Atherosclerosis plus最新文献

{"title":"Fibronectin extra domain a limits liver dysfunction and protects mice during acute inflammation","authors":"Vivek Krishna Pulakazhi Venu ,&nbsp;Annalisa Moregola ,&nbsp;Lorenzo Da Dalt ,&nbsp;Patrizia Uboldi ,&nbsp;Fabrizia Bonacina ,&nbsp;Andrés Fernando Muro ,&nbsp;Giuseppe Danilo Norata","doi":"10.1016/j.athplu.2023.05.002","DOIUrl":"10.1016/j.athplu.2023.05.002","url":null,"abstract":"<div><h3>Background and aim</h3><p>The primary transcript of fibronectin (FN) undergoes alternative splicing to generate different isoforms, including FN containing the Extra Domain A (FN_EDA+), whose expression is regulated spatially and temporarily during developmental and disease conditions including acute inflammation. The role of FN_EDA+ during sepsis, however, remains elusive.</p></div><div><h3>Methods</h3><p>Mice constitutively express the EDA domain of fibronectin (EDA^+/+); lacking the FN EDA domain (EDA^−/−) or with a conditional ablation of EDA + inclusion only in liver produced FN (alb-CRE⁺EDA floxed mice) thus expressing normal plasma FN were used. Systemic inflammation and sepsis were induced by either LPS injection (70 mg/kg) or by cecal ligation and puncture (CLP) Neutrophils isolated from septic patients were tested for neutrophil binding ability.</p></div><div><h3>Results</h3><p>We observed that EDA^+/+ were protected toward sepsis as compared to EDA^−/− mice. Also alb-CRE⁺EDA floxed mice presented reduced survival, thus indicating a key role for EDA in protecting toward sepsis. This phenotype was associated with improved liver and spleen inflammatory profile. Ex vivo experiments showed that neutrophils bind to a larger extent to an FN_EDA + coated surface as compared to FN, thus potentially limiting their over-reactivity.</p></div><div><h3>Conclusions</h3><p>Our study demonstrates that the inclusion of the EDA domain in fibronectin dampens the nflammatoryi consequences of sepsis.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"52 ","pages":"Pages 23-31"},"PeriodicalIF":1.6,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/11/7b/main.PMC10242638.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9652994","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":"Characteristics of peripheral blood cells are independently related to major adverse cardiovascular events after carotid endarterectomy","authors":"L. Malin Overmars ,&nbsp;Joost M. Mekke ,&nbsp;Wouter W. van Solinge ,&nbsp;Saskia C.A. De Jager ,&nbsp;Cornelia A.R. Hulsbergen-Veelken ,&nbsp;Imo E. Hoefer ,&nbsp;Dominique P.V. de Kleijn ,&nbsp;Gert J. de Borst ,&nbsp;Sander W. van der Laan ,&nbsp;Saskia Haitjema","doi":"10.1016/j.athplu.2023.05.003","DOIUrl":"10.1016/j.athplu.2023.05.003","url":null,"abstract":"<div><h3>Background and aims</h3><p>Patients who underwent carotid endarterectomy (CEA) still have a residual risk of 13% of developing a major adverse cardiovascular event (MACE) within 3 years. Inflammatory processes leading up to MACE are not fully understood. Therefore, we examined blood cell characteristics (BCCs), possibly reflecting inflammatory processes, in relation to MACE to identify BCCs that may contribute to an increased risk.</p></div><div><h3>Methods</h3><p>We analyzed 75 pretreatment BCCs from the Sapphire analyzer, and clinical data from the Athero-Express biobank in relation to MACE after CEA using Random Survival Forests, and a Generalized Additive Survival Model. To understand biological mechanisms, we related the identified variables to intraplaque hemorrhage (IPH).</p></div><div><h3>Results</h3><p>Of 783 patients, 97 (12%) developed MACE within 3 years after CEA. Red blood cell distribution width (RDW) (HR 1.23 [1.02, 1.68], p = 0.022), CV of lymphocyte size (LACV) (HR 0.78 [0.63, 0.99], p = 0.043), neutrophil complexity of the intracellular structure (NIMN) (HR 0.80 [0.64, 0.98], p = 0.033), mean neutrophil size (NAMN) (HR 0.67 [0.55, 0.83], p &lt; 0.001), mean corpuscular volume (MCV) (HR 1.35 [1.09, 1.66], p = 0.005), eGFR (HR 0.65 [0.52, 0.80], p &lt; 0.001); and HDL-cholesterol (HR 0.62 [0.45, 0.85], p = 0.003) were related to MACE. NAMN was related to IPH (OR 0.83 [0.71–0.98], p = 0.02).</p></div><div><h3>Conclusions</h3><p>This is the first study to present a higher RDW and MCV and lower LACV, NIMN and NAMN as biomarkers reflecting inflammatory processes that may contribute to an increased risk of MACE after CEA.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"52 ","pages":"Pages 32-40"},"PeriodicalIF":1.6,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/18/49/main.PMC10300576.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9730170","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":"Long term aortic arch plaque progression in older adults","authors":"David Leibowitz ,&nbsp;Yuriko Yoshida ,&nbsp;Zhezhen Jin ,&nbsp;Carlo Mannina ,&nbsp;Shunichi Homma ,&nbsp;Koki Nakanishi ,&nbsp;Mitchell S.V. Elkind ,&nbsp;Tatjana Rundek ,&nbsp;Marco R. Di Tullio","doi":"10.1016/j.athplu.2023.05.001","DOIUrl":"10.1016/j.athplu.2023.05.001","url":null,"abstract":"<div><h3>Background and aims</h3><p>The presence of aortic arch plaques (AAP) is significantly associated with increased cardiovascular morbidity and mortality. Few studies have examined the incidence of AAP progression and factors which may contribute to it using transthoracic echocardiography (TTE). The objective of this study was to utilize sequential imaging of the aortic arch using TTE to examine the rate of AAP progression and its risk factors in a cohort of older adults.</p></div><div><h3>Methods</h3><p>Participants enrolled in both the Cardiovascular Abnormalities and Brain Lesion study (years 2005–2010) and the Subclinical Atrial Fibrillation and Risk of Ischemic Stroke study (2014–2019) who underwent TTE with assessment of aortic arch plaques at both time points represent the study cohort.</p></div><div><h3>Results</h3><p>300 participants were included in the study. Mean age was 67.8 ± 7.5 years at baseline, and 76.7 ± 6.8 years at follow-up; 197 (65.7%) were women. At baseline, 87 (29%) had no significant AAP, 182 (60.7%) had evidence of small AAP (2.0–3.9 mm) and 31 (10.3%) had evidence of large (≥4 mm) AAP. At the time of follow-up assessment, 157 (52.3%) of participants exhibited progression of AAP with 70 (23.3%) having mild progression and 87 (29%) having severe progression. There were no significant demographic or clinical predictors of AAP progression except baseline plaque thickness itself which was significantly lower in the group with AAP progression.</p></div><div><h3>Conclusions</h3><p>Our study demonstrates a high prevalence of AAP on TTE exam in a population-based cohort of older adults with a high incidence of AAP progression. TTE is a useful test for baseline and follow up imaging of AAP, even in subjects with no or little AAP at baseline.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"52 ","pages":"Pages 18-22"},"PeriodicalIF":1.6,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a7/a5/main.PMC10220301.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9916946","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":"HDL and chronic kidney disease","authors":"Chiara Pavanello,&nbsp;Alice Ossoli","doi":"10.1016/j.athplu.2023.04.001","DOIUrl":"10.1016/j.athplu.2023.04.001","url":null,"abstract":"<div><p>Low HDL-cholesterol (HDL-C) concentrations are a typical trait of the dyslipidemia associated with chronic kidney disease (CKD). In this condition, plasma HDLs are characterized by alterations in structure and function, and these particles can lose their atheroprotective functions, e.g., the ability to promote cholesterol efflux from peripheral cells, anti-oxidant and anti-inflammatory proprieties and they can even become dysfunctional, i.e., exactly damaging. The reduction in plasma HDL-C levels appears to be the only lipid alteration clearly linked to the progression of renal disease in CKD patients. The association between the HDL system and CKD development and progression is also supported by the presence of genetic kidney alterations linked to HDL metabolism, including mutations in the <em>APOA1</em>, <em>APOE</em>, <em>APOL</em> and <em>LCAT</em> genes. Among these, renal disease associated with LCAT deficiency is well characterized and lipid abnormalities detected in LCAT deficiency carriers mirror the ones observed in CKD patients, being present also in acquired LCAT deficiency. This review summarizes the major alterations in HDL structure and function in CKD and how genetic alterations in HDL metabolism can be linked to kidney dysfunction. Finally, the possibility of targeting the HDL system as possible strategy to slow CKD progression is reviewed.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"52 ","pages":"Pages 9-17"},"PeriodicalIF":1.6,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10182177/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9857365","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":"Low HDL-c levels at admission are associated with greater severity and worse clinical outcomes in patients with COVID-19 disease","authors":"Sandra Parra ,&nbsp;Mireia Saballs ,&nbsp;Mark DiNubile ,&nbsp;Mireia Feliu ,&nbsp;Simona Iftimie ,&nbsp;Laia Revuelta ,&nbsp;Raul Pavón ,&nbsp;Alba Àvila ,&nbsp;Susan Levinson ,&nbsp;Antoni Castro","doi":"10.1016/j.athplu.2023.01.002","DOIUrl":"10.1016/j.athplu.2023.01.002","url":null,"abstract":"<div><h3>Background and aims</h3><p>HDL particles may act to buffer host cells from excessive inflammatory mediators. The aim of this study is to investigate if the lipid profile provides a prognostic biomarker for COVID-19 outcomes.</p></div><div><h3>Methods</h3><p>This was a prospective study of the characteristics of 125 adult COVID-19 patients with a lipid profile performed on the day of admission analyzed with regard to clinical outcomes.</p></div><div><h3>Results</h3><p>Seventy-seven patients (61.2%) were men, with a mean age of 66.3 (15.6) years. 54.1% had bilateral pneumonia. The all-cause mortality rate during hospitalization was 20.8%. We found a direct association between more severe disease assessed by the WHO classification, admission to the ICU and death with more pronounced lymphopenia, higher levels of CRP, ferritin (<em>p</em> &lt; 0.001), D-dímer and lactate dehydrogenase (LDH) all statistically significant. Lower leves of HDL-c and LDL-c were also associated with a worse WHO classification, ICU admission, and death,. HDL-c levels were inversely correlated with inflammatory markers CRP (<em>r</em> = −0.333; <em>p</em> &lt; 0.001), ferritin (<em>r</em> = −0.354; <em>p</em> &lt; 0.001), D-dímer (<em>r</em> = −0.214; <em>p</em> &lt; 0.001), LDH (<em>r</em> = −0.209; <em>p</em> &lt; 0.001. LDL-c levels were significantly associated with CRP (<em>r</em> = −0.320; <em>p</em> &lt; 0.001) and LDH (<em>r</em> = −0.269; <em>p</em> &lt; 0.001). ROC curves showed that HDL [AUC = 0.737(0.586–0.887), <em>p</em> = 0.005] and lymphocytes [AUC = 0.672(0.497–0.847], <em>p</em> &lt; 0.043] had the best prognostic accuracy to predict death. In a multivariate analysis, HDL-c (β = −0.146(0.770–0.971), <em>p</em> = 0.014) and urea (β = 0.029(1.003–1.057), <em>p</em> = 0.027) predicted mortality.</p></div><div><h3>Conclusion</h3><p>Hypolipidemia including HDL levels at admission identifies patients with a higher risk of death and worse clinical manifestations who may require more intensive care.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"52 ","pages":"Pages 1-8"},"PeriodicalIF":1.6,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9988188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9096496","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":"Young women with familial hypercholesterolemia have higher LDL-cholesterol burden than men: Novel data using repeated measurements during 12-years follow-up","authors":"Anja K. Johansen ,&nbsp;Martin P. Bogsrud ,&nbsp;Jacob J. Christensen ,&nbsp;Amanda Rundblad ,&nbsp;Ingunn Narverud ,&nbsp;Stine Ulven ,&nbsp;Gisle Langslet ,&nbsp;Kjetil Retterstøl ,&nbsp;Kirsten B. Holven","doi":"10.1016/j.athplu.2023.01.001","DOIUrl":"10.1016/j.athplu.2023.01.001","url":null,"abstract":"<div><h3>Background and aims</h3><p>The concentration and the duration of exposure to low-density lipoprotein cholesterol (LDL-C) (LDL-C burden) is an important determinant of risk for cardiovascular disease and thresholds has recently been estimated. Individuals with familial hypercholesterolemia (FH) have increased risk of premature cardiovascular disease. The overall aim of the present study was to describe differences in LDL-C level and LDL-C burden in females and males with FH visiting an outpatient lipid clinic from a young age, using multiple LDL-C measurements during a follow-up time of 12 years. First, we aimed to study if the LDL-C concentration and the LDL-C burden is different between females and males at ages 0–10, 10–20, 20–30 and &gt;30 years. Second, we aimed to estimate the subject-specific LDL-C burden at age 19 and 30 years, and the proportion of female and male patients that reach suggested LDL-C thresholds indicating high risk of ASCVD.</p></div><div><h3>Methods</h3><p>Data was retrospectively collected from medical records of 438 subjects (207 girls and 231 boys) with FH, referred to the Lipid Clinic, Oslo University Hospital below the age of 19 years. The LDL-C burden was estimated based on repeated LDL-C measurements over time.</p></div><div><h3>Results</h3><p>Subjects were followed over a period of mean 12.0 (SD 7.0) years, with median 10 years (7–17; 25–75 percentiles, minimum 2), with median 6 (4–9; 25–75 percentiles, minimum 2) available LDL-C measurements, starting at mean age 11 (SD 3.9) years. There was a difference in both LDL-C and LDL-C burden between sexes at different ages. On average, males had lower LDL-C over time, although this difference was less pronounced with age and males also had lower estimated LDL-C burden over time, and this difference was further exacerbated with age.</p></div><div><h3>Conclusion</h3><p>Our study shows that young women with FH have a higher LDL-C burden than their male counterparts, potentially explaining the increased excess CVD risk seen among these. It underscores the importance of careful-follow up and early treatment initiation both prior to and after pregnancies in order to limit statin-free periods.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"51 ","pages":"Pages 28-34"},"PeriodicalIF":1.6,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9995918/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9455819","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 urinary isoprostanes with measures of subclinical atherosclerosis: The Multi-Ethnic Study of Atherosclerosis (MESA)","authors":"Ryan L. Wallace ,&nbsp;Oluseye Ogunmoroti ,&nbsp;Di Zhao ,&nbsp;Dhananjay Vaidya ,&nbsp;Amir Heravi ,&nbsp;Eliseo Guallar ,&nbsp;Chiadi E. Ndumele ,&nbsp;Joao A.C. Lima ,&nbsp;Pamela Ouyang ,&nbsp;Matthew J. Budoff ,&nbsp;Matthew Allison ,&nbsp;Isac Thomas ,&nbsp;Oluwaseun E. Fashanu ,&nbsp;Ron Hoogeveen ,&nbsp;Wendy S. Post ,&nbsp;Erin D. Michos","doi":"10.1016/j.athplu.2022.12.002","DOIUrl":"10.1016/j.athplu.2022.12.002","url":null,"abstract":"<div><h3>Background</h3><p>Urinary isoprostanes are markers of systemic oxidative stress, which is implicated in the pathogenesis of atherosclerotic cardiovascular disease (ASCVD). Coronary artery calcium (CAC), thoracic aortic calcium (TAC) and carotid plaque are measure subclinical atherosclerosis and prognosticate ASCVD risk. We examined the associations between urinary isoprostane levels and measures of plaque prevalence, burden, incidence and progression across three vascular beds in a cohort from the Multi-Ethnic Study of Atherosclerosis.</p></div><div><h3>Methods</h3><p>Urinary levels of 8-isoprostane and 2,3-dinor-8-F₂-isoprostane were measured in 1089 participants (mean ± SD 62 ± 8 years, 48% women) at baseline. Participants underwent computed tomography for CAC and TAC, and duplex ultrasound for carotid plaque. TAC and CAC were reassessed at 2.4 and 10 years, respectively. Regression models were adjusted for CVD risk factors.</p></div><div><h3>Results</h3><p>In adjusted models, there were no significant associations between isoprostane levels with CAC prevalence or progression. Highest versus lowest tertile of 8-isoprostane was associated with 28% lower prevalence of descending TAC at baseline [prevalence ratio (PR) 0.72 95% CI (0.56, 0.94)], while 1-SD higher 2,3-dinor-8-F₂-isoprostane was associated with 96% higher incident ascending TAC at follow-up [Relative Risk 1.96 (1.24, 3.09)]. Highest versus lowest tertile of isoprostane measures were associated with 22% higher prevalence of carotid plaque [(PR 1.22 (1.04, 1.45)] and 14% difference [3,26] in greater extent of carotid plaque at baseline.</p></div><div><h3>Conclusions</h3><p>Higher urinary isoprostanes were inconsistently associated with some measures of subclinical atherosclerosis by imaging. This suggests a limited role of urinary isoprostane levels as a prognostic marker for the development of ASCVD.</p></div><div><h3>Trial registration</h3><p>The MESA cohort design is registered at <span>clinicaltrials.gov</span><svg><path></path></svg> as follows: <span>https://clinicaltrials.gov/ct2/show/NCT00005487</span><svg><path></path></svg>.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"51 ","pages":"Pages 13-21"},"PeriodicalIF":1.6,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10037087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9561063","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":"Dyslipidemia and the preventive potential in the Greenlandic population","authors":"Johan Skov Bundgaard ,&nbsp;Marit E. Jørgensen ,&nbsp;Kristine Andersen ,&nbsp;Henning Bundgaard ,&nbsp;Uka Wilhjelm Geisler ,&nbsp;Michael Lynge Pedersen","doi":"10.1016/j.athplu.2022.12.003","DOIUrl":"10.1016/j.athplu.2022.12.003","url":null,"abstract":"<div><h3>Background</h3><p>Low-density lipoprotein cholesterol (LDL-C) is a well-established risk factor for development of cardiovascular diseases. Based on available clinical data, we aimed to investigate the plasma lipid profile in the Greenlandic population, the proportion on cholesterol-lowering treatment and the adherence to local indications for cholesterol-lowering therapy.</p></div><div><h3>Methods</h3><p>This is an observational cross-sectional study of the adult (≥21 years) Greenlandic population with focus on clinically determined lipid levels from 2017 to early 2022. We investigated levels of dyslipidemia and assessed cholesterol-lowering medication usage in individuals with an indication according to current Greenlandic guidelines, which include a) LDL-C &gt;5 mmol/l, b) diabetes, c) diagnosed atherosclerotic disease and 4) a SCORE2 &gt;7.5%.</p></div><div><h3>Results</h3><p>In the adult Greenlandic population of 40,565 individuals a lipid profile was available in 13,895 with a mean LDL-C of 3.0 mmol/L and 976 (7%) had a LDL-C &gt;5 mmol/l. One or more indications for cholesterol-lowering medication was present in 3988 individuals and a total of 5464 adult Greenlanders either fulfilled local criteria for statin therapy or received a statin (some without current indication) and among these, 2232 (41%) individuals received no statin.</p></div><div><h3>Conclusion</h3><p>These findings indicate that clinically significant dyslipidemia is common in the adult Greenlandic population and that the cardiovascular preventive potential of cholesterol-lowering therapy is currently underutilized.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"51 ","pages":"Pages 22-27"},"PeriodicalIF":1.6,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10037086/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9546074","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":"Lp(a) does not affect intima media thickness in hypercholesterolemic children –a retrospective cross sectional study","authors":"Oliver Helk ,&nbsp;Andreas Böck ,&nbsp;Claudia Stefanutti ,&nbsp;Kurt Widhalm","doi":"10.1016/j.athplu.2022.11.001","DOIUrl":"10.1016/j.athplu.2022.11.001","url":null,"abstract":"<div><h3>Purpose</h3><p>Combined hyperlipidaemia results in premature atherosclerosis and a high burden of cardiovascular morbidity and mortality. Early identification of highly affected subjects within this population is of utmost importance to enable informed treatment decisions. The measurement of intima media thickness (IMT) is a readily available, non-invasive method to investigate evidence of early atherosclerosis. To assess the usefulness of this method in pediatric subjects with hypercholesterolemia, we here examined a possible interaction of LDL-C and Lp(a) on IMT.</p></div><div><h3>Methods</h3><p>Blood lipids (Lp(a), LDL-cholesterol, total cholesterol, triglycerides, high density lipoprotein (HDL) -cholesterol, apolipoprotein A1, apolipoprotein B), anthropometric parameters (age, height, weight, body mass index (BMI)) and possibly existing early evidence of atherosclerotic lesions measured by intima media thickness (IMT zscore).as a surrogate parameter was examined retrospectively in 113 children and adolescents (aged 1–18 years) with elevated Lp(a) and/or LDL-cholesterol (Lp(a) &gt; 30 mg/dL, LDL&gt;130 mg/dL). Furthermore, we compared hsCRP levels between groups.</p></div><div><h3>Results</h3><p>There were no significant differences in IMT Zscore or hsCRP between groups. Regression analysis did not reveal a statistically significant interaction between Lp(a) and LDL-C.</p></div><div><h3>Conclusions</h3><p>At the age of 6–18 years, we found no significant differences in early markers of atherosclerosis between subjects with high Lp(a)- and/or high LDL-cholesterol with no detectable synergistic effects between the two lipoproteins.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"51 ","pages":"Pages 1-7"},"PeriodicalIF":1.6,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/fc/54/main.PMC10037085.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9561068","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":"Dendritic cell marker Clec4a4 deficiency limits atherosclerosis progression","authors":"Rossella Bellini ,&nbsp;Annalisa Moregola ,&nbsp;Jasmine Nour ,&nbsp;Yoann Rombouts ,&nbsp;Olivier Neyrolles ,&nbsp;Patrizia Uboldi ,&nbsp;Fabrizia Bonacina ,&nbsp;Giuseppe Danilo Norata","doi":"10.1016/j.athplu.2022.12.001","DOIUrl":"10.1016/j.athplu.2022.12.001","url":null,"abstract":"<div><h3>Background and aims</h3><p>Atherogenesis results from altered lipid metabolism and impaired immune response. Emerging evidence has suggested that dendritic cells (DCs) participate to atherosclerosis-related immune response, but their impact is scarcely characterized. Clec4a4 or DCIR2 (Dendritic cell immunoreceptor 2) is a C-type lectin receptor, mainly expressed by CD8α⁻ DCs, able to modulate T cell immunity. However, whether this DC subset could play a role in the atherogenesis is still poorly understood. Thus, the aim of this study is to investigate whether the absence of Clec4a4 could affect atherosclerosis-related immune response and atherosclerosis itself.</p></div><div><h3>Methods</h3><p><em>Dcir2</em>^{<em>−/−</em>} <em>Ldlr</em>^{<em>−/−</em>} and <em>Ldlr</em>^{<em>−/−</em>} mice were fed a standard diet or cholesterol-enriched diet for 12 weeks. Subsequently, the profile of circulating and lymph nodes-resident immune cells was investigated together with the analysis of plasma lipid levels and atherosclerotic plaque extension in the aorta.</p></div><div><h3>Results</h3><p>Here, we show that <em>Clec4a4</em> expression is downregulated under hypercholesterolemia and its deficiency in <em>Ldlr</em>^−/− mice results in the reduction of atherosclerotic plaque formation, together with altered lipid metabolism and impaired myeloid immune cell distribution.</p></div><div><h3>Conclusions</h3><p>Our findings suggest a pro-atherosclerotic role of Clec4a4 in experimental atherosclerosis.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"51 ","pages":"Pages 8-12"},"PeriodicalIF":1.6,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/07/bf/main.PMC10037088.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9561069","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}