Atherosclerosis plus最新文献

{"title":"HEART UK 2023 Moderated Posters","authors":"","doi":"10.1016/j.athplu.2023.07.010","DOIUrl":"https://doi.org/10.1016/j.athplu.2023.07.010","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"54 ","pages":"Page S11"},"PeriodicalIF":1.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089523000238/pdfft?md5=8ab2ab543e2328f4891ea02b30894c85&pid=1-s2.0-S2667089523000238-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138713289","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":"HEART UK 2023 Oral Presentations","authors":"","doi":"10.1016/j.athplu.2023.07.022","DOIUrl":"https://doi.org/10.1016/j.athplu.2023.07.022","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"54 ","pages":"Pages S5-S6"},"PeriodicalIF":1.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089523000354/pdfft?md5=b63f3a0b2e0e0e35ec4ddf66368bd10d&pid=1-s2.0-S2667089523000354-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138713238","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":"How many individuals with Familial Hypercholesterolaemia (FH) need to be identified to achieve the NHS 2019 Long Term Plan ambition?","authors":"S.E. Humphries , J.Gratton , K. Haralambos , M. Futema","doi":"10.1016/j.athplu.2023.07.016","DOIUrl":"https://doi.org/10.1016/j.athplu.2023.07.016","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"54 ","pages":"Page S3"},"PeriodicalIF":1.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089523000299/pdfft?md5=32cbc6cfa7745c37eaf3ff4a3f35e8ea&pid=1-s2.0-S2667089523000299-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138713304","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":"How many FH genetic tests were performed by the UK Genetic Laboratory Hubs in 2022?","authors":"S.E. Humphries , R. Challis , K. Downes , E. Howard , T. Legerton , C. Macanulty , S. Morgan , A. O’Rouke , D. O’Sullivan , A. Taylor-Beadling , E. Thompson , E. Watson , G. Norbury","doi":"10.1016/j.athplu.2023.07.005","DOIUrl":"https://doi.org/10.1016/j.athplu.2023.07.005","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"54 ","pages":"Page S9"},"PeriodicalIF":1.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089523000184/pdfft?md5=e02bd551faecb97e687ddbb511b0731f&pid=1-s2.0-S2667089523000184-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138713345","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 Chylomicronaemia Syndrome (FCS) Compared to Multifactorial Chylomicronaemia Syndrome (MCS) – Lessons learnt from United Kingdom FCS Registry","authors":"B. Bashir , S. Kwok , A.S. Wierzbicki , A. Jones , C. Dawson , P. Downie , F. Jenkinson , P. Gupta , M. Mansfield , R. Kumari , D. Datta , H. Delaney , Y. Teoh , M. Williams , N. Forrester , D. O’Sullivan , Z. Miedzybrodzka , J. Payne , H. Soran","doi":"10.1016/j.athplu.2023.07.018","DOIUrl":"https://doi.org/10.1016/j.athplu.2023.07.018","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"54 ","pages":"Page S4"},"PeriodicalIF":1.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089523000317/pdfft?md5=c6e645e7bc21bd015414a43806f2cb6d&pid=1-s2.0-S2667089523000317-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138713287","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 Chylomicronaemia Syndrome (FCS) Score Validation in United Kingdom FCS Registry: Can Additional Variables Improve the FCS Score Performance?","authors":"B. Bashir , S. Kwok , A.S. Wierzbicki , A. Jones , C. Dawson , P. Downie , F. Jenkinson , P. Gupta , H. Dealeny , M. Mansfield , R. Kumari , D. Datta , Y. Teoh , M. Williams , N. Forrester , D. O’Sullivan , Z. Miedzybrodzka , A. Gallo , P. Moulin , J. Payne , H. Soran","doi":"10.1016/j.athplu.2023.07.004","DOIUrl":"https://doi.org/10.1016/j.athplu.2023.07.004","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"54 ","pages":"Page S8"},"PeriodicalIF":1.6,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089523000172/pdfft?md5=644746d76cf8a7bc9655fbb8659571e5&pid=1-s2.0-S2667089523000172-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138713219","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":"ITGB2 is a central hub-gene associated with inflammation and early fibro-atheroma development in a swine model of atherosclerosis","authors":"Hadjer Namous ,&nbsp;Maria Giuseppina Strillacci ,&nbsp;Camila Urbano Braz ,&nbsp;Dhanu Shanmuganayagam ,&nbsp;Christian Krueger ,&nbsp;Athanasios Peppas ,&nbsp;William C. Soffregen ,&nbsp;Jess Reed ,&nbsp;Juan F. Granada ,&nbsp;Hasan Khatib","doi":"10.1016/j.athplu.2023.11.001","DOIUrl":"https://doi.org/10.1016/j.athplu.2023.11.001","url":null,"abstract":"<div><h3>Background and aim</h3><p>The complex dynamic interplay between different biological pathways involved in atherosclerosis development has rendered the identification of specific therapeutic targets a challenging quest. We aimed to identify specific genes and mechanistic pathways associated with the early development of fibro-atheromas in a swine model of atherosclerosis.</p></div><div><h3>Methods</h3><p>The Wisconsin Miniature Swine™ model of Familial Hypercholesterolemia (WMS-FH, n = 11) and genetically related WMS controls (WMS-N, n = 11) were used. The infrarenal aorta was harvested from both groups for histopathologic and transcriptomic profiling at 12 months. Bioinformatic analysis was performed to identify hub genes and pathways central to disease pathophysiology. The expression of ITGB2, the top ranked hub gene, was manipulated in cell culture and the expression of interconnected genes was tested.</p></div><div><h3>Results</h3><p>Fibro-atheromatous lesions were documented in all WMS-FH aortic tissues and displayed internal elastic lamina (IEL) disruption, significant reduction of myofibroblast presence and disorganized collagen deposition. No fibro-atheromas were observed in the control group. A total of 266 differentially expressed genes (DEGs) were upregulated in WMS-FH aortic tissues, while 29 genes were downregulated. Top identified hub genes included ITGB2, C1QA, LCP2, SPI1, CSF1R, C5AR1, CTSS, MPEG1, C1QC, and CSF2RB. Overexpression of ITGB2 resulted in elevated expression of other interconnected genes expressed in porcine endothelial cells.</p></div><div><h3>Conclusion</h3><p>In a swine translational model of atherosclerosis, transcriptomic analysis identified ITGB2 as a central hub gene associated inflammation and early fibroatheroma development making it a potential therapeutic target at this stage of disease.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"54 ","pages":"Pages 30-41"},"PeriodicalIF":1.6,"publicationDate":"2023-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089523000433/pdfft?md5=320bdbb10453fa6086111075d9285e05&pid=1-s2.0-S2667089523000433-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138437068","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":"Fetuin-A levels in association with calcific aortic valve disease: A meta-analysis","authors":"Muhammad Omar Larik","doi":"10.1016/j.athplu.2023.09.004","DOIUrl":"10.1016/j.athplu.2023.09.004","url":null,"abstract":"<div><h3>Background and aims</h3><p>Calcific aortic valve disease (CAVD) is a common valvular disease, prevalent particularly within the older age groups. The potential use of biomarkers in diagnosing and assessing the severity of CAVD, in supplementation with imaging techniques, has recently gained momentum within the field of cardiovascular medicine. Therefore, a meta-analysis was performed that assessed the association between the fetuin-A levels, and the presence of CAVD.</p></div><div><h3>Methods</h3><p>PubMed and Cochrane were searched from inception to April 2023. Risk of bias was assessed using the Newcastle-Ottawa scale for cohort studies.</p></div><div><h3>Results</h3><p>This analysis includes a total of 3,280 patients with CAVD, and 7,505 patients as control, resulting in the pooling of 10,785 patients in this meta-analysis. It was observed that the circulating levels of fetuin-A were significantly lowered in patients with CAVD (SMD: -0.20; 95% CI: -0.39, -0.02; P = 0.03). Moreover, the analysis revealed that fetuin-A levels had no significant association with CAVD in patients suffering from kidney disease (SMD: 0.20; 95% CI: -0.46, 0.85; P = 0.56).</p></div><div><h3>Conclusion</h3><p>While initial results demonstrate the potential effectiveness, further research is essential in order to arrive at a robust conclusion regarding the use of fetuin-A as a diagnostic biomarker for calcific aortic valve disease.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"54 ","pages":"Pages 27-29"},"PeriodicalIF":1.6,"publicationDate":"2023-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10562872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41221650","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":"The LIPL study: Postprandial lipid profile, inflammation, and platelet activity in patients with chronic coronary syndrome","authors":"Edita Pogran ,&nbsp;Paul M. Haller ,&nbsp;Claudia Wegberger ,&nbsp;Maximilian Tscharre ,&nbsp;Irena Vujasin ,&nbsp;Christoph C. Kaufmann ,&nbsp;Petra Dick ,&nbsp;Bernhard Jäger ,&nbsp;Johann Wojta ,&nbsp;Kurt Huber","doi":"10.1016/j.athplu.2023.09.002","DOIUrl":"10.1016/j.athplu.2023.09.002","url":null,"abstract":"<div><h3>Background and aims</h3><p>It is suggested that the changes in atherosclerosis happen mainly under the influence of non-fasting lipids. To date, the studies in the postprandial state were primarily performed on healthy subjects. This exploratory, cross-sectional study investigates the change in lipid profile, inflammation, and platelet activation in patients with different cardiovascular risk profiles in the postprandial state.</p></div><div><h3>Methods</h3><p>The studied population consists of 66 patients with different cardiovascular risks: patients with a history of the chronic coronary syndrome (CCS) and diabetes mellitus type 2 (DM2) (n = 20), CCS without DM2 (n = 25), and a healthy control group (n = 21). Lipid variables and markers of platelet function and inflammation were assessed during the fasting state and three and 5 h after a standardized fat meal using a standardized oral fat tolerance test (OFTT), a milkshake with 90 g of fat.</p></div><div><h3>Results</h3><p>Patients with CCS and DM2 were significantly older and had the highest BMI. All patients with CCS were on acetylsalicylic acid, and 95% of CCS patients were on high-dose statins. The absolute leukocyte and neutrophile count increased significantly in the control group during the OFTT in comparison to CCS subjects. There was a significant decrease of HDL and increase of triglycerides during the OFTT, however with no difference between groups. There was no difference in the change of platelet activity between all groups.</p></div><div><h3>Conclusion</h3><p>This study showed that OFTT leads to an increased postprandial inflammation response in healthy group compared to CCS ± DM2 while there was no change in lipid profile and platelet activity.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"54 ","pages":"Pages 14-21"},"PeriodicalIF":1.6,"publicationDate":"2023-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/9d/1e/main.PMC10550804.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41174900","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":"High-density lipoprotein cholesterol and multiple myeloma: A systematic review and meta-analysis","authors":"Anastasios Makris ,&nbsp;Antonia Pagkali ,&nbsp;Emmanouil Nikolousis ,&nbsp;Theodosios D. Filippatos ,&nbsp;Aris P. Agouridis","doi":"10.1016/j.athplu.2023.09.003","DOIUrl":"10.1016/j.athplu.2023.09.003","url":null,"abstract":"<div><h3>Background and aims</h3><p>To systematically investigate all relevant evidence on the association between high-density lipoprotein cholesterol (HDL-C) and multiple myeloma (MM).</p></div><div><h3>Methods</h3><p>We searched PubMed and Cochrane library databases (up to 20 September 2022) for studies with evidence on HDL-C in patients with MM. A qualitative synthesis of published prospective and retrospective studies for the role of HDL-C and other lipid profile parameters in MM was performed. Additionally, a meta-analysis on HDL-C mean differences (MD) between MM cases and controls was performed.</p></div><div><h3>Results</h3><p>Fourteen studies (3 prospective, 11 retrospective) including 895 MM patients were eligible for this systematic review. Ten studies compared HDL-C levels in MM patients with healthy controls. In these 10 studies (n = 17,213), pooled analyses showed that MM patients had significantly lower HDL-C levels compared to healthy controls (MD: −13.07 mg/dl, 95% CI: −17.83, −8.32, p &lt; 0.00001). Regarding secondary endpoints, total cholesterol (TC) (MD: −22.19 mg/dl, 95% CI: −39.08, −5.30) and apolipoprotein A-I (apoA-I) (−40.20 mg/dl, 95% CI: −55.00, −25.39) demonstrated significant decreases, while differences in low-density lipoprotein cholesterol (LDL-C) (MD: −11.33 mg/dl, 95% CI: −36.95, 14.30) and triglycerides (MD: 9.93 mg/dl, 95% CI: −3.40, 23.26) were not shown to be significant.</p></div><div><h3>Conclusions</h3><p>HDL-C, as well as TC and apoA-I, levels are significantly decreased in MM. Hence, lipid profile parameters should be taken into account when assessing such patients.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"54 ","pages":"Pages 7-13"},"PeriodicalIF":1.6,"publicationDate":"2023-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10539640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41175749","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}