Atherosclerosis is a primary cause of vascular disease worldwide, resulting in diverse clinical manifestations that contribute to significant morbidity and mortality. It is widely recognized as a multifactorial condition involving both metabolic and oxidative mechanisms.The initiation of atherosclerotic plaques arises from endothelial injury caused by excess lipid-carrying lipoproteins, which trigger an exaggerated pro-inflammatory response.This response is mediated by proteins such as galectin-3 (Gal-3), secreted by monocytes and macrophages, which stimulate and accelerate plaque formation. Because of its largely asymptomatic progression, atherosclerosis remains difficult to diagnose. In recent years, clinical and preclinical research on Gal-3 has expanded considerably, revealing elevated Gal-3 levels in patients with atheroma. Moreover, preclinical studies demonstrate that Gal-3 inhibition or gene suppression can effectively attenuate the development of atherosclerosis.These findings highlight the involvement of monocytes, macrophages, foam cells, and Gal-3 in the initiation and progression of the disease. Consequently, Gal-3 has emerged as a promising biomarker for endothelial dysfunction and other cardiovascular conditions.This review therefore summarizes current evidence on the role of Gal-3 in the pathogenesis, clinical features, diagnosis, treatment, and prognosis of atherosclerosis, while also encouraging discussion of Gal-3 as a potential therapeutic strategy.

Lipoprotein(a) [Lp(a)] is a genetically determined risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis (CAVS), with plasma levels largely unaffected by lifestyle modification or conventional lipid-lowering therapy. Although international guidelines increasingly recognize Lp(a) as a risk-enhancing factor, in many Asian populations thresholds for high Lp(a) and treatment strategies remain undefined.This Korean position paper, developed by the Lp(a) Task Force of the Korean Society of Lipid and Atherosclerosis, presents an evidence-based summary of the pathophysiology, clinical relevance, and therapeutic landscape surrounding Lp(a), with a focus on Koreanspecific data. It reviews the genetic architecture of Lp(a), ethnic variability in concentrations, and its mechanistic roles in inflammation, thrombosis, and calcification. Based on large Korean cohorts, a 3-tiered classification is proposed of normal (<30 mg/dL), borderline high (30–49 mg/dL), and high (≥50 mg/dL), harmonizing global thresholds with local data. The document also highlights the limitations of current Lp(a) assays in Korea, and calls for standardized, isoform-insensitive testing. Novel therapeutics, including antisense oligonucleotides, small interfering RNAs, and small molecular inhibitors, have shown promising Lp(a)-lowering effects, with multiple phase 3 trials currently ongoing, or in planning. Given the unmet clinical need, the paper recommends incorporating Lp(a) into cardiovascular risk assessment, and calls for Korean-specific longitudinal studies, national screening strategies, and participation in clinical trials. These efforts will help clarify Lp(a)-associated risk in Korean patients and guide the adoption of future targeted therapies.

Coronary artery bypass grafting (CABG) is the standard-of-care surgical treatment for patients with advanced coronary artery disease, particularly those with triple-vessel or left main coronary artery involvement. Over the years, refinements in surgical technique have led to higher success rates and improved outcomes. However, the rapid progression of atherosclerosis in native coronary arteries following CABG remains a persistent concern.Although several studies have documented this phenomenon, the exact pathophysiological processes involved are not yet fully understood. Additionally, the options for further treatment in these patients continue to pose challenges for physicians. In this review, we discuss various studies that have evaluated this phenomenon and its clinical implications, along with the proposed underlying mechanisms. Potential strategies for managing atherosclerosis following CABG are also explored.

Objective: Lipid-lowering drugs are known to cause various muscle-related side effects;however, it remains unclear whether their use contributes to reduced muscle mass and sarcopenia. This study aimed to evaluate the association between the use of lipid-lowering drugs and both muscle mass and the prevalence of sarcopenia. Methods: We conducted a cross-sectional analysis using data from 18,668 adults aged ≥20 years from the Korea National Health and Nutrition Examination Survey 2008–2011.Sarcopenia was defined based on appendicular skeletal muscle mass (ASM), measured using dual-energy X-ray absorptiometry. The association between hyperlipidemia medication and the prevalence of sarcopenia was estimated using complex samples logistic regression. Results: Patients with hyperlipidemia exhibited lower ASM/wt than those without hyperlipidemia. After adjusting for potential confounders, including current lipid profiles, ASM/wt did not differ significantly between the general population and hyperlipidemic patients not receiving medication. However, individuals taking lipid-lowering drugs demonstrated significantly lower ASM/wt. This trend was mirrored in sarcopenia prevalence, with odds ratios of 2.89 (95% confidence interval [CI], 1.95–4.28) in men and 1.68 (95% CI, 1.26–2.24) in women (p<0.01 for both). Notably, only participants on lipid-lowering drugs showed a progressive decline in ASM/wt and an increased risk of sarcopenia with longer duration of hyperlipidemia. Conclusion These results suggest that the use of lipid-lowering drugs may contribute to a decrease in muscle mass and a higher risk of sarcopenia. However, the generalizability of these results is limited, and further longitudinal studies are required to confirm the association.

Objective: Vascular inflammation contributes to the development of many chronic human diseases. Inflammatory stimuli such as interleukin (IL)-1β or disturbed blood flow trigger endothelial activation, thereby promoting leukocyte recruitment and transmigration through inflammatory signaling pathways. This study aimed to identify novel compounds capable of blocking vascular inflammation, with potential therapeutic applications in vascular inflammatory diseases such as atherosclerosis. Methods: A natural compound library was screened to identify drug candidates that inhibit IL-1β-induced endothelial inflammation. The anti-inflammatory effects of tigloylgomisin P, one of the hit compounds, were examined in bovine aortic endothelial cells stimulated with IL-1β or oscillatory (disturbed) flow. Endothelial inflammation was assessed by measuring nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) phosphorylation and nuclear translocation, monocyte adhesion to endothelial monolayers, and Smad1/5/9 phosphorylation in vitro. Vascular inflammation in vivo was evaluated in aortas of apolipoprotein E (ApoE) knockout mice treated with tigloylgomisin P using immunohistochemistry. Results: Tigloylgomisin P suppressed IL-1β-induced NF-κB activation and reduced monocyte adhesion. In addition, it inhibited oscillatory shear stress-induced endothelial inflammation mediated by NF-κB activation and Smad1/5/9 phosphorylation. In ApoE knockout mice, administration of tigloylgomisin P decreased inflammatory marker expression in the atheroprone inner curvature of aortic arches. Conclusion These findings suggest that tigloylgomisin P may represent a potential therapeutic agent for vascular inflammatory diseases such as atherosclerosis.

In familial chylomicronemia syndrome (FCS), a rare lipid disorder, triglycerides rise to extremely high levels because of the inability to utilize lipoprotein lipase (LPL) for fat metabolism. Traditional triglyceride-lowering medications are ineffective, leaving patients dependent on strict low-fat diets. This review examines emerging non-LPL-based therapies for FCS. This narrative review assessed therapeutic strategies targeting key regulators of triglyceride metabolism, including apolipoprotein C-III (APOC3) and angiopoietin-like protein 3 (ANGPTL3), in both animal and human studies. Investigational approaches included monoclonal antibodies, RNA-based therapies, gene therapy modalities, genome editing platforms, and plasmapheresis. Olezarsen effectively lowers triglycerides with greater safety than older options. Other agents, such as ANGPTL3 inhibitors and RNA interference therapies, also reduce lipids and provide additional treatment options. Gene therapy and clustered regularly interspaced short palindromic repeats (CRISPR)-associated protein 9 approaches are expected to become available in the near future, while plasmapheresis remains an intervention for acute pancreatitis. Innovative therapies targeting APOC3, ANGPTL3, or liver-specific genes are transforming the management of FCS. These advances not only address this rare disorder but also offer insights into treating triglyceride-related cardiovascular risk and lipid abnormalities. Although some uncertainties remain, the outlook for FCS therapy appears highly promising.

Objective: This systematic review and meta-analysis of observational studies aimed to update the evidence regarding the association between dietary factors and cardiovascular disease (CVD) and related outcomes in the Korean population. Methods: In total, 151 studies were included: 62 from a previous study and 89 identified through an updated search in PubMed and Embase. A random-effects model was applied to analyze pooled relative risks (RRs) and their 95% confidence intervals (CIs) for the consumption of 19 food items, 5 macronutrients, 14 micronutrients, 18 dietary indices, and 2 dietary patterns. Results: Overall, higher fruit intake was associated with a lower risk of elevated blood pressure (BP)/hypertension (RR, 0.74; 95% CI, 0.65-0.84) and elevated/high triglycerides (TG) (RR, 0.82; 95% CI, 0.71–0.95). Higher vegetable intake was associated with a lower risk of elevated/high TG (RR, 0.92; 95% CI, 0.87–0.97). Inverse associations were observed between higher milk and dairy consumption and elevated BP/hypertension (RR, 0.89; 95% CI, 0.83–0.95), elevated/high TG (RR, 0.82; 95% CI, 0.76–0.89), and lower high-density lipoprotein cholesterol (HDL-C) levels (RR, 0.82; 95% CI, 0.75–0.89). Coffee consumption was inversely associated with the risk of CVD (RR, 0.80; 95% CI, 0.67–0.95) and elevated/ high TG (RR, 0.84; 95% CI, 0.79–0.89). Consumption of sugar-sweetened beverages was positively associated with an increased risk of elevated BP/hypertension (RR, 1.21; 95% CI, 1.09–1.33) and elevated/high TG (RR, 1.20; 95% CI, 1.03–1.41). Conclusion This study suggests that higher intake of fruits, vegetables, milk and dairy, and coffee may confer potential benefits for CVD and its associated risk factors, such as BP and lipid profiles. In contrast, sugar-sweetened beverages appear detrimental to cardiovascular health.

Any dysfunction or obstruction in blood circulation can lead to the development of cardiovascular disease (CVD), which is multifactorial but primarily caused by atherosclerosis.Nutrition is considered as the most significant modifiable environmental factor, with a direct influence on cardiovascular risk mediated by triggering inflammation, oxidative stress, and various physiological, molecular, and biological changes. Despite these well-established mechanisms, targeting nutrition has not led to the expected reduction in CVD mortality rates. This discrepancy is thought to be due to interindividual variability in genetic factors that modulate responses to nutritional interventions. Genetic variants can interact with specific nutrients and dietary components, influencing their effects on cardiovascular health.Advances in nutrigenetics and nutrigenomics which explore nutrient-gene interactions, have led to the development of the concept of personalized nutrition. This approach aims to prevent CVD and other diseases by tailoring dietary treatments to individual genotypes identified through genetic polymorphisms. It is suggested that life expectancy and sustainable healthy living can be enhanced by aligning dietary treatments with specific genetic profiles associated with CVD. Therefore, this review discusses genes linked to CVD and explores how gene-driven differences in dietary responses affect cardiovascular health outcomes.

Objective: Hypertriglyceridemia (HTG), often but not always coexists with type 2 diabetes mellitus (T2DM). Both independently increase the risk of vascular complications, with inflammation serving as the underlying pathology. T-regulatory (Treg) cells, identified as CD4+CD25+forkheadbox-P3(FoxP3)+ cells, mitigate inflammation through secretion of interleukin(IL) 10. We investigated markers of Treg cell function in patients of T2DM with and without HTG. Methods: Patients with T2DM were divided into 2 groups: T2DM with normal triglyceride (TG) levels (n=30), designated as (DNT) and T2DM with HTG (n=30) designated as (DHTg).Expression of the FOXP3 and IL-10 genes were evaluated using quantitative polymerase chain reaction. Serum soluble CD25 (sCD25) levels were measured by enzyme-linked immunosorbent assay. Results: FOXP3 and IL-10 expressions were reduced in DHTg group. Serum sCD25 levels were significantly higher in the DHTg group (p=0.04). FOXP3 and IL-10 expressions correlated positively in both groups. FOXP3 and IL-10 expression were reduced in both DHTg-normal body mass index (NW) and DHTg-overweight and obese (OwO) compared with respective DNT subgroups, although difference was smaller among OwO groups. Conclusion Reduced expression of FOXP3 and IL-10 indicates compromised Treg function in patients with T2DM and HTG. This impairment may contribute to inflammatory stress, thereby increasing the risk of atherosclerosis. Elevated serum sCD25 levels may represent an additional link between TG and immune imbalance. Obesity also appears to influence Treg function, though its precise role remains uncertain. Aggressive management of HTG in T2DM is warranted. Furthermore, Tregs may represent an attractive therapeutic target for mitigating risk of complications.

Objective: We estimated the prevalence of statin intolerance (SI) in a Portuguese primary care population, applying the CLEAR Outcomes trial inclusion criteria. Methods: This retrospective study analyzed electronic health records (EHRs) from the Local Health Unit of Matosinhos, Portugal (from system launch through December 2023).The study included both men and women (postmenopausal, surgically sterile, or using birth control) aged 18–85 years, with a history of atherosclerotic cardiovascular disease (ASCVD) or at high/very-high ASCVD risk, and a low-density lipoprotein cholesterol (LDL-C) level ≥100 mg/dL while receiving lipid-lowering therapies. The index date was defined as the date when each patient met all eligibility criteria. SI (the prescription of ≥2 statins at any dose, or 1 statin at any dose in patients unwilling to try a second statin) was identified through freetext search. Univariate logistic regression analyses were performed. Results: In total, 12,393 patients were eligible for inclusion. SI was observed in 9.6% (n=1,195) of patients, who in December 2023 had a median (1st to 3rd quartiles) age of 73 years (68–78 years) and a median LDL-C of 100 mg/dL (76–129 mg/dL). Most patients were male (55.2%), had ≥3 comorbidities (78.2%), and 42.1% were prescribed a moderateintensity statin. Individuals aged ≥70 years had a higher likelihood of SI (odds ratio [OR], 1.3;95% confidence interval [CI], 1.1–1.4). Women showed a non-significantly higher likelihood of SI (OR, 1.1; 95% CI, 0.9–1.2). Conclusion The prevalence of SI observed in this study is consistent with existing literature and is particularly elevated in older individuals. These findings highlight the need to prioritize alternative therapies for dyslipidemia in this population.