syndrome, obesity, and hypertension. Despite advancements in methods for achieving glycemic control, the CVD burden remains disproportionately high in diabetes. The mechanisms driving elevated risk are complex and variably multifactorial, involving hyperglycemia, insulin resistance, dyslipidemia, inflammation, and a hypercoagulable state. Unfortunately, critical gaps in understanding persist on how these factors interact to promote CVD in type 1 versus type 2 diabetes, particularly across disease stages and age. Addressing these knowledge gaps is essential to developing targeted therapies that can effectively mitigate CVD risk. To meet this need, the National Institute of Diabetes and Digestive and Kidney Diseases, in partnership with the National Heart, Lung, and Blood Institute, recently formed the Cardiovascular Repository for Type 1 Diabetes (CaRe-T1D) program. Its mission is to elucidate the molecular and cellular pathways linking diabetes with CVD through the provision of high-quality human tissues for investigator-led analyses using cutting-edge technologies and collaborative data sharing to advance precision medicine and reduce the global burden of diabetes-associated cardiovascular complications.

CaRe-T1D established a biorepository and scientific consortium to advance research on cardiovascular complications in diabetes. The goal is to determine how cardiovascular disease differs in type 1 versus type 2 diabetes. Heart, kidney, carotid and peripheral arteries, and blood from organ donors with type 1 diabetes, with type 2 diabetes, or without diabetes will be distributed to approved investigators to address the pathogenesis of diabetic cardiovascular disease. CaRe-T1D is a resource of human cardiovascular tissue and a database with the results from tissue analysis.

Diabetes is associated with increased atherosclerotic cardiovascular disease (ASCVD) risk, a leading cause of morbidity and mortality. Disordered lipid metabolism is a major contributor to ASCVD risk in diabetes. Dyslipidemia in type 2 diabetes is characterized by hypertriglyceridemia, low high-density lipoprotein cholesterol and the presence of small, dense low-density lipoprotein particles. Statins have demonstrated longstanding benefit for reducing ASCVD risk in individuals with diabetes. Newer agents for add-on therapies to statins are now available for additional cardiovascular risk reduction. In this clinical overview, we review the pathogenesis of dyslipidemia in both type 1 and 2 diabetes and provide an update on the management of lipids in the individual with diabetes. We discuss the importance of appropriate risk stratification and individualized treatment selection and the need to avoid therapy inertia to mitigate cardiovascular risk. We also address lipid-related effects of glycemic-lowering therapies.

Familial chylomicronemia syndrome (FCS) is a rare Mendelian autosomal recessive disorder (MIM 238600) characterized by extreme and sustained hypertriglyceridemia due to profound reduction of lipoprotein lipase (LPL) activity. This expert opinion statement synthesizes current knowledge on the definition, pathophysiology, genetics, prevalence, diagnosis, and management of FCS. FCS typically manifests at a young age with persistent severe hypertriglyceridemia-defined as ≥10 mmol/L (≥885 mg/dL), or ≥1000 mg/dL (≥11.2 mmol/L) depending on region and whether Systeme International (SI) units are utilized-in the absence of secondary factors, resistance to conventional lipid-lowering therapies, and a high lifetime risk of acute pancreatitis. It is caused by biallelic pathogenic variants in the LPL gene encoding LPL, or 1 of 4 other related genes that encode proteins that interact with LPL. Affected individuals require a strict, lifelong very low-fat diet with <15% of energy from fat. Emerging therapies inhibiting apolipoprotein C-III show promise in reducing serum triglycerides and pancreatitis risk in patients with FCS. A multidisciplinary approach, encompassing dietary management, pharmacotherapy, and patient education, is pivotal in mitigating the significant morbidity associated with FCS.

Hyperlipidemia, a major risk factor for cardiovascular diseases, is associated with limitations in clinical lipid-lowering medications. Drug repurposing strategies expedite the research process and mitigate development costs, offering an innovative approach to drug discovery. This study employed systematic literature and guidelines review to compile a training set comprising 176 lipid-lowering drugs and 3254 non-lipid-lowering drugs. Multiple machine learning models were developed to predict the lipid-lowering potential of drugs. A multi-tiered validation strategy was implemented, encompassing large-scale retrospective clinical data analysis, standardized animal studies, molecular docking simulations and dynamics analyses. Through a comprehensive screening analysis utilizing machine learning, 29 FDA-approved drugs with lipid-lowering potential were identified. Clinical data analysis confirmed that four candidate drugs, with Argatroban as the representative, demonstrated lipid-lowering effects. In animal experiments, the candidate drugs significantly improved multiple blood lipid parameters. Molecular docking and dynamics simulations elucidated the binding patterns and stability of candidate drugs in interaction with related targets. We successfully identified multiple non-lipid-lowering drugs with lipid-lowering potential by integrating state-of-the-art machine learning techniques with multi-level validation methods, thereby providing new insights into lipid-lowering drugs, establishing a paradigm for AI-based drug repositioning research, and expanding the repertoire of lipid-lowering medications available to clinicians.

Most existing studies have primarily focused on the effects of Traditional Chinese Exercises (TCEs) on glycemic control in individuals with prediabetes, while specific recommendations for managing dyslipidemia in this population remain insufficient. Moreover, there is a lack of systematic research and conclusive evidence regarding the optimal exercise dose required to achieve metabolic improvements in individuals with prediabetes. Therefore, this meta-analysis aims to comprehensively evaluate the efficacy of TCEs in improving glycemic and lipid profiles in individuals with prediabetes and to explore the potential impact of exercise dose on these metabolic parameters.

A comprehensive search of six databases (PubMed, Web of Science, Cochrane Library, Embase, CNKI, and WanFang Data) followed PRISMA guidelines to identify randomized controlled trials (RCTs) on TCEs (e.g., "Tai Chi," "Yijinjing," "Baduanjin") and prediabetes (e.g., "impaired glucose tolerance," "impaired glucose regulation") published up to November 10, 2024. Three reviewers independently screened studies, extracted data, and assessed bias risk. Meta-analysis and subgroup/meta-regression analyses were conducted using Stata 17 software. The review protocol is registered in PROSPERO (CRD42024615150).

A total of 15 studies involving 1,839 participants were included. The meta-analysis revealed that TCEs significantly improved HbA1c (MD = -0.28%; 95% CI: -0.38% to -0.18%; P = 0.001), FBG (MD = -0.44 mmol/L; 95% CI: -0.53 to -0.34 mmol/L; P < 0.001), 2hPG (MD = -1.16 mmol/L; 95% CI: -1.48 to -0.85 mmol/L; P < 0.001), TC (MD = -0.31 mmol/L; 95% CI: -0.50 to -0.11 mmol/L; P = 0.002), TG (MD = -0.28 mmol/L; 95% CI: -0.50 to -0.06 mmol/L; P = 0.012), and HDL (MD = -0.28 mmol/L; 95% CI: -0.50 to -0.06 mmol/L; P = 0.012) compared to control groups.

TCEs significantly improve prediabetics' blood glucose and lipid levels. The recommended exercise regimen is 30-50 min per session, 2-3 times per week, for at least three months.

Familial chylomicronemia syndrome (FCS) is a rare, recessive monogenic disorder characterized by severely elevated plasma triglyceride (TG) levels due to absent or markedly impaired lipoprotein lipase activity, leading to a greatly increased risk of acute pancreatitis. Naturally occurring very low levels of apoC-III are associated with low TG levels; thus, apoC-III is a target for TG lowering, and therapies have been developed to reduce apoC-III. Strategies to inhibit hepatic apoC-III synthesis include antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs). In the last decade, technologies have been developed to enhance hepatic delivery of these potential therapeutic agents by conjugation of the ligand triantennary N-acetyl galactosamine to ASO and siRNA for receptor-mediated uptake by hepatocytes, where apoC-III is predominantly expressed. Enhanced delivery of these pharmacological agents to the target tissue has been found to support lower and/or less frequent dosing with consequent lower total systemic exposure. One antisense agent, the ASO olezarsen, is now approved by the US Food and Drug Administration (FDA) as an adjunct to diet to lower triglycerides in adults with FCS, and the other, the siRNA plozasiran, is in late-stage clinical development. Both agents have shown effectiveness in reducing both apoC-III and TG levels across several study populations. Reduced TG, lower rates of acute pancreatitis events, and similar proportions of adverse events in placebo and treated patients were recently demonstrated in placebo-controlled phase 3 trials of patients with FCS treated with olezarsen in Balance and with plozasiran in PALISADE. This review discusses causes and consequences of FCS and the rationale and progress made in developing APOC3 RNA-targeted therapeutics for the treatment of FCS.

Cardiovascular-Renal-Hepatic-Metabolic diseases are on the rise worldwide, creating major challenges for patient care and clinical research. Although these conditions share common mechanisms and often respond to similar treatments-such as lifestyle changes and newer cardiometabolic drugs (e.g., SGLT2 inhibitors, GLP-1 receptor agonists)-clinical management remains divided among multiple specialties. Recently proposed curricula in Cardiometabolic Medicine and Preventive Cardiology reflect an effort to address this fragmentation. In addition, recent studies reveal that hormonal deficiencies may increase cardiovascular risk and worsen heart failure, with emerging data showing that correcting these imbalances can improve exercise capacity and possibly reduce major cardiac events. To overcome gaps in care, we propose a new sub-specialty: Cardiovascular-Endocrine-Metabolic Medicine. This approach unifies three main pillars: (1) Lifestyle medicine, emphasizing nutrition, physical activity, and smoking cessation; (2) the Integrated Medical Management of obesity, diabetes, hypertension, dyslipidemia, heart failure with preserved ejection fraction, early-stage kidney disease, metabolic-associated liver disease, and related conditions; and (3) hormonal therapies, focused on optimizing sex hormones and other endocrine pathways to benefit cardiometabolic health. By bridging cardiology, endocrinology, and metabolic medicine, this sub-specialty offers a more seamless framework for patient care, speeds up the adoption of new treatments, and sets the stage for innovative research-all critical steps in addressing the escalating cardiometabolic pandemic.

To review the evidence and provide updated and new recommendations for the pharmacologic management of adults with dyslipidemia to prevent adverse cardiovascular outcomes. These recommendations are intended for use by clinicians, health care team members, patients, caregivers, and other stakeholders.

This guideline was developed by a multidisciplinary task force of content experts and guideline methodologists based on systematic reviews of randomized controlled trials or cohort studies from database inception to November 7, 2023. An updated literature search was completed for any additional articles published by May 31, 2024. Clinical questions addressing nonstatin medications and patient-important outcomes were prioritized. The task force assessed the certainty of the evidence and developed recommendations using the Grading of Recommendations Assessment, Development, and Evaluation framework. All recommendations were based on the consideration of the certainty of the evidence across patient-important outcomes, in addition to issues of feasibility, acceptability, equity, and patient preferences and values.

This guideline update includes 13 evidence-based recommendations for the pharmacologic management of adults with dyslipidemia focused on patient-important outcomes of atherosclerotic cardiovascular disease (ASCVD) risk reduction. The task force issued a good practice statement to assess the risk of ASCVD events for primary prevention in adults with dyslipidemia. The task force suggested the use of alirocumab, evolocumab, or bempedoic acid for adults who have ASCVD or who are at increased risk for ASCVD in addition to standard care. The task force suggested against the use of these medications in adults without ASCVD. There was insufficient evidence to recommend for or against the addition of inclisiran. For adults with hypertriglyceridemia and ASCVD or increased risk of ASCVD, the task force suggested the use of eicosapentaenoic acid but not eicosapentaenoic acid plus docosahexaenoic acid and strongly recommended against the use of niacin. There was insufficient evidence for recommendations regarding pharmacologic management in adults with severe hypertriglyceridemia (≥500 mg/dL). The task force suggested a low-density lipoprotein cholesterol treatment goal of <70 mg/dL in adults with dyslipidemia and ASCVD or at increased risk of ASCVD.

Pharmacotherapy is recommended in adults with dyslipidemia to reduce the risk of ASCVD events. There are several effective and safe treatment options for adults with dyslipidemia who have ASCVD or at increased risk of ASCVD who need additional lipid-lowering medications. Shared decision-making discussions are essential to determine the best option for each individual.

Metabolic and bariatric surgery (MBS) is the most durable treatment of obesity and can reduce statin use.

We compare statin use trajectories in patients with and without MBS.

Adults with a body mass index ≥ 35kg/m2 were identified using a U.S. employer-based retrospective claims database. Individuals who had MBS were matched 1:1 with those who did not. Trajectories of statin use were stratified by statin use in the year before the index date and examined in the 2 years after the index date.

University Hospital.

Sixteen thousand three hundred fifty-nine adults who had MBS and 16,359 matched adults who did not were analyzed. In both groups, 19.4% filled a statin prescription in the year before the index date. In the 2 years after the index date, individuals using statins remained similar at 20% (year 1) and 19% (year 2) among those who didn't have an MBS and decreased to 12.5% (year 1) and 9.3% (year 2) in the MBS cohort. Among baseline statin users, 35.4% of non-MBS and 60.4% of the MBS cohort stopped using statins within 2 years of the index date. Among statin naïve individuals at baseline, 9.6% of the non-MBS cohort started using statins within 2 years of the index date, compared to 2.6% of those who had MBS.

MBS results in a significant discontinuation of statins among baseline users, and significantly decreased the initiation of medications among individuals who were statin naive at baseline. This demonstrates that MBS is both a treatment and preventative measure for dyslipidemia.

TPE drastically reduces serum triglyceride (sTG), but its role in the treatment of hypertriglyceridemia-induced acute pancreatitis (HTG-AP) or at risk of developing it, is not well established. The objectives were to assess the effectiveness and safety of TPE in the treatment of severe HTG (sHTG), as well as to evaluate the severity of HTG-AP treated with TPE.

Observational-retrospective-single-center study, in which a descriptive analysis of sHTG treated with TPE was conducted, with the aim of treating HTG-AP or preventing its recurrence. TPE was performed if sTG≥ 1000 mg/dL after 24 hours of admission.

42 TPE were performed to treat 35 sHTG in 23 patients: 29 HTG-AP, and 6 sHTG with previous HTG-AP. Among the patients, 37% (13/55) were women, with 37 ± 14 years-old, 74.3% had normal BMI (25/35), 34% (12/35) were drinking > 40 g/alcohol/day and 54% (19/35) were diabetics. TPE significantly reduced the baseline sTG (4425 ± 2782 mg/dL vs. 709 ± 353 mg/dL, p < 0.001) in a single session, achieving a mean percentage reduction of 79 ± 13%; 20% (7/35) of sHTG cases required two TPE sessions to reduce sTG to < 1000 mg/dL. Adverse effects were reported in 4/42 TPE sessions (9,5%). sHTG-AP was observed in 3% of cases (1/29), and there were no deaths. sTG at 24 hours of admission showed no relation with the severity of APs.

The treatment of sHTG with TPE, with the aim of treating HTG-AP or preventing its recurrence, reduces sTG quickly and safety.

Severe hypertriglyceridemia (sHTG) is associated with an increased risk of acute pancreatitis. Prompt recognition and treatment of sHTG is key for prevention of acute pancreatitis and its associated life-threatening complications.

Patients with sHTG at a primary care clinic within the Veterans Affairs Eastern Colorado Health Care System were receiving suboptimal treatment that did not align with evidence-based guidelines.

We initiated a quality improvement (QI) project to improve the management of sHTG in an outpatient primary care clinic. Veterans with a triglyceride level between 500 and 1,500 mg/dl were included in the project.

Project interventions included provider education, patient education, and targeted electronic consultations (e-consults) with treatment recommendations. The primary outcome was to decrease the percentage of patients with triglycerides ≥500 mg/dl by 25%. The secondary outcome was to decrease the mean triglyceride level of the patient population by 15%.

Education on evaluation and treatment of sHTG was given to 100% ( n = 21) of primary care clinicians. Overall, 72.8% (95% CI [62.6-81.6%]) of patients ( n = 67) received appropriate written education materials, and 72.8% (95% CI [62.6-81.6%]) of patients ( n = 67) received a targeted e-consult. The percentage of patients with sHTG decreased by 47%. Average triglyceride level decreased from 651 to 483 mg/dl (25.8% decrease).

A multipronged QI project consisting of provider education, patient education, and targeted e-consults resulted in decreased triglyceride levels and improved access to specialist expertise. Clinical implications include decreased prevalence of sHTG and risk of acute pancreatitis among patients in the project.

The Royal College of Physicians of Thailand (RCPT) published a Clinical Practice Guideline on Pharmacologic Therapy of Dyslipidemia for Atherosclerotic Cardiovascular Disease (ASCVD) Prevention in 2016. The availability of newer classes of medications for dyslipidemia, supported by extensive clinical research findings, indicates a significant need for the updating of the existing clinical practice guideline.

To serve as guidelines on the management of dyslipidemia for Thai adults.

The RCPT Dyslipidemia Guidelines Committee was established with representatives from selected professional societies to revise the 2016 Guideline by critically reviewing the latest evidence. Meetings were conducted from August to December 2023, culminating in a public hearing that engaged various stakeholders in January 2024. The final Thai version received approval in April 2024, while the English translation was completed in October 2024.

Lifestyle modifications and statins remain the cornerstone of therapy for dyslipidemia in adults across various clinical settings. Emerging evidence regarding newer classes of lipid-lowering medications indicates that these treatments are effective in lowering LDL-cholesterol levels and reducing atherosclerotic cardiovascular events. This suggests that they may serve as an add-on therapy for individuals who cannot achieve target levels or who are at high risk for future cardiovascular events. The Thai CV Risk Score is recommended due to its specificity for the Thai population.

The 2024 updated clinical practice guidelines establish a framework, provide recommendations, and serve as a comprehensive resource for the contemporary management of dyslipidemia in adults, with the goal of preventing ASCVD in Thailand.

The present preliminary study aimed to provide a targeted lipidomic analysis of Hashimoto (HT) and non-HT patients with well-controlled hypothyroidism as well as in healthy adults, and is the first to demonstrate the association of several components of the human lipidome with hypothyroidism in relation to the total plasma selenium content. All the patients and age-, sex-, and BMI-matched healthy controls met the very strict qualification criteria. Se levels were analyzed by ICP-MS, and lipidome studies were conducted using TQ-LC/MS. The 40 acylcarnitines, 90 glycerophospholipids, and 15 sphingomyelins were identified and quantified. PCaaC26:0 and PCaaC40:1 were negatively correlated with Se concentrations. Other lipids that were negatively correlated with Se concentrations but did not present significant differences between the three groups in the Kruskal-Wallis ANOVA test were PCaaC32:0, PCaeC30:0, PCaeC36:5, SMC18:0, and SM C18:1. In the multiple linear regression analyses, Se levels showed negative relationship, whereas different phosphatidylcholines: PCaaC24:0, PCaaC26:0, PCaeC30:1, PCaeC34:0, PCaeC36:4, PCaeC42:0 were positively associated with the presence of (H). Different lipidome components were identified in healthy and hypothyroid patients regardless of the cause of that condition. Studies on larger populations are needed to determine cause-and-effect relations and the potential mechanisms underlying these associations.

Hypothyroidism (HT) affects millions worldwide and can lead to various lipid disorders. The metabolic complexity and the influence of toxic elements in autoimmune and non-autoimmune HT subtypes are not fully understood. This study aimed to investigate the relationships between plasma lipidome, toxic elements, and clinical classifications of HT in unexposed individuals.

Samples were collected from 120 adults assigned to a study group with Hashimoto's disease and non-autoimmune HT, and a healthy control group. Quantification of 145 pre-defined lipids was performed by using triple quadrupole tandem mass spectrometry (TQ MS/MS) in multiple reactions monitoring (MRM) mode via positive electrospray ionization (ESI). Levels of toxic elements were determined using inductively coupled plasma mass spectrometry (ICP-MS).

Significant associations between altered levels of several components of the plasma lipidome and Al, Cd, Ni, As, and Pb with HT were found. We show metabolic differences in lysophosphatidylcholines (LPC) and phosphatidylcholines (PC) between HT and controls, with distinct predicted activation patterns for lysolecithin acyltransferase and phospholipase A2.

There are significant changes in the lipidome profiles of healthy subjects compared to euthyroid HT patients treated with L-thyroxine, which are related to the type of hypothyroidism and non-occupational exposure to toxic elements.

Dyslipidemia and type 2 diabetes mellitus (T2DM) are chronic conditions with substantial public health implications. Effective management of lipid metabolism in patients with T2DM is critical. However, there has been insufficient attention given to the relationship between thyroid hormone sensitivity and dyslipidemia in the T2DM population, particularly concerning non-high-density lipoprotein cholesterol (non-HDL-C).

To clarify the association between thyroid hormone sensitivity and dyslipidemia in patients with T2DM.

In this cross-sectional study, thyroid hormone sensitivity indices, the thyroid feedback quantile-based index (TFQI), the thyroid-stimulating hormone index (TSHI), the thyrotrophic T4 resistance index (TT4RI), and the free triiodothyronine (FT3)/free thyroxine (FT4) ratio were calculated. Logistic regression analysis was performed to determine the associations between those composite indices and non-HDL-C levels. Random forest variable importance and Shapley Additive Explanations (SHAP) summary plots were used to identify the strength and direction of the association between hyper-non-HDL-C and its major predictor.

Among the 994 participants, 389 (39.13%) had high non-HDL-C levels. Logistic regression analysis revealed that the risk of hyper-non-HDL-C was positively correlated with the TFQI (OR: 1.584; 95%CI: 1.088-2.304; P = 0.016), TSHI (OR: 1.238; 95%CI: 1.034-1.482; P = 0.02), and TT4RI (OR: 1.075; 95%CI: 1.006-1.149; P = 0.032) but was not significantly correlated with the FT3/FT4 ratio. The relationships between composite indices of the thyroid system and non-HDL-C levels differed according to sex. An increased risk of hyper-non-HDL-C was associated with elevated TSHI levels in men (OR: 1.331; 95%CI: 1.003-1.766; P = 0.048) but elevated TFQI levels in women (OR: 2.337; 95%CI: 1.4-3.901; P = 0.001). Among the analyzed variables, the average SHAP values were highest for TSHI, followed by TT4RI.

Impaired sensitivity to thyroid hormones was associated with high non-HDL-C levels in patients with T2DM.

Hypopituitarism is a heterogenous disorder characterised by a deficiency in one or more anterior pituitary hormones. There are marked sex disparities in the morbidity and mortality experienced by patients with hypopituitarism. In women with hypopituitarism, the prevalence of many cardiovascular risk factors, myocardial infarction, stroke and mortality are significantly elevated compared to the general population, however in men, they approach that of the general population. The hypothalamic-pituitary-gonadal axis (HPG) is the most sexually dimorphic pituitary hormone axis. Gonadotropin deficiency is caused by a deficiency of either hypothalamic gonadotropin-releasing hormone (GnRH) or pituitary gonadotropins, namely follicle-stimulating hormone (FSH) and luteinising hormone (LH). HPG axis dysfunction results in oestrogen and testosterone deficiency in women and men, respectively. Replacement of deficient sex hormones is the mainstay of treatment in individuals not seeking fertility. Oestrogen and testosterone replacement in women and men, respectively, have numerous beneficial health impacts. These benefits include improved body composition, enhanced insulin sensitivity, improved atherogenic lipid profiles and increased bone mineral density. Oestrogen replacement in women also reduces the risk of developing type 2 diabetes mellitus. When women and men are considered together, untreated gonadotropin deficiency is independently associated with an increased mortality risk. However, treatment with sex hormone replacement reduces the mortality risk comparable to those with an intact gonadal axis. The reasons for the sex disparities in mortality remain poorly understood. Potential explanations include the reversal of women's natural survival advantage over men, premature loss of oestrogen's cardioprotective effect, less aggressive cardiovascular risk factor modification and inadequate oestrogen replacement in women with gonadotropin deficiency. Regrettably, historical inertia and unfounded concerns about the safety of oestrogen replacement in women of reproductive age have impeded the treatment of gonadotropin deficiency.

Diabetes is a significant independent risk factor for atherosclerotic cardiovascular disease (ASCVD), with dyslipidemia playing a critical role in the initiation and progression of ASCVD in diabetic patients. In China, the current prevalence of dyslipidemia in diabetes is high, but the control rate remains low. Therefore, to enhance lipid management in patients with diabetes, the Endocrinology and Metabolism Physician Branch of the Chinese Medical Doctor Association, in collaboration with the Experts' Committee of the National Society of Cardiometabolic Medicine, has convened experts to develop a consensus on the management of dyslipidemia in patients with type 1 or type 2 diabetes. The development of this consensus is informed by existing practices in lipid management among Chinese diabetic patients, incorporating contemporary evidence-based findings and guidelines from national and international sources. The consensus encompasses lipid profile characteristics, the current epidemiological status of dyslipidemia, ASCVD risk stratification, and lipid management procedures in diabetic patients. For the first time, both low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol have been recommended as primary targets for lipid intervention in diabetic patients. The consensus also includes a summary and recommendations for lipid management strategies in special diabetic populations, including children and adolescents, individuals aged 75 years and older, patients with chronic kidney disease, metabolic-associated fatty liver disease, and those who are pregnant. This comprehensive consensus aims to improve cardiovascular outcomes in diabetic patients by contributing to the dissemination of key clinical advancements and guiding clinical practice.

The primary objective of this review is to explore the pathophysiological roles and clinical implications of lipoprotein(a) [Lp(a)] in the context of atherosclerotic cardiovascular disease (ASCVD). We seek to understand how Lp(a) contributes to inflammation and arteriosclerosis, aiming to provide new insights into the mechanisms of ASCVD progression.

Recent research highlights Lp(a) as an independent risk factor for ASCVD. Studies show that Lp(a) not only promotes the inflammatory processes but also interacts with various cellular components, leading to endothelial dysfunction and smooth muscle cell proliferation. The dual role of Lp(a) in both instigating and, under certain conditions, mitigating inflammation is particularly noteworthy. This review finds that Lp(a) plays a complex role in the development of ASCVD through its involvement in inflammatory pathways. The interplay between Lp(a) levels and inflammatory responses highlights its potential as a target for therapeutic intervention. These insights could pave the way for novel approaches in managing and preventing ASCVD, urging further investigation into Lp(a) as a therapeutic target.

Hypertriglyceridemia is characterized by elevated triglyceride levels in the blood, which increases the risk of cardiovascular disease and pancreatitis. This condition stems from multiple factors including lifestyle choices, genetics, and conditions such as diabetes and metabolic syndrome. Apolipoprotein C-III (APOC3), a protein for lipid metabolism, hinders enzymes necessary for breaking down triglycerides and thus plays a key role in hypertriglyceridemia. Variations in the APOC3 gene are associated with varying triglyceride levels among individuals. Recent genetic studies and clinical trials have shed light on the potential of targeting APOC3 as a potentially promising therapeutic modality of hypertriglyceridemia. Antisense oligonucleotides like volanesorsen have displayed effectiveness in lowering triglyceride levels in individuals with severe hypertriglyceridemia. This review article delves into how APOC3 influences triglyceride control and its potential use in targeting APOC3 to manage severe hypertriglyceridemia.

Establishing direct reference intervals (RIs) for paediatric patients is a very challenging endeavour. Indirect RIs can address this problem, using existing clinical laboratory databases from real-world data research. Compared to the traditional direct method, the indirect approach is highly practical, widely applicable, and low-cost. Considering the relevance of dyslipidemia in the paediatric age, to provide better laboratory services to the local paediatric population, we established population-specific lipid RIs via data mining.

Our laboratory information system was searched for cholesterol (TC), triglycerides (TG), low-density lipoprotein (LDL) and high-density lipoprotein (HDL) of patients aged less than 18 years, performed from January 2009 until December 2022. RIs were estimated using RefineR algorithm.

Values from 215,594 patients were initially collected. After refining data on the basis of specific exclusion criteria that left 17,933 patients, we determined the RIs for each analyte, including corresponding 95% confidence interval (95% CI). Age and sex partitions were required for proper stratification of the heterogenous subpopulations. Age-related variations in TC and TG values were observed mainly in children until 5 years. RIs were defined for children less than 3 years and for those of 3-18 years. In our population, the obtained RIs were comparable with those of the literature, but the upper TG limit in subjects under the age of 3 (2.03 mmol/L with 95% CI: 1.45-2.86) was lower than that previously reported.

Our RIs, necessary for paediatric lipid monitoring, are tailored to the serviced patient population as should be done whenever possible.

Type 2 diabetes mellitus (T2DM) is a significant risk factor for stroke. Nevertheless, the evidence supporting stringent glycemic control to reduce macrovascular complications, particularly stroke, is not as clear as for microvascular complications. Presently, risk reduction strategies are based on controlling multiple risk factors, including hypertension, dyslipidemia, glycemia, smoking, and weight. Since 2008, new pharmacological therapies for treating T2DM have been required to undergo trials to ensure their cardiovascular safety. Remarkably, several novel therapies have exhibited protective effects against the combined endpoint of major cardiovascular events. Evidence from these trials, with stroke as a secondary endpoint, along with real-world data, suggests potential benefits in stroke prevention, particularly with glucagon-like peptide 1 receptor agonists. Conversely, the data on sodium-glucose cotransporter type 2 inhibitors remains more controversial. Dipeptidyl peptidase 4 inhibitors appear neutral in stroke prevention. More recent pharmacological therapies still lack significant data on this particular outcome. This article provides a comprehensive review of the evidence on the most recent T2DM therapies for stroke prevention and their impact on clinical practice.

Lipoprotein(a) [Lp(a)], a genetically determined macromolecular complex, is independently and causally associated with atherosclerotic cardiovascular disease (ASCVD) and calcific aortic stenosis via proposed proinflammatory, prothrombotic, and proatherogenic mechanisms. While Lp(a) measurement standardization issues are being resolved, several guidelines now support testing Lp(a) at least once in each adult's lifetime for ASCVD risk prediction which can foster implementation of more aggressive primary or secondary prevention therapies. Currently, there are several emerging targeted Lp(a) lowering therapies in active clinical investigation for safety and cardiovascular benefit among both primary and secondary prevention populations. First degree relatives of patients with high Lp(a) should be encouraged to undergo cascade screening. Primary prevention patients with high Lp(a) should consider obtaining a coronary calcium score for further risk estimation and to guide further ASCVD risk factor management including consideration of low dose aspirin therapy. Secondary prevention patients with high Lp(a) levels should consider adding PCSK9 inhibition to statin therapy.

The case of a 47-year-old female patient who underwent sigmoidectomy for metastatic colorectal cancer is reported. Treatment with capecitabine and 5-fluorouracil induced severe hypertriglyceridemia repeatedly.

Based on laboratory tests and clinical evaluations, treatment was suggested by specialists.

After treatment with capecitabine, the patient's triglycerides increased from 19.7 mmol/L to 42 mmol/L. It was proposed that the patient had multifactorial chylomicronemia syndrome triggered by secondary factors. Statins, fenofibrate, ezetimib, and metformin were added to the therapy. After metastases appeared, FOLFIRI (leucovorin calcium [folinic acid], 5-fluorouracil, and irinotecan hydrochloride) chemotherapy and biological treatment (cetuximab) followed and triglycerides increased to 55.3 mmol/L.

Monitoring triglyceride levels before and during therapy is suggested.

Proprotein convertase subtilisin/kexin 9 (PCSK9) plays a crucial role in breaking down the hepatic low-density lipoprotein receptor (LDLR), thereby influencing the levels of circulating low-density lipoprotein cholesterol (LDL-C). Consequently, inhibiting PCSK9 through suitable ligands has been established as a validated therapeutic strategy for combating hypercholesterolemia and cardiovascular diseases.

Patent literature claiming novel compounds inhibiting PCSK9 disclosed from 2018 to June 2023 available in the espacenet database, which contains more than 150 million patent documents from over 100 patent-granting authorities worldwide.

The undisputable beneficial influence of PCSK9 as a pharmacological target has prompted numerous private and public institutions to patent chemical frameworks as inhibitors of PCSK9. While several compounds have advanced to clinical trials for treating hypercholesterolemia, they have not completed these trials yet. These compounds must contend in a complex market where new, costly, and advanced drugs, such as monoclonal antibodies and siRNA, are prescribed instead of inexpensive and less potent statins.

Lipoprotein(a) (Lp(a)) is a unique low-density lipoprotein-like lipoprotein that is considered an independent and causal risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis. The Lp(a) molecule also contains apolipoprotein A and apolipoprotein B, which collectively promote atherosclerosis, thrombosis, and inflammation. Lp(a) is highly genetic and minimally responsive to nonpharmacological measures. Lp(a) serum levels ≥125 nmol/L are associated with increased ASCVD risk, but this threshold has not been accepted universally. Elevated Lp(a) is the most common genetic dyslipidemia affecting approximately 20% of the general population. Certain currently available lipid-lowering drugs, including the proprotein convertase subtilisin/kexin type 9 therapies, produce moderate reductions in Lp(a); however, none are indicated for the treatment of elevated Lp(a). There are currently four investigational RNA-based therapeutic agents that reduce Lp(a) by 70% to 100%. Two of these agents are being evaluated for ASCVD risk reduction in adequately powered outcomes trials, with results expected in 2 to 3 years. Until such therapies become available and demonstrate favorable clinical outcomes, strategies for elevated Lp(a) primarily involve early and intensive ASCVD risk factor management.

Lipid disorders are common in several endocrine conditions. Diabetes mellitus, hypothyroidism and Cushing's syndrome are the common endocrine disorders with dyslipidemia. Dyslipidemia has a significant impact on endocrine and metabolic health and the risk of atherosclerotic cardiovascular disease. In most cases of dyslipidemia, the suspicion of endocrine diseases must be based on clinical symptoms and signs. Optimal management of the dyslipidemia requires treatment of the underlying endocrine condition. Lipid lowering therapy is a useful adjunct or a requirement in many cases. The Indian guidelines provide a pragmatic and practical approach to the management of lipid disorders in endocrine disease, as well as endocrine vigilance with lipid therapy.

Triglyceride-rich remnant lipoproteins (TRLs) are considered atherogenic due to the presence of remnant cholesterol, which is transported by apolipoprotein B. In clinical practice, the concentration of TRLs can be estimated by calculating remnant cholesterol or non-HDL cholesterol levels.

This study aims to investigate the proportion of patients who have low LDL cholesterol (LDL-C) concentration but elevated remnant cholesterol concentration, stratified by the presence of hypertriglyceridaemia and ethnicity, using real-world hospital data. Our secondary aim is to investigate the proportion of patients with elevated non-HDL cholesterol levels using guideline-recommended goals.

A 2-year retrospective study was conducted at a single centre, analyzing lipid blood tests of all patients, including directly measured LDL-C. Fasting for blood tests was not mandatory.

The study included a total of 21,605 consecutive patients with plasma lipid profiles analyzed in our hospital laboratory. The median age was 61 years. In patients with ASCVD (n = 14,704), 23.7% had an LDL-C level of <1.8 mmol/L, 11.3% had elevated remnant cholesterol concentrations at ≥0.65 mmol/L, and 48.8% were at the non-high-density lipoprotein cholesterol (non-HDL-C) goal (<2.6 mmol/L). Among patients diagnosed with atherosclerotic cardiovascular disease (ASCVD) with LDL-C levels of <1.8 mmol/L (n = 3,484), only 11.9% had high levels of remnant cholesterol, but 96% of the ASCVD patients also achieved the recommended non-HDL-C target of <2.6 mmol/L. When the LDL-C level was <1.8 mmol/L, the mean concentration of remnant cholesterol was 0.214 mmol/L when the triglyceride level was <1.7 mmol/L (n = 3,380), vs. 0.70 mmol/L when the triglyceride level was elevated (n = 724), p < 0.001. Among patients with a triglyceride level of ≥1.7 mmol/L and an LDL-C level of <.8 mmol/L, there were 254 patients with elevated remnant cholesterol concentration and 71 patients with suboptimal non-HDL levels. Malays had a higher mean remnant cholesterol concentration compared with both Chinese and Indians across all LDL-C levels, particularly in the presence of hypertriglyceridaemia.

An elevated remnant cholesterol concentration of >0.65 mmol/L was present in 11% of all patients. The current guideline-recommended non-HDL-C goal, which uses a 0.8 mmol/L estimate of remnant cholesterol concentration, was achieved in >92% of patients, suggesting that it is unlikely to be clinically useful for the majority of our patient population except where there is concomitant hypertriglyceridaemia. Further studies are needed to establish the appropriate non-HDL-C goal or calculated remnant cholesterol concentration, paired with the LDL-C goal or otherwise, in a Southeast Asian population.

Lipoprotein(a) [Lp(a)] is a molecule bound to apolipoprotein(a) with some similarity to low-density lipoprotein cholesterol (LDL-C), which has been found to be a risk factor for cardiovascular disease (CVD). Lp(a) appears to induce inflammation, atherogenesis, and thrombosis. Approximately 20% of the world's population has increased Lp(a) levels, determined predominantly by genetics. Current clinical practices for the management of dyslipidemia are ineffective in lowering Lp(a) levels. Evolving RNA-based therapeutics, such as the antisense oligonucleotide pelacarsen and small interfering RNA olpasiran, have shown promising results in reducing Lp(a) levels. Phase III pivotal cardiovascular outcome trials [Lp(a)HORIZON and OCEAN(a)] are ongoing to evaluate their efficacy in secondary prevention of major cardiovascular events in patients with elevated Lp(a). The future of cardiovascular residual risk reduction may transition to a personalized approach where further lowering of either LDL-C, triglycerides, or Lp(a) is selected after high-intensity statin therapy based on the individual risk profile and preferences of each patient.

To characterize the time course of triglyceride (Tg) lowering in hypertriglyceridemic (HTg) pancreatitis according to the initial Tg values, causes, and interventions.

Patients hospitalized from October 2013 through December of 2018 with a diagnosis of pancreatitis associated with HTg (Tg level, ≥500 mg/dL), in the absence of other causes, were identified by medical record review. Tg lowering was retrospectively assessed for differences in relation to the initial Tg values, use of intravenous insulin, ethanol-associated versus nonethanol-associated causes, and time to Tg values of <500 versus <1000 mg/dL.

Sixty-six cases were identified, and 45 had multiple measurements for time-course evaluation. Those with initial Tg values of <4000 mg/dL achieved Tg levels of <1000 mg/dL in <3 days, whereas 18.8% with higher values took 5-9 days. Insulin therapy was associated with a longer duration of HTg, whereas ethanol was associated with a shorter duration. Tg clearance in ethanol-associated HTg appeared independent of insulin treatment. Time to Tg levels of <500 mg/dL versus <1000 mg/dL was significantly longer when the initial Tg levels were >2000 mg/dL.

A threshold of 4000 mg/dL for the initial Tg levels in HTg pancreatitis appears to separate patients who are likely to achieve Tg levels of <1000 mg/dL in <3 versus >3 days, independent of cause or treatment. Insulin therapy is appropriate for patients with hyperglycemia but appears unnecessary for those with isolated ethanol-associated HTg. A threshold Tg level of <1000 mg/dL appears more practical than that of <500 mg/dL for resuming nutritional intake.

Hypertriglyceridemia-associated acute pancreatitis is a disease lacking a standardized management approach.

The main objective of this study was to evaluate the safety and efficacy of a continuous intravenous insulin infusion order set specifically designed for managing hypertriglyceridemia.

This study compared the safety and efficacy of a standardized (postintervention) approach to managing hypertriglyceridemia to a nonstandardized (preintervention) approach. The primary efficacy outcome was the percentage of patients who achieved a triglyceride level less than 500 mg/dL. Additional outcomes included the time to achieving a triglyceride level less than 500 mg/dL and the percent reduction in triglyceride levels. The primary safety outcome was the number of patients who experienced hypoglycemia (glucose less than 70 mg/dL).

Twenty patients were included in both the preintervention and postintervention groups. There was a significantly greater reduction in triglyceride levels observed in the postintervention group. The number of patients who achieved a triglyceride level less than 500 mg/dL in the preintervention and postintervention groups were 10 (50%) and 17 (85%), respectively, P = 0.018. Within the postintervention group, the time to achieving a triglyceride level less than 500 mg/dL in those with and without diabetes was 56.8 hours (38.2-64.0) versus 27.6 hours (19.7-45.0), respectively, P = 0.028.

Our findings demonstrate that insulin infusions are safe and effective when therapy is standardized and accounts for nursing to patient ratios. Our results provide the medical community with a standardized approach to acutely managing hypertriglyceridemia.

Triglycerides are a major source of energy, while high plasma triglycerides are a risk factor for various diseases and premature death. Severely elevated plasma triglycerides are a well-established cause of acute pancreatitis with high mortality, likely due to the presence of elevated levels of chylomicrons and large very low-density lipoproteins in plasma. As markedly elevated levels of these very large lipoproteins are not generally found in mild to moderate hypertriglyceridemia, this was previously not regarded as a cause or marker of increased risk of acute pancreatitis. However, mild to moderate hypertriglyceridemia may identify individuals who at a later timepoint develop severe hypertriglyceridemia and acute pancreatitis.

We describe measurement of plasma triglycerides and studies on plasma triglycerides and risk of acute pancreatitis. Further, we summarize current European and American guidelines for the prevention of acute pancreatitis and, finally, the potential for future prevention of acute pancreatitis through lowering of plasma triglycerides.

Recent observational and genetic studies indicate that mild to moderate hypertriglyceridemia is causally related to increased risk of acute pancreatitis, most likely as a marker of future severe hypertriglyceridemia. Current guidelines do not mention individuals with mild to moderate hypertriglyceridemia, even though newer evidence suggests an unmet medical need. Treatment could include plasma triglyceride-lowering therapy targeting the pathway for lipoprotein lipase as the main triglyceride degrading enzyme in plasma. Angiopoietin-like 3 and apolipoproteinC-III are inhibitors of lipoprotein lipase, and blocking of these 2 inhibitors is showing promising results in relation to marked triglyceride-lowering and could perhaps be used to prevent acute pancreatitis in the future.

The pharmacological treatment of dyslipidemia, a major modifiable risk factor for developing atherosclerotic cardiovascular disease (ASCVD), remains a debated and controversial issue, not only in terms of the most appropriate therapeutic range for lipid levels, but also with regard to the optimal strategy and sequence approach (stepwise vs upstream therapy). Current treatment guidelines for the management of dyslipidemia focus on the intensity of low-density lipoprotein cholesterol (LDL-C) reduction, stratified according to risk for developing ASCVD. Beyond statins and ezetimibe, different medications targeting LDL-C have been recently approved by regulatory agencies with potential innovative mechanisms of action, including proprotein convertase subtilisin/kexin type 9 modulators (monoclonal antibodies such as evolocumab and alirocumab; small interfering RNA molecules such as inclisiran), ATP-citrate lyase inhibitors (bempedoic acid), angiopoietin-like 3 inhibitors (evinacumab), and microsomal triglyceride transfer protein inhibitors (lomitapide). An understanding of their pharmacological aspects, benefit-risk profile, including impact on hard cardiovascular endpoints beyond LDL-C reduction, and potential advantages from the patient perspective (e.g., adherence) - the focus of this evidence-based review - is crucial for practitioners across medical specialties to minimize therapeutic inertia and support clinical practice.

Polycystic ovary syndrome (PCOS) is characterized by hyperandrogenemia, a quite common heterogenous endocrine/hormonal disorder, and accompanied by elevated androgen level, menstrual irregularity, and hirsutism. The consequences include infertility or miscarriage. It is a challenging problem to the physicians. In a one-arm, non-randomized preliminary investigation in fifty premenopausal women, we demonstrated the efficacy of Furocyst®, a patented, standardized Trigonella foenum-graecum extract, in ameliorating the symptoms of PCOS over a period of 90 consecutive days.

In the present study, a double-blind, two-arm, single-center, randomized, comparative study was conducted to assess the efficacy of Furocyst® (2 capsules of 500 mg/day) in 208 pre-menopausal women diagnosed with PCOS.

Ethical committee approval was obtained. A total of 208 subjects (placebo = 95; Furocyst® = 113; age:18-45 years, BMI < 42 kg/m2) completed the investigation. The comparative efficacy of placebo and Furocyst® was assessed on the number of cysts, ovarian volume, hirsutism, LH:FSH ratio, titer of TSH, SHBG, prolactin and free testosterone. Key clinical parameters such as fasting blood glucose levels, HOMA Index, cholesterol, LDL, and triglyceride levels, as well as total blood chemistry were also investigated.

Furocyst® supplementation significantly reduced the number of cysts, ovarian volume, and hirsutism levels, as well as normalized the menstrual cycle in Furocyst®-treated subjects as compared to placebo group. Furocyst® significantly reduced luteinizing hormone (LH) and follicle stimulating hormone (FSH) levels, and thyroid stimulating hormone (TSH) levels, and reduced the prolactin and SHBG levels. Furocyst® significantly reduced the fasting blood glucose levels, HOMA Index, cholesterol, LDL, and triglyceride levels as compared to the placebo group, while the free testosterone levels were significantly decreased in the Furocyst® group.

The studies collectively demonstrated the efficacy of Furocyst® as a safe, natural phytochemical-based formulation to alleviate the symptoms of PCOS. No significant adverse events were observed.

Takayasu's arteritis (TAK) is a rare chronic granulomatous arteritis that mainly affects the aorta and its major branches. Coronary artery (CA) involvement can be observed in 10-25% of TAK patients. We report a 21-year-old young female who was previously diagnosed with TAK and severe left main coronary artery (LMCA) stenosis and underwent numerous percutaneous coronary interventions (PCIs) in our hospital due to in-stent restenosis (ISR). This time, an excimer laser coronary atherectomy (ELCA) and drug-coated balloon (DCB) dilation was taken at the LMCA for the ISR. The blood flow was smooth after the operation, and she was symptom-free after discharge. Unfortunately, 5 months later, severe intimal hyperplasia was still seen in the stent of LMCA and left anterior descending (LAD) coronary artery. A coronary artery bypass graft surgery (CABG) was performed, and she has been symptom-free ever since. ELCA plus DCB is one of the novel ways we first reported. However, ensuring long-term inflammation control is equally important to restore blood flow. The combination of revascularization and anti-inflammation/immunosuppression is recommended to improve the outcomes of TAK patients with CA involvements.

The aim of this study was to highlight the current best practice for atherosclerotic cardiovascular disease (CVD) risk evaluation, including selective use of adjunctive tools for risk stratification [e.g. coronary artery calcium (CAC) scoring] and risk enhancement [e.g. lipoprotein(a) [Lp(a)], polygenic risk scoring (PRS)].

New studies have evaluated the efficacy of various risk assessment tools. These studies demonstrate the role of Lp(a) as a risk-enhancing factor ready for more widespread use. CAC is the gold standard method of assessing subclinical atherosclerosis, enabling true risk stratification of patients, and informing net benefit assessment for initiating or titrating lipid-lowering therapy (LLT).

Lp(a) concentration and CAC scoring, apart from the traditional risk factors, add the most value to the current CVD risk assessment approaches of all available tools, especially in terms of guiding LLT. In addition to new integrative tools such as the MESA CHD Risk Score and Coronary Age calculator, the future of risk assessment may include PRS and more advanced imaging techniques for atherosclerosis burden. Soon, polygenic risk scoring may be used to identify the age at which to begin CAC scoring, with CAC scores guiding preventive strategies.

Cardiovascular disease (CVD) is a major cause of morbidity and mortality in people with type 1 diabetes (PWT1D). We assessed cardiovascular risk factors and pharmacologic treatment in a large Canadian cohort of PWT1D.

This cross-sectional study used data from adult PWT1D in the BETTER registry (n=974). CVD risk factor status, diabetes complications, and treatments (used as proxy for blood pressure and dyslipidemia) were self-reported through online questionnaires. Objective data were available for a subgroup of PWT1D (23%, n=224).

Participants were adults (43.9±14.8 years) with a diabetes duration of 23.3±15.2 years; 34.8% reported glycated hemoglobin (A1C) levels of ≤7%, 67.2% reported a very high cardiovascular risk, and 27.2% reported at least 3 CVD risk factors. Most participants received care for CVD in accordance with the Diabetes Canada Clinical Practice Guidelines (DC-CPG), with a median recommended pharmacologic treatment score of 75.0%. However, 3 subgroups of participants with lower adherence (<70%) to DC-CPG were identified: 1) those with microvascular complications and receiving a statin (60.8%, 208 of 342) or renin-angiotensin axis nephroprotective therapy (52.6%, 180 of 342); 2) those aged ≥40 years and receiving statin therapy (67.1%, 369 of 550); and 3) those aged ≥30 years with a diabetes duration of ≥15 years and receiving statin therapy (58.9%, 344 of 584). Among a subgroup of participants with recent laboratory results, only 24.5% of PWT1D (26 of 106) achieved both A1C and low-density lipoprotein cholesterol targets.

Most PWT1D received recommended pharmacologic cardiovascular protection, but specific subgroups required special attention. Target achievement for key risk factors remains suboptimal.

Hypertriglyceridemia-induced acute pancreatitis (HTG-AP) should be considered in all cases of acute pancreatitis and triglyceride levels measured early, so that appropriate early and long-term treatment can be initiated.

In most cases of HTG-AP, conservative management (nothing by mouth, intravenous fluid resuscitation and analgesia) is sufficient to achieve triglyceride levels less than 500 mg/dl. Intravenous insulin and plasmapheresis are sometimes used, although prospective studies showing clinical benefits are lacking. Pharmacological management of hypertriglyceridemia (HTG) should start early and target triglyceride levels of less than 500 mg/dl to reduce the risk or recurrent acute pancreatitis. In addition to currently used fenofibrate and omega-3 fatty acids, several novel agents are being studied for long-term treatment of HTG. These emerging therapies focus mainly on modifying the action of lipoprotein lipase (LPL) through inhibition of apolipoprotein CIII and angiopoietin-like protein 3. Dietary modifications and avoidance of secondary factors that worsen triglyceride levels should also be pursued. In some cases of HTG-AP, genetic testing may help personalize management and improve outcomes.

Patients with HTG-AP require acute and long-term management of HTG with the goal of reducing and maintaining triglyceride levels to less than 500 mg/dl.

High levels of lipoprotein(a) [Lp(a)] are causal for development of atherosclerotic cardiovascular disease and highly regulated by genetics. Levels are higher in Blacks compared to Whites, and in women compared to men. Lp(a)'s main protein components are apolipoprotein (apo) (a) and apoB100, the latter being the main component of Low-Density Lipoprotein (LDL) particles. Studies have identified Lp(a) to be associated with inflammatory, coagulation and wound healing pathways. Lack of validated and accepted assays to measure Lp(a), risk cutoff values, guidelines for diagnosis, and targeted therapies have added challenges to the field. Scientific efforts are ongoing to address these, including studies evaluating the cardiovascular benefits of decreasing Lp(a) levels with targeted apo(a) lowering treatments. This review will provide a synopsis of evidence-based effects of high Lp(a) on disease presentation, highlight available guidelines and discuss promising therapies in development. We will conclude with current clinical information and future research needs in the field.

There is burgeoning interest in intravenous insulin for hypertriglyceridemia-induced acute pancreatitis (HTG-AP) as a less invasive alternative to plasmapheresis; however, there are few published descriptions of disease-specific insulin protocols.

To compare the efficacy and safety of an insulin infusion-based protocol with nonstandardized medical therapy for HTG-AP.

This is a retrospective analysis before and after creation of an HTG-AP-specific insulin infusion treatment protocol. Inclusion criteria were age ≥18 years, an initial triglyceride level >1000 mg/dL, and a diagnosis of AP. The primary outcome of the study was time to a triglyceride level ≤1000 mg/dL.

Sixty-seven patients were included in this study (26 pre-protocol and 41 in the HTG-AP insulin protocol group). Baseline characteristics between the groups were similar, with median initial triglyceride levels >3500 mg/dL. There was a trend toward patients treated with the HTG-AP-specific infusion reaching a triglyceride level ≤1000 mg/dL faster (43.3 [24.9-72.1] vs 26.9 [17.7-51.1] hours; P = 0.07). Those treated to ≤500 mg/dL achieved this faster with the disease-specific infusion (49.2 [29.4-67.8] vs 70.9 [36.3-107.2] hours, P = 0.04). Hypoglycemia was numerically lower in the HTG-AP-specific insulin infusion group despite higher insulin infusion rates (7.3% vs 19.2%). No patient in the HTG-AP-specific protocol group required plasmapheresis.

The use of an HTG-AP-specific insulin infusion protocol, compared with antecedent nonstandardized care, resulted in prompter achievement of a triglyceride level ≤500 mg/dL and a strong trend toward faster achievement of ≤1000 mg/dL without an increased risk of hypoglycemia. While intravenous insulin may be considered the initial medical therapy for HTG-AP, further studies are needed to determine the optimal dosing.

Thyroid hormones affect lipid metabolism via central and peripheral regulation. However, there have been few studies on the association between thyroid hormone sensitivity and dyslipidemia. We aimed to investigate the association between thyroid hormone sensitivity and dyslipidemia in patients with coronary heart disease (CHD).

A total of 31,678 patients with CHD were included in this large multicenter retrospective study. Central thyroid hormone sensitivity was evaluated using the thyroid feedback quantile-based index (TFQI), parametric thyroid feedback quantile-based index (PTFQI), thyroid-stimulating hormone index (TSHI), and thyrotropin thyroxine resistance index (TT4RI); peripheral thyroid hormone sensitivity was assessed by the ratio of free triiodothyronine (FT3)/free thyroxine (FT4). Logistic regression analysis was used to analyze the association between thyroid hormone sensitivity and dyslipidemia.

Among 31,678 participants, 21,648 (68.34%) had dyslipidemia. In the multi-adjusted models, the risk of dyslipidemia was positively correlated with TFQI (odds ratio [OR]: 1.04; 95% confidence interval [CI]: 1.03-1.05), PTFQI (OR: 1.09; 95% CI: 1.06-1.12), TSHI (OR: 1.08; 95% CI: 1.06-1.11), and TT4RI (OR: 1.08; 95% CI: 1.05-1.11). Conversely, the risk of dyslipidemia was negatively correlated with FT3/FT4 (OR: 0.94; 95% CI: 0.92-0.97). In stratified analyses, the association between thyroid hormone sensitivity and dyslipidemia was statistically significant for different sexes, glucose levels, and blood pressure states.

There is a significant association between sensitivity to thyroid hormones and dyslipidemia, regardless of sex, glucose level, or blood pressure. Graphical abstract.

Hypertriglyceridemia is associated with significant morbidity during pregnancy. Hypertriglyceridemia-induced pancreatitis (HTGP) is associated with genetically determined dyslipidemia or a secondary condition such as diabetes, alcohol, pregnancy, or medication use. The lack of data on the safety of drugs to be used to decrease triglyceride levels during pregnancy dictates that other strategies must be chosen.

We describe a case of a pregnant woman with severe hypertriglyceridemia treated with two different techniques of plasmapheresis (Dual Filtration apheresis and Centrifugal Plasma Separation).

The patient could be treated throughout the pregnancy, with good control of the triglycerides, and a healthy baby was born.

Hypertriglyceridemia is a major issue during pregnancy. The use of plasmapheresis is a safe and efficient tool in that clinical scenario.

We describe and discuss the safety of statins and non-statin drugs in neuromuscular disorders (NMDs). We also propose a pragmatic model of care for the management of such cases.

Patients with both NMD and hypercholesterolemia may be particularly disadvantaged owing to the toxic effects of cholesterol-lowering therapy and the inability to take medication. Specifically, the management of hypercholesterolemia in patients with NMD is complicated by the increased risk of statin-related myotoxicity and concerns that statins may aggravate or possibly induce the onset of a specific NMD. The most severe form of statin-related myotoxicity is immune-mediated necrotizing myopathy. Management of hypercholesterolemia in patients with NMDs include treating modifiable factors, consideration of toxicity risk of statin, use of non-statin lipid lowering agents, noting possible drug interactions, and careful monitoring.

This paper aimed to comprehensively evaluate the effectiveness and safety of Inclisiran in treating hyperlipidemia through an overview of systematic reviews (SRs).

The Cochrane Library, EMBASE, PubMed, CNKI, WANGFANG database, VIP database, ClinicalTrials.gov, and ICRT were searched electronically to collect SRs and meta-analysis of Inclisiran in hyperlipidemia treatment from the establishment of the database till May 2022. Two researchers independently screened the relevant literature, then the assessment of multiple systematic reviews tool was made into assess the methodological quality of the included studies. Data extracted were used to perform the study through RevMan5.3 software. The grading of recommendations assessment, development, and evaluation tool was used to grade the quality of the evidence of the outcomes included in the SRs. Prospero ID: CRD 42022326845.

A total of 10 relevant SRs were included, involving 7 randomized controlled trials. The assessment results of the assessment of multiple systematic reviews tool suggested that the quality of the SRs included needed to be improved. The reduced level of low-density lipoprotein cholesterol of the experimental group was lower than the control group, and the difference in the amount of effectiveness was statistically significant (MD = -50.13, 95%CI: -56.2 to -44.06, P < .00001). The grading of recommendations assessment, development, and evaluation results showed that out of 27 outcomes, 8 were high-quality, 3 were of medium quality, 6 were of low quality, and 10 were of the most inferior quality.

300mg Inclisiran with 2 injections a year has the best therapeutic effect, which can significantly reduce low-density lipoprotein cholesterol and total cholesterol, and increase high-density lipoprotein cholesterol levels in patients with hyperlipidemia. Inclisiran has a favorable safety profile, with no significant difference in the incidence of adverse reactions compared to a placebo. Most of the adverse effects were associated with the reaction on the injection site.