Atherosclerosis plus最新文献

{"title":"The effect of hydroxychloroquine on cholesterol metabolism in statin treated patients after myocardial infarction","authors":"Lotta Ulander ,&nbsp;Piia Simonen ,&nbsp;Heli Tolppanen ,&nbsp;Otto Hartman ,&nbsp;Tuomas T. Rissanen ,&nbsp;Kari K. Eklund ,&nbsp;Marita Kalaoja ,&nbsp;Mika Kurkela ,&nbsp;Mikko Neuvonen ,&nbsp;Mikko Niemi ,&nbsp;Janne T. Backman ,&nbsp;Helena Gylling ,&nbsp;Juha Sinisalo ,&nbsp;on behalf of the OXI pilot trial","doi":"10.1016/j.athplu.2023.06.003","DOIUrl":"10.1016/j.athplu.2023.06.003","url":null,"abstract":"<div><h3>Background and aims</h3><p>To evaluate the effect of hydroxychloroquine (HCQ) on serum and lipoprotein lipids and serum biomarkers of cholesterol synthesis and absorption in myocardial infarction patients with a high-dose statin.</p></div><div><h3>Methods</h3><p>Myocardial infarction patients (n = 59) with a constant statin dose were randomized to receive hydroxychloroquine 300 mg (n = 31) or placebo (n = 28) daily for six months and followed up for one year.</p></div><div><h3>Results</h3><p>Statin reduced total-c (−26 ± 22% in hydroxychloroquine and −28 ± 19% in placebo group, P = 0.931), LDL-c (−38 ± 26% vs. −44 ± 23%, respectively, P = 0.299), and cholesterol synthesis biomarkers zymostenol, desmosterol, and lathosterol ratios from baseline to one year (e.g., serum lathosterol ratio −17 ± 45% vs. −15 ± 41%, respectively, P &lt; 0.001 for both, P = 0.623 between groups). Compensatorily, cholesterol absorption increased during the intervention (e.g., serum campesterol ratio 125 ± 90% vs. 113 ± 72%, respectively, P &lt; 0.001 for both, P = 0.488 between groups). Hydroxychloroquine did not affect cholesterol concentrations or cholesterol absorption. It prevented the statin-induced increase in cholesterol precursor, desmosterol ratio, from six months to one year in the hydroxychloroquine group (P = 0.007 at one year compared to placebo).</p></div><div><h3>Conclusions</h3><p>Combined with a high-dose statin, hydroxychloroquine had no additional effect on serum cholesterol concentration or cholesterol absorption. However, the findings suggest that hydroxychloroquine interferes with lanosterol synthesis, and thereafter, it temporarily interferes with the cholesterol synthesis pathway, best seen in halting the increase of the desmosterol ratio.</p><p>Trial Registration ClinicalTrials.gov Identifier: NCT02648464.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"53 ","pages":"Pages 26-32"},"PeriodicalIF":1.6,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10336266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9822958","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":"SARS-CoV-2 reinfection: Adding insult to dysfunctional endothelium in patients with atherosclerotic cardiovascular disease","authors":"Petri T. Kovanen ,&nbsp;Alpo Vuorio","doi":"10.1016/j.athplu.2023.06.002","DOIUrl":"10.1016/j.athplu.2023.06.002","url":null,"abstract":"<div><p>In this short narrative review, we aim at defining the pathophysiological role endothelial dysfunction in the observed COVID-19–associated rise in risk of cardiovascular disease. Variants of the SARS-CoV-2 virus have caused several epidemic waves of COVID-19, and the emergence and rapid spread of new variants and subvariants are likely. Based on a large cohort study, the incidence rate of SARS-CoV-2 reinfection is about 0.66 per 10 000 person-weeks. Both the first infection and reinfection with SARS-CoV-2 increase cardiac event risk, particularly in vulnerable patients with cardiovascular risk factors and the accompanying systemic endothelial dysfunction. By worsening pre-existing endothelial dysfunction, both the first infection and reinfection with ensuing COVID-19 may turn the endothelium procoagulative and prothrombotic, and ultimately lead to local thrombus formation. When occurring in an epicardial coronary artery, the risk of an acute coronary syndrome increases, and when occurring in intramyocardial microvessels, scattered myocardial injuries will ensue, both predisposing the COVID-19 patients to adverse cardiovascular outcomes. In conclusion, considering weakened protection against the cardiovascular risk-enhancing reinfections with emerging new subvariants of SARS-CoV-2, treatment of COVID-19 patients with statins during the illness and thereafter is recommended, partly because the statins tend to reduce endothelial dysfunction.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"53 ","pages":"Pages 1-5"},"PeriodicalIF":1.6,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10238112/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10100484","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 lipoproteins and non-alcoholic fatty liver disease","authors":"Menno Hoekstra ,&nbsp;Miranda Van Eck","doi":"10.1016/j.athplu.2023.08.001","DOIUrl":"10.1016/j.athplu.2023.08.001","url":null,"abstract":"<div><h3>Background and aims</h3><p>Non-alcoholic fatty liver disease (NAFLD), a high incidence liver pathology, is associated with a ∼1.5-fold higher cardiovascular disease risk. This phenomenon is generally attributed to the NAFLD-associated increase in circulating levels of pro-atherogenic apolipoprotein B100-containing small dense low-density lipoprotein and plasma hypertriglyceridemia. However, also a significant reduction in cholesterol transported by anti-atherogenic high-density lipoproteins (HDL) is frequently observed in subjects suffering from NAFLD as compared to unaffected people. In this review, we summarize data regarding the relationship between NAFLD and plasma HDL-cholesterol levels, with a special focus on highlighting potential causality between the NAFLD pathology and changes in HDL metabolism.</p></div><div><h3>Methods and results</h3><p>Publications in PUBMED describing the relationship between HDL levels and NAFLD susceptibility and/or disease severity, either in human clinical settings or genetically-modified mouse models, were critically reviewed for subsequent inclusion in this manuscript. Furthermore, relevant literature describing effects on lipid loading in cultured hepatocytes of models with genetic alterations related to HDL metabolism have been summarized.</p></div><div><h3>Conclusions</h3><p>Although in vitro observations suggest causality between HDL formation by hepatocytes and protection against NAFLD-like lipid accumulation, current literature remains inconclusive on whether relative HDL deficiency is actually driving the development of fatty liver disease in humans. In light of the current obesity pandemic and the associated marked rise in NAFLD incidence, it is of clear scientific and societal interest to gain further insight into the relationship between HDL-cholesterol levels and fatty liver development to potentially uncover the therapeutic potential of pharmacological HDL level and/or function modulation.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"53 ","pages":"Pages 33-41"},"PeriodicalIF":1.6,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10469384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10208204","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 German CaRe high registry for familial hypercholesterolemia – Sex differences, treatment strategies, and target value attainment","authors":"Winfried März ,&nbsp;Nina Schmidt ,&nbsp;Ira an Haack ,&nbsp;Alexander Dressel ,&nbsp;Tanja B. Grammer ,&nbsp;Marcus E. Kleber ,&nbsp;Andrea Baessler ,&nbsp;F. Ulrich Beil ,&nbsp;Ioanna Gouni-Berthold ,&nbsp;Ulrich Julius ,&nbsp;Ursula Kassner ,&nbsp;Julius L. Katzmann ,&nbsp;Gerald Klose ,&nbsp;Christel König ,&nbsp;Wolfgang Koenig ,&nbsp;Ann-Cathrin Koschker ,&nbsp;Ulrich Laufs ,&nbsp;Martin Merkel ,&nbsp;Britta Otte ,&nbsp;Klaus G. Parhofer ,&nbsp;Ulrike Schatz","doi":"10.1016/j.athplu.2023.06.001","DOIUrl":"10.1016/j.athplu.2023.06.001","url":null,"abstract":"<div><h3>Background and aims</h3><p>Familial hypercholesterolemia (FH) is among the most common genetic disorders in primary care. However, only 15% or less of patients are diagnosed, and few achieve the goals for low-density lipoprotein cholesterol (LDL-C). In this analysis of the German Cascade Screening and Registry for High Cholesterol (CaRe High), we examined the status of lipid management, treatment strategies, and LDL-C goal attainment according to the ESC/EAS dyslipidemia guidelines.</p></div><div><h3>Methods</h3><p>We evaluated consolidated datasets from 1501 FH patients diagnosed clinically and seen either by lipid specialists or general practitioners and internists. We conducted a questionnaire survey of both the recruiting physicians and patients.</p></div><div><h3>Results</h3><p>Among the 1501 patients, 86% regularly received lipid-lowering drugs. LDL-C goals were achieved by 26% and 10% of patients with atherosclerotic cardiovascular disease (ASCVD) according to the 2016 and 2019 ESC/EAS dyslipidemia guidelines, respectively. High intensity lipid-lowering was administered more often in men than in women, in patients with ASCVD, at higher LDL-C and in patients with a genetic diagnosis of FH.</p></div><div><h3>Conclusions</h3><p>FH is under-treated in Germany compared to guideline recommendations. Male gender, genetic proof of FH, treatment by a specialist, and presence of ASCVD appear to be associated with increased treatment intensity. Achieving the LDL-C goals of the 2019 ESC/EAS dyslipidemia guidelines remains challenging if pre-treatment LDL-C is very high.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"53 ","pages":"Pages 6-15"},"PeriodicalIF":1.6,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10331285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9804814","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":"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}