Pub Date : 2026-03-01Epub Date: 2026-01-20DOI: 10.1016/j.atherosclerosis.2026.120641
Lale Tokgozoglu , Meral Kayıkcioglu , Jeanine Roeters van Lennep
Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of mortality in both sexes globally. However, sex-specific differences in risk factor prevalence, pathophysiology, clinical presentation, and treatment outcomes demand nuanced understanding and tailored management approaches. This review examines the biological and gender-related drivers of ASCVD risk, focusing on hypertension, dyslipidemia, diabetes, obesity, smoking, inflammation, and female-specific factors such as pregnancy complications and menopause. The underrepresentation of women in cardiovascular research, combined with therapeutic inertia and gaps in preventive care, has led to suboptimal outcomes. We discuss current evidence, highlight knowledge gaps, and call for more research initiatives to reduce the burden of ASCVD in women.
{"title":"Sex-specific differences in cardiovascular risk factors and their management","authors":"Lale Tokgozoglu , Meral Kayıkcioglu , Jeanine Roeters van Lennep","doi":"10.1016/j.atherosclerosis.2026.120641","DOIUrl":"10.1016/j.atherosclerosis.2026.120641","url":null,"abstract":"<div><div>Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of mortality in both sexes globally. However, sex-specific differences in risk factor prevalence, pathophysiology, clinical presentation, and treatment outcomes demand nuanced understanding and tailored management approaches. This review examines the biological and gender-related drivers of ASCVD risk, focusing on hypertension, dyslipidemia, diabetes, obesity, smoking, inflammation, and female-specific factors such as pregnancy complications and menopause. The underrepresentation of women in cardiovascular research, combined with therapeutic inertia and gaps in preventive care, has led to suboptimal outcomes. We discuss current evidence, highlight knowledge gaps, and call for more research initiatives to reduce the burden of ASCVD in women.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"414 ","pages":"Article 120641"},"PeriodicalIF":5.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146037357","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}
Pub Date : 2026-03-01Epub Date: 2025-07-10DOI: 10.1016/j.atherosclerosis.2025.120433
Giuseppe Patti, Leonardo Grisafi, Danila Azzolina, Luca Cumitini, Domenico D'Amario, Marco Mennuni
Background and aims: The specific relationship between changes in coronary plaque phenotype by optical coherence tomography (OCT) and decrease in major adverse cardiovascular events (MACE) among patients receiving lipid-lowering therapies (LLTs) is unknown. Aim was to quantify the relationship between LLTs-related improvement of coronary plaque phenotype (e.g. coronary plaque stabilization, as assessed by OCT) and MACE occurrence.
Methods: A comprehensive, systematic search of publications in PubMed, Embase, Cochrane Central Register of Controlled Trials and Web of Science was performed to identify eligible studies. A total of 8 studies (5 randomized and 3 observational) on LLTs reporting mean maximum lipid arc (LA) and mean minimum fibrous cap thickness (FCT) at baseline and during follow-up, as assessed by OCT, and incidence of MACE were selected, encompassing a total of 652 patients.
Results: Mean follow-up duration was 8.6 months. Meta-regression analysis revealed a significant direct relationship between absolute change in LA and MACE occurrence (coefficient 0.055, I2 0 %, p < 0.001), with each 10° decrease in LA being related to a 39 % MACE reduction (OR 0.61, 95 % CI 0.44-0.77). The indirect relationship between absolute change in FCT and risk of MACE was not significant (coefficient -0.011, I2 59 %, p = 0.136).
Conclusions: This analysis quantifies the potential of LLT-related modifications of coronary plaque phenotype in terms of LA decrease for reducing the risk of MACE within the first year of treatment. These findings suggest that LA changes might be a surrogate for changes in MACE.
背景和目的：在接受降脂治疗（LLTs）的患者中，光学相干断层扫描（OCT）冠状动脉斑块表型的变化与主要不良心血管事件（MACE）的减少之间的具体关系尚不清楚。目的是量化llt相关的冠状动脉斑块表型改善（如冠状动脉斑块稳定，由OCT评估）与MACE发生之间的关系。方法：对PubMed、Embase、Cochrane Central Register of Controlled Trials和Web of Science的出版物进行全面、系统的检索，以确定符合条件的研究。共选择了8项关于llt的研究（5项随机研究和3项观察性研究），报告了基线和随访期间平均最大脂质弧（LA）和平均最小纤维帽厚度（FCT），通过OCT评估，以及MACE的发生率，共包括652例患者。结果：平均随访时间8.6个月。meta回归分析显示LA的绝对变化与MACE的发生有显著的直接关系（系数0.055,i20 %, p 2 59 %, p = 0.136）。结论：该分析量化了llt相关的冠状动脉斑块表型改变的潜力，即在治疗的第一年内降低MACE的风险。这些发现表明LA的变化可能是MACE变化的替代指标。
{"title":"Modifications of coronary plaque phenotype on lipid-lowering therapies and risk of cardiovascular events: a systematic review and meta-regression analysis.","authors":"Giuseppe Patti, Leonardo Grisafi, Danila Azzolina, Luca Cumitini, Domenico D'Amario, Marco Mennuni","doi":"10.1016/j.atherosclerosis.2025.120433","DOIUrl":"10.1016/j.atherosclerosis.2025.120433","url":null,"abstract":"<p><strong>Background and aims: </strong>The specific relationship between changes in coronary plaque phenotype by optical coherence tomography (OCT) and decrease in major adverse cardiovascular events (MACE) among patients receiving lipid-lowering therapies (LLTs) is unknown. Aim was to quantify the relationship between LLTs-related improvement of coronary plaque phenotype (e.g. coronary plaque stabilization, as assessed by OCT) and MACE occurrence.</p><p><strong>Methods: </strong>A comprehensive, systematic search of publications in PubMed, Embase, Cochrane Central Register of Controlled Trials and Web of Science was performed to identify eligible studies. A total of 8 studies (5 randomized and 3 observational) on LLTs reporting mean maximum lipid arc (LA) and mean minimum fibrous cap thickness (FCT) at baseline and during follow-up, as assessed by OCT, and incidence of MACE were selected, encompassing a total of 652 patients.</p><p><strong>Results: </strong>Mean follow-up duration was 8.6 months. Meta-regression analysis revealed a significant direct relationship between absolute change in LA and MACE occurrence (coefficient 0.055, I<sup>2</sup> 0 %, p < 0.001), with each 10° decrease in LA being related to a 39 % MACE reduction (OR 0.61, 95 % CI 0.44-0.77). The indirect relationship between absolute change in FCT and risk of MACE was not significant (coefficient -0.011, I<sup>2</sup> 59 %, p = 0.136).</p><p><strong>Conclusions: </strong>This analysis quantifies the potential of LLT-related modifications of coronary plaque phenotype in terms of LA decrease for reducing the risk of MACE within the first year of treatment. These findings suggest that LA changes might be a surrogate for changes in MACE.</p>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"120433"},"PeriodicalIF":5.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648408","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}
Pub Date : 2026-03-01Epub Date: 2026-01-16DOI: 10.1016/j.atherosclerosis.2026.120644
Aksaan Arif , Irene Karungi , Christophe A.T. Stevens , Amany Elshorbagy , Kausik K. Ray , the DA VINCI study group
Background
Non-high-density lipoprotein-cholesterol (non-HDL-C) provides prognostic information on cardiovascular disease (CVD) risk, even when low-density lipoprotein-cholesterol (LDL-C) appears controlled, and is a secondary target in guidelines. We evaluated non-HDL-C goal-attainment across Europe using European Society of Cardiology/European Atherosclerosis Society (ESC/EAS) guidelines, explored factors influencing goal-attainment and assessed lipid-lowering therapy (LLT) practices.
Methods
Cross-sectional secondary analysis of the DA VINCI study data from 2041 primary and 1923 secondary prevention patients receiving LLT across 18 European countries between 2017 and 2018. Non-HDL-C goal-attainment was evaluated using 2016 and retrospectively applied 2019 ESC/EAS guidelines, overall and across CVD risk categories and treatment regimens. Multivariable logistic regression was used to identify independent predictors of goal-attainment.
Results
Overall, 59 % (95 %CI:57–60 %) of patients attained their 2016 non-HDL-C goals, vs. 54 % (95 %CI:53–56 %) for LDL-C; 50 % (95 %CI:48–51 %) attained both. Under stricter 2019 guidelines applied retrospectively, goal-attainment was 40 % (95 %CI:39–42 %), vs. 34 % (95 %CI:32–35 %) for LDL-C, and 30 % (95 %CI:28–32 %) for dual-goals. Non-HDL-C goal-attainment decreased with increasing CVD risk. Use of combination LLT was low, especially in very-high-risk patients. Older age (OR:1.60) and male sex (OR:1.35) were positively associated with non-HDL-C goal attainment; smoking (OR:0.71) and hypertriglyceridemia (OR:0.35) were negatively associated. Those at LDL-C-goal only had higher triglycerides, BMI, and T2DM burden than those achieving both goals, highlighting residual risk.
Conclusions
Despite widespread statin use, many patients treated under 2017–2018 practice would not have met the more stringent 2019 non-HDL-C targets. This highlights the need for risk-based treatment intensification, improved targeting of triglyceride-rich lipoproteins, and broader adoption of combination LLTs to optimise guideline-based care.
{"title":"Attainment of non-high-density lipoprotein cholesterol targets in secondary and primary care: A secondary-analysis of the DA VINCI study","authors":"Aksaan Arif , Irene Karungi , Christophe A.T. Stevens , Amany Elshorbagy , Kausik K. Ray , the DA VINCI study group","doi":"10.1016/j.atherosclerosis.2026.120644","DOIUrl":"10.1016/j.atherosclerosis.2026.120644","url":null,"abstract":"<div><h3>Background</h3><div>Non-high-density lipoprotein-cholesterol (non-HDL-C) provides prognostic information on cardiovascular disease (CVD) risk, even when low-density lipoprotein-cholesterol (LDL-C) appears controlled, and is a secondary target in guidelines. We evaluated non-HDL-C goal-attainment across Europe using European Society of Cardiology/European Atherosclerosis Society (ESC/EAS) guidelines, explored factors influencing goal-attainment and assessed lipid-lowering therapy (LLT) practices.</div></div><div><h3>Methods</h3><div>Cross-sectional secondary analysis of the DA VINCI study data from 2041 primary and 1923 secondary prevention patients receiving LLT across 18 European countries between 2017 and 2018. Non-HDL-C goal-attainment was evaluated using 2016 and retrospectively applied 2019 ESC/EAS guidelines, overall and across CVD risk categories and treatment regimens. Multivariable logistic regression was used to identify independent predictors of goal-attainment.</div></div><div><h3>Results</h3><div>Overall, 59 % (95 %CI:57–60 %) of patients attained their 2016 non-HDL-C goals, vs. 54 % (95 %CI:53–56 %) for LDL-C; 50 % (95 %CI:48–51 %) attained both. Under stricter 2019 guidelines applied retrospectively, goal-attainment was 40 % (95 %CI:39–42 %), vs. 34 % (95 %CI:32–35 %) for LDL-C, and 30 % (95 %CI:28–32 %) for dual-goals. Non-HDL-C goal-attainment decreased with increasing CVD risk. Use of combination LLT was low, especially in very-high-risk patients. Older age (OR:1.60) and male sex (OR:1.35) were positively associated with non-HDL-C goal attainment; smoking (OR:0.71) and hypertriglyceridemia (OR:0.35) were negatively associated. Those at LDL-C-goal only had higher triglycerides, BMI, and T2DM burden than those achieving both goals, highlighting residual risk.</div></div><div><h3>Conclusions</h3><div>Despite widespread statin use, many patients treated under 2017–2018 practice would not have met the more stringent 2019 non-HDL-C targets. This highlights the need for risk-based treatment intensification, improved targeting of triglyceride-rich lipoproteins, and broader adoption of combination LLTs to optimise guideline-based care.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"414 ","pages":"Article 120644"},"PeriodicalIF":5.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147353357","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}
Pub Date : 2026-03-01Epub Date: 2026-01-08DOI: 10.1016/j.atherosclerosis.2026.120638
Daniel G. Brieger , Michael P. Gray , Sina Fathieh , Christina Magnussen , Gemma A. Figtree
The identification and targeting of standard modifiable risk factors (SMuRFs) - hypertension, dyslipidaemia, diabetes, and smoking - have led to significant improvements in cardiovascular outcomes over the past decades. However, clinical algorithms that rely on these SMuRFs only provide part of the solution, with 14–25 % of myocardial infarction patients presenting without these risk factors, and these factors accounting for only 53–56 % of incident cardiovascular disease (CVD) events globally. These algorithms perform particularly poorly in women, with SMuRFless women who suffer myocardial infarction (MI) experiencing a nearly threefold higher risk of early mortality compared to men with at least one risk factor. As the decline in global cardiovascular mortality has slowed markedly for women over the past decade, there is a pressing need for new solutions that extend beyond population-level risk factor models.
Advances in CT coronary angiography allow for the non-invasive detection of coronary atherosclerosis; the causal disease underlying MI. When combined with blood-based biomarkers, this holds promise for a shift towards precision preventative cardiology. To enable scalable and equitable implementation, coordinated global efforts are needed to couple biomarker discovery with implementation into clinical pathways capable of detecting subclinical CAD before events occur. Such strategies hold potential not only for more individualized treatment, but also for monitoring of disease activity and remission, and for accelerating the translation of novel therapeutics. This review outlines emerging innovations in risk stratification, diagnostics, clinical pathways and drug development, with an emphasis on the critical need to incorporate sex as a biological variable throughout.
{"title":"Coronary artery disease in the absence of standard modifiable risk factors (SMuRFs): The impact of sex","authors":"Daniel G. Brieger , Michael P. Gray , Sina Fathieh , Christina Magnussen , Gemma A. Figtree","doi":"10.1016/j.atherosclerosis.2026.120638","DOIUrl":"10.1016/j.atherosclerosis.2026.120638","url":null,"abstract":"<div><div>The identification and targeting of standard modifiable risk factors (SMuRFs) - hypertension, dyslipidaemia, diabetes, and smoking - have led to significant improvements in cardiovascular outcomes over the past decades. However, clinical algorithms that rely on these SMuRFs only provide part of the solution, with 14–25 % of myocardial infarction patients presenting without these risk factors, and these factors accounting for only 53–56 % of incident cardiovascular disease (CVD) events globally. These algorithms perform particularly poorly in women, with SMuRFless women who suffer myocardial infarction (MI) experiencing a nearly threefold higher risk of early mortality compared to men with at least one risk factor. As the decline in global cardiovascular mortality has slowed markedly for women over the past decade, there is a pressing need for new solutions that extend beyond population-level risk factor models.</div><div>Advances in CT coronary angiography allow for the non-invasive detection of coronary atherosclerosis; the causal disease underlying MI. When combined with blood-based biomarkers, this holds promise for a shift towards precision preventative cardiology. To enable scalable and equitable implementation, coordinated global efforts are needed to couple biomarker discovery with implementation into clinical pathways capable of detecting subclinical CAD before events occur. Such strategies hold potential not only for more individualized treatment, but also for monitoring of disease activity and remission, and for accelerating the translation of novel therapeutics. This review outlines emerging innovations in risk stratification, diagnostics, clinical pathways and drug development, with an emphasis on the critical need to incorporate sex as a biological variable throughout.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"414 ","pages":"Article 120638"},"PeriodicalIF":5.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146006640","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}
Pub Date : 2026-03-01Epub Date: 2026-02-04DOI: 10.1016/j.atherosclerosis.2026.120657
Frederick J. Raal , Susanne Greber-Platzer , Laurens F. Reeskamp , Gabriella Iannuzzo , Robert S. Rosenson , Samir Saheb , Claudia Stefanutti , Erik Stroes , Eric Bruckert , Alpana Waldron , Poulabi Banerjee , Robert Pordy , Pinay Kainth , Richard Jones , Daniel Gaudet
Background and aims
Homozygous familial hypercholesterolaemia (HoFH) is a rare genetic disorder caused primarily by variants in both alleles of the gene encoding the low-density lipoprotein receptor (LDLR). This subanalysis of the ELIPSE open-label extension (OLE) study assessed the efficacy of evinacumab, an angiopoietin-like 3 inhibitor, by genotype and LDLR function in patients with HoFH.
Methods
Patients aged ≥12 years with HoFH on stable lipid-lowering therapies received evinacumab 15 mg/kg intravenously every 4 weeks. Patients were grouped according to genotype: bi-allelic monogenic identical variants (true homozygous) or bi-allelic monogenic different LDLR variants (compound heterozygous); and by LDLR function: null/null variants resulting in <15% LDLR activity or negative/negative variants predicted to result in <2% LDLR activity.
Results
One hundred and sixteen patients enrolled in the OLE. At baseline, 55 (47.4%) had either identical bi-allelic variants in LDLR (n = 53) or LDLRAP1 (n = 2), and 41 (35.3%) had different bi-allelic LDLR variants. Median (Q1, Q3) LDL-C levels were reduced by −53.8% (−42.6%, −67.0%) and −58.1% (−41.5%, −65.9%) by Week 8 of evinacumab treatment in the identical (LDLR or LDLRAP1) and different (LDLR) bi-allelic variant groups, respectively, and remained low at Week 104 (−50.9% [-34.9%, −60.3%] and −47.3% [-34.8%, −67.5%], respectively). At baseline, 36 (31.0%) patients had null/null LDLR variants, and 19 (16.4%) patients had negative/negative LDLR variants. Evinacumab treatment also resulted in rapid and sustained decreases in median LDL-C levels to Week 104 in these subgroups.
Conclusions
Evinacumab treatment resulted in sustained LDL-C reduction in patients with HoFH irrespective of genotype or LDLR function.
{"title":"Efficacy of evinacumab by genotype and low-density lipoprotein receptor function in patients with homozygous familial hypercholesterolaemia: A subanalysis from the ELIPSE open-label extension study","authors":"Frederick J. Raal , Susanne Greber-Platzer , Laurens F. Reeskamp , Gabriella Iannuzzo , Robert S. Rosenson , Samir Saheb , Claudia Stefanutti , Erik Stroes , Eric Bruckert , Alpana Waldron , Poulabi Banerjee , Robert Pordy , Pinay Kainth , Richard Jones , Daniel Gaudet","doi":"10.1016/j.atherosclerosis.2026.120657","DOIUrl":"10.1016/j.atherosclerosis.2026.120657","url":null,"abstract":"<div><h3>Background and aims</h3><div>Homozygous familial hypercholesterolaemia (HoFH) is a rare genetic disorder caused primarily by variants in both alleles of the gene encoding the low-density lipoprotein receptor (<em>LDLR</em>). This subanalysis of the ELIPSE open-label extension (OLE) study assessed the efficacy of evinacumab, an angiopoietin-like 3 inhibitor, by genotype and LDLR function in patients with HoFH.</div></div><div><h3>Methods</h3><div>Patients aged ≥12 years with HoFH on stable lipid-lowering therapies received evinacumab 15 mg/kg intravenously every 4 weeks. Patients were grouped according to genotype: bi-allelic monogenic identical variants (true homozygous) or bi-allelic monogenic different <em>LDLR</em> variants (compound heterozygous); and by LDLR function: null/null variants resulting in <15% LDLR activity or negative/negative variants predicted to result in <2% LDLR activity.</div></div><div><h3>Results</h3><div>One hundred and sixteen patients enrolled in the OLE. At baseline, 55 (47.4%) had either identical bi-allelic variants in <em>LDLR</em> (n = 53) or <em>LDLRAP1</em> (n = 2), and 41 (35.3%) had different bi-allelic <em>LDLR</em> variants. Median (Q1, Q3) LDL-C levels were reduced by −53.8% (−42.6%, −67.0%) and −58.1% (−41.5%, −65.9%) by Week 8 of evinacumab treatment in the identical (<em>LDLR</em> or <em>LDLRAP1</em>) and different (<em>LDLR)</em> bi-allelic variant groups, respectively, and remained low at Week 104 (−50.9% [-34.9%, −60.3%] and −47.3% [-34.8%, −67.5%], respectively). At baseline, 36 (31.0%) patients had null/null <em>LDLR</em> variants, and 19 (16.4%) patients had negative/negative <em>LDLR</em> variants. Evinacumab treatment also resulted in rapid and sustained decreases in median LDL-C levels to Week 104 in these subgroups.</div></div><div><h3>Conclusions</h3><div>Evinacumab treatment resulted in sustained LDL-C reduction in patients with HoFH irrespective of genotype or LDLR function.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"414 ","pages":"Article 120657"},"PeriodicalIF":5.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146163839","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}
Pub Date : 2026-03-01DOI: 10.1016/j.atherosclerosis.2026.120643
Viviane Zorzanelli Rocha, Raul D Santos
{"title":"C-reactive protein in secondary prevention: Clarifying residual risk in individuals already at high risk.","authors":"Viviane Zorzanelli Rocha, Raul D Santos","doi":"10.1016/j.atherosclerosis.2026.120643","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2026.120643","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"414 ","pages":"120643"},"PeriodicalIF":5.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147484396","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}
Pub Date : 2026-03-01Epub Date: 2025-06-13DOI: 10.1016/j.atherosclerosis.2025.120405
Ole Fröbert, Ida B Pedersen, Astrid J Hjelholt, Christian Erikstrup, Sara Cajander
Influenza infection is a well-established trigger of acute cardiovascular events, particularly myocardial infarction, mediated by systemic inflammation, endothelial dysfunction, and thrombosis. In this review, we examine the evidence supporting influenza vaccination as a preventive strategy in cardiovascular disease. Observational studies and randomized trials consistently show reduced cardiovascular event rates among vaccinated individuals, with the most pronounced benefit seen after myocardial infarction. Emerging data suggest that the effects of vaccination extend beyond infection prevention, involving immunomodulatory effects, including regulatory T cell activity, features of trained innate immunity, and mechanisms promoting resolution of inflammation. Unlike conventional anti-inflammatory therapies, vaccination appears to rebalance immune responses without compromising host defence. We also consider an evolutionary perspective, proposing that historical influenza exposure may have contributed to the genetic architecture of atherosclerosis. Taken together, current evidence positions influenza vaccination as a safe, low-cost, and biologically plausible intervention in the prevention of cardiovascular events. However, important questions remain. Whether revaccination during hospitalization provides added benefit in previously immunized individuals, and the potential of high-dose or next-generation vaccine platforms such as mRNA, warrant further study. Dedicated outcome trials conducted outside the influenza season are especially needed to clarify nonspecific cardiovascular benefits. Cardiologists and other stakeholders share a responsibility to implement existing guidelines with the same commitment given to statins and platelet inhibitors.
{"title":"The flu shot and cardiovascular Protection: Rethinking inflammation in ischemic heart disease.","authors":"Ole Fröbert, Ida B Pedersen, Astrid J Hjelholt, Christian Erikstrup, Sara Cajander","doi":"10.1016/j.atherosclerosis.2025.120405","DOIUrl":"10.1016/j.atherosclerosis.2025.120405","url":null,"abstract":"<p><p>Influenza infection is a well-established trigger of acute cardiovascular events, particularly myocardial infarction, mediated by systemic inflammation, endothelial dysfunction, and thrombosis. In this review, we examine the evidence supporting influenza vaccination as a preventive strategy in cardiovascular disease. Observational studies and randomized trials consistently show reduced cardiovascular event rates among vaccinated individuals, with the most pronounced benefit seen after myocardial infarction. Emerging data suggest that the effects of vaccination extend beyond infection prevention, involving immunomodulatory effects, including regulatory T cell activity, features of trained innate immunity, and mechanisms promoting resolution of inflammation. Unlike conventional anti-inflammatory therapies, vaccination appears to rebalance immune responses without compromising host defence. We also consider an evolutionary perspective, proposing that historical influenza exposure may have contributed to the genetic architecture of atherosclerosis. Taken together, current evidence positions influenza vaccination as a safe, low-cost, and biologically plausible intervention in the prevention of cardiovascular events. However, important questions remain. Whether revaccination during hospitalization provides added benefit in previously immunized individuals, and the potential of high-dose or next-generation vaccine platforms such as mRNA, warrant further study. Dedicated outcome trials conducted outside the influenza season are especially needed to clarify nonspecific cardiovascular benefits. Cardiologists and other stakeholders share a responsibility to implement existing guidelines with the same commitment given to statins and platelet inhibitors.</p>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"120405"},"PeriodicalIF":5.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324328","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}
Pub Date : 2026-02-25DOI: 10.1016/j.atherosclerosis.2025.120520
F Lozano Vigario, J Molenaar, I Simó Vesperinas, M van der Zon, N S A Crone, M J M deJong, E Hemme, M A C Depuydt, L Delfos, J de Mol, M N Bernabé Kleijn, J A H M Peeters, A Wezel, H J Smeets, R T N Tjokrodirijo, A H deRu, A Kros, P H A Quax, M R de Vries, J Kuiper, I Bot, P van Veelen, B Slütter
{"title":"Corrigendum to immunopeptidomics analysis of human atherosclerosis plaques identifies antigenic drivers of atherosclerosis[Atherosclerosis, (409), October 2025, 120509].","authors":"F Lozano Vigario, J Molenaar, I Simó Vesperinas, M van der Zon, N S A Crone, M J M deJong, E Hemme, M A C Depuydt, L Delfos, J de Mol, M N Bernabé Kleijn, J A H M Peeters, A Wezel, H J Smeets, R T N Tjokrodirijo, A H deRu, A Kros, P H A Quax, M R de Vries, J Kuiper, I Bot, P van Veelen, B Slütter","doi":"10.1016/j.atherosclerosis.2025.120520","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2025.120520","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"120520"},"PeriodicalIF":5.7,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147301284","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}
Pub Date : 2026-02-01Epub Date: 2026-02-04DOI: 10.1016/j.atherosclerosis.2025.120629
Yang Shen, Weijie Hu
{"title":"Considerations on statistical analysis of NHANES data in oral microbiome diversity and mortality study","authors":"Yang Shen, Weijie Hu","doi":"10.1016/j.atherosclerosis.2025.120629","DOIUrl":"10.1016/j.atherosclerosis.2025.120629","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"413 ","pages":"Article 120629"},"PeriodicalIF":5.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131164","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}
Pub Date : 2026-02-01Epub Date: 2026-02-04DOI: 10.1016/j.atherosclerosis.2025.120626
Philippe Moulin MD PhD
{"title":"Is there a new dark side of persistent chylomicronemia?","authors":"Philippe Moulin MD PhD","doi":"10.1016/j.atherosclerosis.2025.120626","DOIUrl":"10.1016/j.atherosclerosis.2025.120626","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"413 ","pages":"Article 120626"},"PeriodicalIF":5.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131183","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}
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