Atherosclerosis最新文献

{"title":"2025 Focused Update of the 2019 ESC/EAS Guidelines for the management of dyslipidaemias.","authors":"François Mach, Konstantinos C Koskinas, Jeanine E Roeters van Lennep, Lale Tokgözoğlu, Lina Badimon, Colin Baigent, Marianne Benn, Christoph J Binder, Alberico L Catapano, Guy G De Backer, Victoria Delgado, Natalia Fabin, Brian A Ference, Ian M Graham, Ulf Landmesser, Ulrich Laufs, Borislava Mihaylova, Børge Grønne Nordestgaard, Dimitrios J Richter, Marc S Sabatine","doi":"10.1016/j.atherosclerosis.2025.120479","DOIUrl":"10.1016/j.atherosclerosis.2025.120479","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"120479"},"PeriodicalIF":5.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lp(a) variability untangled: It's the benchwork, not the biology.","authors":"Elias Björnson","doi":"10.1016/j.atherosclerosis.2025.120477","DOIUrl":"10.1016/j.atherosclerosis.2025.120477","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"120477"},"PeriodicalIF":5.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144844285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Residual cardiovascular risk in CKD: Reevaluating remnant cholesterol and inflammation.","authors":"Haiting Huang, Guirong Dong","doi":"10.1016/j.atherosclerosis.2025.120453","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2025.120453","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"120453"},"PeriodicalIF":5.7,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145079566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipoprotein(a) concentrations and secondary outcomes following first-time acute coronary syndrome: The Multi-Ethnic New Zealand Study of Acute Coronary Syndromes (MENZACS)","authors":"Malcolm E. Legget ,&nbsp;Nikki J. Earle ,&nbsp;Katrina K. Poppe ,&nbsp;Kathryn E. Bradbury ,&nbsp;Anna P. Pilbrow ,&nbsp;Greer Logue ,&nbsp;Yeunhyang Choi ,&nbsp;Gerry Devlin ,&nbsp;Patrick A. Gladding ,&nbsp;Corina Grey ,&nbsp;Wil Harrison ,&nbsp;Kimiora Henare ,&nbsp;Joanna MM. Howson ,&nbsp;Gregory T. Jones ,&nbsp;Andrew J. Kerr ,&nbsp;Thomas Lumley ,&nbsp;Vijaya Pera ,&nbsp;Graeme Porter ,&nbsp;A Mark Richards ,&nbsp;Ralph Stewart ,&nbsp;Robert N. Doughty","doi":"10.1016/j.atherosclerosis.2025.120516","DOIUrl":"10.1016/j.atherosclerosis.2025.120516","url":null,"abstract":"<div><h3>Background and aims</h3><div>Lipoprotein(a) (Lp[a]) is an established predictor of cardiovascular risk but associations with secondary events are less certain, and data on understudied ethnic groups are scarce. This study aimed to assess the association between Lp(a) and secondary events and explore variation in Lp(a) levels by ethnicity in first-time acute coronary syndrome (ACS) patients, to inform future risk prediction models.</div></div><div><h3>Methods</h3><div>The Multi-Ethnic New Zealand Study of Acute Coronary Syndromes (MENZACS) is a longitudinal multi-centre cohort study of 1900 patients enrolled during their ACS admission. Baseline plasma Lp(a) concentrations were measured using an isoform-insensitive assay measured in nmol/L. The primary outcome was a composite of all-cause mortality or cardiovascular readmission, ascertained through national health datasets. Cox regression models were used to assess the association between Lp(a) levels and outcomes, adjusted for clinical risk factors.</div></div><div><h3>Results</h3><div>The mean age was 61 years, 20 % were female, and 73 % were European, 14 % Māori, 5 % Pacific peoples, 4 % Indian and 3 % other ethnicities. Of 1890 alive at discharge, 493 (26 %) experienced the primary outcome over a median follow-up of 4.9 years. Higher Lp(a) levels were associated with increased risk of secondary events. Compared to the lowest quartile (≤7 nmol/L), the adjusted hazard ratio for the highest quartile (&gt;92 nmol/L) was 1.46 (95 %CI 1.12–1.89, p = 0.004). In this ACS cohort, Lp(a) concentrations varied by ethnicity, being highest amongst Indian participants (median 27 nmol/L) and lowest amongst Māori participants (median 12 nmol/L).</div></div><div><h3>Conclusions</h3><div>Elevated Lp(a) concentrations are associated with secondary events following ACS. Further research is needed to define optimal thresholds for increased risk and explore ethnic-specific implications for secondary prevention.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"410 ","pages":"Article 120516"},"PeriodicalIF":5.7,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145079590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Patient perspectives on statin intolerance, attribution of the nocebo effect and use of N=1-interventions: a qualitative focus group study","authors":"Ruben J.M. Mijnster ,&nbsp;Marte F. van der Bijl ,&nbsp;Amber Niesthoven ,&nbsp;Leonieke W. Kranenburg ,&nbsp;P. Hugo M. van der Kuy ,&nbsp;Inge Merkelbach ,&nbsp;Melvin Lafeber ,&nbsp;Jeanine E. Roeters van Lennep","doi":"10.1016/j.atherosclerosis.2025.120514","DOIUrl":"10.1016/j.atherosclerosis.2025.120514","url":null,"abstract":"<div><h3>Background and aims</h3><div>Statin-associated symptoms often occur under therapy, though N=1-interventions suggest most symptoms may not be attributable to the therapy itself and might be related to the nocebo effect. This study explores patient perspectives on statin intolerance, the nocebo effect and factors influencing participation in N=1-interventions.</div></div><div><h3>Methods</h3><div>We conducted qualitative online focus groups among patients with statin intolerance from a university hospital. Collection of data persisted until data saturation was reached. Analysis was performed following the principles of thematic analysis.</div></div><div><h3>Results</h3><div>Eighteen patients (median age 65.5 [IQR 11.5] years; 56 % men) participated in four focus groups. While acknowledging the nocebo effect as a mental construct mainly driven by imagination, none attributed their symptoms to it. Participants cited early symptom onset, severity, initial optimism about statins, and symptom relief after discontinuation as reasons to dismiss the nocebo effect. Barriers to N=1-intervention participation included dissatisfaction with statins, contentment with current therapy, uncertainty about lipid goals during placebo phases, and concerns that short treatment periods might not trigger symptoms. Facilitators included early intervention, altruism, potential health benefits, and research importance. Patients emphasized the need for clear guidance, personalized results, peer comparison, communication on causes beyond the nocebo effect, and therapeutic options for managing symptoms.</div></div><div><h3>Conclusions</h3><div>Statin-intolerant patients perceive the nocebo effect as unrelated to their symptoms and feel inadequately informed. Focus on the neurobiological component of the nocebo effect and introduction of N=1-interventions early in the patient journey combined with personalized information including practical nocebo coping tools can facilitate participation in N=1-interventions.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"409 ","pages":"Article 120514"},"PeriodicalIF":5.7,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145118466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRIM39 reinforces E2-ESR1 signaling through SUMOylation of ESR1 to hinder the progression of aortic dissection","authors":"Deming Zhang ,&nbsp;Di Liu ,&nbsp;Renxi Gong ,&nbsp;Zikang Liu,&nbsp;Yalun Yang,&nbsp;Lizhen Lv,&nbsp;Kuang Xiao,&nbsp;Chenggang Lei,&nbsp;Kun Tian,&nbsp;Qian Zhou,&nbsp;Haiyun Qian,&nbsp;Shengwei Ma,&nbsp;Fenghe Cui,&nbsp;Xianghui Wang","doi":"10.1016/j.atherosclerosis.2025.120513","DOIUrl":"10.1016/j.atherosclerosis.2025.120513","url":null,"abstract":"<div><h3>Background and aims</h3><div>Aortic dissection (AD) is one of the most dangerous and tricky diseases in the field of cardiovascular surgery, severely affecting public health. Recent studies have found that SUMOylation is linked to the pathogenesis of cardiovascular diseases. However, we know very little about the molecular mechanisms of SUMOylation in AD.</div></div><div><h3>Methods</h3><div>Clinical samples of AD and normal aorta were collected for transcriptome sequencing analysis. qPCR and Western blot were utilized to examine the expression of TRIM39 in clinical samples. AD mouse model and cell model were constructed to test the effect of TRIM39 overexpression on the progression of AD. With the help of bioinformatics analysis tools UBIBROWSER, BIOGRID, and GPS-SUMO, the substrate protein ESR1 of TRIM39 was predicted. Combined with CO-IP, we verified whether TRIM39 SUMOylated ESR1 and how SUMOylation affected ESR1 protein.</div></div><div><h3>Results</h3><div>TRIM39 was greatly downregulated in AD samples, and ESR1 is a downstream target protein of TRIM39. <em>In vivo</em> and <em>in vitro</em> experiments revealed that TRIM39 overexpression alleviated the phenotype of AD by changing the contractile phenotype and cell function of aortic smooth muscle cells, and this process depended on the activation of ESR1 by E2. Mechanistically, TRIM39 mediated the SUMOylation of ESR1, thereby enhancing its protein stability and strengthening E2-ESR1 signaling.</div></div><div><h3>Conclusions</h3><div>TRIM39 modifies ESR1 through SUMOylation and enhances its stability, facilitating E2-ESR1 signaling and alleviating AD progression.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"409 ","pages":"Article 120513"},"PeriodicalIF":5.7,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145007486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Repurposing statin treatment for the prevention of gallstone disease","authors":"Søren N. Rønborg ,&nbsp;Faiza Qayyum ,&nbsp;Bo K. Lauridsen ,&nbsp;Ruth Frikke-Schmidt ,&nbsp;Børge G. Nordestgaard ,&nbsp;Mette Christoffersen ,&nbsp;Anne Tybjærg-Hansen","doi":"10.1016/j.atherosclerosis.2025.120507","DOIUrl":"10.1016/j.atherosclerosis.2025.120507","url":null,"abstract":"<div><h3>Background and aims</h3><div>In observational studies, statin treatment has been associated with low risk of gallstone disease (GSD) or cholecystectomy. We tested the hypothesis that genetic variation in <em>HMGCR</em>, mimicking statin treatment, causally lowers risk of GSD and cholecystectomy in the general population.</div></div><div><h3>Methods</h3><div>A drug-target Mendelian randomization analysis was conducted using individual participant data on 101,809 and 375,094 individuals from the Copenhagen General Population Study (CGPS) and the UK Biobank (UKBB), followed for a median 44 and 26 years, respectively, with external validation using summary level data from up to 1,319,534 individuals. The exposure was <em>HMGCR</em> rs12654264A&gt;T, a GWAS variant strongly associated with LDL cholesterol (LDL-C) in the Global Lipids Genetics Consortium. Endpoints were incident GSD and cholecystectomy, with myocardial infarction (MI) as a positive control.</div></div><div><h3>Results</h3><div>Using instrumental variable analysis, a 1 standard deviation (SD) lower LDL-C due to statin treatment was observationally associated with a 21 % and 16 % lower risk of GSD [Odds Ratio (OR) = 0.79(95 % CI:0.66–0.95)]; 0.84(0.78–0.91)] in the CGPS and UKBB, respectively. The corresponding risk of cholecystectomy was lower by 12 % [0.88(0.69–1.11)] and 23 % [0.77(0.71–0.84)] in the CGPS and UKBB, respectively. In meta-analyses, the ORs per 1 SD lower LDL-C via <em>HMGCR</em> were 0.63(0.46–0.86) for GSD and 0.68(0.52–0.88) for cholecystectomy, similar to the OR for MI of 0.75(0.63–0.88).</div></div><div><h3>Conclusions</h3><div>Statin treatment likely causally reduces risk of GSD and cholecystectomy in the general population. Furthermore, lowering LDL-C by statin treatment may be as effective in the prevention of GSD and cholecystectomy as in the prevention of MI.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"409 ","pages":"Article 120507"},"PeriodicalIF":5.7,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145026390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunopeptidomics analysis of human atherosclerosis plaques identifies antigenic drivers of atherosclerosis","authors":"F. Lozano Vigario ,&nbsp;J. Molenaar ,&nbsp;I. Simó Vesperinas ,&nbsp;M. van der zon ,&nbsp;N.S.A. Crone ,&nbsp;M.J.M. de Jong ,&nbsp;E. Hemme ,&nbsp;M.A.C. Depuydt ,&nbsp;L. Delfos ,&nbsp;J. de Mol ,&nbsp;M.N. Bernabé Kleijn ,&nbsp;J.A.H.M. Peeters ,&nbsp;A. Wezel ,&nbsp;H.J. Smeets ,&nbsp;R.T.N. Tjokrodirijo ,&nbsp;A.H. de Ru ,&nbsp;A. Kros ,&nbsp;P.H.A. Quax ,&nbsp;M.R. de Vries ,&nbsp;J. Kuiper ,&nbsp;B. Slütter","doi":"10.1016/j.atherosclerosis.2025.120509","DOIUrl":"10.1016/j.atherosclerosis.2025.120509","url":null,"abstract":"<div><h3>Background and aim</h3><div>Atherosclerosis has an auto-immune component driven by self-reactive T and B cells. Identifying their antigenic drivers may lead to new diagnosis and treatment approaches. Here, we aim to identify immunogenic T cell epitopes derived from atherosclerosis-relevant proteins such as ApoB100 by studying the repertoire of peptides presented by HLA in human plaques.</div></div><div><h3>Methods</h3><div>We used immunopeptidomics to identify peptides presented by HLA-DR molecules from plaques of patients that underwent endarterectomy surgery. We selected a set of 20 peptides derived from ApoB100 and studied the presence and cytokine profile of ApoB100-specific CD4⁺ T cells in peripheral blood mononuclear cells (PBMCs) from atherosclerosis patients.</div></div><div><h3>Results</h3><div>revealed significant CD4⁺ T cell activation in response to these ApoB100 peptides in 22–39 % of the patients, and this T cell response correlated positively with plaque vulnerability. These cells were characterized by production of both pro- and anti-inflammatory cytokines.</div></div><div><h3>Conclusion</h3><div>We show that immunopeptidomics can be a valid approach to new discover antigens in atherosclerosis.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"409 ","pages":"Article 120509"},"PeriodicalIF":5.7,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145004339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated triglycerides are related to higher residual cardiovascular disease and mortality risk independent of lipid targets and intensity of lipid-lowering therapy in patients with established cardiovascular disease","authors":"Pauline C.E. Schuitema ,&nbsp;Frank L.J. Visseren ,&nbsp;Børge G. Nordestgaard ,&nbsp;Martin Teraa ,&nbsp;Manon G. van der Meer ,&nbsp;Ynte M. Ruigrok ,&nbsp;N Charlotte Onland-Moret ,&nbsp;Charlotte Koopal ,&nbsp;the UCC-SMART Study Group","doi":"10.1016/j.atherosclerosis.2025.120411","DOIUrl":"10.1016/j.atherosclerosis.2025.120411","url":null,"abstract":"<div><h3>Background and aims</h3><div>Despite optimal management of low-density lipoprotein cholesterol (LDL-C), substantial residual cardiovascular risk persists in patients with cardiovascular disease (CVD), which may be attributed to other atherogenic lipoproteins. We tested the hypotheses that elevated triglycerides (TGs) are related to higher residual CVD and mortality risk in patients with established CVD, and that such relationships depend on guideline-recommended lipid target achievement, high-density lipoprotein cholesterol (HDL-C) levels, and intensity of lipid-lowering therapy (LLT).</div></div><div><h3>Methods</h3><div>In a prospective cohort study of 9436 patients with manifest CVD, the relationships between log-transformed TG levels and recurrent cardiovascular events and all-cause mortality were analyzed overall using Cox regression models. Subsequently, analyses were stratified by achievement of low-density lipoprotein cholesterol (LDL-C) and non-HDL-C treatment goals, HDL-C levels, and LLT intensity.</div></div><div><h3>Results</h3><div>During a median follow-up of 9.0 years (IQR 4.5–14.1), 2075 recurrent cardiovascular events, 736 myocardial infarctions, 586 strokes, 1231 cardiovascular deaths, and 2729 all-cause deaths occurred. Per 1-unit higher log-TG level, the hazard ratio was 1.17 (95 % CI: 1.07–1.28) for recurrent cardiovascular events, 1.34 (1.16–1.56) for myocardial infarction, 1.10 (0.92–1.30) for stroke, 1.23 (1.09–1.38) for cardiovascular mortality, and 1.12 (1.03–1.21) for all-cause mortality. These hazard ratios did not depend on achievement of LDL-C and non-HDL-C treatment goals, HDL-C levels, or LLT intensity (all <em>p</em> for interaction ≥0.05).</div></div><div><h3>Conclusions</h3><div>Elevated TGs are related to higher residual CVD and mortality risk in patients with established CVD. These relationships were unrelated to guideline-recommended lipid target achievement, HDL-C levels, and LLT intensity.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"408 ","pages":"Article 120411"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144511484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Does statin matter when it comes to Lipoprotein(a) levels?","authors":"Aris P. Agouridis ,&nbsp;Theodosios D. Filippatos ,&nbsp;Christina Kostara ,&nbsp;Michalis S. Kostapanos ,&nbsp;Vasilios Tsimihodimos","doi":"10.1016/j.atherosclerosis.2025.120466","DOIUrl":"10.1016/j.atherosclerosis.2025.120466","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"408 ","pages":"Article 120466"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}