Atherosclerosis plus最新文献

{"title":"LDL-C lowering in patients treated with bempedoic acid in a real-world cohort","authors":"James Nelson ,&nbsp;LeAnne Bloedon ,&nbsp;Dave Lewandowski ,&nbsp;Muthiah Vaduganathan ,&nbsp;Maryam Ajose ,&nbsp;Mac Bonafede ,&nbsp;Evelyn Sarnes","doi":"10.1016/j.athplu.2026.01.007","DOIUrl":"10.1016/j.athplu.2026.01.007","url":null,"abstract":"<div><h3>Background</h3><div>Elevated low-density lipoprotein cholesterol (LDL-C) is directly associated with cardiovascular disease, with the risk level determined by the magnitude and duration of exposure. In routine practice, there are limited data on the expected LDL-C lowering with bempedoic acid (BA) alone or in combination with ezetimibe (BA + EZE).</div></div><div><h3>Methods</h3><div>Patients initiating BA or BA + EZE were identified in the Veradigm Network EHR linked to claims (index). LDL-C levels were evaluated at baseline, 3, 6, and 12 months. To further examine BA and BA + EZE efficacy, patients were stratified by background statin use (12 months pre-index) and by continuous index therapy use (no therapy gap &gt;45 days).</div></div><div><h3>Results</h3><div>Of the 900 BA and 615 BA + EZE patients identified, median baseline LDL-C was 137 mg/dL and 127 mg/dL, respectively. By 3 months, BA (21%) and BA + EZE (33%, <em>p</em> &lt; 0.0001 for both) were associated with significant reductions in median LDL-C levels. At baseline, only 6.3% of BA and 8.5% of BA + EZE patients had LDL-C &lt;70 mg/dL; by 3 months, this increased to 16.8% and 33.3%. Over 12 months, 18.0% and 27.5% of patients had LDL-C &lt;70 mg/dL. When stratified, the median reductions by 3 months highlighted use of BA and BA + EZE in patients without background statin use (BA: 24.2%; BA + EZE: 36.7%) and with continuous use (BA: 26.1%; BA + EZE: 40.2%).</div></div><div><h3>Conclusions</h3><div>Patients initiating BA and BA + EZE experienced early and sustained LDL-C improvements. The greatest reductions were in patients with continuous use and patients with no evidence of prior statin use, underscoring the importance of long-term adherence and treating patients not on statin therapy.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"63 ","pages":"Pages 58-66"},"PeriodicalIF":2.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147312093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Poecilobdella manillensis ameliorates atherosclerosis by inhibiting endothelial cell pyroptosis","authors":"Chunxia Guo,&nbsp;Yudong Rao,&nbsp;Hao Zhou,&nbsp;Yiran Feng,&nbsp;Ganyu Deng,&nbsp;Lin Yang,&nbsp;Ying Zhang,&nbsp;Xueya Zhang","doi":"10.1016/j.athplu.2025.12.004","DOIUrl":"10.1016/j.athplu.2025.12.004","url":null,"abstract":"<div><h3>Objective</h3><div>Leeches and other herbs may improve atherosclerosis symptoms. This study explores <em>Poecilobdella manillensis</em>'effect on AS.</div></div><div><h3>Methods</h3><div>In vivo used high-fat diet + rabbit carotid balloon injury model, with <em>Poecilobdella manillensis</em> at 0.1, 0.4, 0.8 g/day. In vitro, aortic endothelial cells were treated with ox-LDL to establish AS model, then with animal group sera to assess P.manillensis effects on AS and explore mechanisms.</div></div><div><h3>Results</h3><div>The in vivo findings indicated that P.manillensis is capable of lowering blood lipid levels and exhibiting anti-thrombotic properties. Additionally, P.manillensis significantly alleviated pathological damage and lipid deposition in the common carotid artery, and reduced apoptosis of the common carotid artery smooth muscle cells. Further assays revealed that P.manillensis markedly decreased the levels of PI3K, p-AKT, NF-κB p65, NLRP3, Caspase-1, eNOS, GSDMD, IL-1β, and IL-18. In vitro results demonstrated that serum containing P.manillensis significantly enhanced cell activity and ATP production while decreasing the apoptosis rate, IL-1β, IL-18, LDH, and ROS, PI3K, p-AKT, NF-κB p65, NLRP3, Caspase-1, GSDMD, and ASC levels.</div></div><div><h3>Conclusion</h3><div>Both in vivo and in vitro studies have confirmed that P.manillensis ameliorates endothelial damage and inflammatory responses in AS, with involvement of the PI3K/AKT and NF-κB signaling pathways.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"63 ","pages":"Pages 1-13"},"PeriodicalIF":2.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145754097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to Neural network model outperforms conventional equations in LDL cholesterol estimation: A comparative study of 188,887 Chinese individuals with focus on hypertriglyceridemia [Atherosclerosis Plus, (62), December 2025, Pages 38-46]","authors":"Hao Xue ,&nbsp;Yu Lin ,&nbsp;Youlin Liu ,&nbsp;Lin Li ,&nbsp;Pengzhen Chen ,&nbsp;Mingyang Li ,&nbsp;Ling Ji ,&nbsp;Yong Xia","doi":"10.1016/j.athplu.2026.01.004","DOIUrl":"10.1016/j.athplu.2026.01.004","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"63 ","pages":"Page 43"},"PeriodicalIF":2.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146173597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of abnormal phosphatidylcholine metabolism in endoplasmic reticulum stress-induced carotid artery plaque destabilization","authors":"Qifei Hu ,&nbsp;Haoran Zhang ,&nbsp;Xianwei Wang ,&nbsp;Jiaming Huang ,&nbsp;Xiaohui Jiang ,&nbsp;Mei Li ,&nbsp;Dong Chen","doi":"10.1016/j.athplu.2026.02.001","DOIUrl":"10.1016/j.athplu.2026.02.001","url":null,"abstract":"<div><h3>Background and aims</h3><div>The imbalance of carotid plaque stability is a key cause of acute cardiovascular and cerebrovascular events. Lipid metabolism disorder and endoplasmic reticulum stress (ERS) are both involved in the progression of atherosclerotic plaque. This study aims to reveal the role and molecular mechanism of abnormal phosphatidylcholine metabolism in ERS-induced carotid plaque instability, and to provide theoretical basis for plaque stabilization intervention.</div></div><div><h3><strong>Methods</strong></h3><div>With carotid plaques intima-media specimens as the research object, by HE staining is divided into a stable plaque group (group S) and unstable plaque group (U); The differences of metabolic profiles between the two groups were analyzed by principal component analysis (PCA) and orthogonal partial least squares-discriminant analysis (OPLS-DA). The differential metabolites were screened by cluster heat map and volcano map. Metabolic pathway enrichment analysis and IPA pathway analysis were used to identify key pathways. Finally, Western blot and RT-qPCR were used to verify the protein and mRNA expression levels of key molecules in ERS pathway.</div></div><div><h3>Results</h3><div>Two groups of baseline characteristics have no statistical difference (P &gt; 0.05); PCA and OPLS-DA showed that the metabolic profiles of group S and group U were significantly separated. A total of 198 potential biomarkers were identified. Among them, changes in phospholipid metabolites (including phosphatidylcholine) were significant, and these are the core markers for differentiating plaque stability. Metabolic pathway enrichment analysis showed that glycerophospholipid metabolic pathway was the key core pathway regulating plaque stability. The protein and mRNA expressions of key molecules of ERS pathway (GRP78, ATF6, PERK, CHOP and IRE1) in group U were significantly higher than those in group S.</div></div><div><h3>Conclusion</h3><div>Abnormal metabolism of phosphatidylcholine can drive the transformation of carotid plaques to an unstable phenotype by activating the ER stress (ERS) pathway (especially the PERK/CHOP branch pathway); this study verified the association mechanism between abnormal phosphatidylcholine metabolism and the activation of the ER stress pathway and the occurrence of unstable carotid plaques, providing experimental evidence for the study of the mechanism of unstable carotid plaques and the formulation of targeted clinical intervention strategies<u>.</u></div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"63 ","pages":"Pages 67-76"},"PeriodicalIF":2.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prelamin A accumulation overlaps increased vascular calcification in peripheral artery disease and regulates vascular smooth muscle cells mineralization in diabetes mellitus","authors":"Eduardo Varejão Díaz Placencia ,&nbsp;Elisângela Farias-Silva ,&nbsp;Melissa Regina Fessel ,&nbsp;Maria Claudina de Andrade ,&nbsp;Luciana Simão Carmo ,&nbsp;Cynthia de Almeida Mendes ,&nbsp;Nelson Wolosker ,&nbsp;Alexandre Leme Godoy dos Santos ,&nbsp;Tulio Diniz Fernandes ,&nbsp;Marcel Liberman","doi":"10.1016/j.athplu.2026.01.002","DOIUrl":"10.1016/j.athplu.2026.01.002","url":null,"abstract":"<div><div>This study investigated the mechanistic intersection between aging, diabetes mellitus (DM), and prelamin A accumulation in vascular calcification (VC) progression in patients with peripheral arterial disease (PAD) undergoing lower limb amputation. Arterial segments were collected from amputated PAD patients with (PAD + DM, n = 10) and without DM (PAD, n = 8), as well as from non-vascular amputated patients (CTRL, n = 3). Additional in vivo and <em>in vitro</em> experiments were conducted to investigate early-stages of VC and the impact of insulin resistance on prelamin A accumulation and ZMPSTE24 expression. PAD and PAD + DM patients exhibited greater VC than CTRL patients. Prelamin A accumulation was higher in PAD (6.3 ± 5.0 %) and PAD + DM (10.9 ± 6.4 %) than in CTRL (1.2 ± 1.3 %), while ZMPSTE24 expression was lower in PAD (5.2 ± 2.6 %) and PAD + DM (3.1 ± 3.2 %) than in CTRL (20.0 ± 3.8 %), indicating impaired prelamin A processing. Investigation in a murine VC model, aortae from leptin-deficient ob/ob mice showed increased prelamin A accumulation, independently of calcifying stimulation. Increased prelamin A expression was also observed insulin-resistant ob/ob VSMCs, independently of calcifying stimulation. These findings suggest that aging-related mechanisms, such as prelamin A accumulation, may synergistically contribute to VC progression, particularly in diabetic PAD patients. Targeting prelamin A processing may unveil a potential therapeutic approach to mitigate VC and reduce amputation risk in diabetic PAD patients.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"63 ","pages":"Pages 34-42"},"PeriodicalIF":2.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing Service quality for Homozygous Familial Hypercholesterolaemia (HoFH) in the UK: Insights from a Multi-Centre Survey","authors":"Maryam Ferdousi ,&nbsp;Bilal Bashir ,&nbsp;Raabya Pasha ,&nbsp;Atiqah Aspiyan ,&nbsp;Anoushka Kammath ,&nbsp;Handrean Soran","doi":"10.1016/j.athplu.2025.10.017","DOIUrl":"10.1016/j.athplu.2025.10.017","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"62 ","pages":"Page 9"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145808443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polygenic predisposition to increased LDL-cholesterol concentration and Carotid Artery Intima Media Thickness in childhood and early adulthood","authors":"M. Futema ,&nbsp;T. Ingegneri ,&nbsp;M. Sharifi ,&nbsp;F. Drenos ,&nbsp;S.E. Humphries","doi":"10.1016/j.athplu.2025.10.004","DOIUrl":"10.1016/j.athplu.2025.10.004","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"62 ","pages":"Page 3"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145808510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Introduction of a new stroke lipid specialist nurse to improve lipid optimisation for acute ischaemic stroke patients","authors":"Aravind Udayan ,&nbsp;Lucy Barton ,&nbsp;Soma Banerjee ,&nbsp;Joseph Kwan ,&nbsp;Jaimini Cegla","doi":"10.1016/j.athplu.2025.10.021","DOIUrl":"10.1016/j.athplu.2025.10.021","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"62 ","pages":"Page 11"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145808507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural network model outperforms conventional equations in LDL cholesterol estimation: A comparative study of 188,887 Chinese individuals with focus on hypertriglyceridemia","authors":"Hao Xue ,&nbsp;Yu Lin ,&nbsp;Youlin Liu ,&nbsp;Lin Li ,&nbsp;Pengzhen Chen ,&nbsp;Mingyang Li ,&nbsp;Ling Ji ,&nbsp;Yong Xia","doi":"10.1016/j.athplu.2025.11.003","DOIUrl":"10.1016/j.athplu.2025.11.003","url":null,"abstract":"<div><h3>Background</h3><div>Accurate estimation of low-density lipoprotein cholesterol (LDL-C) is crucial for atherosclerotic cardiovascular disease (ASCVD) risk management. Extensive international validation studies have demonstrated that traditional formulas (Friedewald, Martin/Hopkins, Sampson) often yield significant errors under conditions of extreme hypertriglyceridemia. This study aimed to assess the performance of these conventional formulas in Chinese populations and develop a novel neural network–based LDL-C estimation model [LDL-C(NN)].</div></div><div><h3>Methods</h3><div>In this retrospective study, we analyzed 188,887 lipid profiles—including total cholesterol, triglycerides, high-density lipoprotein cholesterol, and directly measured LDL-C—from Peking University Shenzhen Hospital using Mindray (outpatients, n = 83,731) and Beckman (inpatients, n = 105,156) systems. The test results from the two detection systems are non-overlapping. We used stratified random sampling based on TG levels to select 30,000 profiles from each of the two systems as the training dataset (60,000 profiles in total). Within this training dataset, 70 % of profiles were used for parameter learning, 15 % were used for early-stopping validation, and 15 % were used for post-training testing. The remaining profiles constituted the independent test set for the final performance evaluation (Mindray: n = 53,731; Beckman: n = 75,156). We then compared the performance of LDL-C(NN) with the Friedewald, Martin/Hopkins, and Sampson formulas using correlation coefficient (r), root mean square error (RMSE), Concordance Correlation Coefficient (CCC) and clinical risk stratification accuracy.</div></div><div><h3>Results</h3><div>Compared with directly measured LDL-C, LDL-C(NN) demonstrated higher correlation and lower RMSE than other traditional LDL-C equations in the Mindray system (r = 0.9778, RMSE = 0.1762 mmol/L; vs Friedewald quation: r = 0.8894, RMSE = 0.4783 mmol/L; vs Martin/Hopkins quation: r = 0.9658, RMSE = 0.2463 mmol/L; vs Sampson quation: r = 0.9548, RMSE = 0.2934 mmol/L, particularly patients with high triglycerides (TG levels, 9.03–13.56 mmol/L, neural network Model: CCC = 0.8750, vs Friedewald quation: CCC = 0.3320; vs Martin/Hopkins quation: CCC = 0.7278; vs Sampson quation: CCC = 0.4176). Beckman database shows the same performance. The clinical classification accuracy for LDL-C(NN) reached 87.5 % (Mindray) and 83.4 % (Beckman), surpassing that of other traditional LDL-C equations (66.6–78.7 %).</div></div><div><h3>Conclusions</h3><div>By overcoming the linear assumptions of conventional equations, the neural network–based model significantly improves LDL-C estimation in hypertriglyceridemia (especially≥9.03 mmol/L) and complex lipid profiles, thereby expanding the applicability of traditional formulas, while demonstrating robust performance across multiple analytical systems.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"62 ","pages":"Pages 38-46"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145618037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inclisiran for fast-track lipid-lowering treatment early after an acute coronary syndrome: a pilot study","authors":"Alessandro Lupi ,&nbsp;Martino Baluci ,&nbsp;Simone Persampieri ,&nbsp;Iacopo Perversi ,&nbsp;Davide Presutti ,&nbsp;Alberto Somaschini ,&nbsp;Giovanni Vincenzo Gaudio ,&nbsp;Luigina Guasti ,&nbsp;Marc Ferrini ,&nbsp;Alberto Corsini ,&nbsp;Roberto De Ponti","doi":"10.1016/j.athplu.2025.09.005","DOIUrl":"10.1016/j.athplu.2025.09.005","url":null,"abstract":"<div><h3>Background</h3><div>Elevated low-density lipoprotein cholesterol (LDL-C) after acute coronary syndrome (ACS) significantly increases cardiovascular risk. Timely reduction of LDL-C is crucial, but it takes several weeks to achieve optimal LDL-C levels with standard therapy. Monoclonal antibodies that inhibit PCSK9 have been demonstrated in some small randomised trials to rapidly abate LDL-C levels when used early after hospital admission for ACS. Inclisiran, a PCSK9-inhibiting siRNA, has recently been introduced into clinical practice; however, no information is available about its effectiveness and safety as a fast-track lipid-lowering agent in this clinical context.</div></div><div><h3>Methods</h3><div>We conducted a prospective, real-world study evaluating a fast-track lipid-lowering approach starting inclisiran on top of standard therapy in 16 consecutive ACS patients admitted to our cardiac intensive care unit with a high baseline LDL-C level (147.2 ± 35.7 mg/dL). Patients started inclisiran as add-on therapy as soon as baseline LDL-C levels were available. We assessed LDL-C levels and the mean change of LDL-C at baseline, discharge, 15-day and 30-day follow-up.</div></div><div><h3>Results</h3><div>Inclisiran, added to standard therapy, reduced LDL-C levels to 30.3 ± 13.0 mg/dL at 30-day follow-up. The guideline-recommended LDL-C levels (≤55 mg/dL, ≥50 % reduction) were achieved in 73.3 % of patients at 15 days and in 100 % of patients at 30 days, with no adverse effects.</div></div><div><h3>Conclusion</h3><div>This pilot study shows promise for inclisiran as a novel therapeutic option to improve cardiovascular outcomes in patients with ACS by contributing to achieving an early and sustained reduction in LDL-C levels.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"62 ","pages":"Pages 9-14"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145159687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}