Current Atherosclerosis Reports最新文献

{"title":"Bridging Prevention and Imaging: The Influence of Statins on CAC and CCTA Findings.","authors":"Soumya Kambalapalli, Mrinal Bhandari, Natdanai Punnanithinont, Beshoy Iskander, Muneeb A Khan, Matthew Budoff","doi":"10.1007/s11883-025-01287-x","DOIUrl":"https://doi.org/10.1007/s11883-025-01287-x","url":null,"abstract":"<p><p>To evaluate the impact of statins on CHD prevention, role of CAC scoring and CCTA in guiding statin therapy for both primary and secondary prevention in ASCVD. Coronary artery calcium (CAC) scoring and coronary computed tomography angiography (CCTA) have emerged as vital non-invasive imaging tools for refining cardiovascular risk assessment and guiding statin therapy in patients with atherosclerotic cardiovascular disease (ASCVD). CAC scoring helps stratify patients based on subclinical atherosclerosis burden, while CCTA provides detailed insights into plaque composition and distribution. Multiple studies, including the Multi-Ethnic Study of Atherosclerosis (MESA) and the CONFIRM registry, have demonstrated the utility of CAC scoring in identifying individuals at risk of major adverse cardiovascular events (MACE) and guiding personalized statin therapy. CAC scores, categorized into risk-based thresholds, enable clinicians to determine when statins should be initiated or deferred. CCTA complements CAC scoring by assessing plaque characteristics, including non-calcified plaque (NCP), calcified plaque, and high-risk features such as low-attenuation plaques, spotty calcifications, and positive remodeling. Serial CCTA imaging has further highlighted the effect of high-intensity statin therapy on plaque progression, demonstrating reductions in NCP and stabilization through increased calcification. CAC scoring effectively identifies patients with subclinical atherosclerosis who would benefit from statin therapy, particularly those with CAC scores > 100 or in the ≥ 75th percentile for age and sex. Statin therapy has been shown to promote plaque stabilization by increasing calcified plaque volume while reducing the progression of non-calcified plaques, thereby mitigating the risk of plaque rupture. CCTA provides additional value by identifying vulnerable plaque features and monitoring the impact of statin therapy over time. Studies have demonstrated significant reductions in total plaque volume and low-attenuation plaques in patients undergoing intensive lipid-lowering therapy, reinforcing the role of CCTA in guiding statin decisions for patients with established ASCVD. CAC scoring serves as a powerful tool to refine risk stratification and guide statin therapy initiation, particularly in asymptomatic individuals. CCTA enhances this approach by providing comprehensive plaque assessment and monitoring the response to statin therapy. Integrating CAC scoring and CCTA into clinical practice allows for a personalized approach to ASCVD management, improving patient outcomes through optimized statin therapy and targeted risk reduction.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"27 1","pages":"50"},"PeriodicalIF":5.7,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810681","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":"Anti-Inflammatory Lipid Mediators from Polyunsaturated Fatty Acids: Insights into their Role in Atherosclerosis Microenvironments.","authors":"Hongqin Wang, Yuan Li, Lei Zhang, Mengkai Lu, Chao Li, Yunlun Li","doi":"10.1007/s11883-025-01285-z","DOIUrl":"https://doi.org/10.1007/s11883-025-01285-z","url":null,"abstract":"<p><strong>Purpose of review: </strong>Inflammation has become a major residual risk factor for atherosclerotic cardiovascular disease (ASCVD). Certain lipid mediators, known as specialized proresolving mediators (SPMs), are mainly derived from polyunsaturated fatty acids (PUFAs) and can promote inflammation resolution while maintaining host autoimmunity. This review investigates the synthesis and ligand action pathways of these lipid mediators, as well as their regulatory mechanisms in the microenvironment of atherosclerotic plaques. Furthermore, it explores their clinical therapeutic potential, aiming to offer new insights into novel anti-inflammatory drug targets for the treatment of ASCVD.</p><p><strong>Recent findings: </strong>Reduced levels of SPMs are associated with the progression of atherosclerosis. SPMs inhibit inflammatory responses in the plaque microenvironment by limiting immune cell infiltration, reducing oxidative stress, and promoting the clearance of apoptotic cells, all of which contribute to plaque stabilization. Tyrosine-protein kinase Mer (MerTK), TRIF-related adaptor molecule (TRAM), and high mobility group box 1 (HMGB1) play crucial roles in the modulation of SPM production. Clinical use of ω-3 PUFAs has been shown to reduce the incidence of fatal cardiovascular events. Furthermore, aspirin not only initiates the synthesis of specific SPMs but also extends their activity within the body. The enhanced production of SPMs promotes inflammation resolution in the plaque microenvironment without inducing immunosuppression. This characteristic highlights MerTK, TRAM, and HMGB1 as potential targets for the development of anti-inflammatory drugs. Investigating targets and compounds that enhance the production of SPMs presents a promising strategy for developing future anti-inflammatory agents.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"27 1","pages":"48"},"PeriodicalIF":5.7,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810679","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":"Role of Aspirin in Reducing Risk for Atherosclerotic Cardiovascular Disease in Individuals with Elevated Lipoprotein(a).","authors":"Alexander C Razavi, Harpreet S Bhatia","doi":"10.1007/s11883-025-01296-w","DOIUrl":"https://doi.org/10.1007/s11883-025-01296-w","url":null,"abstract":"<p><strong>Purpose of review: </strong>Elevated Lp(a) is associated with increased risk for atherosclerotic cardiovascular disease (ASCVD), and there is currently a lack of targeted therapies for treating individuals with elevated Lp(a). The purpose of this review is to evaluate the current evidence for aspirin therapy for the primary prevention of ASCVD in individuals with elevated Lp(a).</p><p><strong>Recent findings: </strong>Prior studies demonstrated an association between aspirin use and a reduction in cardiovascular events among carriers of particular high-risk LPA single nucleotide polymorphisms. More recent studies have extended these findings by incorporating the more clinically available Lp(a) levels, observing an approximately 50% reduction in risk for coronary heart disease events and ASCVD mortality with aspirin use among individuals with Lp(a) > 50 mg/dL. There is growing evidence for a benefit with aspirin therapy in individuals with elevated Lp(a) without clinical ASCVD. The limitations of the available data must be acknowledged, and shared decision making should be used when discussing with patients, particularly when balancing potential bleeding risk. Future studies are needed to provide more definitive guidance regarding primary prevention aspirin therapy in this population.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"27 1","pages":"49"},"PeriodicalIF":5.7,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810683","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 Atherosclerotic Plaque Microenvironment as a Therapeutic Target.","authors":"Rajan Pandit, Arif Yurdagul","doi":"10.1007/s11883-025-01294-y","DOIUrl":"10.1007/s11883-025-01294-y","url":null,"abstract":"<p><strong>Purpose of review: </strong>Atherosclerosis is traditionally viewed as a disease triggered by lipid accumulation, but growing evidence underscores the crucial role of the plaque microenvironment in disease progression. This review explores recent advances in understanding how cellular and extracellular components of the plaque milieu drive atherosclerosis, with a focus on leveraging these microenvironmental factors for therapeutic intervention. This review highlights recent advances in cell-cell crosstalk and matrix remodeling, offering insights into innovative therapeutic strategies for atherosclerotic cardiovascular disease.</p><p><strong>Recent findings: </strong>While atherosclerosis begins with the subendothelial retention of apolipoprotein B (ApoB)-containing lipoproteins​, its progression is increasingly recognized as a consequence of complex cellular and extracellular dynamics within the plaque microenvironment. Soluble factors and extracellular matrix proteins shape mechanical properties and the biochemical landscape, directly influencing cell behavior and inflammatory signaling. For instance, the deposition of transitional matrix proteins, such as fibronectin, in regions of disturbed flow primes endothelial cells for inflammation​. Likewise, impaired clearance of dead cells and chronic extracellular matrix remodeling contribute to lesion expansion and instability, further exacerbating disease severity. Targeting the plaque microenvironment presents a promising avenue for stabilizing atherosclerotic lesions. Approaches that enhance beneficial cellular interactions, such as boosting macrophage efferocytosis to resolve inflammation while mitigating proatherogenic signals like integrin-mediated endothelial activation, may promote fibrous cap formation and reduce plaque vulnerability. Harnessing these mechanisms may lead to novel therapeutic approaches aimed at modifying the plaque microenvironment to combat atherosclerotic cardiovascular disease.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"27 1","pages":"47"},"PeriodicalIF":5.7,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11965263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763280","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":"The Role of Non-Statin Lipid Lowering Therapies to Reduce ASCVD Events in Primary Prevention.","authors":"Chukwuemezie Kamanu, Dean G Karalis","doi":"10.1007/s11883-025-01283-1","DOIUrl":"10.1007/s11883-025-01283-1","url":null,"abstract":"<p><strong>Purpose of review: </strong>Atherosclerotic cardiovascular disease (ASCVD) remains a leading global health challenge, with low-density lipoprotein (LDL) cholesterol a pivotal risk factor. While statins are cornerstone therapy for lowering LDL cholesterol, many high-risk primary prevention patients are unable to tolerate statin therapy and do not achieve their guideline directed LDL cholesterol goal. For these patients, non-statin therapies offer complementary and alternative approaches to LDL cholesterol reduction.</p><p><strong>Recent findings: </strong>Recent advancements in non-statin therapies have expanded the options available to clinicians to lower LDL cholesterol in high-risk primary prevention patients. Yet these medications are often under-utilized in clinical practice. Observational studies, Mendelian randomization studies, and randomized clinical trials support the role of non-statin LDL cholesterol lowering therapies in the primary prevention of ASCVD. This review summarizes the evidence supporting their use for the primary prevention of ASCVD and offers practical suggestions as to how clinicians can integrate these medications into their clinical practice.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"27 1","pages":"46"},"PeriodicalIF":5.7,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11965143/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763284","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":"Familial Combined Hyperlipidemia: Myth or Reality?","authors":"M C G J Brouwers, B Klop, J Ribalta, M Castro Cabezas","doi":"10.1007/s11883-025-01289-9","DOIUrl":"10.1007/s11883-025-01289-9","url":null,"abstract":"<p><strong>Purpose of review: </strong>Familial combined hyperlipidemia (FCHL) was first described by Goldstein and co-workers in 1973 as a multiple-type hyperlipidemia in pedigrees with premature myocardial infarction. However, it can be questioned what actually defines FCHL.</p><p><strong>Recent findings: </strong>Although initially regarded as an autosomal dominant disorder, quantitative trait linkage analyses have revealed multiple genes that are associated with the FCHL phenotype. With the advent of genome-wide association studies and next generation sequencing it has been confirmed that FCHL is a polygenic disorder and the associated gene variants, mostly with a triglyceride-raising effect, are not unique to FCHL. Furthermore, epidemiological studies have demonstrated that the multiple-type hyperlipidemia is also not specifically confined to FCHL. This review provides a historical overview of the metabolic and genetic abnormalities that characterize FCHL. Integration of these findings with recent population-based, genetic studies results in a new pathophysiological concept of FCHL. This model provides practical guidance on how to approach an individual patient with an 'FCHL phenotype'.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"27 1","pages":"45"},"PeriodicalIF":5.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11961474/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751426","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":"Remnant Cholesterol: Should it be a Target for Prevention of ASCVD?","authors":"Takahito Doi, Anne Langsted, Børge Grønne Nordestgaard","doi":"10.1007/s11883-025-01288-w","DOIUrl":"https://doi.org/10.1007/s11883-025-01288-w","url":null,"abstract":"<p><strong>Purpose of review: </strong>To summarize studies analyzing whether remnant cholesterol should be a target for prevention of atherosclerotic cardiovascular disease (ASCVD).</p><p><strong>Recent findings: </strong>There is a growing body of evidence from epidemiologic and Mendelian randomization studies implicating remnant cholesterol as a causal risk factor for ASCVD. However, the results of randomized controlled trials, particularly those conducted in the current high-intensity statin era, have been inconsistent. Most recently, the PROMINENT trial failed to show a beneficial effect of 0.4 mg/day of pemafibrate on the risk of ASCVD. In the Copenhagen General Population Study (CGPS), which mimics PROMINENT, the estimated hazard ratio for ASCVD was 1.05 (0.96-1.14) when absolute changes in remnant cholesterol, LDL cholesterol, and apolipoprotein B were combined, whereas the hazard ratio for ASCVD in PROMINENT was 1.03 (0.91-1.15). Further trials are warranted to ascertain the efficacy of novel remnant cholesterol- and triglyceride-lowering agents in the prevention of ASCVD. To reduce ASCVD, active agents need to reduce total atherogenic cholesterol (LDL and remnant cholesterol) and apolipoprotein B.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"27 1","pages":"44"},"PeriodicalIF":5.7,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708953","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":"Correction to: Built Environment and Cardiovascular Diseases - Insights from a Global Review.","authors":"Ali Aahil Noorali, Asma Altaf Hussain Merchant, Noreen Afzal, Rupshikha Sen, Vashma Junaid, Adeel Khoja, Sadeer Al-Kindi, Elizabeth M Vaughan, Unab I Khan, Nilofer F Safdar, Salim S Virani, Sana Sheikh","doi":"10.1007/s11883-025-01293-z","DOIUrl":"https://doi.org/10.1007/s11883-025-01293-z","url":null,"abstract":"","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"27 1","pages":"43"},"PeriodicalIF":5.7,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699900","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":"Inflammation-Driven Plaque Erosion in Atherosclerosis: A Focus on Complement System Pathways.","authors":"Davide Ramoni, Federico Carbone, Simon Kraler, Davide Di Vece, Fabrizio Montecucco, Luca Liberale","doi":"10.1007/s11883-025-01279-x","DOIUrl":"10.1007/s11883-025-01279-x","url":null,"abstract":"<p><strong>Purpose of review: </strong>Complement system activation is implicated in various stages of atherogenesis, from fatty streak formation to plaque destabilization and thrombus formation, with its dreadful clinical sequelae such as myocardial infarction, stroke and premature death. In this review, we consider these issues and explore recent studies on complement activation in atherosclerotic plaque initiation and progression.</p><p><strong>Recent findings: </strong>Complement pathways impact plaque stability and healing through the modulation of inflammatory processes. Recent studies indicate that complement components, notably C3 and C5b-9, accelerate atherosclerosis progression through their interactions with endothelial cells, smooth muscle cells, and immune cells. Nonetheless, the beneficial versus deleterious effects of complement activation at different stages of atherogenesis remains a matter of ongoing debates. Research also investigates therapies targeting the complement cascade to mitigate plaque erosion and rupture. This review explores the ongoing debates surrounding complement activation in atherogenesis. We bring forward controversial findings and therapeutic strategies aimed at modulating complement cascade activation with the ultimate goal to reduce the burden of atherosclerotic cardiovascular disease..</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"27 1","pages":"42"},"PeriodicalIF":5.7,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11928383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143676771","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":"Managing Dyslipidemia in Chronic Kidney Disease: Implications for Cardiovascular and Renal Risk.","authors":"Panagiotis Theofilis, Panayotis K Vlachakis, Paschalis Karakasis, Rigas G Kalaitzidis","doi":"10.1007/s11883-025-01290-2","DOIUrl":"https://doi.org/10.1007/s11883-025-01290-2","url":null,"abstract":"<p><strong>Purpose of review: </strong>The review aims to address the complex relationship between dyslipidemia and chronic kidney disease (CKD), emphasizing its dual role in driving cardiovascular disease (CVD) risk and contributing to CKD progression. It explores pathophysiological mechanisms, highlights recent biomarker discoveries, and evaluates contemporary and emerging lipid-lowering therapies tailored for CKD patients.</p><p><strong>Recent findings: </strong>Recent studies have highlighted the inadequacy of traditional lipid markers like LDL-C in reflecting cardiovascular risk in CKD. Novel biomarkers, such as remnant cholesterol and lipoprotein(a), demonstrate stronger associations with adverse outcomes. Emerging lipid-lowering agents, including bempedoic acid, pemafibrate, and PCSK9 inhibitors, show promise for risk reduction, especially in non-dialysis-dependent CKD. However, evidence remains limited for advanced stages of CKD and dialysis patients. Furthermore, alterations in lipid metabolism, such as dysfunctional HDL and triglyceride-rich lipoproteins, are now recognized as significant contributors to CVD and renal damage in CKD populations. Dyslipidemia is a pivotal modifiable risk factor in CKD, exacerbating both cardiovascular risk and disease progression. While statins remain the cornerstone of therapy in early-to-moderate CKD, their efficacy diminishes in advanced stages. The advent of novel therapeutic options and a deeper understanding of dyslipidemia's pathophysiology hold potential for improving outcomes. Future research should prioritize personalized approaches, focusing on the unique metabolic derangements of CKD and advancing treatments for high-risk and dialysis-dependent patients.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"27 1","pages":"41"},"PeriodicalIF":5.7,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673558","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}