Antiplatelet Therapy in Coronary Artery Disease: Now and Then

Tscharre, Maximilian; Gremmel, Thomas

doi:10.1055/s-0042-1758821

Cited by 5 publications

(3 citation statements)

References 131 publications

(136 reference statements)

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“…Its pathogenesis involves endothelial cell dysfunction, lipid deposition, macrophage activation, and proliferation with the migration of smooth muscle cells [1][2][3] . Current treatments for CHD include pharmacologic therapy drugs, including antiplatelet agents, lipid-lowering agents, and vasodilators, as well as procedures such as percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) [4][5][6] . PCI involves the use of cardiac catheterization to open narrowed or occluded coronary arteries, while CABG involves the use of veins or arteries to bypass narrowed coronary arteries.…”

Section: Introductionmentioning

confidence: 99%

SGK1 contributes to endothelial cell ferroptosis in coronary heart disease through the NEDD4L/NF-κB pathway

Peng,

Jiang,

Zhou

et al. 2024

Preprint

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The prevalence of coronary heart disease (CHD) has increased significantly with the aging population worldwide. It is unclear whether ferroptosis occurs during CHD. Hence, we aimed to investigate the potential mechanisms associated with ferroptosis in CHD. Bioinformatics was used to characterize differentially expressed genes (DEGs) in CHD-related datasets (GSE21610 and GSE66360), and enrichment analysis was performed via protein‒protein interaction (PPI) network analysis. Proteins that interact with SGK1 as predicted by the String database. Flow cytometry and western blot analysis revealed alterations in lipid peroxidation, Fe accumulation, and ferroptosis-related marker expression in MAECs following lentivirus-mediated modulation of SGK1 and NEDD4L expression. A total of 76 and 689 DEGs were involved in pathways associated with immune and inflammatory responses, respectively. DDX3Y, EIF1AY, KDM5D, RPS4Y1, SGK1, USP9Y, and NSG1 showed intersecting DEGs. The differences in the number of circulating endothelial cells (ECs) between healthy individuals and CHD patients are consistent with the results of bioinformatics analysis. SGK1 may interact with NEDD4L and promote NEDD4L and p-P65 expression in MAECs according to the String database. Additionally, SGK1 knockdown alleviated the Erastin-induced downregulation of SLC7A11, GPX4, GSH, and GSSG, as well as the upregulation of lipid peroxidation, Fe accumulation, p-P65 expression, and mitochondrial damage. NEDD4L and PMA (NF-κB pathway activator) were rescued with overexpression. SGK1 contributes to EC ferroptosis by regulating the NEDD4L-NF-κB pathway. SGK1 could be recognized as a therapeutic target related to ferroptosis in CHD.

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Section: Introductionmentioning

confidence: 99%

SGK1 contributes to endothelial cell ferroptosis in coronary heart disease through the NEDD4L/NF-κB pathway

Peng,

Jiang,

Zhou

et al. 2024

Preprint

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“…Aspirin is a fundamental component of antiplatelet therapy and is extensively employed in the management and prophylaxis of cardiovascular and cerebrovascular ailments (7,8). In AF mice, aspirin administration impeded pathological atrial remodeling, mitigated fibrosis, and safeguarded mitochondrial function, thereby leading to a marked decrease in the occurrence of spontaneous AF.…”

Section: Introductionmentioning

confidence: 99%

Association between aspirin and mortality in critically ill patients with atrial fibrillation: a retrospective cohort study based on mimic-IV database

Zhang,

Zuo,

Jiao

2024

Front. Cardiovasc. Med.

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BackgroundAtrial fibrillation (AF) is a prevalent issue among critically ill patients, and the availability of effective treatment strategies for AF is limited.AimThe objective of this study was to evaluate the mortality rate associated with AF in critically ill patients who were either aspirin or non-aspirin users.MethodsThis cohort study incorporated critically ill patients with AF from the Medical Information Mart for Intensive Care database. The study compared incidences of 28-day mortality, 90-day mortality, and 1-year mortality between patients with and without aspirin prescriptions. To assess the association between aspirin and the endpoints, Kaplan-Meier analysis and Cox proportional hazards regression analyses were conducted.ResultsIn this study, a total of 13,330 critically ill patients with atrial fibrillation (AF) were included, of which 4,421 and 8,909 patients were categorized as aspirin and non-aspirin users, respectively. The 28-day, 90-day, and 1-year mortality rates were found to be 17.5% (2,330/13,330), 23.9% (3,180/13,330), and 32.9% (4,379/13,330), respectively. The results of a fully-adjusted Cox proportional hazard model indicated that aspirin use was negatively associated with the risk of death after adjusting for confounding factors (28-day mortality, HR 0.64, 95% CI 0.55–0.74; 90-day mortality, HR 0.65, 95% CI 0.58–0.74; 1-year mortality, HR 0.67, 95%CI 0.6∼0.74). The results of the subgroup analysis indicate a more robust correlation, specifically among patients under the age of 65 and those without a history of congestive heart failure or myocardial infarction.ConclusionsThe utilization of aspirin may exhibit a correlation with a reduction in risk-adjusted mortality from all causes in critically ill patients diagnosed with atrial fibrillation. However, additional randomized controlled trials are necessary to elucidate and confirm this potential association.

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“…Another historical review, this time on antiplatelet therapy, as specifically applied to coronary artery disease (CAD), follows from the team of Tscharre and Gremmel. 14 Cardiovascular disease, particularly CAD, remains the leading cause of mortality and morbidity in industrialized countries. Platelet activation and aggregation at the site of endothelial injury plays a key role in the processes ultimately resulting in thrombus formation with vessel occlusion and subsequent end-organ damage.…”

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confidence: 99%