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Reply to: “Correspondence on: “Subclinical atherosclerosis: More data – More insights into prevention” ” 答复关于 "亚临床动脉粥样硬化"亚临床动脉粥样硬化:更多数据 - 更多预防见解" "
IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-11-06 DOI: 10.1016/j.atherosclerosis.2024.118634
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引用次数: 0
Complement factor B, not the membrane attack complex component C9, promotes neointima formation after arterial wire injury 促进动脉导线损伤后新生内膜形成的是补体因子 B,而非膜攻击复合物成分 C9
IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-23 DOI: 10.1016/j.atherosclerosis.2024.118586

Background and aims

Vascular restenosis due to neointima hyperplasia limits the long-term patency of stented arteries, resulting in angioplasty failure. The complement system has been implicated in restenosis. This study aimed to investigate the role of complement factor B (fB), an essential component of the alternative pathway of complement activation, in neointima formation.

Methods

Angioplasty wire injury was conducted using 12-week-old mice deficient in fB or C9 (the main component of the membrane attacking complex, C5b-9) and littermate controls and neointima formation were assessed. Vascular smooth muscle cell (SMC) and endothelial cell (EC) proliferation and migration were examined in vitro.

Results

fB was mainly detected in SMCs of stenotic arteries from humans and mice. Deletion of fB substantially reduced the neointima area and intima-to-media area ratio without affecting the media area at 28 days after injury. At 7 days after injury, fB deficiency decreased SMC proliferation, unaltering neointimal macrophage infiltration and EC reendothelialization. Vascular SMC-expressed fB, not the circulation-sourced fB, played an essential role in SMC proliferation and migration in vitro. fB deficient mice exhibited lower levels of the soluble form of C5b-9, however, deletion of C9 did not alter neointima formation after wire injury, consistent with the null impact of C9 deficiency on SMC proliferation in vitro.

Conclusions

fB promotes neointima formation following wire-induced artery injury independent of forming the membrane-attacking complex. This is attributable to fB-dependent SMC proliferation and migration without affecting EC function. Targeting fB might protect against restenosis after percutaneous coronary intervention.
背景和目的 新内膜增生引起的血管再狭窄限制了支架动脉的长期通畅,导致血管成形术失败。补体系统与血管再狭窄有关。本研究旨在探讨补体激活替代途径的重要组成部分--补体因子 B(fB)在新生内膜形成中的作用。方法使用缺乏 fB 或 C9(膜攻击复合物 C5b-9 的主要成分)的 12 周大小鼠和同窝对照组进行血管成形术线损伤,并评估新生内膜的形成。在体外检测了血管平滑肌细胞(SMC)和内皮细胞(EC)的增殖和迁移。损伤后 28 天,缺失 fB 可显著减少新生内膜面积和内膜与中膜面积比,但不影响中膜面积。损伤后 7 天,缺乏 fB 会减少 SMC 的增殖,但不会改变新生内膜巨噬细胞的浸润和 EC 的再内皮化。血管SMC表达的fB,而非循环来源的fB,在体外SMC增殖和迁移中发挥了重要作用。fB缺乏的小鼠表现出较低水平的可溶性C5b-9,然而,C9的缺失并没有改变钢丝损伤后新内膜的形成,这与C9缺乏对体外SMC增殖的无效影响一致。这归因于 fB 依赖于 SMC 的增殖和迁移,而不影响 EC 的功能。以 fB 为靶点可预防经皮冠状动脉介入治疗后的再狭窄。
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引用次数: 0
ERICH4 is not involved in the assembly and secretion of intestinal lipoproteins ERICH4不参与肠道脂蛋白的组装和分泌。
IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-18 DOI: 10.1016/j.atherosclerosis.2024.118635

Background and aims

The small intestine plays a central role in lipid metabolism, most notably the uptake of dietary fats that are packaged into chylomicrons and secreted into the circulation for utilisation by peripheral tissues. While microsomal triglyceride transfer protein (MTP) is known to play a key role in this pathway, the intracellular assembly, trafficking, and secretion of chylomicrons is incompletely understood.

Methods and Results

Using human transcriptome datasets to find genes co-regulated with MTTP, we identified ERICH4 as a top hit. The gene encodes for glutamate-rich protein 4, a protein of unknown function. REACTOME gene-function prediction tools indicated that ERICH4 is involved in intestinal lipid metabolism. In addition, GWAS data point to a strong relationship between ERICH4 and plasma lipids. To validate ERICH4 as a lipid gene, we generated whole-body Erich4 knockout (Erich4−/−) mice. ERICH4 deficiency, however, did not result in changes in body weight and composition, food intake, circulating plasma lipids, energy absorption and excretion, and tissue weights compared to controls. Additionally, there were no morphological abnormalities seen in the small intestine. Challenging mice with a high-fat diet did not give rise to a phenotype either.

Conclusions

Despite prediction tools indicating ERICH4 as a strong candidate gene in intestinal lipid metabolism, we here show that ERICH4 does not play a role in intestinal lipid metabolism in mice. It remains to be established whether ERICH4 plays a role in human lipid metabolism.
背景和目的:小肠在脂质代谢中起着核心作用,其中最主要的是吸收饮食中的脂肪,这些脂肪被包装成乳糜微粒并分泌到血液循环中供外周组织利用。众所周知,微粒体甘油三酯转移蛋白(MTP)在这一途径中发挥着关键作用,但人们对乳糜微粒的细胞内组装、贩运和分泌却知之甚少:利用人类转录组数据集寻找与MTTP共调的基因,我们发现ERICH4是最热门的基因。该基因编码富谷氨酸蛋白 4,这是一种功能未知的蛋白质。REACTOME 基因功能预测工具表明,ERICH4 参与了肠道脂质代谢。此外,GWAS 数据表明 ERICH4 与血浆脂质之间存在密切关系。为了验证ERICH4是一个脂质基因,我们产生了全身Erich4基因敲除(Erich4-/-)小鼠。然而,与对照组相比,ERICH4 基因缺失不会导致体重和组成、食物摄入量、循环血浆脂质、能量吸收和排泄以及组织重量发生变化。此外,小肠也未出现形态异常。用高脂肪饮食挑战小鼠也没有产生表型:结论:尽管预测工具显示ERICH4是肠道脂质代谢的一个强有力的候选基因,但我们在这里发现ERICH4在小鼠肠道脂质代谢中并没有发挥作用。ERICH4是否在人类脂质代谢中发挥作用,还有待进一步证实。
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引用次数: 0
Publication bias in pharmacogenetics of statin-associated muscle symptoms: A meta-epidemiological study. 他汀类药物相关肌肉症状药物遗传学的发表偏差:一项荟萃流行病学研究。
IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-18 DOI: 10.1016/j.atherosclerosis.2024.118624
A Gougeon, I Aribi, S Guernouche, J C Lega, J M Wright, C Verstuyft, A Lajoinie, F Gueyffier, G Grenet

Background and aims: Statin-associated muscle symptoms (SAMS) are a major cause of treatment discontinuation. Clinical Pharmacogenetics Implementation Consortium (CPIC) recommend dose adjustment for statin treatment according to known SLCO1B1 genotype to reduce SAMS. We hypothesized that the association between SLCO1B1 genotype and SAMS is misestimated because of publication bias.

Methods: We searched published systematic reviews on the association between SLCO1B1 genotype and SAMS. To assessed publication bias, we used funnel plot visual inspection, Egger's test, and the Bayes Factor (BFPublication-bias) from Robust Bayesian Meta-Analysis (RoBMA). We compared the odds ratios (ORUncorrected) from meta-analyses before and after correcting for publication bias using trim-and-fill (ORTrim&Fill) and RoBMA (ORRoBMA) methods.

Results: We included 8 cohort and 11 case-control studies, totaling 62 OR of three SLCO1B1 genotypes and six statin drugs. In the primary analysis, the funnel plot was suggestive of publication bias, confirmed by Egger's test (p=0.001) and RoBMA (BFPublication-bias = 18). Correcting the estimate for publication bias resulted in loss of the association, from a significant ORUncorrected (1.31 95%CI [1.13-1.53]) to corrected ORs suggesting no difference: ORTrim&Fill (1.07 95%CI [0.89-1.30]) and ORRoBMA (1.02 95%CI [1.00-1.33]). This suggested that publication bias overestimated the association by 18 % and 23 %, respectively. Similar results were found for genotype rs4149056, simvastatin and atorvastatin.

Conclusions: The effect of the SLCO1B1 genotype on the risk of developing SAMS is overestimated in the published literature, especially rs4149056. This could lead prescribers to incorrectly decreasing statin doses or even avoiding statin use, leading to a loss of the potential cardiovascular benefit of statins.

背景和目的:他汀类药物相关肌肉症状(SAMS)是导致治疗中断的主要原因。临床药物遗传学实施联合会(CPIC)建议根据已知的 SLCO1B1 基因型调整他汀类药物治疗剂量,以减少 SAMS。我们假设,由于发表偏倚,SLCO1B1 基因型与 SAMS 之间的关联被错误估计:我们检索了已发表的有关 SLCO1B1 基因型与 SAMS 之间关系的系统综述。为了评估发表偏倚,我们使用了漏斗图目测、Egger 检验和稳健贝叶斯荟萃分析(Robust Bayesian Meta-Analysis,RoBMA)中的贝叶斯因子(BFPublication-bias)。我们比较了使用修剪与填充(ORTrim&Fill)和RoBMA(ORRoBMA)方法纠正发表偏倚前后荟萃分析的几率比(ORUncorrected):我们纳入了 8 项队列研究和 11 项病例对照研究,共计 62 个 OR,涉及 3 种 SLCO1B1 基因型和 6 种他汀类药物。在主要分析中,漏斗图提示存在发表偏倚,Egger 检验(P=0.001)和 RoBMA(BFP 发表偏倚 = 18)证实了这一点。对发表偏倚的估计值进行校正后,相关性消失,从显著的未校正 OR(1.31 95%CI [1.13-1.53])变为校正 OR,表明没有差异:ORTrim&Fill(1.07 95%CI [0.89-1.30])和 ORRoBMA(1.02 95%CI [1.00-1.33])。这表明,发表偏倚分别高估了 18% 和 23% 的相关性。基因型 rs4149056、辛伐他汀和阿托伐他汀也发现了类似的结果:结论:在已发表的文献中,SLCO1B1 基因型对罹患 SAMS 风险的影响被高估了,尤其是 rs4149056。这可能会导致处方者错误地减少他汀类药物的剂量,甚至避免使用他汀类药物,从而失去他汀类药物对心血管的潜在益处。
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引用次数: 0
Unraveling the complex interplay of PPARα and age in cardiac metabolism: Implications for managing age-related cardiac dysfunctions. 揭示 PPARα 和年龄在心脏新陈代谢中的复杂相互作用:对控制与年龄相关的心脏功能障碍的启示。
IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-11 DOI: 10.1016/j.atherosclerosis.2024.118627
Sina Rashedi, Mohammad Keykhaei
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引用次数: 0
Single bolus PCSK9 Inhibition: A new approach to plaque stabilisation. 单次注射 PCSK9 抑制剂:稳定斑块的新方法。
IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-11 DOI: 10.1016/j.atherosclerosis.2024.118628
Stephen J Nicholls, Gavin Pr Manmathan
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引用次数: 0
Comparison of pooled cohort equation and PREVENT™ risk calculator for statin treatment allocation 用于他汀类药物治疗分配的汇集队列方程与 PREVENT™ 风险计算器的比较。
IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-10 DOI: 10.1016/j.atherosclerosis.2024.118626

Background and aims

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.

Methods

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.

Results

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.
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.

Conclusions

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.
背景和目的:有效的高胆固醇血症管理与降低全因死亡率和心血管死亡率有关。2018 年 AHA/ACC 指南建议使用集合队列方程 (PCE) 进行血脂管理,但这些方程可能会高估风险,对某些种族群体的准确性较低。美国心脏病学会的新 PREVENT 方程省略了种族因素并包含了心脏代谢因素,旨在为不同人群提供更准确的风险评估。然而,该方程尚未应用于具有全国代表性的美国人群,也缺乏实施指南。我们的研究旨在评估使用 PREVENT 方程而非 PCE 进行一级预防时高胆固醇血症管理的潜在变化:通过分析大流行前的 NHANES 2017-2020 年数据,使用 PCE 和 PREVENT 方程确定了年龄在 40-75 岁、既往未接受过降脂治疗或无其他强制指征的参与者的高风险(≥7.5%)。我们对两种风险方程进行了比较,评估了他汀类药物治疗的风险转移和适应症。为了获得具有美国全国代表性的估计值,我们遵循了 NHANES 的加权指南:在 77 647 807(未加权 = 2494)名参与者中,81.0% 的风险没有变化。PCE标记了18.8%(n=14,614,094)未被PREVENT识别的高风险参与者,而0.20%(n=107,813)仅被PREVENT标记。仅通过 PCE 确定的参与者年龄较大,收缩压较高,估计肾小球滤过率较高。他汀类药物治疗的适应症基本未变(81.0%)。PREVENT 新发现(0.20%)可接受中等强度治疗的患者,没有发现可接受高强度治疗的患者。有 74.59% 符合 PCE 中度治疗条件的参与者被重新分类为无需治疗,25.41% 保持不变。93.97%的病例被重新分类为中度治疗,6.03%的病例被重新分类为无治疗:与 PCE 相比,PREVENT 方程在确定高胆固醇血症候选者方面存在显著差异。结论:与 PCE 相比,PREVENT 方程在确定高胆固醇血症候选者方面存在显著差异,它的采用将影响降低心血管风险疗法的建议,因此需要进行全面研究以了解其长期影响,并重新评估治疗策略的阈值,以改善患者的预后。
{"title":"Comparison of pooled cohort equation and PREVENT™ risk calculator for statin treatment allocation","authors":"","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":null,"pages":null},"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}
引用次数: 0
Statin use is associated with less ST-elevation versus non-ST-elevation myocardial infarction in a nationwide study 在一项全国性研究中,使用他汀类药物可减少ST段抬高与非ST段抬高心肌梗死的发生率。
IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-09 DOI: 10.1016/j.atherosclerosis.2024.118625

Background and aims

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.

Methods

In a nationwide study, including 66,896 patients with first-time myocardial infarction between 2010 and 2021, we obtained multivariable risk estimates for STEMI versus 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.

Results

Odds ratios for STEMI versus 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 <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 >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 versus non-STEMI was 2.24 (2.13–2.37).

Conclusions

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.
背景和目的:他汀类药物治疗可降低心肌梗死发生率,但它是否与ST段抬高型心肌梗死(STEMI)向非ST段抬高型心肌梗死(非STEMI)的转变有关仍是未知数。因此,我们对他汀类药物的使用与首次心肌梗死中STEMI相对于非STEMI的减少有关这一假设进行了检验:在一项全国性研究(包括 2010 年至 2021 年间的 66,896 例首次心肌梗死患者)中,我们根据是否使用过他汀类药物、累计使用他汀类药物的情况以及他汀类药物的日剂量,得出了 STEMI 与非 STEMI 的多变量风险估计值。此外,我们还根据心肌梗死类型得出了心肌梗死后 60 天死亡率(5545 例死亡)的危险比:与从未使用过他汀类药物的患者相比,目前和曾经使用过他汀类药物的患者STEMI与非STEMI的危险比分别为0.81(95 % CI:0.77-0.85)和1.07(1.01-1.13)。与从未使用过他汀类药物者相比,累积他汀类药物暴露 10 年的几率比为 0.96(0.87-1.07)。他汀类药物剂量强度的相应几率比分别为:低强度 0.89(0.84-0.95),中强度 0.77(0.73-0.82),高强度 0.70(0.63-0.77)。多重敏感性分析和队列设计的结果相似。首次 STEMI 后 60 天死亡率与非 STEMI 后 60 天死亡率的危险比为 2.24(2.13-2.37):在这项全国性研究中,他汀类药物的使用剂量与STEMI的发生率相关,而非STEMI的发生率较低。这表明他汀类药物治疗除了能降低心肌梗死的发生率外,还能减少心肌梗死的严重程度。
{"title":"Statin use is associated with less ST-elevation versus non-ST-elevation myocardial infarction in a nationwide study","authors":"","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":null,"pages":null},"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}
引用次数: 0
Shear stress is uncoupled from atheroprotective KLK10 in atherosclerotic plaques 剪切应力与动脉粥样硬化斑块中具有动脉粥样硬化保护作用的 KLK10 脱钩
IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-04 DOI: 10.1016/j.atherosclerosis.2024.118622

Background and aims

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 versus atherosclerotic conditions.

Methods

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 (Apoe−/− normal diet) mice, and highly diseased (Apoe−/− high fat diet) mice. The transcriptomes of Nos3high cells (exposed to physiological shear stress) were compared among the groups.

Results

Nos3high EC were associated with several markers of physiological shear stress in healthy arteries. Clustering of Nos3high 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 Nos3high 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 Nos3high EC in healthy arteries but markedly reduced in severely diseased arteries.

Conclusions

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.
背景和目的生理性剪切应力通过诱导内皮细胞(EC)中的保护性分子促进血管稳态。然而,在一些心血管风险较高的人群中,生理性剪切应力却与动脉粥样硬化的进展有关。为了解决这一明显的悖论,我们假设,病变动脉可能对生理性剪切应力的保护作用反应迟钝。因此,我们比较了健康动脉和动脉粥样硬化条件下暴露于生理性剪切应力的EC的转录组。方法利用三维光片成像和计算流体动力学,我们确定了NOS3是健康和动脉粥样硬化鼠动脉中生理性剪切应力的标志物。我们对健康(C57BL/6)小鼠、轻度患病(载脂蛋白-/-正常饮食)小鼠和高度患病(载脂蛋白-/-高脂饮食)小鼠的动脉血管进行了单细胞RNA测序。结果Nos3高的EC与健康动脉中生理剪切应力的几个标记相关。对Nos3高的心肌细胞进行聚类发现了8个不同的心肌细胞亚群,它们在健康动脉和患病动脉中的比例各不相同。基因本体论术语的簇特异性嵌套功能富集显示,患病动脉中的Nos3高EC富含炎症和凋亡基因表达。这些变化伴随着几种机械感受器的变化,其中包括动脉粥样硬化保护因子 KLK10,它在健康动脉的 Nos3high EC 中富集,但在严重病变动脉中则明显减少。这揭示了剪切应力、内皮功能和心血管并发症高危人群动脉粥样硬化进展之间复杂的相互作用。
{"title":"Shear stress is uncoupled from atheroprotective KLK10 in atherosclerotic plaques","authors":"","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><sup><em>−/−</em></sup> normal diet) mice, and highly diseased (<em>Apoe</em><sup><em>−/−</em></sup> high fat diet) mice. The transcriptomes of <em>Nos3</em><sup>high</sup> cells (exposed to physiological shear stress) were compared among the groups.</div></div><div><h3>Results</h3><div><em>Nos3</em><sup>high</sup> EC were associated with several markers of physiological shear stress in healthy arteries. Clustering of <em>Nos3</em><sup>high</sup> 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><sup>high</sup> 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><sup>high</sup> 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":null,"pages":null},"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}
引用次数: 0
Role of fatty acids in the pathogenesis of ß-cell failure and Type-2 diabetes. 脂肪酸在 ß 细胞衰竭和 2 型糖尿病发病机制中的作用。
IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-04 DOI: 10.1016/j.atherosclerosis.2024.118623
Cecilia Jiménez-Sánchez, Lucie Oberhauser, Pierre Maechler

Pancreatic ß-cells are glucose sensors in charge of regulated insulin delivery to the organism, achieving glucose homeostasis and overall energy storage. The latter function promotes obesity when nutrient intake chronically exceeds daily expenditure. In case of ß-cell failure, such weight gain may pave the way for the development of Type-2 diabetes. However, the causal link between excessive body fat mass and potential degradation of ß-cells remains largely unknown and debated. Over the last decades, intensive research has been conducted on the role of lipids in the pathogenesis of ß-cells, also referred to as lipotoxicity. Among various lipid species, the usual suspects are essentially the non-esterified fatty acids (NEFA), in particular the saturated ones such as palmitate. This review describes the fundamentals and the latest advances of research on the role of fatty acids in ß-cells. This includes intracellular pathways and receptor-mediated signaling, both participating in regulated glucose-stimulated insulin secretion as well as being implicated in ß-cell dysfunction. The discussion extends to the contribution of high glucose exposure, or glucotoxicity, to ß-cell defects. Combining glucotoxicity and lipotoxicity results in the synergistic and more deleterious glucolipotoxicity effect. In recent years, alternative roles for intracellular lipids have been uncovered, pointing to a protective function in case of nutrient overload. This requires dynamic storage of NEFA as neutral lipid droplets within the ß-cell, along with active glycerolipid/NEFA cycle allowing subsequent recruitment of lipid species supporting glucose-stimulated insulin secretion. Overall, the latest studies have revealed the two faces of the same coin.

胰腺ß-细胞是葡萄糖传感器,负责向机体输送胰岛素,实现葡萄糖平衡和总体能量储存。当营养摄入长期超过每日消耗时,胰腺ß细胞的后一种功能会导致肥胖。如果ß细胞功能失效,体重增加可能会为发展成2型糖尿病铺平道路。然而,过多的体内脂肪量与ß细胞的潜在退化之间的因果关系在很大程度上仍不为人所知,也存在争议。过去几十年来,人们一直在深入研究脂质在ß细胞发病机制中的作用,这也被称为脂毒性。在各种脂质中,最常见的是非酯化脂肪酸(NEFA),尤其是饱和脂肪酸,如棕榈酸酯。本综述介绍了脂肪酸在ß细胞中作用的基本原理和最新研究进展。这包括细胞内途径和受体介导的信号传导,两者都参与调节葡萄糖刺激的胰岛素分泌,并与ß细胞功能障碍有关。讨论延伸到高葡萄糖暴露或葡萄糖毒性对ß细胞缺陷的影响。将葡萄糖毒性和脂肪毒性结合在一起,会产生协同作用和更具破坏性的葡萄糖脂肪毒性效应。近年来,人们发现了细胞内脂质的另一种作用,即在营养过剩的情况下发挥保护功能。这就需要在ß细胞内以中性脂滴的形式动态储存 NEFA,同时进行活跃的甘油脂/NEFA 循环,以便随后招募脂质物种支持葡萄糖刺激的胰岛素分泌。总之,最新研究揭示了同一枚硬币的两面。
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引用次数: 0
期刊
Atherosclerosis
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