Ischemic heart disease is a significant risk factor that threatens human health, and antiplatelet drugs are routinely used to treat cases in clinical settings. Chinese medicine for promoting blood circulation and removing blood stasis (PBCRBSCM) can often be combined with antiplatelet drugs to treat ischemic heart disease. PBCRBSCM can inhibit platelet adhesion, activation, and aggregation; moreover, PBCRBSCM in combination with antiplatelet drugs exerts antiplatelet effects. The mechanism is related to several factors, including the inhibition of platelet activation and aggregation, improvement of the hemodynamic status and coagulation function, and correction of metabolism and inflammation. PBCRBSCM can also regulate the absorption and metabolism of conventional antiplatelet drugs and protect the gastric mucosal epithelial cells against damage induced by conventional antiplatelet drugs. Randomized controlled trials have confirmed that PBCRBSCM preparations and the active ingredients in these preparations can reduce resistance to aspirin and clopidogrel so that the combination of these drugs can exert their antiplatelet effects. In the perioperative treatment of patients with stable angina pectoris, unstable angina pectoris, and acute coronary syndrome undergoing percutaneous coronary intervention therapy, preparations of the active ingredients of PBCRBSCM combined with antiplatelet drugs and other conventional Western medicine treatments have been proven effective. The efficacy and safety of such combinations have also been extensively verified. Considerable progress has been made to understand the antiplatelet mechanism of PBCRBSCM. However, most clinical studies had problems, such as limited sample size and inappropriate research design, which has limited the translational use of PBCRBSCM in antiplatelet therapy. A large-scale, multicenter, randomized controlled study with cardiovascular events as the endpoint is still to be conducted to provide evidence for the combined application of PBCRBSCM and antiplatelet drugs in the prevention and treatment of ischemic heart disease.

Although low-density lipoprotein cholesterol (LDL-C) can now be effectively reduced, substantial residual risk of acute ischemic cardiovascular events persists. Lipoprotein(a) [Lp(a)] is an established causal risk factor for atherosclerotic cardiovascular disease (ASCVD), yet its mechanistic links to plaque vulnerability and their clinical implications remain incompletely understood. Clinical imaging studies have associated elevated Lp(a) with plaque progression and features of vulnerability, including lipid-rich necrotic cores, macrophage accumulation, and thin fibrous caps, suggesting that Lp(a)-associated risk may involve destabilization during plaque progression. This review draws on imaging and pathological evidence to examine the potential mechanisms underlying these associations and their implications for clinical risk stratification and preventive decision-making. The apolipoprotein(a) [apo(a)] component unique to Lp(a), together with the oxidized phospholipids (OxPL) it carries, may contribute to plaque vulnerability by sustaining vascular inflammation, promoting necrotic core expansion, and influencing fibrous cap stability and intraplaque neovascularization. Integrating circulating Lp(a) levels with plaque imaging features and baseline cardiovascular risk may help identify individuals at high risk in primary prevention and evaluate residual risk in secondary prevention, informing earlier or more intensive efforts to manage modifiable risk factors. Alongside established preventive measures, therapies aimed at lowering Lp(a) may provide an additional approach to reducing residual risk. In trials conducted to date, substantial reductions in Lp(a) have been observed with antisense oligonucleotides, small interfering RNAs, and oral small-molecule inhibitors; some agents have demonstrated sustained effects and favorable safety profiles. However, whether therapies targeting Lp(a) reduce cardiovascular event risk remains to be established through robust evidence from large cardiovascular outcome trials.

Glucagon-like peptide-1 receptor agonists (GLP-1RAs), initially developed for type 2 diabetes, have demonstrated cardiovascular benefits. However, evidence

Atherosclerosis (AS) is a chronic inflammatory disorder of the medium and large arteries, characterized by lipid accumulation within the arterial wall and a sustained inflammatory milieu, and it remains a leading cause of cardiovascular morbidity and mortality worldwide. Glycolysis and neutrophil extracellular traps (NETs) are both involved in the initiation and progression of AS in part through effects on endothelial function, platelet activation, lipid metabolism, and the inflammatory microenvironment. This article reviews the roles of NETs and glycolysis in AS, elucidates the mechanisms underlying NETosis, and discusses the association between glycolysis and NETosis. Finally, the article discusses the potential value of glycolytic inhibitors in the treatment of AS, with the aim of providing new perspectives for the diagnosis and treatment of AS and related cardiovascular diseases.

Background: Polydatin has shown anti-inflammatory, antioxidant, and cytoprotective effects in preclinical studies. Its development is limited by low oral bioavailability, extensive metabolism, and poorly defined tissue exposure. Objectives: This review summarizes the pharmacology and delivery systems of polydatin, distinguishes nano from non-nano formulations, and examines the evidence for improved exposure, tissue delivery, safety, and clinical translation. Methods: Relevant studies were identified through a structured PubMed search and assessed by formulation type, administration route, comparator, and reported endpoints. Results: Delivery strategies include liposomes, polymeric and polysaccharide nanoparticles, lipid-based formulations, inclusion complexes, solid-state systems, hydrogels, local matrices, and targeted systems. Only a few oral formulations have been compared directly with free polydatin using quantitative pharmacokinetic measurements. Many injectable and local studies report release, cellular uptake, fluorescence distribution, or pharmacodynamic effects, but these findings do not by themselves demonstrate improved bioavailability or drug-specific targeting. Evidence on repeat-dose toxicity, immunogenicity, carrier clearance, and manufacturing consistency remains limited. No clinical study of a polydatin nanocarrier was identified. Conclusions: Further development requires appropriate free-polydatin controls, measurement of polydatin and its metabolites, exposure–response analysis, fuller safety assessment, and reproducible product characterization.