Atherosclerosis plus最新文献

{"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}

{"title":"Prediabetes is an incremental risk factor for adverse cardiac events: A nationwide analysis","authors":"Dhairya Nanavaty ,&nbsp;Rhea Green ,&nbsp;Ankushi Sanghvi ,&nbsp;Rishav Sinha ,&nbsp;Sohrab Singh ,&nbsp;Tushar Mishra ,&nbsp;Pradeep Devarakonda ,&nbsp;Kendall Bell ,&nbsp;Cesar Ayala Rodriguez ,&nbsp;Kanwal Gambhir ,&nbsp;Chadi Alraies ,&nbsp;Sarath Reddy","doi":"10.1016/j.athplu.2023.08.002","DOIUrl":"10.1016/j.athplu.2023.08.002","url":null,"abstract":"<div><h3>Background and aims</h3><p>Prediabetes is defined as a state of impaired glucose metabolism with hemoglobin A1c (HbA1c) levels that precede those of a diabetic state. There is increasing evidence that suggests that hyperglycemic derangement in prediabetes leads to microvascular and macrovascular complications even before progression to overt diabetes mellitus. We aim to identify the association of prediabetes with acute cardiovascular events.</p></div><div><h3>Methods</h3><p>We utilized the National inpatient sample 2018-2020 to identify adult hospitalizations with prediabetes after excluding all hospitalizations with diabetes. Demographics and prevalence of other cardiovascular risk factors were compared in hospitalizations with and without prediabetes using the chi-square test for categorical variables and the <em>t</em>-test for continuous variables. Multivariate regression analysis was further performed to study the impact of prediabetes on acute coronary syndrome, acute ischemic stroke, intracranial hemorrhage, and acute heart failure.</p></div><div><h3>Results</h3><p>Hospitalizations with prediabetes had a higher prevalence of cardiovascular risk factors like hypertension, hyperlipidemia, obesity, and tobacco abuse. In addition, the adjusted analysis revealed that hospitalizations with prediabetes were associated with higher odds of developing acute coronary syndrome (OR-2.01; C.I:1.94-2.08; P&lt;0.001), acute ischemic stroke (OR-2.21; 2.11-2.31; p&lt;0.001), and acute heart failure (OR-1.41; C.I.: 1.29-1.55; p&lt;0.001) as compared to hospitalizations without prediabetes.</p></div><div><h3>Conclusions</h3><p>Our study suggests that prediabetes is associated with a higher odds of major cardiovascular events. Further prospective studies should be conducted to identify prediabetes as an independent causative factor for these events. In addition, screening and lifestyle modifications for prediabetics should be encouraged to improve patient outcomes.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"54 ","pages":"Pages 22-26"},"PeriodicalIF":1.6,"publicationDate":"2023-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a0/7a/main.PMC10543778.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41141530","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), Interleukin-6 inhibitors, and atherosclerotic cardiovascular disease: Is there an association?","authors":"Anastasios Makris ,&nbsp;Fotios Barkas ,&nbsp;Petros P. Sfikakis ,&nbsp;Evangelos Liberopoulos ,&nbsp;Theodosios D. Filippatos ,&nbsp;Kausik K. Ray ,&nbsp;Aris P. Agouridis","doi":"10.1016/j.athplu.2023.09.001","DOIUrl":"10.1016/j.athplu.2023.09.001","url":null,"abstract":"<div><h3>Background and aims</h3><p>Lipoprotein(a) [Lp(a)] and interleuking-6 (IL-6), an inflammation biomarker, have been established as distinct targets of the residual atherosclerotic cardiovascular disease (ASCVD) risk. We aimed to investigate the association between them, and the potential clinical implications in ASCVD prevention.</p></div><div><h3>Methods</h3><p>A literature search was conducted in PubMed until December 31st, 2022, using relevant keywords.</p></div><div><h3>Results</h3><p>Elevated lipoprotein(a) [Lp(a)] levels constitute the most common inherited lipid disorder associated with ASCVD. Although Lp(a) levels are mostly determined genetically by the LPA gene locus, they may be altered by acute conditions of stress and chronic inflammatory diseases. Considering its resemblance with low-density lipoproteins, Lp(a) is involved in atherosclerosis, but it also exerts oxidative, thrombotic, antifibrinolytic and inflammatory properties. The cardiovascular efficacy of therapies lowering Lp(a) by &gt;90% is currently investigated. On the other hand, interleukin (IL)-1b/IL-6 pathway also plays a pivotal role in atherosclerosis and residual ASCVD risk. IL-6 receptor inhibitors [IL-6(R)i] lower Lp(a) by 16–41%, whereas ongoing trials are investigating their potential anti-atherosclerotic effect. The Lp(a)-lowering effect of IL-6(R)i might be attributed to the inhibition of the IL-6 response elements in the promoter region of the LPA gene.</p></div><div><h3>Conclusions</h3><p>Although the effect of IL-6(R)i on Lp(a) levels is inferior to that of available Lp(a)-lowering therapies, the dual effect of the former on both inflammation and apolipoprotein (a) synthesis may prove of equal or even greater significance when it comes ASCVD outcomes. More trials are required to establish IL-6(R)i in ASCVD prevention and elucidate their interplay with Lp(a) as well as its clinical significance.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"54 ","pages":"Pages 1-6"},"PeriodicalIF":1.6,"publicationDate":"2023-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/04/ba/main.PMC10500445.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10279978","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":"Increased extracellular vesicles (EVs) related to T cell-mediated inflammation and vascular function in familial hypercholesterolemia","authors":"Morten Hjuler Nielsen ,&nbsp;Rikke Bæk ,&nbsp;Malene Moller Jorgensen ,&nbsp;Maiken Mellergaard ,&nbsp;Aase Handberg","doi":"10.1016/j.athplu.2023.06.004","DOIUrl":"10.1016/j.athplu.2023.06.004","url":null,"abstract":"<div><h3>Background and aims</h3><p>OxLDL modulates innate and adaptive immunity, and extracellular vesicles (EVs) released from both non-immune and immune cells are proposed key players in atherosclerosis development. In the present study, we aimed to investigate EVs expressing markers related to adaptive immunity-driven inflammation and endothelial activation/dysfunction in hypercholesterolemic patients.</p></div><div><h3>Methods</h3><p>EVs were phenotyped in thirty patients with familial hypercholesterolemia (FH) and twenty-three healthy controls using the Extracellular Vesicle (EV) Array with antibodies targeting proteins expressed on B and T cells, and endothelial cells.</p></div><div><h3>Results</h3><p>FH patients had a higher atherosclerotic burden, as determined by the mean carotid intima-media thickness (IMT) (0.64 ± 0.12 mm vs. 0.58 ± 0.07 mm; p = 0.033), higher oxLDL levels (p &lt; 0.0001), and showed increased levels of EV-specific markers: CD9 (p = 0.017), CD63 (p = 0.045), CD81 (p = 0.003), Annexin V (p = 0.018), and EV markers related to adaptive/lymphocyte immunity: CD28 (p = 0.034), CD4 (p = 0.049), CD152 (p = 0.029), LFA-1 (p = 0.024), and endothelial function: CD62E (p = 0.032), CD144 (p = 0.018), tPA (p = 0.017), CD31 (p = 0.024). Linear regression revealed a positive relationship between carotid IMT and several of the increased markers observed within the FH group, including CD9 (β = 0.33; p = 0.022), CD63 (β = 0.35; p 225 = 0.026), CD28 (β = 0.37; p = 0.026), CD4 (β = 0.40; p = 0.025), CD152 (β = 0.41; p = 0.017), LFA-1 (β = 0.42; p = 0.014) and CD62E (β = 0.38; p = 0.024).</p></div><div><h3>Conclusion</h3><p>EVs associated with adaptive immunity and endothelial dysfunction are elevated in FH patients, and several markers related to a higher atherosclerotic burden.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"53 ","pages":"Pages 16-25"},"PeriodicalIF":1.6,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10457578/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10165046","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 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}