Atherosclerosis最新文献

{"title":"Unraveling the complex interplay of PPARα and age in cardiac metabolism: Implications for managing age-related cardiac dysfunctions.","authors":"Sina Rashedi, Mohammad Keykhaei","doi":"10.1016/j.atherosclerosis.2024.118627","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2024.118627","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"118627"},"PeriodicalIF":4.9,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single bolus PCSK9 Inhibition: A new approach to plaque stabilisation.","authors":"Stephen J Nicholls, Gavin Pr Manmathan","doi":"10.1016/j.atherosclerosis.2024.118628","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2024.118628","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"118628"},"PeriodicalIF":4.9,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of pooled cohort equation and PREVENT™ risk calculator for statin treatment allocation","authors":"Joseph Heaton ,&nbsp;Abbas Alshami ,&nbsp;Steven Imburgio ,&nbsp;Vandan Upadhyaya ,&nbsp;Matthew Saybolt ,&nbsp;Renato Apolito ,&nbsp;Riple Hansalia ,&nbsp;Jeffrey Selan ,&nbsp;Jesus Almendral ,&nbsp;Brett Sealove","doi":"10.1016/j.atherosclerosis.2024.118626","DOIUrl":"10.1016/j.atherosclerosis.2024.118626","url":null,"abstract":"<div><h3>Background and aims</h3><div>Effective hypercholesterolemia management is linked to lower all-cause and cardiovascular mortality. The 2018 AHA/ACC guidelines recommended using the Pooled Cohort Equations (PCE) for lipid management, but these may overestimate risk and be less accurate for certain racial groups. The AHA's new PREVENT equation, which omits race and includes cardiometabolic factors, aims to provide a more accurate risk assessment for a diverse population. However, it has not yet been applied to a nationally representative US population, and implementation guidelines are still lacking. Our study aimed to evaluate potential changes in hypercholesterolemia management for primary prevention by using the PREVENT equation instead of the PCE.</div></div><div><h3>Methods</h3><div>Analyzing pre-pandemic NHANES 2017–2020 data, participants aged 40–75 without prior lipid-lowering treatment or other compelling indication were identified for elevated risk (≥7.5 %) using the PCE and PREVENT equations. We assessed risk shifts and indications for statin therapy, comparing the two risk equations. NHANES guidelines with weighting were followed to obtain US nationally representative estimates.</div></div><div><h3>Results</h3><div>Out of 77, 647, 807 (unweighted = 2494) participants, 81.0 % had no change in risk. The PCE flagged 18.8 % (n = 14,614,094) of participants at elevated risk not identified by PREVENT, while 0.20 % (n = 107,813) were flagged only by PREVENT. Participants identified solely by the PCE were older, with higher systolic blood pressure and increased estimated glomerular filtration rates.</div><div>Indications for statin therapy were largely unchanged (81.0 %). PREVENT newly identified (0.20 %) for moderate-intensity therapy and none for high-intensity therapy. Participants qualifying for moderate intensity therapy by the PCE were reclassified to no therapy in 74.59 % of cases, while 25.41 % remained unchanged. Participants qualifying for high-intensity therapy by the PCE were reclassified to moderate therapy in 93.97 % of cases, and 6.03 % were reclassified to no therapy.</div></div><div><h3>Conclusions</h3><div>The PREVENT equation notably differs in identifying hypercholesterolemia candidates compared to the PCE. Its adoption would influence cardiovascular risk reduction therapy recommendations, emphasizing the need for comprehensive studies to understand its long-term impact and reevaluate the threshold of treatment strategies for improved patient outcomes.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"399 ","pages":"Article 118626"},"PeriodicalIF":4.9,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Statin use is associated with less ST-elevation versus non-ST-elevation myocardial infarction in a nationwide study","authors":"Sofie B. Simony ,&nbsp;Anne Langsted ,&nbsp;Martin B. Mortensen ,&nbsp;Børge G. Nordestgaard ,&nbsp;Shoaib Afzal","doi":"10.1016/j.atherosclerosis.2024.118625","DOIUrl":"10.1016/j.atherosclerosis.2024.118625","url":null,"abstract":"<div><h3>Background and aims</h3><div>Statin therapy reduces myocardial infarction rate but whether it is associated with a shift of ST-elevation myocardial infarction (STEMI) towards non-ST-elevation myocardial infarction (non-STEMI) remains unknown. Thus, we tested the hypothesis that statin use is associated with less STEMI relative to non-STEMI in first-time myocardial infarction.</div></div><div><h3>Methods</h3><div>In a nationwide study, including 66,896 patients with first-time myocardial infarction between 2010 and 2021, we obtained multivariable risk estimates for STEMI <em>versus</em> non-STEMI according to any statin use, cumulated statin use, and daily statin dose. Furthermore, we obtained hazard ratios for 60-day mortality (5545 deaths) following myocardial infarction according to type of infarction.</div></div><div><h3>Results</h3><div>Odds ratios for STEMI <em>versus</em> non-STEMI were 0.81 (95 % CI:0.77–0.85) and 1.07 (1.01–1.13) in current and previous statin users compared to never statin users. Cumulated statin exposure yielded odds ratios of 0.96 (0.87–1.07) for &lt;2 statin-years, 0.87 (0.79–0.95) for 2–4.9 statin-years, 0.80 (0.74–0.87) for 5–10 statin-years, and 0.75 (0.70–0.80) for &gt;10 statin-years compared to never users. Corresponding odds ratios for statin dose intensity were 0.89 (0.84–0.95) for low-intensity, 0.77 (0.73–0.82) for moderate-intensity, and 0.70 (0.63–0.77) for high-intensity. Results were similar in multiple sensitivity analyses and using a cohort design. The hazard ratio for 60-day mortality after first-time STEMI <em>versus</em> non-STEMI was 2.24 (2.13–2.37).</div></div><div><h3>Conclusions</h3><div>In this nationwide study, prior statin use is associated with less STEMI relative to non-STEMI in a dose dependent manner. This indicates that statin therapy, in addition to reducing myocardial infarction event rates, also result in a less severe presentation of myocardial infarctions.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"399 ","pages":"Article 118625"},"PeriodicalIF":4.9,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Shear stress is uncoupled from atheroprotective KLK10 in atherosclerotic plaques","authors":"Ziqi Zhou ,&nbsp;Suze-Anne Korteland ,&nbsp;Blanca Tardajos-Ayllon ,&nbsp;Junxi Wu ,&nbsp;Emily Chambers ,&nbsp;Julia Weninck ,&nbsp;Michael Simons ,&nbsp;Mark Dunning ,&nbsp;Torsten Schenkel ,&nbsp;Mannekomba Diagbouga ,&nbsp;Jolanda Wentzel ,&nbsp;Maria Fragiadaki ,&nbsp;Paul C. Evans","doi":"10.1016/j.atherosclerosis.2024.118622","DOIUrl":"10.1016/j.atherosclerosis.2024.118622","url":null,"abstract":"<div><h3>Background and aims</h3><div>Physiological shear stress promotes vascular homeostasis by inducing protective molecules in endothelial cells (EC). However, physiological shear stress has been linked to atherosclerosis progression in some individuals with heightened cardiovascular risk. To address this apparent paradox, we hypothesized that diseased arteries may exhibit reduced responsiveness to the protective effects of physiological shear stress. Consequently, we compared the transcriptome of EC exposed to physiological shear stress in healthy arteries <em>versus</em> atherosclerotic conditions.</div></div><div><h3>Methods</h3><div>Employing 3D light sheet imaging and computational fluid dynamics, we identified NOS3 as a marker of physiological shear stress in both healthy and atherosclerotic murine arteries. Single-cell RNA sequencing was performed on EC from healthy (C57BL/6) mice, mildly diseased (<em>Apoe</em>^{<em>−/−</em>} normal diet) mice, and highly diseased (<em>Apoe</em>^{<em>−/−</em>} high fat diet) mice. The transcriptomes of <em>Nos3</em>^high cells (exposed to physiological shear stress) were compared among the groups.</div></div><div><h3>Results</h3><div><em>Nos3</em>^high EC were associated with several markers of physiological shear stress in healthy arteries. Clustering of <em>Nos3</em>^high EC revealed 8 different EC subsets that varied in proportion between healthy and diseased arteries. Cluster-specific nested functional enrichment of gene ontology terms revealed that <em>Nos3</em>^high EC in diseased arteries were enriched for inflammatory and apoptotic gene expression. These alterations were accompanied by changes in several mechanoreceptors, including the atheroprotective factor KLK10, which was enriched in <em>Nos3</em>^high EC in healthy arteries but markedly reduced in severely diseased arteries.</div></div><div><h3>Conclusions</h3><div>Physiological shear stress is uncoupled from atheroprotective KLK10 within atherosclerotic plaques. This sheds light on the complex interplay between shear stress, endothelial function, and the progression of atherosclerosis in individuals at risk of cardiovascular complications.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"398 ","pages":"Article 118622"},"PeriodicalIF":4.9,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142441174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age drives the impact of vascular disease on ischemic stroke in patients with atrial fibrillation: Role of hypertension and prediabetes.","authors":"Pasquale Mone, Florindo D'Onofrio, Tommaso Dazzetti, Thais Luma De Oliveira Roza, Germano Guerra, Gaetano Santulli","doi":"10.1016/j.atherosclerosis.2024.118619","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2024.118619","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"118619"},"PeriodicalIF":4.9,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142493738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeted plasma multi-omics propose glutathione, glycine and serine as biomarkers for abdominal aortic aneurysm growth on serial CT scanning","authors":"Alexander Vanmaele ,&nbsp;Elke Bouwens ,&nbsp;Sanne E. Hoeks ,&nbsp;Alida Kindt ,&nbsp;Lieke Lamont ,&nbsp;Bram Fioole ,&nbsp;Ricardo PJ. Budde ,&nbsp;Sander ten Raa ,&nbsp;Burhan Hussain ,&nbsp;José Oliveira-Pinto ,&nbsp;Arne S. Ijpma ,&nbsp;Felix van Lier ,&nbsp;K. Martijn Akkerhuis ,&nbsp;Danielle F. Majoor-Krakauer ,&nbsp;Jorg L. de Bruin ,&nbsp;Thomas Hankemeier ,&nbsp;Yolanda de Rijke ,&nbsp;Hence JM. Verhagen ,&nbsp;Eric Boersma ,&nbsp;Isabella Kardys","doi":"10.1016/j.atherosclerosis.2024.118620","DOIUrl":"10.1016/j.atherosclerosis.2024.118620","url":null,"abstract":"<div><h3>Background and aims</h3><div>Abdominal aortic aneurysm (AAA) patients undergo uniform imaging surveillance until reaching the surgical threshold. In spite of the ongoing exploration of AAA pathophysiology, biomarkers for personalized surveillance are lacking. This study aims to identify potential circulating biomarkers for AAA growth on serial CT scans.</div></div><div><h3>Methods</h3><div>Patients with an AAA (maximal diameter ≥40 mm) were included in this multicentre, prospective cohort study. Participants underwent baseline blood sampling and yearly CT-imaging to determine AAA diameter and volume. Proteins and metabolites were measured using proximity extension assay (Olink Cardiovascular III) or separate ELISA panels, and mass-spectrometry (LC-TQMS), respectively. Linear mixed-effects, orthogonal partial least squares, and Cox regression were used to explore biomarker associations with AAA volume growth rate and the risk of surpassing the surgical threshold, as formulated by current guidelines.</div></div><div><h3>Results</h3><div>271 biomarkers (95 proteins, 176 metabolites) were measured in 109 (90.8 % male) patients with mean age 72. Median baseline maximal AAA diameter was 47.8 mm, volume 109 mL. Mean annual AAA volume growth rate was 11.5 %, 95 % confidence interval (CI) (10.4, 12.7). Median follow-up time was 23.2 months, 49 patients reached the surgical threshold. Patients with one standard deviation (SD) higher glutathione and glycine levels at baseline had an AAA volume growth rate that respectively was 1.97 %, 95%CI (0.97, 2.97) and 1.74 %, 95%CI (0.78, 2.71) larger, relative to the actual aneurysm size. Serine was associated with the risk of reaching the surgical threshold, independent of age and baseline AAA size (cause-specific hazard ratio per SD difference 1.78, 95%CI (1.30, 2.44)).</div></div><div><h3>Conclusions</h3><div>Among multiple intertwined biomarkers related to AAA pathophysiology and progression, glutathione, glycine and serine were most promising.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"398 ","pages":"Article 118620"},"PeriodicalIF":4.9,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142387543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the adaptive immune continuum in atherosclerosis and post-MI injury","authors":"Viktoria Juhasz ,&nbsp;Fiona T. Charlier ,&nbsp;Tian X. Zhao ,&nbsp;Dimitrios Tsiantoulas","doi":"10.1016/j.atherosclerosis.2024.118616","DOIUrl":"10.1016/j.atherosclerosis.2024.118616","url":null,"abstract":"<div><div>Atherosclerotic disease is a cholesterol-rich lipoprotein particle-driven disease resulting in the formation of atherosclerotic plaques in large and medium size arteries. Rupture or erosion of atherosclerotic plaques can trigger the formation of a thrombus causing the obstruction of the blood flow in the coronary artery and thereby leading to myocardial infarction (MI). Inflammation is a crucial pillar of the mechanisms leading to atherosclerosis and governing the cardiac repair post-MI. Dissecting the complex and sophisticated networks of the immune responses underlying the formation of atherosclerotic plaques and affecting the healing of the heart after MI will allow the designing of highly precise immunomodulatory therapies for these settings. Notably, MI also accelerates atherosclerosis via modulating the response of the immune system. Therefore, for the identification of effective and safe therapeutic targets, it is critical to consider the inflammatory continuum that interconnects the two pathologies and identify immunomodulatory strategies that confer a protective effect in both settings or at least, affect each pathology independently. Adaptive immunity, which consists of B and T lymphocytes, is a major regulator of atherosclerosis and post-MI cardiac repair. Here, we review and discuss the effect of potential adaptive immunity-targeting therapies, such as cell-depleting therapies, in atherosclerosis and post-MI cardiac injury.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"399 ","pages":"Article 118616"},"PeriodicalIF":4.9,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142638312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy and safety of statins, ezetimibe and statins-ezetimibe therapies for children and adolescents with heterozygous familial hypercholesterolaemia: Systematic review, pairwise and network meta-analyses of randomised controlled trials.","authors":"Alexis Llewellyn, Mark Simmonds, David Marshall, Melissa Harden, Beth Woods, Steve E Humphries, Uma Ramaswami, Lorraine Priestley-Barnham, Mark Fisher, Laila J Tata, Nadeem Qureshi","doi":"10.1016/j.atherosclerosis.2024.118598","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2024.118598","url":null,"abstract":"<p><strong>Background and aims: </strong>Statins, ezetimibe and statins-ezetimibe combination therapy are recommended lipid-lowering therapies (LLTs) in children with heterozygous familial hypercholesterolaemia (HeFH). However, their relative effectiveness is not well understood. We aimed to compare the safety and efficacy of these therapies using direct and indirect comparisons.</p><p><strong>Methods: </strong>We conducted systematic review, pairwise and network meta-analyses (NMAs) of randomised-controlled trials (RCTs) of statins, ezetimibe and statins-ezetimibe combination therapy in people <18 years with HeFH. Comprehensive bibliographic searches were conducted in December 2022, and a Medline update in January 2024. NMA models accounted for drug class, statin type and dosage.</p><p><strong>Results: </strong>Thirteen RCTs were included (n = 1649, median age 13 years, follow-up 6 weeks-2 years). All LLTs reduced low-density lipoprotein cholesterol (LDL-C) and total cholesterol; statins led to increases in high-density lipoprotein cholesterol and reductions in triglycerides. Statins reduced LDL-C by 33.61 % against placebo (95 % CI 27.58 to 39.63, I² = 83 %). Adding ezetimibe to statins reduced LDL-C by an additional 15.85 % (95 % CI 11.91 to 19.79). NMAs showed intermediate-dose statins reduced LDL-C by an additional 4.77 % compared with lower-doses statins (95 % CrI -11.22 to 1.05); higher-dose statins and intermediate-dose statins + ezetimibe may be similarly effective and are probably superior to ezetimibe, intermediate-and lower-dose statins. There was no evidence of differences in maturation, safety or tolerability between LLTs and placebo.</p><p><strong>Conclusions: </strong>Statins, ezetimibe and statins-ezetimibe are all effective treatments for children with HeFH, but the magnitude of LDL-C reductions varies and may depend on treatment dosage and combination. No safety or tolerability issues were found. Longer-term safety and effectiveness are uncertain.</p>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"118598"},"PeriodicalIF":4.9,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of HDL cholesterol with all-cause and cardiovascular mortality in primary hypercholesterolemia.","authors":"Ana M Bea, Anton González-Guerrero, Ana Cenarro, Itziar Lamiquiz-Moneo, Elisenda Climent, Estibaliz Jarauta, Irene Gracia-Rubio, David Benaiges, Martín Laclaustra, Teresa Tejedor, Juan Pedro-Botet, Fernando Civeira, Victoria Marco-Benedí","doi":"10.1016/j.atherosclerosis.2024.118617","DOIUrl":"10.1016/j.atherosclerosis.2024.118617","url":null,"abstract":"<p><strong>Background and aims: </strong>Recent reports have shown that subjects with high high-density lipoprotein cholesterol (HDLc) levels are paradoxically at increased risk for all-cause and cardiovascular mortality. The aim was to study the association of HDLc concentration with mortality in subjects with high cholesterol.</p><p><strong>Methods: </strong>We analyzed total mortality, cardiovascular mortality, and non-cardiovascular mortality in a cohort of 2992 subjects with primary hypercholesterolemia, who were followed for 10.2 years (range 1-25 years), with a total of 30,602 subject-years of follow-up.</p><p><strong>Results: </strong>During follow-up, 168 subjects died, with 52 (13.7 %), 105 (4.80 %), and 11 (2.60 %) in the low, normal, and high HDLc groups, respectively (p < 0.001). The risk of death was 2.89 times higher (95 % confidence interval (CI), 1.50-5.57, p < 0.001) in subjects in the low HDLc group compared to those in the high HDLc group and 1.48 times higher (95 % CI 0.80-2.76, p = 0.214) in the normal HDLc group compared to the high HDLc group. However, HDLc concentration and HDLc groups based on HDLc concentration were not independently associated with mortality in Cox regression analysis. Cardiovascular and non-cardiovascular mortalities showed similar results.</p><p><strong>Conclusions: </strong>All types of mortality were lower in subjects with primary hypercholesterolemia and with high HDLc in univariate analysis. Elevated HDLc was not associated with total, cardiovascular, and non-cardiovascular mortality when adjusted for major cardiovascular risk factors.</p>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"118617"},"PeriodicalIF":4.9,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}