Atherosclerosis plus最新文献

{"title":"Emerging oral therapeutic strategies for inhibiting PCSK9","authors":"Nicola Ferri ,&nbsp;Giorgia Marodin","doi":"10.1016/j.athplu.2024.11.003","DOIUrl":"10.1016/j.athplu.2024.11.003","url":null,"abstract":"<div><div>Pharmacological inhibition of Proprotein Convertase Subtilisin/Kexin 9 (PCSK9) have been firmly established to be an effective approach to reduce low-density lipoprotein (LDL) cholesterol levels and cardiovascular events. Subcutaneous administration of monoclonal antibodies (evolocumab and alirocumab) every 2 or 4 weeks determined a 60 % reduction of LDL cholesterol levels, while the GalNac-siRNA anti PCSK9 (inclisiran) provided an effective lipid lowering activity (−50 %) after an initial subcutaneous dose, repeated after 3 months and followed by a maintenance dose every 6 months. Although these two approaches have the potentiality to bring the majority of patients at high and very-high cardiovascular risk to the appropriate LDL cholesterol targets, their cost and subcutaneous administration represent a strong limitation for their large-scale use. These problems could be overcome by the development of small chemical molecules anti PCSK9 as oral therapy for controlling hypercholesterolemia. In the present review, we summarized the pharmacological properties of oral anti PCSK9 molecules that are currently under clinical development (DC371739, CVI-LM001, and AZD0780), including the mimetic peptides enlicitide decanoate (MK-0616) and NNC0385-0434.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"59 ","pages":"Pages 25-31"},"PeriodicalIF":1.4,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11722601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973585","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":"Familial hypercholesterolemia – Targeted whole gene sequencing as a diagnostic approach","authors":"Emma Adolfsson ,&nbsp;Nils Johan Fredriksson ,&nbsp;Jon Jonasson ,&nbsp;Anna Nordenskjöld ,&nbsp;Anna Green","doi":"10.1016/j.athplu.2024.12.001","DOIUrl":"10.1016/j.athplu.2024.12.001","url":null,"abstract":"<div><h3>Background and aims</h3><div>Familial hypercholesterolemia (FH) and other disorders with similar features are common genetic disorders that remain underdiagnosed and undertreated, due in part to the cost of screening. The aim of this study was to design and implement a whole gene targeted NGS panel for the molecular diagnosis of FH and statin intolerance with an emphasis on high quality variant calling, including copy number analysis.</div></div><div><h3>Methods</h3><div>A whole gene panel for hybridisation-based short read NGS was designed for the dominant FH-genes low density lipoprotein receptor (<em>LDLR</em>), apolipoprotein B (APOB), proproteinconvertas subtilisin/kexin type 9 (PCSK9), apolipoprotein E (APOE) and the recessive FH-genes low density lipoprotein receptor adaptor protein 1 (<em>LDLRAP1</em>), ATP binding cassette subfamily member 5/8 (ABCG5/8) and lipase A, lysosomal acid type (<em>LIPA</em>), as well as solute carrier organic anion transporter family member 1B1 (<em>SLCO1B1</em>), not an FH gene but linked to statin intolerance. Polygenetic risk score markers were also included. The panel was used for screening of a Swedish FH-study population (n = 133).</div></div><div><h3>Results</h3><div>The panel sequencing resulted in high coverage and confident variant calling of included genes. Known causal variants were found in common dominant FH-genes in 43 % of the cohort. Copy number variants were found in <em>LDLR</em> in 10 individuals and a whole gene deletion of <em>SLCO1B1</em> in one individual. In addition, coding variants in recessive genes and rare non-coding intronic and untranslated region variants were found in a large proportion of the study individuals highlighting the need for extended gene panels.</div></div><div><h3>Conclusions</h3><div>This new tool can be used for a comprehensive high-quality molecular genetic analysis according to guidelines for the diagnosis and treatment of FH.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"59 ","pages":"Pages 1-9"},"PeriodicalIF":1.4,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11719334/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973592","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 cross-tissue transcriptome-wide association study identifies WDPCP as a potential susceptibility gene for coronary atherosclerosis","authors":"Xinyue Hu ,&nbsp;Guanglei Chen ,&nbsp;Xiaofang Yang ,&nbsp;Jin Cui ,&nbsp;Ning Zhang","doi":"10.1016/j.athplu.2024.11.002","DOIUrl":"10.1016/j.athplu.2024.11.002","url":null,"abstract":"<div><h3>Background</h3><div>Coronary atherosclerosis (CAS) is a complex chronic inflammatory disease with significant genetic and environmental contributions. While genome-wide association studies (GWAS) have pinpointed many risk loci, over 75 % are in non-coding regions, complicating functional analysis and understanding gene-disease mechanisms.</div></div><div><h3>Methods</h3><div>We conducted a cross-tissue transcriptome-wide association study (TWAS) using data from the GWAS Catalog (16,041 cases, 440,307 controls) and the Genotype-Tissue Expression (GTEx) v8 eQTL dataset. Initially, we used the Unified Test for Molecular Signatures (UTMOST) for analysis, followed by validation with Functional Summary-based Imputation (FUSION) and conditional and joint (COJO) analyses. Candidate genes were further refined using Multi-marker Analysis of Genomic Annotation (MAGMA). Causal relationships were assessed through Summary Data-Based Mendelian Randomization (SMR), colocalization analysis (COLOC), and Mendelian Randomization (MR). GeneMANIA was used to identify interacting genes, and Phenome-Wide Association Study (PheWAS) was employed to enhance the results.</div></div><div><h3>Results</h3><div>UTMOST identified 33 susceptibility genes for CAS. Out of these, 17 met stringent criteria in both UTMOST and FUSION analyses. Combining results from UTMOST, FUSION, and MAGMA, we identified four critical candidate genes. WDPCP was the only gene to pass SMR, COLOC, and MR analyses, confirming its causal role in CAS. GeneMANIA revealed additional interacting genes, and PheWAS validated WDPCP's role as a susceptibility gene.</div></div><div><h3>Conclusion</h3><div>WDPCP is a potential novel susceptibility gene for CAS, influencing endothelial function, lipid metabolism, and coronary artery development. This study extends GWAS findings, highlighting WDPCP's potential as a therapeutic target and its consistent expression across different tissues. Further validation studies are warranted.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"58 ","pages":"Pages 59-74"},"PeriodicalIF":1.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142742945","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 data lipid profiles in one million colombian adults: The LiPAC million person study","authors":"Claudia C. Colmenares-Mejía ,&nbsp;Marcela Godoy-Corredor ,&nbsp;Esteban Morales-Mendoza ,&nbsp;Diego Alejandro Pinto-Pinzón ,&nbsp;José Medardo Rozo-Vanstrahlen ,&nbsp;Jairo Acuña-Olmos ,&nbsp;Liliana Hilarión-Gaitán ,&nbsp;María del Pilar Suarez-Ramos ,&nbsp;Diego Alberto Ruiz-Amaya ,&nbsp;Fredy Rolando Salazar-Heredia ,&nbsp;Johana Vargas-Rodríguez ,&nbsp;Mario A. Isaza-Ruget","doi":"10.1016/j.athplu.2024.11.001","DOIUrl":"10.1016/j.athplu.2024.11.001","url":null,"abstract":"<div><h3>Background and aims</h3><div>Lipid profile results are of clinical interest for assessing the presence of dyslipidemia and the risk of cardiovascular disease. This study aimed to characterize lipid profile parameters in a large adult population from different regions of Colombia.</div></div><div><h3>Methods</h3><div>Cross-sectional study. Adults with a complete lipid profile [TC, c-HDL, non-c-HDL, c-LDL, Triglycerides] from a national reference laboratory between 2018 and 2022 were included. Lipid profile levels are reported as medians and adjusted means and are also presented according to different guideline thresholds. Mixed dyslipidemia frequencies are also reported.</div></div><div><h3>Results</h3><div>1,030,195 subjects were included, with a median age of 49 years (IQR 36–61 years); 59.8 % were females. Adjusted mean value for TC was 188.1 mg/dl (CI95 % 188.0–188.2), 110.1 mg/dl (CI95 % 110.0–110.1) for c-LDL, 45.9 mg/dl (CI95 % 45.9–46.0) for c-HDL, 139.1 mg/dl (CI95 % 139.0–139.2) for non-c-HDL and 129.5 mg/dl (CI95 % 129.4–129.6) for triglycerides. The most frequent single dyslipidemia was c-HDL &lt;40 mg/dL (n = 86,725, 8.4 %), and the most common mixed dyslipidemia was TC ≥ 200 mg/dL + c-LDL &gt;130 mg/dL (n = 138,366, 17.0 %). Elevated c-LDL (≥130 mg/dL) was found in 32.4 % of the population, while c-LDL levels ≥190 mg/dL were observed in 2.0 % (n = 21,045). Triglyceride levels ≥500 mg/dL were identified in 0.3 % (n = 3103).</div></div><div><h3>Conclusion</h3><div>This large study on lipid markers from a selected sample of Colombian adults’ highlights variations in dyslipidemia by gender, age, and region. The findings emphasize the need for targeted interventions to reduce cardiovascular risk. Identifying high-risk groups is essential to improving outcomes in developing countries.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"58 ","pages":"Pages 51-58"},"PeriodicalIF":1.4,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142703592","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 collaborative effort across Africa to investigate risk factors and outcomes of premature acute coronary syndrome: Protocol for the EAS Lipid Registry of Africa (LIPRA)","authors":"Ashraf Reda ,&nbsp;Alexander R.M. Lyons ,&nbsp;Alberto Zambon ,&nbsp;Ahmed Bendary ,&nbsp;Mutaz Al-Khnifsawi ,&nbsp;Habib Gamra ,&nbsp;David Marais ,&nbsp;Okechukwu S. Ogah ,&nbsp;Tigist Seleshi ,&nbsp;Ahmed A.A. Suliman ,&nbsp;Julius C. Mwita ,&nbsp;Albertino Damasceno ,&nbsp;Anastase Dzudie ,&nbsp;Atef Elbahry ,&nbsp;Elsayed Farag ,&nbsp;Chala Fekadu ,&nbsp;Lilian Mbau ,&nbsp;Mohammed Mujahed ,&nbsp;Rosemary P. Minja ,&nbsp;Bernard Samia ,&nbsp;Alexandros Tselepis","doi":"10.1016/j.athplu.2024.10.002","DOIUrl":"10.1016/j.athplu.2024.10.002","url":null,"abstract":"<div><div>Data on acute coronary syndrome (ACS) is lacking in Africa where cases of premature ACS seem to be on the rise. Africa would benefit from an epidemiological assessment of premature ACS to determine its risk factors and management in this demographic to inform guidelines and practice. The European Atherosclerosis Society recognised this urgency and formed a growing network across 11 African countries to create the Lipid Registry of Africa (EAS-LIPRA). This article is based on the EAS-LIPRA protocol and presents the aims, concept and methodological considerations, and the operations and collaborative governance structure of this project. EAS-LIPRA aims to report risk factors and outcomes of premature ACS in Africa to further understand its prevalence and management via collating and pooling multinational prospective data on premature ACS across multiple sites in Africa into a standardised registry. Data will be stratified into subgroups based on country-level income as defined by the World Bank, and within country residence of urban versus rural areas. Valid statistical procedures will be employed to compare and observe trends in the pooled data based on demographics, clinical and laboratory variables, and disparities in its management. Being the first multinational lipid registry in Africa, it is envisaged that the network will expand to other African countries and sites yet to participate, facilitate other epidemiological studies in preventive cardiology, and set a precedent for other developing countries and regions.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"58 ","pages":"Pages 46-50"},"PeriodicalIF":1.4,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142552686","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":"Adherence to the Healthy Nordic Food Index is associated with reduced plasma levels of inflammatory markers in patients with heterozygous familial hypercholesterolemia","authors":"Eirin B. Løvheim ,&nbsp;Kjetil Retterstøl ,&nbsp;Ingunn Narverud ,&nbsp;Martin P. Bogsrud ,&nbsp;Bente Halvorsen ,&nbsp;Thor Ueland ,&nbsp;Pål Aukrust ,&nbsp;Kirsten B. Holven","doi":"10.1016/j.athplu.2024.10.003","DOIUrl":"10.1016/j.athplu.2024.10.003","url":null,"abstract":"<div><h3>Background and aims</h3><div>Familial hypercholesterolemia (FH) is an inherited disease associated with hypercholesterolemia, and dietary treatment is part of the treatment. We aimed to assess the dietary pattern in relation to the Healthy Nordic Food Index (HNFI) in adults with and without heterozygous FH (HeFH), and to examine the associations between dietary quality and biomarkers related to cardiovascular disease in adults with HeFH.</div></div><div><h3>Methods</h3><div>We included 205 adults (≥18 years) with HeFH who received follow-up at the Lipid Clinic in Oslo and compared them to controls (n = 228). Dietary intake was assessed using a food frequency questionnaire and dietary quality was assessed using the HNFI. Blood samples were analysed for levels of blood lipids, plasma fatty acids (FAs), and markers of inflammation and platelet activation.</div></div><div><h3>Results</h3><div>The HeFH patients (median 60 years; 50.2 % female; 25.9 % in secondary prevention) had lower intake of total and saturated fat compared to controls (32.6 energy percent (E%) vs. 34.9 E%, and 9.6 E% vs 12.0 E%, respectively; p &lt; 0.001 for both). In the HeFH patients, increasing dietary quality was associated with increased plasma levels of the n-3 polyunsaturated FAs (PUFAs) eicosapentaenoic acid and docosahexaenoic acid, and the n-6 PUFA linoleic acid, and lower plasma levels of the inflammatory cytokines Tumor Necrosis Factor and interleukin-6, and of the platelet-derived inflammatory cytokines Platelet Factor 4 and Neutrophil-Activating Peptide-2.</div></div><div><h3>Conclusion</h3><div>Norwegian patients with HeFH followed up at a Lipid Clinic eat healthier than controls. Adherence to a healthy dietary pattern is associated with higher plasma levels of n-3 and n-6 PUFA, and lower levels of inflammatory markers, including platelet markers. This may suggest that adherence to an overall healthy dietary pattern might be beneficial for HeFH patients independent of the cholesterol-lowering effect of the diet.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"58 ","pages":"Pages 38-45"},"PeriodicalIF":1.4,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142552685","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":"Efficacy and safety of lipid-lowering therapies in combination with or without statin to reduce the cardiovascular risk: A systematic review of randomised controlled trials","authors":"Gabriella Iannuzzo ,&nbsp;Geetank Kamboj ,&nbsp;Parinita Barman ,&nbsp;Shirish Dongare ,&nbsp;Shantanu Jawla","doi":"10.1016/j.athplu.2024.10.001","DOIUrl":"10.1016/j.athplu.2024.10.001","url":null,"abstract":"<div><h3>Background and aims</h3><div>Cardiovascular diseases (CVD) pose a significant global health burden. Lowering low-density lipoprotein-cholesterol is the primary therapeutic aim for preventing primary and secondary CVD events. While statins are the standard treatments, their limitations, such as side effects and intolerance in certain patient groups, necessitate exploration of alternative lipid-lowering therapies (LLTs). We systematically reviewed randomised controlled trials (RCTs) evaluating cardiovascular outcomes associated with non-statin LLTs (bempedoic acid, alirocumab, evolocumab, ezetimibe, and inclisiran) in adults with CVD or high cardiovascular risk.</div></div><div><h3>Methods</h3><div>EMBASE, Medline, Cochrane Library, and clinical trial registries were systematically searched for eligible studies, from inception until February 08, 2023. Two reviewers independently screened the studies, with discrepancies resolved by a third reviewer. Data extraction and validation were conducted, and the risk of bias was assessed using the Cochrane Risk-of-Bias tool-2 for RCTs.</div></div><div><h3>Results</h3><div>The search strategy yielded 2104 citations. Post screening for eligibility, nine unique trials/studies (84 publications) were identified. Among these, one trial each was identified for bempedoic acid and alirocumab, three for evolocumab, and four for ezetimibe. No published literature documenting the cardiovascular outcomes of inclisiran was identified. Only one trial (CLEAR Outcomes) included statin-intolerant patients at baseline. Most studies evaluated a 3-component, 4-component, or 5-component major adverse cardiovascular events composite as an outcome along with individual components. The quality of the included trials was found to be fair-to-good.</div></div><div><h3>Conclusions</h3><div>The systematic review findings emphasise the significance of considering non-statin LLTs as viable treatment options for individuals with CVD or high cardiovascular risk who cannot tolerate or achieve optimal lipid control with statin therapy alone.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"58 ","pages":"Pages 24-37"},"PeriodicalIF":1.4,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142532846","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":"Lipoprotein(a) and the atherosclerotic burden – Should we wait for clinical trial evidence before taking action?","authors":"Isabella Fichtner ,&nbsp;Chiara Macchi ,&nbsp;Alessandra Stefania Rizzuto ,&nbsp;Stefano Carugo ,&nbsp;Alberto Corsini ,&nbsp;Massimiliano Ruscica","doi":"10.1016/j.athplu.2024.09.004","DOIUrl":"10.1016/j.athplu.2024.09.004","url":null,"abstract":"<div><div>The fact that lipoprotein(a) levels should be regarded as a causal residual risk factor in the atherosclerotic cardiovascular diseases (ASCVD) is now a no-brainer. This review article aims to summarize the latest evidence supporting the causal role of lipoprotein(a) in ASCVD and the potential strategies to reduce the lipoprotein(a) burden until clinical trial results are available. Epidemiological and genetic data demonstrate the causal link between lipoprotein(a) and increased ASCVD risk. That being said, a specific question comes to mind: “must we wait for outcome trials in order to take action?”. Given that lipoprotein(a) levels predict incident ASCVD in both primary and secondary prevention contexts, with a linear risk gradient across its distribution, measuring lipoprotein(a) can unequivocally help identify patients who may later benefit from specific lipoprotein(a)-lowering therapies. This understanding has led various National Societies to recommend dosing lipoprotein(a) in high-risk individuals and to support the recommendation of measuring lipoprotein(a) levels at least once in every adult for risk stratification.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"58 ","pages":"Pages 16-23"},"PeriodicalIF":1.4,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142421783","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":"Coronary artery calcification score and 19 biomarkers on cardiovascular events; a 10-year follow-up DanRisk substudy","authors":"Mie Schæffer ,&nbsp;Jeppe Holm Rasmussen ,&nbsp;Maise Høigaard Fredgart ,&nbsp;Selma Hasific ,&nbsp;Frederikke Nørregaard Jakobsen ,&nbsp;Flemming Hald Steffensen ,&nbsp;Jess Lambrechtsen ,&nbsp;Niels Peter Rønnow Sand ,&nbsp;Lars Melholt Rasmussen ,&nbsp;Axel CP. Diederichsen","doi":"10.1016/j.athplu.2024.09.003","DOIUrl":"10.1016/j.athplu.2024.09.003","url":null,"abstract":"<div><h3>Aim</h3><div>The SCORE2 algorithm is recommended to estimate risk of cardiovascular disease (CVD). Coronary artery calcification (CAC) score is expensive but improves the risk prediction. This study aims to determine and compare the additive value of CAC-score and 19 biomarkers in risk prediction.</div></div><div><h3>Methods</h3><div>Traditional cardiovascular (CV) risk factors, CAC-score, and a wide range of biomarkers (including lipids, calcium-phosphate metabolism, troponin, inflammation, kidney function and ankle brachial index (ABI)) were collected from 1211 randomly selected middle-aged men and women in this multicenter prospective cohort in 2009–2010. 10-year follow-up data on CV-events were obtained via the Danish Health Registries. CV-event was defined as stroke, myocardial infarction, hospitalization for heart failure, coronary artery revascularization or death from CVD. The association between SCORE2, CAC-score, biomarkers, and CV-events was assessed using cox proportional hazard rates (HR) and compared using AUC-calculation of ROC-curves. Finally, net reclassification improvement (NRI) was calculated.</div></div><div><h3>Results</h3><div>92 participants had CV-events. Adjusted for risk factors, CAC-score was significantly associated with events (adjusted HR 1.9 (95%CI:1.1; 3.3), 3.6 (95%CI:1.9; 6.8), and 5. (95%CI:2.6; 10.3) for CAC-score 1–99, CAC-score 100–399 and CAC-score ≥400, respectively. HR for the highest quartile of CRP was 2.3 (95%CI:1.2; 4.5), while none of the remaining biomarkers improved HR. Adjusted for SCORE2, the CAC-score improved AUC (AUC_CAC: 0.72, AUC_SCORE2: 0.67, <em>p&lt;</em>0.01). A combination of selected biomarkers (total cholesterol, low-density lipoprotein, phosphate, troponin, CRP, and creatinine) borderline improved AUC (AUC_{Biomarkers + SCORE2}: 0.71, AUC_SCORE2: 0.67, <em>p=</em>0.06). NRI for CAC score was 63 % (<em>p&lt;</em>0.0001).</div></div><div><h3>Conclusion</h3><div>CAC-score improved prediction of CV-events, however the selected biomarkers did not.</div></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"58 ","pages":"Pages 9-15"},"PeriodicalIF":1.4,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142327729","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":"Eligibility for marine omega-3 fatty acid supplementation after acute coronary syndromes","authors":"Cédric Follonier ,&nbsp;Gabriel Rabassa ,&nbsp;Mattia Branca ,&nbsp;David Carballo ,&nbsp;Konstantinos Koskinas ,&nbsp;Dik Heg ,&nbsp;David Nanchen ,&nbsp;Lorenz Räber ,&nbsp;Roland Klingenberg ,&nbsp;Moa Lina Haller ,&nbsp;Sebastian Carballo ,&nbsp;Stephan Windecker ,&nbsp;Christian M. Matter ,&nbsp;Nicolas Rodondi ,&nbsp;François Mach ,&nbsp;Baris Gencer","doi":"10.1016/j.athplu.2024.09.002","DOIUrl":"10.1016/j.athplu.2024.09.002","url":null,"abstract":"<div><h3>Background and aims</h3><p>The 2019 European Society of Cardiology guidelines for the management of dyslipidemia consider the use of high-dose marine omega-3 fatty acid (FA) eicosapentaenoic acid (EPA) supplementation (icosapent ethyl 2 × 2g/day) to lower residual cardiovascular risk in high-risk patients with hypertriglyceridemia. This study aimed to assess the eligibility for omega-3 FA-EPA supplementation in patients with acute coronary syndromes (ACS).</p></div><div><h3>Methods</h3><p>In a prospective Swiss cohort of patients hospitalized for ACS, eligibility for marine omega-3 FA-EPA, defined as plasma triglyceride levels ranging from 1.5 to 5.6 mmol/l, was assessed at baseline and one-year follow-up and compared across subgroups. Lipid-lowering therapy intensification with statin and ezetimibe was modelled to simulate a hypothetical systematic treatment and its effect on omega-3 FA-EPA supplementation eligibility.</p></div><div><h3>Results</h3><p>Of 2643 patients, 98 % were prescribed statin therapy at discharge, including 62 % at a high-intensity regimen; 93 % maintained it after one year, including 53 % at a high-intensity regimen. The use of ezetimibe was 3 % at discharge and 7 % at one year. Eligibility was observed in 32 % (32 % men, 29 % women) one year post-ACS. After modelling systematic treatment with statins, ezetimibe, and both, eligibility decreased to 31 %, 25 % and 24 %, respectively. Eligibility was higher in individuals aged &lt;70 (34 vs 25 %), smokers (38 vs 28 %), diabetics (46 vs 29 %), hypertensive (35 vs 29 %), and obese patients (46 vs 22 % for normal weight), all with p-values &lt;0.001.</p></div><div><h3>Conclusion</h3><p>In a contemporary Swiss cohort of patients with ACS, up to 32 % would be eligible for omega-3 FA-EPA supplementation one year after ACS, highlighting an opportunity to mitigate residual cardiovascular risk in patients with ACS and hypertriglyceridemia.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"58 ","pages":"Pages 1-8"},"PeriodicalIF":1.4,"publicationDate":"2024-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089524000439/pdfft?md5=140a849556d7934c58fbe2caf2c9759a&pid=1-s2.0-S2667089524000439-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142270704","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}