Atherosclerosis plus最新文献

{"title":"Ketogenic Diet – a culinary delight but is there a cautionary tale?","authors":"R. Valaiyapathi ∗ , N. Rao , R. Chandra , R.P. Vincent , R. Ranasinghe","doi":"10.1016/j.athplu.2024.08.011","DOIUrl":"10.1016/j.athplu.2024.08.011","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Page 10"},"PeriodicalIF":1.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142423698","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 tale of 2 pregnancies: the biochemical trends, medical management, and outcomes of hypertriglyceridemia in pregnancy secondary to multi-factorial chylomicronaemia syndrome (MCS) and extreme ketogenic/carnivorous diet","authors":"N.W.P. Cantley ∗ , S. Tapley , K. Antwi , P. Downie , E. Willis","doi":"10.1016/j.athplu.2024.08.003","DOIUrl":"10.1016/j.athplu.2024.08.003","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Pages 6-7"},"PeriodicalIF":1.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142416450","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":"Variants in LPA are associated with mutation-negative Familial Hypercholesterolaemia: whole genome sequencing analysis in the 100,000 Genomes Project","authors":"Martin Bird , Antoine Rimbert , Alan M. Pittman , Steve E. Humphries , Marta Futema ∗","doi":"10.1016/j.athplu.2024.08.015","DOIUrl":"10.1016/j.athplu.2024.08.015","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Page 2"},"PeriodicalIF":1.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142423456","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":"Lomitapide in paediatric patients with homozygous familial hypercholesterolaemia (HoFH) – Analysis of patient-level LDL-C reduction, fat-soluble vitamins, lipoproteins and patient maturation from the APH-19 study","authors":"Luis Masana , Alberto Zambon , Claus Peter Schmitt , Christina Taylan , Joenna Driemeyer , Hofit Cohen , Paola Sabrina Buonuomo , Abdullah Alashwal , Mohammed Al-Dubayee , José Luis Diaz-Diaz , Faouzi Maatouk , Sergio Martinez-Hervas , Brian Mangal , Naji Kholaif , Sandra Löwe , Zsuzsanna Tamas ∗","doi":"10.1016/j.athplu.2024.08.020","DOIUrl":"10.1016/j.athplu.2024.08.020","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Page 4"},"PeriodicalIF":1.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142423460","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":"Genetic Landscape of Familial Chylomicronaemia Syndrome (FCS) and Multifactorial Chylomicronaemia Syndrome (MCS) in United Kingdom","authors":"Bilal Bashir , Natalie Forrester , Paul Downie , Carolyn Dent , Dawn O’Sullivan , Sarah Marsh , Raabya Pasha , Anoushka Kamath , Haya Haso , Maryam Ferdousi , Jian Wang , Robert Hegele , Handrean Soran","doi":"10.1016/j.athplu.2024.08.013","DOIUrl":"10.1016/j.athplu.2024.08.013","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Page 1"},"PeriodicalIF":1.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142423253","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":"Extreme founder effect associated with hyperglycemia and hyperlipidemia on the island of NIAS/Indonesia","authors":"Ingo Kennerknecht ,&nbsp;Johannes M. Hämmerle ,&nbsp;Manfred Fobker ,&nbsp;Jerzy-Roch Nofer","doi":"10.1016/j.athplu.2024.07.002","DOIUrl":"10.1016/j.athplu.2024.07.002","url":null,"abstract":"<div><p>The island of Nias/Indonesia shows an extremely reduced genetic diversity indicating a strong founder effect. As a consequence, the prevalence of some disease genes should significantly differ among populations depending on the gene pool passed on to the founder population and their successive expansion as it has already been documented for several monogenic diseases. Results of the current study based on routine laboratory blood examination give rise to the notion that this might also hold true for polygenic disorders. We observed very high prevalence of hyperglycemia (non-fasting glucose above 200 mg/dL in 14 % Nias population compared to 1.5 % in the population of the neighboring island of Sumatra) accompanied by hypertriglyceridemia, high non-HDL-cholesterol, and low HDL-cholesterol levels. These findings suggest that the Nias population may be disproportionally affected by prediabetes and type 2 diabetes mellitus. By contrast, laboratory parameters potentially indicative of other polygenic disorders such as total plasma cholesterol, electrolytes, creatinine, urea, and uric acid were comparable between the inhabitants of Nias and Sumatra islands. To our knowledge this is the first study suggesting that the extremely strong genetic bottleneck seen in the Nias population translates into the widespread metabolic disease with potentially deleterious influence on public health.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Pages 26-29"},"PeriodicalIF":1.4,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089524000178/pdfft?md5=308d0b8c2f1c0734c601c409bf9639ac&pid=1-s2.0-S2667089524000178-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141846605","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":"Associations of very low Lipoprotein(a) levels with risks of new-onset diabetes and non-alcoholic liver disease","authors":"Ming Wai Yeung ,&nbsp;M. Abdullah Said ,&nbsp;Yordi J. van de Vegte ,&nbsp;Niek Verweij ,&nbsp;Robin P.F. Dullaart ,&nbsp;Pim van der Harst","doi":"10.1016/j.athplu.2024.07.001","DOIUrl":"https://doi.org/10.1016/j.athplu.2024.07.001","url":null,"abstract":"<div><h3>Background and aims</h3><p>We aimed to study the association of very low serum Lipoprotein(a) [Lp(a)] concentrations with new-onset type 2 diabetes (T2D) and non-alcoholic liver disease (NAFLD) in the context of statin usage in the UK Biobank, a large prospective population cohort.</p></div><div><h3>Methods</h3><p>Using an extended biomarker dataset, we identified 47,362 participants with very low Lp(a) concentrations (&lt;3.8 nmol/L) from a total of 451,479 participants. With a median follow-up of 12.3 years, we assessed the risk of new-onset cardiometabolic diseases in participants stratified by statin usage with Cox proportional hazards models. We performed two-sample Mendelian randomization MR analyses to test causal relationship between genetically predicted Lp(a) and T2D and NAFLD.</p></div><div><h3>Results</h3><p>Taking the participants with Lp(a) within reportable range as the reference group, the hazard ratios (HR) for T2D were 1.07 (95 % confidence interval, CI 1.01–1.13) and for NAFLD 1.30 (95 % CI 1.20–1.41) respectively for participants with very low Lp(a) (&lt;3.8 nmol/L). The risk for new-onset T2D was higher in participants using statins (adjusted HR 1.15; 95 % CI 1.05–1.27). The risk estimates for new-onset NAFLD were comparable in the analysis stratified by statin use. There was no evidence for causal links between genetically predicted Lp(a) and T2D nor NAFLD in two-sample MR analyses.</p></div><div><h3>Conclusions</h3><p>Very low Lp(a) was associated with higher risks of T2D and NAFLD in a prospective analysis of the UK Biobank. The association with T2D was influenced by lipid lowering medication usage. MR analyses did not support causality for these inverse associations.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Pages 19-25"},"PeriodicalIF":1.4,"publicationDate":"2024-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089524000166/pdfft?md5=c3a6777b13986ebec4c5e9321f64810d&pid=1-s2.0-S2667089524000166-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141607836","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) in children and adolescents with genetically confirmed familial hypercholesterolemia followed up at a specialized lipid clinic","authors":"Anja K. Johansen ,&nbsp;Martin P. Bogsrud ,&nbsp;Magne Thoresen ,&nbsp;Jacob J. Christensen ,&nbsp;Ingunn Narverud ,&nbsp;Gisle Langslet ,&nbsp;Tone Svilaas ,&nbsp;Kjetil Retterstøl ,&nbsp;Kirsten B. Holven","doi":"10.1016/j.athplu.2024.06.002","DOIUrl":"https://doi.org/10.1016/j.athplu.2024.06.002","url":null,"abstract":"<div><h3>Background and aim</h3><p>Many children with an FH mutation also exhibit elevated lipoprotein(a) levels, which is an independent risk factor for atherosclerotic cardiovascular disease. Studies have reported higher levels of lipoprotein(a) in adult and middle-aged women than men. There is limited knowledge on the concentration and change of lipoprotein(a) levels in children with genetic FH, and therefore we investigated sex-differences in lipoprotein(a) level and change in lipoprotein(a) in girls and boys with genetically confirmed FH.</p></div><div><h3>Methods</h3><p>Medical records were reviewed retrospectively in 438 subjects with heterozygous FH that started follow-up below the age of 19 years at the Lipid Clinic, Oslo University Hospital in Norway, and of these we included 386 subjects with at least one Lp(a) measurement.</p></div><div><h3>Results</h3><p>Mean (SD) age at baseline was 13.8 (7.3) years and the age was similar between sexes. Girls had a higher lipoprotein(a) level than boys at baseline: median (25–75 percentile) 223 (108–487) vs. 154 (78–360) mg/L, respectively (<em>p</em> &lt; 0.01). From baseline to follow-up measurement (mean [SD] 8.9 [6.1] years apart), the mean (95 % CI) absolute and percentage change in Lp(a) level in girls was 151.4 (54.9–247.8) mg/L and 44.8 (16.4–73.1) %, respectively, and in boys it was 66.8 (22.9–110.8) mg/L and 50.5 (8.8–92.3) %, respectively (both p &gt; 0.05).</p></div><div><h3>Conclusions</h3><p>We found an increase in Lp(a) levels in children with genetic FH with age, and higher levels in girls than boys, which could impact risk assessment and future ASCVD. Further research is needed to elucidate whether subjects with FH could benefit from lipoprotein(<em>a</em>)-lowering therapies that are under current investigations.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Pages 13-18"},"PeriodicalIF":1.4,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089524000154/pdfft?md5=15f96828203462a10735210142d91fb5&pid=1-s2.0-S2667089524000154-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141478933","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":"NAD+ metabolism and therapeutic strategies in cardiovascular diseases","authors":"Chongxu Shi ,&nbsp;Zhaozhi Wen ,&nbsp;Yihang Yang ,&nbsp;Linsheng Shi ,&nbsp;Dong Liu","doi":"10.1016/j.athplu.2024.06.001","DOIUrl":"https://doi.org/10.1016/j.athplu.2024.06.001","url":null,"abstract":"<div><p>Nicotinamide adenine dinucleotide (NAD+) is a central and pleiotropic metabolite involved in cellular energy metabolism, cell signaling, DNA repair, and protein modifications. Cardiovascular diseases (CVDs) are the leading cause of death worldwide. Metabolic stress and aging directly affect the cardiovascular system. Compelling data suggest that NAD + levels decrease with age, obesity, and hypertension, which are all notable risk factors for CVD. In addition, the therapeutic elevation of NAD + levels reduces chronic low-grade inflammation, reactivates autophagy and mitochondrial biogenesis, and enhances oxidative metabolism in vascular cells of humans and rodents with vascular disorders. In preclinical models, NAD + boosting can also expand the health span, prevent metabolic syndrome, and decrease blood pressure. Moreover, NAD + storage by genetic, pharmacological, or natural dietary NAD + -increasing strategies has recently been shown to be effective in improving the pathophysiology of cardiac and vascular health in different animal models, and human health. Here, we review and discuss NAD + -related mechanisms pivotal for vascular health and summarize recent experimental evidence in NAD + research directly related to vascular disease, including atherosclerosis, and coronary artery disease. Finally, we comparatively assess distinct NAD + precursors for their clinical efficacy and the efficiency of NAD + elevation in the treatment of major CVD. These findings may provide ideas for new therapeutic strategies to prevent and treat CVD in the clinic.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Pages 1-12"},"PeriodicalIF":1.6,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089524000142/pdfft?md5=5c934b362462e68508d9d5357b0a38dc&pid=1-s2.0-S2667089524000142-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141313913","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":"Trends in cardiovascular disease among Inuit in Greenland from 1994 to 2021","authors":"Hjalte Erichsen Larsen ,&nbsp;Uka Wilhjelm Geisler ,&nbsp;Finn Gustafsson ,&nbsp;Michael Lynge Pedersen ,&nbsp;Marit Eika Jørgensen","doi":"10.1016/j.athplu.2024.04.002","DOIUrl":"10.1016/j.athplu.2024.04.002","url":null,"abstract":"<div><h3>Background and aims</h3><p>Cardiovascular disease (CVD) poses significant health challenges globally. While substantial data exists for most populations, the Arctic Inuit's CVD incidence rates remain understudied. This research aimed to change this by estimating CVD incidence and mortality rates in Greenland from 1994 to 2021.</p></div><div><h3>Methods</h3><p>Using nationwide registers, a retrospective observational study was conducted, focusing on individuals born in Greenland to Greenlandic-born parents. Data were sourced from the Greenlandic Hospital Discharge Register and the nationwide electronic medical record.</p></div><div><h3>Results</h3><p>A total of 65,824 individuals were included. the age- and sex-specific incidence rates (IR) of ischemic heart disease, stroke, and heart failure (HF) declined from 1994 to 2021, with the most substantial decline observed for HF among women. Conversely, the IR of atrial fibrillation/flutter increased in both men and women, while the IR of myocardial infarction rose among men. The IR for stroke was particularly elevated compared to other CVD subgroups. Mortality rates for those diagnosed with CVD were 2.4 times higher than those without. Men exhibited a 40 % elevated mortality risk relative to women.</p></div><div><h3>Conclusion</h3><p>The study provides pivotal insights into CVD trends within the Arctic Inuit population, highlighting both positive developments and areas of concern. Given the increasing elderly demographic in Greenland, proactive health strategies are crucial. Emphasizing primary prevention and addressing specific CVD risks, particularly the elevated stroke IR, is imperative for future public health efforts.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"56 ","pages":"Pages 12-20"},"PeriodicalIF":1.6,"publicationDate":"2024-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089524000129/pdfft?md5=9d4d7793df96d29ba2f3fbeec3cb849c&pid=1-s2.0-S2667089524000129-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140763717","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}