Atherosclerosis最新文献

{"title":"Simvastatin ameliorates senescence-induced mitochondrial dysfunction in vascular smooth muscle cells","authors":"C. Rossi ,&nbsp;C. Macchi ,&nbsp;C. D'Alonzo ,&nbsp;M. Venturin ,&nbsp;M. Ruscica ,&nbsp;A. Corsini ,&nbsp;C. Battaglia ,&nbsp;S. Bellosta","doi":"10.1016/j.atherosclerosis.2025.119176","DOIUrl":"10.1016/j.atherosclerosis.2025.119176","url":null,"abstract":"<div><h3>Background and aims</h3><div>Senescence and mitochondrial dysfunction are two major indicators of aging. Mitochondria are potential drivers of aging phenotypes and dysfunctional mitochondria are associated with several age-related diseases. There is evidence that senescence induces changes in mitochondrial structure, dynamics, and function. Moreover, senescent vascular smooth muscle cells (VSMCs) are present in atherosclerotic plaques and contribute to their instability. The anti-atherosclerotic effects of simvastatin are well known, but recently other benefits, such as promoting mitochondrial quality and senostatic effects, have been hypothesized. We aimed to analyze simvastatin's senostatic effects in senescent VSMCs.</div></div><div><h3>Methods</h3><div>We established and characterized mitochondrial dysfunction in doxorubicin-induced senescent VSMCs (doxorubicin) or VSMCs serially passaged to induce replicative senescence (old).</div></div><div><h3>Results</h3><div>We observed in both senescent models few typical senescence markers such as altered cell morphology, cell cycle inhibitors, laminB1, an accumulation of dysfunctional mitochondria characterized by reduced mitochondrial membrane potential (MMP) and respiration, accumulation of reactive oxygen species (ROS), and an altered mitochondria morphology. Down-regulation of TFAM and TOM70 expression was observed only in old cells suggesting a reduction of mitochondrial biogenesis. Next, we investigated whether simvastatin could ameliorate age‐associated phenotypes in senescent VSMCs. Simvastatin 0.1 μM reduces the senescence-associated secretory phenotype (SASP) and ROS production and improves mitochondrial respiration in doxorubicin and old VSMCs. Interestingly, the effects of simvastatin on mitochondrial respiration and SASP were replicated by using a siRNA for the hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase, and abolished by adding mevalonic acid, suggesting that these effects are mediated through the inhibition of HMG-CoA reductase.</div></div><div><h3>Conclusions</h3><div>Our results suggest that simvastatin controls SASP and exerts potentially beneficial therapeutic effects by ameliorating senescence-induced mitochondrial dysfunction in senescent VSMCs.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119176"},"PeriodicalIF":4.9,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143715161","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":"Low-density lipoprotein-cholesterol subfractions as predictors for coronary artery calcium incidence and progression – The Brazilian longitudinal study of Adult Health (ELSA – Brasil)","authors":"Shamroz Farooq ,&nbsp;Giuliano Generoso ,&nbsp;Isabela M. Bensenor ,&nbsp;Raul D. Santos ,&nbsp;Steven R. Jones ,&nbsp;Eugenio Moraes ,&nbsp;Michael J. Blaha ,&nbsp;Peter P. Toth ,&nbsp;Paulo A. Lotufo ,&nbsp;Henrique L. Staniak ,&nbsp;Marcio S. Bittencourt","doi":"10.1016/j.atherosclerosis.2025.119171","DOIUrl":"10.1016/j.atherosclerosis.2025.119171","url":null,"abstract":"<div><h3>Background and aims</h3><div>Low-density lipoprotein-cholesterol (LDL-c) subfractions may play different roles in atherogenesis. Our objective was to evaluate the association between LDL-c subfractions and coronary artery calcium (CAC) incidence in individuals with a baseline CAC = 0 and CAC progression in those with CAC &gt; 0 at baseline.</div></div><div><h3>Methods</h3><div>We include 2632 participants from the Brazilian Longitudinal Study of Adult Health cohort, all of whom underwent two repeated CAC score measurements and had LDL-c subfraction measurements. The LDL-c subfraction concentrations were measured by the vertical auto profile method and categorized as small dense LDL-c (sdLDL-c) and large buoyant LDL-c (lbLDL-c). We constructed logistic regression analyses to examine CAC incidence and CAC progression. Additionally, CAC progression was analyzed using linear regression analyses as continuous variables.</div></div><div><h3>Results</h3><div>At baseline, a total of 2066 individuals (47.2 years, 62.2% female) had CAC = 0 and 566 (53.63 years, 36.9% female) had CAC &gt; 0. The mean interscan interval was (5.15 ± 2.37 years). We found a significant association between sdLDL-c and CAC incidence (OR, 1.29 [95% CI, 1.13–1.47]) but not for lbLDL-c (<em>p</em> = 0.28) after adjustment for confounders. We found no association of the sdLDL-c fraction with CAC progression in any of the analyses. However, lbLDL-c concentrations were inversely associated with CAC progression on both logistic and linear regression analyses (all <em>p</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>There is a positive association between incidence of CAC and sdLDL-c but not lbLDL-c. CAC progression was inversely associated with lbLDL-c but not with sdLDL-c.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119171"},"PeriodicalIF":4.9,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143704959","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":"Association between statin adherence and arterial stiffness in young adult patients with familial hypercholesterolemia: A cross-sectional study","authors":"Sibbeliene E. van den Bosch ,&nbsp;Barbara A. Hutten ,&nbsp;Alma Revers ,&nbsp;Eric M. Schrauben ,&nbsp;Pim van Ooij ,&nbsp;Aart J. Nederveen ,&nbsp;Willemijn E. Corpeleijn ,&nbsp;Albert Wiegman","doi":"10.1016/j.atherosclerosis.2025.119175","DOIUrl":"10.1016/j.atherosclerosis.2025.119175","url":null,"abstract":"<div><h3>Background</h3><div>Familial hypercholesterolemia (FH) causes elevated low-density lipoprotein cholesterol (LDL-C) levels, leading to an increased risk for premature atherosclerotic cardiovascular disease (ASCVD). To prevent ASCVD, lipid-lowering therapy (LLT), such as statins, is needed from childhood on, to lower LDL-C levels. Arterial stiffness can serve as a surrogate marker for atherosclerosis. The aim of this study is to determine the association between statin adherence and arterial stiffness in young adults with FH.</div></div><div><h3>Methods</h3><div>The cohort for this cross-sectional study originally consisted of 214 children with heterozygous FH who participated in a placebo-controlled trial on the efficacy and safety of pravastatin, and all continued on LLT. After 20 years, these patients were invited for a follow-up visit, including a questionnaire where they reported the percentage of prescribed LLT they had taken over the past month, as well as a 4D flow MRI examination to assess carotid pulse wave velocity (PWV), in m/s.</div></div><div><h3>Results</h3><div>We included 134 patients with FH (mean (SD) age: 31.7 (3.2) years; 67 (50.0 %) males). A higher adherence (%) to statin therapy was significantly associated with lower PWV (beta [β] −0.003 (95 % confidence interval [CI] −0.007 to −0.000); <em>P</em> = 0.039)<strong>.</strong> After adjustment for potential confounders, this association remained similar (β −0.003 (95 % CI -0.007 to −0.000), <em>P</em> = 0.031).</div></div><div><h3>Conclusions</h3><div>The results of our study suggest that higher adherence to statin therapy is associated with less arterial stiffness, thereby reducing the risk for ASCVD compared to lower levels of adherence. These findings highlight the importance of adherence to LLT in patients with FH.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"404 ","pages":"Article 119175"},"PeriodicalIF":4.9,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143833254","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":"The emerging role of glycans and the importance of sialylation in cardiovascular disease","authors":"Naomi E. Wattchow ,&nbsp;Benjamin J. Pullen ,&nbsp;Anuk D. Indraratna ,&nbsp;Victoria Nankivell ,&nbsp;Arun Everest-Dass ,&nbsp;Peter J. Psaltis ,&nbsp;Daniel Kolarich ,&nbsp;Stephen J. Nicholls ,&nbsp;Nicolle H. Packer ,&nbsp;Christina A. Bursill","doi":"10.1016/j.atherosclerosis.2025.119172","DOIUrl":"10.1016/j.atherosclerosis.2025.119172","url":null,"abstract":"<div><div>Glycosylation is the process by which glycans (i.e. ‘sugars’) are enzymatically attached to proteins or lipids to form glycoconjugates. Growing evidence points to glycosylation playing a central role in atherosclerosis. Glycosylation occurs in all human cells and post-translationally modifies many signalling molecules that regulate cardiovascular disease, affecting their binding and function. Glycoconjugates are present in abundance on the vascular endothelium and on circulating lipoproteins, both of which have well-established roles in atherosclerotic plaque development. Sialic acid is a major regulator of glycan function and therefore the process of sialylation, in which sialic acid is added to glycans, is likely to be entwined in any regulation of atherosclerosis. Glycans and sialylation regulators have the potential to present as new biomarkers that predict atherosclerotic disease or as targets for pharmacological intervention, as well as providing insights into novel cardiovascular mechanisms. Moreover, the asialoglycoprotein receptor 1 (ASGR1), a glycan receptor, is emerging as an exciting new regulator of lipid metabolism and coronary artery disease. This review summarises the latest advances in the growing body of evidence that supports an important role for glycosylation and sialylation in the regulation of atherosclerosis.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119172"},"PeriodicalIF":4.9,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679607","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":"Ethnic variations in neutrophil count as predictors of prognosis following acute myocardial infarction","authors":"Matthew Sadler ,&nbsp;Antonio Cannata ,&nbsp;Sarah Mackie ,&nbsp;Rupavidhya Mondi Anandhakrishna ,&nbsp;Fulye Argunhan ,&nbsp;Emma Ferone ,&nbsp;Al-Agil Mohammad ,&nbsp;Jamila Salim ,&nbsp;Narun Tantichirasakul ,&nbsp;Mei Tung Lam ,&nbsp;Josel Ambon ,&nbsp;Aamir Shamsi ,&nbsp;Susan Piper ,&nbsp;Giorgio Napolitani ,&nbsp;Ajay M. Shah ,&nbsp;Theresa McDonagh ,&nbsp;Paul A. Scott ,&nbsp;Lynn Quek ,&nbsp;Daniel I. Bromage","doi":"10.1016/j.atherosclerosis.2025.119169","DOIUrl":"10.1016/j.atherosclerosis.2025.119169","url":null,"abstract":"<div><h3>Aims</h3><div>Elevated neutrophils are associated with a poor prognosis after acute myocardial infarction (AMI) but it is not known if ethnicity influences the association between neutrophil count and outcome. We aimed to describe the temporal dynamics of neutrophils after AMI, and assess the interaction between ethnicity, neutrophil count, and outcomes after AMI.</div></div><div><h3>Methods</h3><div>Consecutive patients presenting with AMI between 2016 and 2023 were divided into two groups according to their median neutrophil count. Ethnicity was dichotomised as white and other ethnic groups combined (referred to as ‘ethnic minorities’). The primary outcome was in-hospital mortality, with a secondary outcome of 60-day mortality.</div></div><div><h3>Results</h3><div>In our study of 3062 AMI patients (76 % white, 24 % from ethnic minority groups), we found that neutrophil counts rose early post AMI, which coincided with a nadir of the other cell groups. We identified a relative baseline neutropenia in ethnic minority individuals, compared to white individuals (6.85 vs 8.42 × 10⁹/L). We observed a significant, independent association between elevated neutrophils at baseline and the primary outcome of in-hospital mortality (OR 2.06, p &lt; 0.001) and secondary outcome of 60-day all-cause mortality (HR 1.08, p = 0.002). Sub-group analysis revealed a significant interaction between ethnicity and elevated neutrophils (p = 0.004), indicating that a comparable neutrophil count conferred an increased risk for ethnic minority patients for both outcomes.</div></div><div><h3>Conclusions</h3><div>We report ethnicity-specific leucocyte dynamics after AMI. Furthermore, neutrophil count is associated with a disproportionate risk in ethnic minority compared with white individuals. Understanding post-AMI inflammation and its interaction with ethnicity is essential in providing personalised prognostication and patient management.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119169"},"PeriodicalIF":4.9,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143715108","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":"Global deletion of the LXR-regulated gene EEPD1 reveals macrophage-specific changes in lipid metabolism and cholesterol efflux","authors":"Suzanne A.E. van Wouw ,&nbsp;Melanie Loix ,&nbsp;Roelof Ottenhoff ,&nbsp;Jenina Kingma ,&nbsp;Aldo Jongejan ,&nbsp;Jeroen Bogie ,&nbsp;Menno Hoekstra ,&nbsp;Noam Zelcer","doi":"10.1016/j.atherosclerosis.2025.119163","DOIUrl":"10.1016/j.atherosclerosis.2025.119163","url":null,"abstract":"<div><h3>Background and aims</h3><div>We recently reported that Endonuclease/Exonuclease/Phosphatase family Domain containing 1 (EEPD1) is a transcriptional target of the sterol-responsive nuclear Liver X Receptors (LXR) in macrophages. The aim of this study is to clarify the <em>in vivo</em> role of EEPD1 in whole-body and macrophage lipid handling, and in the development of atherosclerosis.</div></div><div><h3>Methods</h3><div>We developed mice with global deletion of <em>Eepd1</em> and challenged them with a high-fat- and a Western-type diet. Bone marrow-derived macrophages (BMDM) were used for profiling transcriptomic and lipidomic changes, and evaluating cholesterol efflux in the absence of <em>Eepd1</em>. We transplanted bone marrow from wildtype and <em>Eepd1</em>^<em>KO</em> mice into <em>Ldlr</em>^<em>KO</em> recipients to assess the role of myeloid-specific EEPD1 in atherogenesis.</div></div><div><h3>Results</h3><div><em>Eepd1</em>^<em>KO</em> mice were indistinguishable from wildtype controls when fed a low-fat diet. However, when challenged with a high-fat diet or a cholesterol-containing western diet, <em>Eepd1</em>^<em>KO</em> displayed enhanced weight gain, with no evident changes in plasma and hepatic lipid levels observed. Consistent with our earlier report, BMDM isolated from <em>Eepd1</em>^<em>KO</em> mice had attenuated LXR-stimulated cholesterol efflux to high density lipoprotein and Apolipoprotein A1 when compared to wildtype cells. The transcriptomic and lipidomic landscape of these cells revealed a small reduction in expression of cholesterol biosynthetic genes in LXR-stimulated <em>Eepd1</em>^<em>KO</em> cells, and prominent changes in diacylglycerol and hexosylceramides level and species. Changes were also observed in triglyceride and cholesterol-ester species. Myeloid-specific loss of <em>Eepd1</em> did not alter atherosclerotic plaque size and collagen content in bone marrow-transplanted <em>Ldlr</em>^<em>KO</em> recipients.</div></div><div><h3>Conclusions</h3><div>Loss of <em>Eepd1</em> results in an altered lipidomic landscape and reduced LXR-stimulated cholesterol efflux in BMDM, but myeloid-specific loss of <em>Eepd1</em> does not influence atherogenesis in mice.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119163"},"PeriodicalIF":4.9,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679611","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":"Liver and atherosclerotic risk of alcohol consumption in patients with metabolic dysfunction-associated Steatotic Liver Disease","authors":"Shao-Wen Wang ,&nbsp;Ching Wang ,&nbsp;Yu-Ming Cheng ,&nbsp;Tsung-Han Hsieh ,&nbsp;Chia-Chi Wang ,&nbsp;Jia-Horng Kao","doi":"10.1016/j.atherosclerosis.2025.119161","DOIUrl":"10.1016/j.atherosclerosis.2025.119161","url":null,"abstract":"<div><h3>Background/purpose</h3><div>A new disease name, \"Steatotic Liver Disease (SLD)\" was proposed in 2023. Within this algorithm, combined metabolic and alcoholic liver disease (MetALD) was named as a new specific subgroup. The clinical profiles and outcomes of MetALD patients are unknown.</div></div><div><h3>Methods</h3><div>Participants from Taiwan Biobank database after exclusion those with positive for HBsAg, anti-HCV, and former drinkers were selected. MASLD was diagnosed if having hepatic steatosis on ultrasound plus at least one of cardiometabolic criteria. Increased or moderate alcohol intake was defined as continuous drinkers with alcohol consumption exceeding 210 g for men and 140 g for women weekly or below the levels, respectively. The fibrosis 4 (FIB-4) score was used to assess the severity of liver fibrosis, and carotid plaques on duplex ultrasound were employed to diagnose atherosclerosis.</div></div><div><h3>Results</h3><div>In a total of 18,160 (mean age 55.28 ± 10.41; 33.2 % males) participants, there were 7316 (40.3 %) MASLD patients and 209 (1.2 %) MetALD patients. The participants with MetALD were younger and male predominant. After propensity score matching for age and gender, MetALD patients had higher AST, GGT, fatty liver index (FLI), and FIB-4 score and tended to have a higher proportion of carotid plaques than MASLD patients. Among MASLD patients, those with moderate alcohol intake had higher values of GGT, FLI, and FIB-4 score and a higher proportion of carotid plaques than those with no or social alcohol intake.</div></div><div><h3>Conclusions</h3><div>MetALD patients have a higher risk of liver injury than those with MASLD. Moreover, moderatet alcohol intake also increases the risk of liver injury and atherosclerotic in MASLD patients, suggesting MASLD patients should refrain from alcohol intake.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119161"},"PeriodicalIF":4.9,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143629094","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":"Pericoronary adipose tissue attenuation on coronary computed tomography angiography: Possibilities and challenges","authors":"Alexander C. Razavi ,&nbsp;Seamus P. Whelton ,&nbsp;Mouaz H. Al-Mallah","doi":"10.1016/j.atherosclerosis.2025.119105","DOIUrl":"10.1016/j.atherosclerosis.2025.119105","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"402 ","pages":"Article 119105"},"PeriodicalIF":4.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143254471","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":"Incremental prognostic value of pericoronary adipose tissue attenuation beyond conventional features in patients with nonobstructive coronary artery disease","authors":"Nan Zheng ,&nbsp;Zinuan Liu ,&nbsp;Yipu Ding ,&nbsp;Xi Wang ,&nbsp;Jing Li ,&nbsp;Guanhua Dou ,&nbsp;Ran Xin ,&nbsp;Ziqiang Guo ,&nbsp;Guanxi Chen ,&nbsp;Jing Jing ,&nbsp;Bai He ,&nbsp;Dongkai Shan ,&nbsp;Junjie Yang","doi":"10.1016/j.atherosclerosis.2024.119075","DOIUrl":"10.1016/j.atherosclerosis.2024.119075","url":null,"abstract":"<div><h3>Background and aims</h3><div>It remains uncertain whether pericoronary adipose tissue attenuation (PCATa) is associated with clinical outcome in patients with nonobstructive coronary artery disease (CAD). We aim to investigate the incremental prognostic value of PCATa beyond clinical and coronary computed tomographic angiography (CCTA) features in patients with nonobstructive CAD.</div></div><div><h3>Methods</h3><div>Consecutive patients with chest pain suspected of CAD referred for CCTA from January 2017 to December 2018 were prospectively included. Multivariable Cox proportional hazard regression analysis was employed to identify the predictive factors for major adverse cardiovascular events (MACE), while the receiver operating characteristics (ROC) curve was utilized to assess the discriminatory capacity of PCATa. Kaplan-Meier curves were ultilized to visually represent event-free survival and were compared using Log-rank tests among groups stratified by high-risk plaque (HRP) and PCATa.</div></div><div><h3>Results</h3><div>Of the 1614 patients (mean age 59.0 years, 55.6 % male) with nonobstructive CAD, 68 (4.2 %) suffered MACE during a median follow-up of 28.6 months. After multivariable adjustment, PCATa was identified as an independent predictor (HR: 1.060, 95%CI: 1.025–1.096, <em>p</em> = 0.001). The inclusion of PCATa significantly enhanced the discrimination capacity [AUC:0.72 (0.66–0.78), <em>p</em> = 0.041] and risk reclassification (NRI = 1.99, <em>p</em> &lt; 0.001; IDI = 0.93, <em>p</em> &lt; 0.001) beyond the influence of clinical and CCTA factors. In the presence of HRP, a higher PCATa was found to be associated with a relatively higher risk of MACE compared to a lower PCATa (HR: 2.45, 95%CI: 1.09–5.52, <em>p</em> = 0.031).</div></div><div><h3>Conclusions</h3><div>PCATa is positively correlated with adverse outcome in patients with nonobstructive CAD, and it offers incremental predictive value beyond clinical variables and CCTA characteristics.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"402 ","pages":"Article 119075"},"PeriodicalIF":4.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794302","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":"Ferroptosis: A novel paradigm in the pathophysiology of MINOCA","authors":"Uğur Özkan ,&nbsp;Meral Kayıkçıoğlu ,&nbsp;Servet Altay","doi":"10.1016/j.atherosclerosis.2024.119097","DOIUrl":"10.1016/j.atherosclerosis.2024.119097","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"402 ","pages":"Article 119097"},"PeriodicalIF":4.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142998888","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}