Atherosclerosis plus最新文献

{"title":"Proposed lipidology and preventive cardiology research priorities in Africa; Results of a Delphi survey","authors":"Alexander R.M. Lyons ,&nbsp;Frederick J. Raal ,&nbsp;Brett S. Mansfield ,&nbsp;David Marais ,&nbsp;Neusa P.J. Jessen ,&nbsp;Lambert T. Appiah ,&nbsp;Lilian Mbau ,&nbsp;Bernard Samia ,&nbsp;Ashraf Reda ,&nbsp;Tigist S. Mekonnen ,&nbsp;Albertino Damasceno ,&nbsp;Chala F. Oljira ,&nbsp;Meral Kayikcioglu ,&nbsp;Alberto Zambon","doi":"10.1016/j.athplu.2025.05.003","DOIUrl":"10.1016/j.athplu.2025.05.003","url":null,"abstract":"<div><div>Despite a population of over 1.5 billion, lipidology and preventive cardiology research of African origin is lacking in quantity and impact, and accounts for a small percentage of outputs globally due to limited resources to address the full breadth of unexplored research areas. We therefore conducted a Delphi survey on an expert panel of African clinical investigators to ascertain the proposed areas of priority to provide guidance on the future direction of African research in this field. Round one of the survey generated 58 proposed unanswered questions, and subsequent priority ratings of 1–5 of the proposed questions in two further rounds resulted in 42 priority research questions (PRQs) based on a two-thirds majority rating of 3–5 with 5 being the highest rating. Common themes amongst the 42 PRQs included mostly prevalence and distribution studies on hyperlipidaemia and lipid profiles and their risk of cardiovascular disease with emphasis on atherosclerotic cardiovascular disease, aortic stenosis, coronary artery disease, and acute coronary syndrome. The need for a cardiovascular risk score calculator appropriate for the different, diverse African populations was also emphasised. In conclusion, the results of this Delphi survey highlight a number of unanswered PRQs in lipidology and preventive cardiology in Africa that may be helpful to inform the strategic direction of future studies, education and funding in that underrepresented part of the world based on current priorities and may also have relevance globally.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"61 ","pages":"Pages 18-22"},"PeriodicalIF":1.4,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307523","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":"Association of uric acid with all-cause mortality in acute coronary syndrome patients with T2DM","authors":"Bing-Yang Zhou ,&nbsp;Jian-Jun Yan ,&nbsp;Cui-Ying Zhang ,&nbsp;Qi Zhang ,&nbsp;Hong-Liang Cong ,&nbsp;Le Wang","doi":"10.1016/j.athplu.2025.06.001","DOIUrl":"10.1016/j.athplu.2025.06.001","url":null,"abstract":"<div><h3>Background</h3><div>The specific prognostic value of hyperuricemia for all-cause mortality in patients with concurrent type 2 diabetes mellitus (T2DM) and acute coronary syndrome (ACS) remains unclear, particularly regarding the modifying effect of glycemic control status (HbA1c levels). This study elucidated the uric acid (UA)-mortality association in ACS patients with T2DM and examined this relationship across different HbA1c subgroups.</div></div><div><h3>Methods and results</h3><div>The study included 2265 ACS patients with T2DM who were assigned to four groups based on UA quartiles. During a median follow-up period of 4.4 years, 203 all-cause deaths occurred. Significant positive associations were found in patients with HbA1c level above 7 (Quartile 1 group: Hazard Ratio (HR): 3.215, 95 % confidence interval (CI): 1.525–6.780, p = 0.002; Quartile 3 group: HR: 2.725, 95 % CI: 1.308–5.678, p = 0.007; Quartile 4 group: HR: 3.369, 95 % CI: 1.644–6.905, p = 0.001). Interaction analysis between UA quartiles and HbA1c subgroups showed no statistical significance (p-interaction = 0.648). Restricted cubic splines revealed a J-shaped relationship between UA and all-cause mortality. Kaplan–Meier analysis demonstrated higher event-free survival rates in the Quartile 2 group (log-rank test: p &lt; 0.001).</div></div><div><h3>Conclusions</h3><div>A J-shaped curve characterizes the association between UA levels and all-cause mortality in patients with T2DM and ACS. Patients with an appropriate UA level exhibited better prognosis. Post-hoc analyses revealed stronger point estimates for the prognostic effect of UA in patients with suboptimal glycemic control, although interaction testing did not achieve statistical significance. Further studies with larger subgroup samples are warranted.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"61 ","pages":"Pages 12-17"},"PeriodicalIF":1.4,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144261455","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":"The role and mechanism of PGC-1α in oxLDL-induced ferroptosis of vascular endothelial cells","authors":"Jiao Li ,&nbsp;Pingping He ,&nbsp;Yu Zhang ,&nbsp;Ranzun Zhao,&nbsp;Changyin Shen,&nbsp;Chaofu Li,&nbsp;Weiwei Liu,&nbsp;Zhijiang Liu,&nbsp;Xianping Long,&nbsp;Yan Wang,&nbsp;Bei Shi","doi":"10.1016/j.athplu.2025.05.002","DOIUrl":"10.1016/j.athplu.2025.05.002","url":null,"abstract":"<div><div>Ferroptosis is a regulated form of cell death that is dependent on reactive oxygen species (ROS) and iron metabolism. Ferroptosis can participate in the formation and rupture of atherosclerotic plaque by regulating apoptosis. However, the mechanism of vascular endothelial cells (VECs) ferroptosis in the occurrence and development of atherosclerosis (AS) requires further exploration. Previous studies have shown that peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) can improve mitochondrial dysfunction and apoptosis induced by oxidized low-density lipoprotein (oxLDL), but its specific role in VECs ferroptosis remains unclear. In this study, we found that oxLDL can induce VECs ferroptosis, and mitochondria are key to oxLDL-induced VECs ferroptosis. As a key regulator of mitochondrial function, the protein expression of PGC-1α was lower in oxLDL-treated VECs. Moreover, overexpression of PGC-1α inhibited oxLDL-induced VECs ferroptosis, whereas the role of PGC-1α was affected by its upstream regulatory molecule AMPK in this process. This study explores the new idea of oxLDL-induced VECs ferroptosis mediated by AMPK/PGC-1α to better understand the pathogenesis of vascular lesions caused by high lipid levels and provides a theoretical basis for the early prevention of AS.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"61 ","pages":"Pages 1-11"},"PeriodicalIF":1.4,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144243467","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":"Fucosterol exerts an anti-atherosclerotic action via NF-κB and p38/Erk MAPK signaling pathways","authors":"Tiancheng Liu ,&nbsp;Mengli Zhang ,&nbsp;Xian Wu ,&nbsp;Zhenxing Liu ,&nbsp;Huan Peng ,&nbsp;Feng Gui ,&nbsp;Wen Xiong ,&nbsp;Qijuan Liu ,&nbsp;Guojun Du ,&nbsp;Bo Liu ,&nbsp;Chenchen Zhang ,&nbsp;Junfeng Ma ,&nbsp;Quan Yuan ,&nbsp;Wei Li ,&nbsp;Zhen Chen","doi":"10.1016/j.athplu.2025.05.001","DOIUrl":"10.1016/j.athplu.2025.05.001","url":null,"abstract":"<div><h3>Background</h3><div>Fucosterol is a sterol isolated from brown algae and has various biological properties, such anti-inflammatory and antidiabetic effects. In this study, we investigated the anti-atherosclerosis effects of fucosterol <em>in vivo</em> and <em>in vitro</em>.</div></div><div><h3>Methods</h3><div>ApoE^−/− mice were fed a high fat diet for 12 weeks with or without fucosterol treatment. H&amp;E staining and Oil Red O staining were performed to detect atherosclerotic lesion and lipid content in the aorta of mice. The lipid metabolism indexes in the mouse serum were measured. Macrophage infiltration into the aortic wall was detected using immunohistochemistry of CD68. Human umbilical vein endothelial cells (HUVECs) were treated with 100 μg/mL ox-LDL to establish a cell model of atherosclerosis <em>in vitro</em>. The expression and protein levels of adhesion molecules and inflammatory cytokines in the aorta and HUVECs were measured using RT-qPCR and western blot, respectively. The levels of oxidative stress-related markers in the mouse serum and HUVECs were measured using corresponding detection kits. The effects of fucosterol on the viability and apoptosis of HUVECs were detected using CCK-8 and flow cytometry, respectively. The levels of NF-κB and p38/Erk MAPK pathway-related proteins in HUVECs were assessed by western blot.</div></div><div><h3>Results</h3><div>Fucosterol reduced atherosclerotic plaques and lipid levels in apoE^−/− mice. Fucosterol alleviated macrophage infiltration, inflammatory response, and oxidative stress in apoE^−/− mice. The ox-LDL-induced inflammatory response, oxidative stress, and apoptosis in HUVECs were attenuated by fucosterol. Additionally, fucosterol reduced the expression of proprotein convertase subtilisin/kexin type 9 (PCSK9) in <em>vivo</em> and <em>in vitro</em>. Moreover, the ox-LDL-induced activation of the NF-κB and p38/Erk MAPK signaling in HUVECs was suppressed by fucosterol.</div></div><div><h3>Conclusion</h3><div>The current investigation revealed that fucosterol attenuates atherosclerotic plaques in apoE^−/− mice through the inhibition of hyperlipidemia, inflammation, and oxidative stress.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"60 ","pages":"Pages 51-59"},"PeriodicalIF":1.4,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144131755","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":"Plasma apolipoprotein concentrations and occurrence of cardiovascular events in the general population: an exploratory analysis","authors":"Avedis Torossian ,&nbsp;Annelise Genoux ,&nbsp;Zichun Cai ,&nbsp;Nathan Jolivet ,&nbsp;Mikaël Croyal ,&nbsp;Arsênio Rodrigues Oliveira ,&nbsp;Sébastien Dejean ,&nbsp;Nathalie Viguerie ,&nbsp;Cendrine Cabou ,&nbsp;Bertrand Perret ,&nbsp;Jean Ferrières ,&nbsp;Vanina Bongard ,&nbsp;Laurent O. Martinez","doi":"10.1016/j.athplu.2025.04.003","DOIUrl":"10.1016/j.athplu.2025.04.003","url":null,"abstract":"<div><h3>Background and aims</h3><div>The role of many apolipoproteins in cardiovascular disease (CVD) pathophysiology and their predictive potential remains unclear. This study examined the association between plasma concentrations of a broad panel of apolipoproteins and the occurrence of cardiovascular events in a general population.</div></div><div><h3>Methods</h3><div>A nested case-control study was conducted within a cohort from Southwestern France. Baseline concentrations of apolipoproteins A-I, A-II, A-IV, B100, C-I, C-II, C-III, D, E, H, J, L1 and M were analyzed in 65 cases who experienced a cardiovascular event during the follow-up period, and in 65 controls matched for age and sex (mean age 60.9 ± 10.7 years; 66.9 % men; median follow up 9.3 years for controls, 6.2 years for cases). Baseline correlations were assessed using Spearman's coefficients.</div><div>Logistic regression and partial least squares discriminant analysis (PLS-DA) were used to evaluate associations with the occurrence of cardiovascular events.</div></div><div><h3>Results</h3><div>Concentrations of apolipoproteins A-I, A-IV, C-I, D, H, J and M differed significantly between cases and controls. All expect apoM remained independently associated with cardiovascular events after adjustment for known risk factors. Additionally, PLS-DA revealed that the entire apolipoprotein panel explained 64 % of variance in case-control status with 60 % predictive accuracy, with apolipoproteins D, J, A-IV, H, and C-I contributing the most to group discrimination.</div></div><div><h3>Conclusions</h3><div>This study identifies a novel panel of apolipoproteins (A-I, A-IV, C-I, D, H, and J) whose levels are associated with occurrence of cardiovascular diseases, independently of traditional risk factors. Further research is needed to confirm these findings and explore underlying mechanisms.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"60 ","pages":"Pages 35-42"},"PeriodicalIF":1.4,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144069266","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":"Association of dietary preferences with cardiovascular disease: a Mendelian randomization study","authors":"Mia D. Lee ,&nbsp;Benjamin F. Voight","doi":"10.1016/j.athplu.2025.04.002","DOIUrl":"10.1016/j.athplu.2025.04.002","url":null,"abstract":"<div><h3>Background and aims</h3><div>Susceptibility to cardiovascular disease (CVD) is driven by genetic and environmental risk factors. Diet is a modifiable and largely environmental risk factor for CVD. Genetic factors associated with a variety of dietary preferences revealed via recent genome-wide association studies (GWAS) allow further investigate the role of diet in liability to disease that has been limited to observational and epidemiologic studies with mixed findings.</div></div><div><h3>Method</h3><div>We obtained publicly available genome-wide association data for 38 dietary preference traits and seven common CVDs to investigate causal hypotheses between diet as the exposure to CVD as outcomes using the statistical framework of Mendelian randomization (MR) for hypothesis testing and sensitivity analyses. We also conducted mediation analyses to evaluate the effects of dietary preferences on CVDs to elucidate potential causal graphs and estimate the effects of dietary preferences mediated by potential mediators.</div></div><div><h3>Results</h3><div>Across all methods, we identified 10 significant causal effects, which included eight dietary preferences across three CVD endpoints (Bonferroni-corrected P &lt; 1.88 × 10⁻⁴). In sensitivity MR and mediation analysis, we observed that obesity - quantified by body mass index (BMI) - was a common mediator that contributed to many of these observed effects. We also found that educational attainment was an exclusive, additional mediator for the effect of preference for muesli with risk to peripheral artery disease (PAD).</div></div><div><h3>Conclusions</h3><div>Our results provide genetic evidence for a link between diet and CVD that aligns with obesity-mediated risk of CVD in individuals in relation to their specific preferences for food.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"60 ","pages":"Pages 43-50"},"PeriodicalIF":1.4,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144107075","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":"Trends of atherosclerosis-related mortality in adults with diabetes: A cross-sectional analysis of U.S. national data","authors":"Yusuf Hasan Ali ,&nbsp;Fakhar Latif ,&nbsp;Fatimah Hoda ,&nbsp;Azeem Hassan ,&nbsp;Huda Ahmed ,&nbsp;Raheel Ahmed ,&nbsp;Vikash Jaiswal","doi":"10.1016/j.athplu.2025.04.001","DOIUrl":"10.1016/j.athplu.2025.04.001","url":null,"abstract":"<div><h3>Background</h3><div>Diabetes mellitus is a rapidly growing global health issue, projected to affect 643 million adults by 2030. Atherosclerosis, a prevalent complication of diabetes, significantly contributes to morbidity and mortality among affected individuals. This study aimed to analyze mortality trends associated with atherosclerosis in diabetic patients aged ≥45 years, with particular focus on variations by sex, race, urban-rural classification, and geographical regions in the US from 1999 to 2020.</div></div><div><h3>Methods</h3><div>We conducted a study using data from the CDC WONDER database, identifying atherosclerosis-related deaths in diabetic patients. We calculated age-adjusted mortality rates (AAMRs) per 100,000 population and analyzed trends over time using Joinpoint regression to assess annual percentage changes (APC) and average annual percentage changes (AAPC).</div></div><div><h3>Results</h3><div>A total of 674,582 atherosclerosis-related deaths were recorded in diabetic patients from 1999 to 2020, with a higher prevalence in men (57.40 %). The majority of deaths occurred in NH White individuals (81.70 %). Overall, AAMRs declined from 32.8 in 1999 to 25.8 in 2020. A significant decrease was observed from 1999 to 2014 (APC: −2.61, p &lt; 0.05), followed by stability (2014–2018) and a subsequent rise (APC: 6.97, p &lt; 0.05) till 2020. Sex-stratified analysis indicated persistently higher AAMRs in men, with a significant increase from 2018 to 2020 (APC: 7.33, p &lt; 0.05). Racial disparities were evident, with NH Black individuals demonstrating the highest AAMRs. Geographic analysis revealed higher AAMRs in nonmetropolitan areas, with notable state-level variations. All census regions exhibited an initial decline, followed by a significant rise in AAMRs post-2018 (p &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>Despite initial declines, recent trends indicate a resurgence in atherosclerosis-related mortality among diabetic patients, particularly in specific racial groups, rural areas, and certain regions. These findings underscore the need for targeted interventions to address disparities and improve cardiovascular outcomes in diabetic populations.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"60 ","pages":"Pages 27-34"},"PeriodicalIF":1.4,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143935996","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":"ApoE [−/−] CA1-overexpressing knock-in mice aggravated atherosclerosis by increasing M1 macrophages","authors":"Jinbao Zong ,&nbsp;Changyuan Wang ,&nbsp;Hongji Zhou ,&nbsp;Yu Song ,&nbsp;Kehua Fang ,&nbsp;Xiaotian Chang","doi":"10.1016/j.athplu.2025.03.003","DOIUrl":"10.1016/j.athplu.2025.03.003","url":null,"abstract":"<div><h3>Background</h3><div>Carbonic anhydrase I (CA1) has been reported to be a diagnostic and therapeutic target for atherosclerosis (AS). This study aimed to verify the essential role of CA1 in AS progression in CA1-overexpressing mice.</div></div><div><h3>Methods</h3><div>A ApoE [−/−] CA1-overexpressing knock-in mouse model was constructed via CRISPR/Cas9-mediated genome engineering. AS was then induced in these transgenic mice via the administration of a high-fat diet, and a second group simultaneously received treatment with methazolamide (MTZ), a carbonic anhydrase inhibitor.</div></div><div><h3>Results</h3><div>Compared with ApoE [−/−] mice without CA1 overexpression, CA1-overexpressing mice had a greater average body weight, regardless of whether their treatment with MTZ or their AS induction status. Sudan IV, hematoxylin and eosin and Oil Red O staining revealed more plaques and fat deposits in the cardiac aortas of CA1-overexpressing mice than in those of ordinary ApoE−/− mice when AS was induced. Moreover, the atherogenic index; low-density lipoprotein, total cholesterol and triglyceride levels were significantly elevated, and high-density lipoprotein levels were declined in the peripheral blood of CA1-overexpressing mice than in that of ordinary ApoE [−/−] mice, regardless of whether these animals were induced to AS. Immunohistochemistry, <em>Von Kossa</em> staining and fluorescence immunohistochemistry revealed increases in CA1 expression, calcium deposition and M1 macrophages in the aortic tissues of CA1-overexpressing mice with AS. MTZ treatment significantly suppressed AS pathologies in the above experiments.</div></div><div><h3>Conclusion</h3><div>These findings revealed aggravated AS in ApoE [−/−] CA1-overexpressing mice and suggest that CA1 aggravates AS by increasing M1-type macrophages, a proinflammatory macrophage subtype.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"60 ","pages":"Pages 6-19"},"PeriodicalIF":1.4,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143738059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real-world management of hypercholesterolemia in patients after acute coronary syndrome in Greece","authors":"Despoina Massia ,&nbsp;Periklis Giovas ,&nbsp;Nikolaos Papadopoulos ,&nbsp;Georgios Katsimagklis ,&nbsp;Evangelos Pissimisis ,&nbsp;Sotirios Patsilinakos ,&nbsp;Evgenia Pappa ,&nbsp;Giannis Baltogiannis ,&nbsp;Nikolaos Kouremenos ,&nbsp;Christos Dontas ,&nbsp;Evangelos Liberopoulos","doi":"10.1016/j.athplu.2025.03.002","DOIUrl":"10.1016/j.athplu.2025.03.002","url":null,"abstract":"<div><h3>Background</h3><div>Prompt initiation of lipid-lowering therapy (LLT) following acute coronary syndrome (ACS) is crucial for preventing secondary cardiovascular events. However, there are gaps in clinical implementation of the 2019 ESC/EAS guideline-recommended low-density lipoprotein cholesterol (LDL-C) goal of &lt;55 mg/dL in patients post-ACS.</div></div><div><h3>Methods</h3><div>This multicenter, real-world, retrospective, 12-month study of adult patients in Greece hospitalized for ACS from September 2019 to November 2022 assessed the attainment of target LDL-C (&lt;55 mg/dL) during the first year post-ACS. Eligible patients had elevated LDL-C at hospitalization (&gt;130 mg/dL if LLT naïve; &gt;100 mg/dL if on statin monotherapy; &gt;70 mg/dL if on a statin plus ezetimibe) and ≥1 LDL-C measurement within 12 months post-ACS.</div></div><div><h3>Results</h3><div>Overall, 212 eligible patients of mean (SD) age 59.9 (±11.1) years were enrolled. Type 2 diabetes and hypertension were reported in 19.8 % (42/212) and 50.9 % (108/212) of patients, respectively. Median (Q1, Q3) LDL-C was 138.0 (106.5, 158.0) mg/dL at hospitalization (n = 212). In patients with LDL-C availability at 12 months posthospitalization (n = 197), median (Q1, Q3) LDL-C was 64.0 (53.0, 76.0) mg/dL, with 27.9 % of patients (55/197) attaining LDL-C &lt;55 mg/dL. Although 73.9 % of patients (199/212) were discharged from the hospital on statin monotherapy, 50 % of patients (106/212) were receiving statin-ezetimibe LLT and 1.4 % (3/212) were receiving statin-ezetimibe-PCSK9 inhibitor LLT 12 months posthospitalization.</div></div><div><h3>Conclusion</h3><div>LDL-C goal attainment is suboptimal in the first year after ACS hospitalization in Greece, indicating an unmet need to improve the treatment of patients with hypercholesterolemia during the post-ACS period by optimizing lipid management through earlier LLT intensification.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"60 ","pages":"Pages 20-26"},"PeriodicalIF":1.4,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143746184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A male patient with pseudoxanthoma elasticum caused by isodisomy of chromosome 16 containing a nonsense variant of the ABCC6 gene: A quarter-century treatment experience","authors":"Minoru Wakasa ,&nbsp;Chihiro Nakagawa ,&nbsp;Taka-aki Takamura ,&nbsp;Kosuke Fujibayashi ,&nbsp;Hironobu Akao ,&nbsp;Michihiko Kitayama ,&nbsp;Akira Shimizu ,&nbsp;Yo Niida ,&nbsp;Kouji Kajinami","doi":"10.1016/j.athplu.2025.03.001","DOIUrl":"10.1016/j.athplu.2025.03.001","url":null,"abstract":"<div><div>Pseudoxanthoma elasticum (PXE) is a rare autosomal recessive disorder characterized by fragmentation and calcification of the elastic fibers of the skin, eyes, and various arteries with highly variable clinical expression. PXE is predominantly caused by pathogenic variants of the <em>ABCC6</em> gene, which encodes the ABCC6 efflux transporter; however, the precise mechanism responsible for clinical manifestation remains unclear. We herein report the case of a male patient with PXE with premature coronary stenosis as his first presentation requiring catheter intervention, in association with typical ocular and skin lesions; the latter was confirmed histologically. A molecular analysis revealed an isodisomy of 6.8 Mb in the 16p13.11 region containing the nonsense mutation p.(Gln199Ter) in the <em>ABCC6</em> gene. We also describe the 25-year clinical course of this case, while focusing on cardiovascular lesions.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"60 ","pages":"Pages 1-5"},"PeriodicalIF":1.4,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143696213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}