Pub Date : 2024-09-01Epub Date: 2024-07-03DOI: 10.1007/s11883-024-01223-5
Priyanka Banerjee, Khanh Chau, Sivareddy Kotla, Eleanor L Davis, Estefani Berrios Turcios, Shengyu Li, Zhang Pengzhi, Guangyu Wang, Gopi Krishna Kolluru, Abhishek Jain, John P Cooke, Junichi Abe, Nhat-Tu Le
Purpose of review: Major Depressive Disorder (MDD) is characterized by persistent symptoms such as fatigue, loss of interest in activities, feelings of sadness and worthlessness. MDD often coexist with cardiovascular disease (CVD), yet the precise link between these conditions remains unclear. This review explores factors underlying the development of MDD and CVD, including genetic, epigenetic, platelet activation, inflammation, hypothalamic-pituitary-adrenal (HPA) axis activation, endothelial cell (EC) dysfunction, and blood-brain barrier (BBB) disruption.
Recent findings: Single nucleotide polymorphisms (SNPs) in the membrane-associated guanylate kinase WW and PDZ domain-containing protein 1 (MAGI-1) are associated with neuroticism and psychiatric disorders including MDD. SNPs in MAGI-1 are also linked to chronic inflammatory disorders such as spontaneous glomerulosclerosis, celiac disease, ulcerative colitis, and Crohn's disease. Increased MAGI-1 expression has been observed in colonic epithelial samples from Crohn's disease and ulcerative colitis patients. MAGI-1 also plays a role in regulating EC activation and atherogenesis in mice and is essential for Influenza A virus (IAV) infection, endoplasmic reticulum stress-induced EC apoptosis, and thrombin-induced EC permeability. Despite being understudied in human disease; evidence suggests that MAGI-1 may play a role in linking CVD and MDD. Therefore, further investigation of MAG-1 could be warranted to elucidate its potential involvement in these conditions.
{"title":"A Potential Role for MAGI-1 in the Bi-Directional Relationship Between Major Depressive Disorder and Cardiovascular Disease.","authors":"Priyanka Banerjee, Khanh Chau, Sivareddy Kotla, Eleanor L Davis, Estefani Berrios Turcios, Shengyu Li, Zhang Pengzhi, Guangyu Wang, Gopi Krishna Kolluru, Abhishek Jain, John P Cooke, Junichi Abe, Nhat-Tu Le","doi":"10.1007/s11883-024-01223-5","DOIUrl":"10.1007/s11883-024-01223-5","url":null,"abstract":"<p><strong>Purpose of review: </strong>Major Depressive Disorder (MDD) is characterized by persistent symptoms such as fatigue, loss of interest in activities, feelings of sadness and worthlessness. MDD often coexist with cardiovascular disease (CVD), yet the precise link between these conditions remains unclear. This review explores factors underlying the development of MDD and CVD, including genetic, epigenetic, platelet activation, inflammation, hypothalamic-pituitary-adrenal (HPA) axis activation, endothelial cell (EC) dysfunction, and blood-brain barrier (BBB) disruption.</p><p><strong>Recent findings: </strong>Single nucleotide polymorphisms (SNPs) in the membrane-associated guanylate kinase WW and PDZ domain-containing protein 1 (MAGI-1) are associated with neuroticism and psychiatric disorders including MDD. SNPs in MAGI-1 are also linked to chronic inflammatory disorders such as spontaneous glomerulosclerosis, celiac disease, ulcerative colitis, and Crohn's disease. Increased MAGI-1 expression has been observed in colonic epithelial samples from Crohn's disease and ulcerative colitis patients. MAGI-1 also plays a role in regulating EC activation and atherogenesis in mice and is essential for Influenza A virus (IAV) infection, endoplasmic reticulum stress-induced EC apoptosis, and thrombin-induced EC permeability. Despite being understudied in human disease; evidence suggests that MAGI-1 may play a role in linking CVD and MDD. Therefore, further investigation of MAG-1 could be warranted to elucidate its potential involvement in these conditions.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141491204","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 : 2024-08-27DOI: 10.1007/s11883-024-01232-4
Daphney Kernizan, Sean Connolly, Dima Turpin, Abbas Zaidi, Carissa M Baker-Smith
Purpose of review: Family history of premature cardiovascular disease is a strong predictor of individual cardiovascular risk. However, family history is not always available and not always reliable. Roughly 80% of health outcomes are influenced not by genetic risk but by societal factors, including adverse health behaviors and environment. Furthermore, in the present age of genetic testing, laboratory evaluations, and imaging, a key question remains: What is the contemporary relevance of family history screening in the management of cardiovascular disease in youth?
Recent findings: Knowledge of an individual's family history can help clinicians identify not only inherited risk but also familial clustering of unhealthy behaviors and environmental adversity contributing to enhanced cardiovascular disease risk in youth. For those at greatest risk, prevention strategies can be applied sooner and more conservatively. Integrating family history into clinical practice is crucial for cardiovascular risk assessment and for optimizing outcomes, but, in some cases, is more reflective of social factors.
{"title":"Is Family History for the Management of Cardiovascular Health in Youth Still Relevant in Clinical Practice?","authors":"Daphney Kernizan, Sean Connolly, Dima Turpin, Abbas Zaidi, Carissa M Baker-Smith","doi":"10.1007/s11883-024-01232-4","DOIUrl":"https://doi.org/10.1007/s11883-024-01232-4","url":null,"abstract":"<p><strong>Purpose of review: </strong>Family history of premature cardiovascular disease is a strong predictor of individual cardiovascular risk. However, family history is not always available and not always reliable. Roughly 80% of health outcomes are influenced not by genetic risk but by societal factors, including adverse health behaviors and environment. Furthermore, in the present age of genetic testing, laboratory evaluations, and imaging, a key question remains: What is the contemporary relevance of family history screening in the management of cardiovascular disease in youth?</p><p><strong>Recent findings: </strong>Knowledge of an individual's family history can help clinicians identify not only inherited risk but also familial clustering of unhealthy behaviors and environmental adversity contributing to enhanced cardiovascular disease risk in youth. For those at greatest risk, prevention strategies can be applied sooner and more conservatively. Integrating family history into clinical practice is crucial for cardiovascular risk assessment and for optimizing outcomes, but, in some cases, is more reflective of social factors.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072277","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 : 2024-08-16DOI: 10.1007/s11883-024-01230-6
Lucia Barbieri, Gabriele Tumminello, Isabella Fichtner, Alberto Corsini, Raul D Santos, Stefano Carugo, Massimiliano Ruscica
Purpose of review: Although the clinical benefit of reducing low-density lipoprotein cholesterol (LDLc) in patients with coronary artery disease (CAD) is well-established, the impact on plaque composition and stability is less clear. Our narrative review aimed to assess the clinical effects of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors on coronary plaque characteristics specifically focusing from atheroma progression to regression and stabilization.
Recent findings: The combination of statin therapy and PCSK9 inhibitors (evolocumab and alirocumab) promotes plaque stability in patients following an acute coronary syndrome. The GLAGOV study highlighted the relationship between achieved LDLc levels and changes in percentage atheroma volume. Similarly, the PACMAN-AMI study concluded that the qualitative and quantitative changes in coronary plaque were associated with the levels of LDLc. Assessing the severity of coronary artery stenosis and the extent of atherosclerotic burden by means of imaging techniques (e.g., IVUS, OCT and near-infrared spectroscopic) have significantly advanced our understanding of the benefits from promoting plaque regression and achieving to features of plaque stabilization through increasingly intensive lipid-lowering strategies.
{"title":"PCSK9 and Coronary Artery Plaque-New Opportunity or Red Herring?","authors":"Lucia Barbieri, Gabriele Tumminello, Isabella Fichtner, Alberto Corsini, Raul D Santos, Stefano Carugo, Massimiliano Ruscica","doi":"10.1007/s11883-024-01230-6","DOIUrl":"https://doi.org/10.1007/s11883-024-01230-6","url":null,"abstract":"<p><strong>Purpose of review: </strong>Although the clinical benefit of reducing low-density lipoprotein cholesterol (LDLc) in patients with coronary artery disease (CAD) is well-established, the impact on plaque composition and stability is less clear. Our narrative review aimed to assess the clinical effects of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors on coronary plaque characteristics specifically focusing from atheroma progression to regression and stabilization.</p><p><strong>Recent findings: </strong>The combination of statin therapy and PCSK9 inhibitors (evolocumab and alirocumab) promotes plaque stability in patients following an acute coronary syndrome. The GLAGOV study highlighted the relationship between achieved LDLc levels and changes in percentage atheroma volume. Similarly, the PACMAN-AMI study concluded that the qualitative and quantitative changes in coronary plaque were associated with the levels of LDLc. Assessing the severity of coronary artery stenosis and the extent of atherosclerotic burden by means of imaging techniques (e.g., IVUS, OCT and near-infrared spectroscopic) have significantly advanced our understanding of the benefits from promoting plaque regression and achieving to features of plaque stabilization through increasingly intensive lipid-lowering strategies.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141987609","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 : 2024-08-16DOI: 10.1007/s11883-024-01231-5
Bliss Chang, Luke J Laffin, Ashish Sarraju, Steven E Nissen
Purpose of review: To provide perspective on the current development status, and potential future role, of obicetrapib, a third-generation cholesterylester transfer protein (CETP) inhibitor. Obicetrapib has received recent attention following positive Phase II clinical trial data and initiation of Phase III trials for the treatment of dyslipidemia and atherosclerotic cardiovascular disease (ASCVD).
Recent findings: The ROSE and ROSE2 trials are Phase II studies that examined the lipid lowering effects of obicetrapib in patients on pre-existing high-intensity statin therapy. Obicetrapib significantly reduced key dyslipidemia biomarkers including low density lipoprotein cholesterol (LDL-C), Apolipoprotein B (Apo B), and non-high-density lipoprotein cholesterol (non-HDL-C) while increasing high-density lipoprotein cholesterol (HDL-C). Four phase III clinical trials, including a cardiovascular outcomes trial, are ongoing. Preliminary data for obicetrapib shows favorable effects on dyslipidemia, which could theoretically lead to a decrease in ASCVD clinical events. Short-term safety data in preliminary studies shows no significant safety signals.
综述的目的:透视第三代胆固醇酯转移蛋白 (CETP) 抑制剂 Obicetrapib 的研发现状和未来可能发挥的作用。在获得积极的II期临床试验数据并启动治疗血脂异常和动脉粥样硬化性心血管疾病(ASCVD)的III期试验后,奥比塞替匹最近受到了关注:ROSE和ROSE2试验是一项II期研究,考察了奥比曲匹对已接受高强度他汀类药物治疗的患者的降脂效果。Obicetrapib 能显著降低主要的血脂异常生物标志物,包括低密度脂蛋白胆固醇 (LDL-C)、载脂蛋白 B (Apo B) 和非高密度脂蛋白胆固醇 (non-HDL-C),同时提高高密度脂蛋白胆固醇 (HDL-C)。目前正在进行四项 III 期临床试验,包括一项心血管预后试验。obicetrapib 的初步数据显示其对血脂异常有良好的影响,理论上可减少 ASCVD 临床事件。初步研究的短期安全性数据未显示出明显的安全性信号。
{"title":"Obicetrapib-the Rebirth of CETP Inhibitors?","authors":"Bliss Chang, Luke J Laffin, Ashish Sarraju, Steven E Nissen","doi":"10.1007/s11883-024-01231-5","DOIUrl":"https://doi.org/10.1007/s11883-024-01231-5","url":null,"abstract":"<p><strong>Purpose of review: </strong>To provide perspective on the current development status, and potential future role, of obicetrapib, a third-generation cholesterylester transfer protein (CETP) inhibitor. Obicetrapib has received recent attention following positive Phase II clinical trial data and initiation of Phase III trials for the treatment of dyslipidemia and atherosclerotic cardiovascular disease (ASCVD).</p><p><strong>Recent findings: </strong>The ROSE and ROSE2 trials are Phase II studies that examined the lipid lowering effects of obicetrapib in patients on pre-existing high-intensity statin therapy. Obicetrapib significantly reduced key dyslipidemia biomarkers including low density lipoprotein cholesterol (LDL-C), Apolipoprotein B (Apo B), and non-high-density lipoprotein cholesterol (non-HDL-C) while increasing high-density lipoprotein cholesterol (HDL-C). Four phase III clinical trials, including a cardiovascular outcomes trial, are ongoing. Preliminary data for obicetrapib shows favorable effects on dyslipidemia, which could theoretically lead to a decrease in ASCVD clinical events. Short-term safety data in preliminary studies shows no significant safety signals.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141987608","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 : 2024-08-12DOI: 10.1007/s11883-024-01229-z
Juan Wang, Qiang Wu, Xinyu Wang, Hongbin Liu, Mulei Chen, Li Xu, Ze Zhang, Kuibao Li, Weiming Li, Jiuchang Zhong
Purpose of the review: Macrophage accumulation and activation function as hallmarks of atherosclerosis and have complex and intricate dynamics throughout all components and stages of atherosclerotic plaques. In this review, we focus on the regulatory roles and underlying mechanisms of macrophage phenotypes and metabolism in atherosclerosis. We highlight the diverse range of macrophage phenotypes present in atherosclerosis and their potential roles in progression and regression of atherosclerotic plaque. Furthermore, we discuss the challenges and opportunities in developing therapeutic strategies for preventing and treating atherosclerotic cardiovascular disease.
Recent findings: Dysregulation of macrophage polarization between the proinflammatory M1 and anti-inflammatory M2 phenotypealters the immuno-inflammatory response during atherosclerosis progression, leading to plaque initiation, growth, and ultimately rupture. Altered metabolism of macrophage is a key feature for their function and the subsequent progression of atherosclerotic cardiovascular disease. The immunometabolism of macrophage has been implicated to macrophage activation and metabolic rewiring of macrophages within atherosclerotic lesions, thereby shifting altered macrophage immune-effector and tissue-reparative function. Targeting macrophage phenotypes and metabolism are potential therapeutic strategies in the prevention and treatment of atherosclerosis and atherosclerotic cardiovascular diseases. Understanding the precise function and metabolism of specific macrophage subsets and their contributions to the composition and growth of atherosclerotic plaques could reveal novel strategies to delay or halt development of atherosclerotic cardiovascular diseases and their associated pathophysiological consequences. Identifying biological stimuli capable of modulating macrophage phenotypes and metabolism may lead to the development of innovative therapeutic approaches for treating patients with atherosclerosis and coronary artery diseases.
{"title":"Targeting Macrophage Phenotypes and Metabolism as Novel Therapeutic Approaches in Atherosclerosis and Related Cardiovascular Diseases.","authors":"Juan Wang, Qiang Wu, Xinyu Wang, Hongbin Liu, Mulei Chen, Li Xu, Ze Zhang, Kuibao Li, Weiming Li, Jiuchang Zhong","doi":"10.1007/s11883-024-01229-z","DOIUrl":"https://doi.org/10.1007/s11883-024-01229-z","url":null,"abstract":"<p><strong>Purpose of the review: </strong>Macrophage accumulation and activation function as hallmarks of atherosclerosis and have complex and intricate dynamics throughout all components and stages of atherosclerotic plaques. In this review, we focus on the regulatory roles and underlying mechanisms of macrophage phenotypes and metabolism in atherosclerosis. We highlight the diverse range of macrophage phenotypes present in atherosclerosis and their potential roles in progression and regression of atherosclerotic plaque. Furthermore, we discuss the challenges and opportunities in developing therapeutic strategies for preventing and treating atherosclerotic cardiovascular disease.</p><p><strong>Recent findings: </strong>Dysregulation of macrophage polarization between the proinflammatory M1 and anti-inflammatory M2 phenotypealters the immuno-inflammatory response during atherosclerosis progression, leading to plaque initiation, growth, and ultimately rupture. Altered metabolism of macrophage is a key feature for their function and the subsequent progression of atherosclerotic cardiovascular disease. The immunometabolism of macrophage has been implicated to macrophage activation and metabolic rewiring of macrophages within atherosclerotic lesions, thereby shifting altered macrophage immune-effector and tissue-reparative function. Targeting macrophage phenotypes and metabolism are potential therapeutic strategies in the prevention and treatment of atherosclerosis and atherosclerotic cardiovascular diseases. Understanding the precise function and metabolism of specific macrophage subsets and their contributions to the composition and growth of atherosclerotic plaques could reveal novel strategies to delay or halt development of atherosclerotic cardiovascular diseases and their associated pathophysiological consequences. Identifying biological stimuli capable of modulating macrophage phenotypes and metabolism may lead to the development of innovative therapeutic approaches for treating patients with atherosclerosis and coronary artery diseases.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141916303","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 : 2024-08-01Epub Date: 2024-06-01DOI: 10.1007/s11883-024-01219-1
Benjamin De Ornelas, Vincenzo Sucato, Giuseppe Vadalà, Andrea Buono, Alfredo Ruggero Galassi
Purpose of review: This review investigates the relationship between myocardial bridges (MBs), intimal thickening in coronary arteries, and Atherosclerotic cardiovascular disease. It focuses on the role of mechanical forces, such as circumferential strain, in arterial wall remodeling and aims to clarify how MBs affect coronary artery pathology.
Review findings: MBs have been identified as influential in modulating coronary artery intimal thickness, demonstrating a protective effect against thickening within the MB segment and an increase in thickness proximal to the MB. This is attributed to changes in mechanical stress and hemodynamics. Research involving arterial hypertension models and vein graft disease has underscored the importance of circumferential strain in vascular remodeling and intimal hyperplasia. Understanding the complex dynamics between MBs, mechanical strain, and vascular remodeling is crucial for advancing our knowledge of coronary artery disease mechanisms. This could lead to improved management strategies for cardiovascular diseases, highlighting the need for further research into MB-related vascular changes.
{"title":"Myocardial Bridge and Atherosclerosis, an Intimal Relationship.","authors":"Benjamin De Ornelas, Vincenzo Sucato, Giuseppe Vadalà, Andrea Buono, Alfredo Ruggero Galassi","doi":"10.1007/s11883-024-01219-1","DOIUrl":"10.1007/s11883-024-01219-1","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review investigates the relationship between myocardial bridges (MBs), intimal thickening in coronary arteries, and Atherosclerotic cardiovascular disease. It focuses on the role of mechanical forces, such as circumferential strain, in arterial wall remodeling and aims to clarify how MBs affect coronary artery pathology.</p><p><strong>Review findings: </strong>MBs have been identified as influential in modulating coronary artery intimal thickness, demonstrating a protective effect against thickening within the MB segment and an increase in thickness proximal to the MB. This is attributed to changes in mechanical stress and hemodynamics. Research involving arterial hypertension models and vein graft disease has underscored the importance of circumferential strain in vascular remodeling and intimal hyperplasia. Understanding the complex dynamics between MBs, mechanical strain, and vascular remodeling is crucial for advancing our knowledge of coronary artery disease mechanisms. This could lead to improved management strategies for cardiovascular diseases, highlighting the need for further research into MB-related vascular changes.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141186238","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 : 2024-08-01Epub Date: 2024-06-15DOI: 10.1007/s11883-024-01215-5
Ting Qin, Tian-Yi Ma, Kang Huang, Shi-Juan Lu, Jiang-Hua Zhong, Jian-Jun Li
Purpose of review: The primary objective of this review is to explore the pathophysiological roles and clinical implications of lipoprotein(a) [Lp(a)] in the context of atherosclerotic cardiovascular disease (ASCVD). We seek to understand how Lp(a) contributes to inflammation and arteriosclerosis, aiming to provide new insights into the mechanisms of ASCVD progression.
Recent findings: Recent research highlights Lp(a) as an independent risk factor for ASCVD. Studies show that Lp(a) not only promotes the inflammatory processes but also interacts with various cellular components, leading to endothelial dysfunction and smooth muscle cell proliferation. The dual role of Lp(a) in both instigating and, under certain conditions, mitigating inflammation is particularly noteworthy. This review finds that Lp(a) plays a complex role in the development of ASCVD through its involvement in inflammatory pathways. The interplay between Lp(a) levels and inflammatory responses highlights its potential as a target for therapeutic intervention. These insights could pave the way for novel approaches in managing and preventing ASCVD, urging further investigation into Lp(a) as a therapeutic target.
{"title":"Lipoprotein (a)-Related Inflammatory Imbalance: A Novel Horizon for the Development of Atherosclerosis.","authors":"Ting Qin, Tian-Yi Ma, Kang Huang, Shi-Juan Lu, Jiang-Hua Zhong, Jian-Jun Li","doi":"10.1007/s11883-024-01215-5","DOIUrl":"10.1007/s11883-024-01215-5","url":null,"abstract":"<p><strong>Purpose of review: </strong>The primary objective of this review is to explore the pathophysiological roles and clinical implications of lipoprotein(a) [Lp(a)] in the context of atherosclerotic cardiovascular disease (ASCVD). We seek to understand how Lp(a) contributes to inflammation and arteriosclerosis, aiming to provide new insights into the mechanisms of ASCVD progression.</p><p><strong>Recent findings: </strong>Recent research highlights Lp(a) as an independent risk factor for ASCVD. Studies show that Lp(a) not only promotes the inflammatory processes but also interacts with various cellular components, leading to endothelial dysfunction and smooth muscle cell proliferation. The dual role of Lp(a) in both instigating and, under certain conditions, mitigating inflammation is particularly noteworthy. This review finds that Lp(a) plays a complex role in the development of ASCVD through its involvement in inflammatory pathways. The interplay between Lp(a) levels and inflammatory responses highlights its potential as a target for therapeutic intervention. These insights could pave the way for novel approaches in managing and preventing ASCVD, urging further investigation into Lp(a) as a therapeutic target.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11236888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141327320","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}
Pub Date : 2024-08-01Epub Date: 2024-05-30DOI: 10.1007/s11883-024-01217-3
Guojiao Shang, Qi Shao, Kai Lv, Wenxiu Xu, Jing Ji, Shuning Fan, Xiangdong Kang, Fafeng Cheng, Xueqian Wang, Qingguo Wang
Purpose of review: Vascular dementia (VaD) is the second most prevalent type of dementia after Alzheimer's disease.Hypercholesterolemia may increase the risk of dementia, but the association between cholesterol and cognitive function is very complex. From the perspective of peripheral and brain cholesterol, we review the relationship between hypercholesterolemia and increased risk of VaD and how the use of lipid-lowering therapies affects cognition.
Recent findings: Epidemiologic studies show since 1980, non-HDL-C levels of individuals has increased rapidly in Asian countries.The study has suggested that vascular risk factors increase the risk of VaD, such as disordered lipid metabolism. Dyslipidemia has been found to interact with chronic cerebral hypoperfusion to promote inflammation resulting in cognitive dysfunction in the brain.Hypercholesterolemia may be a risk factor for VaD. Inflammation could potentially serve as a link between hypercholesterolemia and VaD. Additionally, the potential impact of lipid-lowering therapy on cognitive function is also worth considering. Finding strategies to prevent and treat VaD is critical given the aging of the population to lessen the load on society. Currently, controlling underlying vascular risk factors is considered one of the most effective methods of preventing VaD. Understanding the relationship between abnormal cholesterol levels and VaD, as well as discovering potential serum biomarkers, is important for the early prevention and treatment of VaD.
综述的目的:血管性痴呆(VaD)是仅次于阿尔茨海默病的第二大痴呆类型。高胆固醇血症可能会增加痴呆的风险,但胆固醇与认知功能之间的关系非常复杂。从外周胆固醇和脑胆固醇的角度,我们回顾了高胆固醇血症与老年痴呆症风险增加之间的关系,以及降脂疗法的使用如何影响认知功能:流行病学研究显示,自1980年以来,亚洲国家非高密度脂蛋白胆固醇水平迅速上升。研究表明,血管危险因素会增加罹患VaD的风险,如血脂代谢紊乱。研究发现,血脂异常与慢性脑灌注不足相互作用,促进炎症,从而导致大脑认知功能障碍。炎症可能是高胆固醇血症与 VaD 之间的潜在联系。此外,降脂治疗对认知功能的潜在影响也值得考虑。随着人口老龄化的加剧,找到预防和治疗退行性脑损伤的策略对于减轻社会负担至关重要。目前,控制潜在的血管风险因素被认为是预防先天性心脏病最有效的方法之一。了解胆固醇水平异常与血管性脑损伤之间的关系以及发现潜在的血清生物标志物,对于早期预防和治疗血管性脑损伤非常重要。
{"title":"Hypercholesterolemia and the Increased Risk of Vascular Dementia: a Cholesterol Perspective.","authors":"Guojiao Shang, Qi Shao, Kai Lv, Wenxiu Xu, Jing Ji, Shuning Fan, Xiangdong Kang, Fafeng Cheng, Xueqian Wang, Qingguo Wang","doi":"10.1007/s11883-024-01217-3","DOIUrl":"10.1007/s11883-024-01217-3","url":null,"abstract":"<p><strong>Purpose of review: </strong>Vascular dementia (VaD) is the second most prevalent type of dementia after Alzheimer's disease.Hypercholesterolemia may increase the risk of dementia, but the association between cholesterol and cognitive function is very complex. From the perspective of peripheral and brain cholesterol, we review the relationship between hypercholesterolemia and increased risk of VaD and how the use of lipid-lowering therapies affects cognition.</p><p><strong>Recent findings: </strong>Epidemiologic studies show since 1980, non-HDL-C levels of individuals has increased rapidly in Asian countries.The study has suggested that vascular risk factors increase the risk of VaD, such as disordered lipid metabolism. Dyslipidemia has been found to interact with chronic cerebral hypoperfusion to promote inflammation resulting in cognitive dysfunction in the brain.Hypercholesterolemia may be a risk factor for VaD. Inflammation could potentially serve as a link between hypercholesterolemia and VaD. Additionally, the potential impact of lipid-lowering therapy on cognitive function is also worth considering. Finding strategies to prevent and treat VaD is critical given the aging of the population to lessen the load on society. Currently, controlling underlying vascular risk factors is considered one of the most effective methods of preventing VaD. Understanding the relationship between abnormal cholesterol levels and VaD, as well as discovering potential serum biomarkers, is important for the early prevention and treatment of VaD.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141174921","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 : 2024-08-01Epub Date: 2024-06-03DOI: 10.1007/s11883-024-01218-2
Kartik Gupta, Bharat Rawlley, Chelsea Meloche, Abdul Mannan Khan Minhas, Melody Hermel, Leandro Slipczuk, Sana Sheikh, Adeel Khoja, Elizabeth M Vaughan, Mayank Dalakoti, Salim S Virani
Purpose of review: To summarize selected late-breaking science on cardiovascular (CV) disease prevention presented at the 2024 Scientific Session of the American College of Cardiology (ACC) conference.
Recent findings: The LIBerate-HR trial showed the efficacy and safety of lerodalcibep, a subcutaneous injection that prevents binding of Pro-Protein Convertase Subtilisin/Kexin (PCSK) 9 to low-density lipoprotein (LDL)-receptors resulting in LDL-cholesterol (LDL-C) lowering in patients at very high risk or high risk of atherosclerotic CV disease (ASCVD). The AEGIS-II randomized patients with type 1 myocardial infarction (MI) with multivessel coronary artery disease and additional CV risk factors and found no benefit in major adverse CV events (MACE) with CSL112, an apolipoprotein A1 infusion shown to increase cholesterol efflux capacity. The Bridge-TIMI 73a trial showed a significant reduction in triglyceride (TG) levels with olezarsen, an antisense mRNA, in patients with moderate hyperTG with elevated CV risk. The BE ACTIVE trial showed significant improvement in step counts in patients given behavioral and financial incentives. The DRIVE study showed a significant increase in the prescription of either sodium-glucose co-transporter-2 inhibitors or glucagon-like peptide-1 receptor agonists in patients with type 2 diabetes mellitus (T2DM) at elevated CV or renal risk with a remote team-based, non-licensed navigator and clinical pharmacist approach. The TACTiC trial showed increased and sustained use of statin therapy by patient-driven use of a web-based portal that calculated the ASCVD risk score and gave prompts. The VICTORIAN-INITIATE trial showed efficacy and safety in early use of inclisiran in patients with ASCVD who did not reach target LDL-C < 70 mg/dL despite maximally tolerated statin therapy. The ARISE-HF trial showed no difference in change of peak oxygen consumption with the use of an oral aldose reductase inhibitor, AT-001, in patients with well-controlled T2DM and diabetic cardiomyopathy with high-risk features compared to placebo. The PREVENT trial showed a significant reduction in target vessel failure at 2 years in patients with non-flow limiting vulnerable plaques with percutaneous coronary intervention and optimal medical therapy (OMT) compared to OMT alone. The late-breaking clinical science presented at the 2024 Scientific Session of the ACC paves the way for an evidence-based alternative to statin therapy and provides data on several common clinical scenarios encountered in daily practice.
{"title":"Highlights of Cardiovascular Disease Prevention Studies Presented at the 2024 American College of Cardiology Conference.","authors":"Kartik Gupta, Bharat Rawlley, Chelsea Meloche, Abdul Mannan Khan Minhas, Melody Hermel, Leandro Slipczuk, Sana Sheikh, Adeel Khoja, Elizabeth M Vaughan, Mayank Dalakoti, Salim S Virani","doi":"10.1007/s11883-024-01218-2","DOIUrl":"10.1007/s11883-024-01218-2","url":null,"abstract":"<p><strong>Purpose of review: </strong>To summarize selected late-breaking science on cardiovascular (CV) disease prevention presented at the 2024 Scientific Session of the American College of Cardiology (ACC) conference.</p><p><strong>Recent findings: </strong>The LIBerate-HR trial showed the efficacy and safety of lerodalcibep, a subcutaneous injection that prevents binding of Pro-Protein Convertase Subtilisin/Kexin (PCSK) 9 to low-density lipoprotein (LDL)-receptors resulting in LDL-cholesterol (LDL-C) lowering in patients at very high risk or high risk of atherosclerotic CV disease (ASCVD). The AEGIS-II randomized patients with type 1 myocardial infarction (MI) with multivessel coronary artery disease and additional CV risk factors and found no benefit in major adverse CV events (MACE) with CSL112, an apolipoprotein A1 infusion shown to increase cholesterol efflux capacity. The Bridge-TIMI 73a trial showed a significant reduction in triglyceride (TG) levels with olezarsen, an antisense mRNA, in patients with moderate hyperTG with elevated CV risk. The BE ACTIVE trial showed significant improvement in step counts in patients given behavioral and financial incentives. The DRIVE study showed a significant increase in the prescription of either sodium-glucose co-transporter-2 inhibitors or glucagon-like peptide-1 receptor agonists in patients with type 2 diabetes mellitus (T2DM) at elevated CV or renal risk with a remote team-based, non-licensed navigator and clinical pharmacist approach. The TACTiC trial showed increased and sustained use of statin therapy by patient-driven use of a web-based portal that calculated the ASCVD risk score and gave prompts. The VICTORIAN-INITIATE trial showed efficacy and safety in early use of inclisiran in patients with ASCVD who did not reach target LDL-C < 70 mg/dL despite maximally tolerated statin therapy. The ARISE-HF trial showed no difference in change of peak oxygen consumption with the use of an oral aldose reductase inhibitor, AT-001, in patients with well-controlled T2DM and diabetic cardiomyopathy with high-risk features compared to placebo. The PREVENT trial showed a significant reduction in target vessel failure at 2 years in patients with non-flow limiting vulnerable plaques with percutaneous coronary intervention and optimal medical therapy (OMT) compared to OMT alone. The late-breaking clinical science presented at the 2024 Scientific Session of the ACC paves the way for an evidence-based alternative to statin therapy and provides data on several common clinical scenarios encountered in daily practice.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141198975","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}
Purpose of review: Our work is to establish more distinct association between specific stress and vascular smooth muscle cells (VSMCs) phenotypes to alleviate atherosclerotic plaque burden and delay atherosclerosis (AS) progression.
Recent finding: In recent years, VSMCs phenotypic transition has received significant interests. Different stresses were found to be associated with VSMCs phenotypic transition. However, the explicit correlation between VSMCs phenotype and specific stress has not been elucidated clearly yet. We discover that VSMCs phenotypic transition, which is widely involved in the progression of AS, is associated with specific stress. We discuss approaches targeting stresses to intervene VSMCs phenotypic transition, which may contribute to develop innovative therapies for AS.
{"title":"Stress, Vascular Smooth Muscle Cell Phenotype and Atherosclerosis: Novel Insight into Smooth Muscle Cell Phenotypic Transition in Atherosclerosis.","authors":"Xiuya Guan, Yuanlong Hu, Jiaqi Hao, Mengkai Lu, Zhiyuan Zhang, Wenxian Hu, Dongxiao Li, Chao Li","doi":"10.1007/s11883-024-01220-8","DOIUrl":"10.1007/s11883-024-01220-8","url":null,"abstract":"<p><strong>Purpose of review: </strong>Our work is to establish more distinct association between specific stress and vascular smooth muscle cells (VSMCs) phenotypes to alleviate atherosclerotic plaque burden and delay atherosclerosis (AS) progression.</p><p><strong>Recent finding: </strong>In recent years, VSMCs phenotypic transition has received significant interests. Different stresses were found to be associated with VSMCs phenotypic transition. However, the explicit correlation between VSMCs phenotype and specific stress has not been elucidated clearly yet. We discover that VSMCs phenotypic transition, which is widely involved in the progression of AS, is associated with specific stress. We discuss approaches targeting stresses to intervene VSMCs phenotypic transition, which may contribute to develop innovative therapies for AS.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":null,"pages":null},"PeriodicalIF":5.7,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141174924","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}