Pub Date : 2025-10-23DOI: 10.1007/s11886-025-02284-x
Shivesh Anand, Gaoxian Chen, Astha Khanna, Ngan F Huang
Purpose of review: To provide an overview of human induced pluripotent stem cell (hiPSC)-derived cardiovascular lineages and describe their impact on drug testing in vitro.
Recent findings: hiPSCs have garnered tremendous interest over the last decade due to their potential for unlimited proliferation and differentiation into cardiovascular lineages. Technologies using tissue engineering, 3D bioprinting, and organ-on-a-chip platforms composed of hiPSC derivatives can produce cardiovascular tissue mimetics that enhance drug screening applications. hiPSC-derived cardiovascular lineages advance drug screening efforts by using autologous cells that are more therapeutically relevant. Established approaches to reproducibly generate hiPSC-derived cardiovascular lineages and their subsequent organization into 3D constructs more accurately mimic the physiological organization of cardiac tissue, leading to improved identification of potential drug targets for therapeutic testing.
{"title":"Human iPSC-Based in Vitro Cardiovascular Tissue Models for Drug Screening Applications.","authors":"Shivesh Anand, Gaoxian Chen, Astha Khanna, Ngan F Huang","doi":"10.1007/s11886-025-02284-x","DOIUrl":"10.1007/s11886-025-02284-x","url":null,"abstract":"<p><strong>Purpose of review: </strong>To provide an overview of human induced pluripotent stem cell (hiPSC)-derived cardiovascular lineages and describe their impact on drug testing in vitro.</p><p><strong>Recent findings: </strong>hiPSCs have garnered tremendous interest over the last decade due to their potential for unlimited proliferation and differentiation into cardiovascular lineages. Technologies using tissue engineering, 3D bioprinting, and organ-on-a-chip platforms composed of hiPSC derivatives can produce cardiovascular tissue mimetics that enhance drug screening applications. hiPSC-derived cardiovascular lineages advance drug screening efforts by using autologous cells that are more therapeutically relevant. Established approaches to reproducibly generate hiPSC-derived cardiovascular lineages and their subsequent organization into 3D constructs more accurately mimic the physiological organization of cardiac tissue, leading to improved identification of potential drug targets for therapeutic testing.</p>","PeriodicalId":10829,"journal":{"name":"Current Cardiology Reports","volume":"27 1","pages":"145"},"PeriodicalIF":3.3,"publicationDate":"2025-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12971102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-21DOI: 10.1007/s11886-025-02288-7
Aleksandr Talishinsky, Olujimi A Ajijola, Sahib S Khalsa
Purpose of the review: This review provides a framework for understanding autonomic neural regulation of cardiac function and dysfunction, highlighting the anatomical and functional organization of the autonomic nervous system, from intrinsic cardiac neurons to central cortical control centers. We review pathways leading to autonomic dysregulation in heart failure (HF) and cardiomyopathy (CMY), and we discuss the potential for precision neuromodulation informed by biomarkers and neuroimaging.
Recent findings: We synthesize emerging insights into the molecular, inflammatory, and psychological mechanisms contributing to autonomic dysregulation in HF, and examine the clinical implications of impaired reflex arcs and persistent neurohormonal activation. Recent advances in neuromodulation, including vagus nerve stimulation, baroreflex activation therapy, spinal cord stimulation, cardiac sympathetic denervation and cortical neuromodulation demonstrate the potential to restore autonomic balance and improve HF outcomes. Autonomic imbalance, characterized by sympathetic overactivation and parasympathetic withdrawal, is a hallmark of HF and CMY, contributing to disease progression and adverse outcomes. While traditional pharmacotherapies target downstream neurohormonal pathways, neuromodulation offers the opportunity to intervene upstream, directly at pathophysiological nexus points. Ultimately, a shift toward personalized, circuit-specific neuromodulation strategies may offer new opportunities for treating autonomic dysregulation in HF and CMY.
{"title":"Autonomic Imbalance in Cardiomyopathy and Heart Failure: From Neurobiology to Precision Neuromodulation.","authors":"Aleksandr Talishinsky, Olujimi A Ajijola, Sahib S Khalsa","doi":"10.1007/s11886-025-02288-7","DOIUrl":"10.1007/s11886-025-02288-7","url":null,"abstract":"<p><strong>Purpose of the review: </strong>This review provides a framework for understanding autonomic neural regulation of cardiac function and dysfunction, highlighting the anatomical and functional organization of the autonomic nervous system, from intrinsic cardiac neurons to central cortical control centers. We review pathways leading to autonomic dysregulation in heart failure (HF) and cardiomyopathy (CMY), and we discuss the potential for precision neuromodulation informed by biomarkers and neuroimaging.</p><p><strong>Recent findings: </strong>We synthesize emerging insights into the molecular, inflammatory, and psychological mechanisms contributing to autonomic dysregulation in HF, and examine the clinical implications of impaired reflex arcs and persistent neurohormonal activation. Recent advances in neuromodulation, including vagus nerve stimulation, baroreflex activation therapy, spinal cord stimulation, cardiac sympathetic denervation and cortical neuromodulation demonstrate the potential to restore autonomic balance and improve HF outcomes. Autonomic imbalance, characterized by sympathetic overactivation and parasympathetic withdrawal, is a hallmark of HF and CMY, contributing to disease progression and adverse outcomes. While traditional pharmacotherapies target downstream neurohormonal pathways, neuromodulation offers the opportunity to intervene upstream, directly at pathophysiological nexus points. Ultimately, a shift toward personalized, circuit-specific neuromodulation strategies may offer new opportunities for treating autonomic dysregulation in HF and CMY.</p>","PeriodicalId":10829,"journal":{"name":"Current Cardiology Reports","volume":"27 1","pages":"144"},"PeriodicalIF":3.3,"publicationDate":"2025-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12540530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145336565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-20DOI: 10.1007/s11886-025-02301-z
Seung Yeon Jeon, Chan Young Lee, Yun-Hee Lee, Hyojeong Kim, Jiwon Kim, Soo Kyung Cho, Han Soo Noh, Mo-Yeol Kang
Purpose of review: Cardiovascular disease (CVD) remains a leading cause of morbidity and mortality worldwide, with occupational factors emerging as significant yet modifiable risk factors. This comprehensive review evaluates the association between various occupational exposures-including job stress, long working hours, shift work, physical activity at work, and exposure to hazardous substances-and CVD risk. Using the GRADE framework, we assessed the strength of evidence for each risk factor.
Recent findings: Job stress, long working hours, night shift work, and carbon monoxide exposure demonstrated moderate evidence linking them to increased CVD risk, while occupational noise, air pollutants, and extreme temperatures had limited evidence. Physical activity at work and exposure to toxic metals showed inconclusive findings due to inconsistencies and indirectness in study populations. This review suggests that evaluating occupational exposures is essential for the early identification and management of individuals at elevated cardiovascular risk, and emphasizes that workplace interventions and health policies should prioritize reducing specific risk factors-such as job stress, long working hours, and hazardous exposures-to prevent CVD at both individual and population levels.
{"title":"Occupational Risk Factors for Cardiovascular Disease: A Comprehensive Review.","authors":"Seung Yeon Jeon, Chan Young Lee, Yun-Hee Lee, Hyojeong Kim, Jiwon Kim, Soo Kyung Cho, Han Soo Noh, Mo-Yeol Kang","doi":"10.1007/s11886-025-02301-z","DOIUrl":"10.1007/s11886-025-02301-z","url":null,"abstract":"<p><strong>Purpose of review: </strong>Cardiovascular disease (CVD) remains a leading cause of morbidity and mortality worldwide, with occupational factors emerging as significant yet modifiable risk factors. This comprehensive review evaluates the association between various occupational exposures-including job stress, long working hours, shift work, physical activity at work, and exposure to hazardous substances-and CVD risk. Using the GRADE framework, we assessed the strength of evidence for each risk factor.</p><p><strong>Recent findings: </strong>Job stress, long working hours, night shift work, and carbon monoxide exposure demonstrated moderate evidence linking them to increased CVD risk, while occupational noise, air pollutants, and extreme temperatures had limited evidence. Physical activity at work and exposure to toxic metals showed inconclusive findings due to inconsistencies and indirectness in study populations. This review suggests that evaluating occupational exposures is essential for the early identification and management of individuals at elevated cardiovascular risk, and emphasizes that workplace interventions and health policies should prioritize reducing specific risk factors-such as job stress, long working hours, and hazardous exposures-to prevent CVD at both individual and population levels.</p>","PeriodicalId":10829,"journal":{"name":"Current Cardiology Reports","volume":"27 1","pages":"143"},"PeriodicalIF":3.3,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145336586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-14DOI: 10.1007/s11886-025-02285-w
Jonathan X Fang, Leo Kar Lok Lai, Gennaro Giustino, Jaffar M Khan, Pedro Engel Gonzalez, Brian P O'Neill, Tiberio M Frisoli, James C Lee, Ahmad Jabri, Dee Dee Wang, William W O'Neill, Pedro A Villablanca
Purpose of review: Lithotripsy, first applied to treating nephrolithiasis, has an evolving role in cardiovascular disease, including intravascular treatment of calcified coronary and peripheral artery disease. Its role is expanding to the management of valvular and structural heart disease. This narrative review provides an overview of the emerging role of lithotripsy in various valvular and structural heart interventions.
Recent findings: We have conducted a comprehensive literature review of all publications on lithotripsy in structural heart interventions found in PubMed and Google Scholar. We have also included a series of case examples of lithotripsy in structural heart interventions from a tertiary referral center in the United States (Henry Ford Health, Michigan). Lithotripsy has been used to facilitate large-bore access in both transfemoral and alternative access procedures, to treat valvular stenosis of mitral and aortic valves, manage paravalvular leak closure, aid transcatheter electrosurgery, and manage endovascular, congenital, and structural electrophysiology procedures. While a nationwide registry is available for large-bore access facilitation, the current data on valvular stenosis is limited to a single-center registry. Data on most other applications is restricted to case reports and case series and is subject to publication bias. Only two studies have been published on ex vivo and translational models. Lithotripsy is increasingly used off-label in structural heart interventions, with early clinical successes being reported. Translational research and bench-testing models are necessary to determine the optimal energy transfer conditions for valvular and annular lithotripsy. Multi-center studies and randomized controlled trials are needed to assess the efficacy of these novel procedures.
回顾目的:碎石术最初用于治疗肾结石,在心血管疾病中的作用不断发展,包括血管内治疗钙化冠状动脉和外周动脉疾病。它的作用正在扩展到瓣膜病和结构性心脏病的治疗。本文综述了碎石术在各种瓣膜和结构性心脏干预中的作用。最近发现:我们对PubMed和谷歌Scholar上发现的所有关于结构性心脏干预中碎石术的出版物进行了全面的文献回顾。我们还纳入了一系列来自美国三级转诊中心(密歇根州Henry Ford Health)的结构性心脏介入碎石病例。在经股动脉和其他途径中,碎石已被用于促进大口径通路,治疗二尖瓣和主动脉瓣狭窄,处理瓣旁泄漏,辅助经导管电外科手术,以及处理血管内、先天性和结构性电生理手术。虽然有一个全国性的大口径通道便利登记,但目前关于瓣膜狭窄的数据仅限于单中心登记。大多数其他应用程序的数据仅限于病例报告和病例系列,并受到发表偏倚的影响。只有两项关于离体和转化模型的研究发表。碎石术越来越多地在非适应症下用于结构性心脏干预,有早期临床成功的报道。为了确定瓣膜和环形碎石的最佳能量传递条件,有必要进行平移研究和台架试验模型。需要多中心研究和随机对照试验来评估这些新方法的疗效。
{"title":"The Emerging Role of Lithotripsy in Structural Heart Interventions.","authors":"Jonathan X Fang, Leo Kar Lok Lai, Gennaro Giustino, Jaffar M Khan, Pedro Engel Gonzalez, Brian P O'Neill, Tiberio M Frisoli, James C Lee, Ahmad Jabri, Dee Dee Wang, William W O'Neill, Pedro A Villablanca","doi":"10.1007/s11886-025-02285-w","DOIUrl":"10.1007/s11886-025-02285-w","url":null,"abstract":"<p><strong>Purpose of review: </strong>Lithotripsy, first applied to treating nephrolithiasis, has an evolving role in cardiovascular disease, including intravascular treatment of calcified coronary and peripheral artery disease. Its role is expanding to the management of valvular and structural heart disease. This narrative review provides an overview of the emerging role of lithotripsy in various valvular and structural heart interventions.</p><p><strong>Recent findings: </strong>We have conducted a comprehensive literature review of all publications on lithotripsy in structural heart interventions found in PubMed and Google Scholar. We have also included a series of case examples of lithotripsy in structural heart interventions from a tertiary referral center in the United States (Henry Ford Health, Michigan). Lithotripsy has been used to facilitate large-bore access in both transfemoral and alternative access procedures, to treat valvular stenosis of mitral and aortic valves, manage paravalvular leak closure, aid transcatheter electrosurgery, and manage endovascular, congenital, and structural electrophysiology procedures. While a nationwide registry is available for large-bore access facilitation, the current data on valvular stenosis is limited to a single-center registry. Data on most other applications is restricted to case reports and case series and is subject to publication bias. Only two studies have been published on ex vivo and translational models. Lithotripsy is increasingly used off-label in structural heart interventions, with early clinical successes being reported. Translational research and bench-testing models are necessary to determine the optimal energy transfer conditions for valvular and annular lithotripsy. Multi-center studies and randomized controlled trials are needed to assess the efficacy of these novel procedures.</p>","PeriodicalId":10829,"journal":{"name":"Current Cardiology Reports","volume":"27 1","pages":"142"},"PeriodicalIF":3.3,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12521296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145285861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-10DOI: 10.1007/s11886-025-02305-9
Zaid Shahrori, Michel Chedid El Helou, Sherin Sallam, Gianluca Iacobellis, Ian J Neeland
Purpose of review: This review explores the unique anatomy and pathophysiology of pericardial fat (including both epicardial adipose tissue [EAT] and paracardial fat), its clinical significance, and its potential role as a therapeutic target. It addresses key questions regarding the contribution of EAT to cardiometabolic conditions such as coronary artery disease, heart failure, atrial fibrillation, and ventricular arrhythmias, and explores interventions that reduce EAT to possibly improve cardiovascular outcomes.
Recent findings: Recent studies have established EAT as a metabolically active, pro-inflammatory fat depot directly affecting the myocardium and coronary arteries. Imaging and metabolomic studies have advanced the assessment of EAT burden. Clinical evidence supports lifestyle modification, pharmacologic therapies including GLP-1 RA and SGLT2i, and bariatric surgery to effectively reduce EAT volume. Emerging data link EAT reduction with improved cardiac function and arrhythmia risk, although causality remains unclear. EAT is a modifiable cardiometabolic risk factor associated with adverse outcomes in coronary artery disease, heart failure, atrial fibrillation, and ventricular arrhythmias. Targeting EAT through cardiometabolic risk reduction strategies may improve prognosis. Future research should focus on determining whether reducing EAT directly improves clinical outcomes.
{"title":"The Role of Pericardial Fat in Cardiometabolic Disease: Emerging Evidence and Therapeutic Potential.","authors":"Zaid Shahrori, Michel Chedid El Helou, Sherin Sallam, Gianluca Iacobellis, Ian J Neeland","doi":"10.1007/s11886-025-02305-9","DOIUrl":"10.1007/s11886-025-02305-9","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review explores the unique anatomy and pathophysiology of pericardial fat (including both epicardial adipose tissue [EAT] and paracardial fat), its clinical significance, and its potential role as a therapeutic target. It addresses key questions regarding the contribution of EAT to cardiometabolic conditions such as coronary artery disease, heart failure, atrial fibrillation, and ventricular arrhythmias, and explores interventions that reduce EAT to possibly improve cardiovascular outcomes.</p><p><strong>Recent findings: </strong>Recent studies have established EAT as a metabolically active, pro-inflammatory fat depot directly affecting the myocardium and coronary arteries. Imaging and metabolomic studies have advanced the assessment of EAT burden. Clinical evidence supports lifestyle modification, pharmacologic therapies including GLP-1 RA and SGLT2i, and bariatric surgery to effectively reduce EAT volume. Emerging data link EAT reduction with improved cardiac function and arrhythmia risk, although causality remains unclear. EAT is a modifiable cardiometabolic risk factor associated with adverse outcomes in coronary artery disease, heart failure, atrial fibrillation, and ventricular arrhythmias. Targeting EAT through cardiometabolic risk reduction strategies may improve prognosis. Future research should focus on determining whether reducing EAT directly improves clinical outcomes.</p>","PeriodicalId":10829,"journal":{"name":"Current Cardiology Reports","volume":"27 1","pages":"141"},"PeriodicalIF":3.3,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145273822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-09DOI: 10.1007/s11886-025-02306-8
Deirdre E O'Neill, Daniel E Forman
Purpose of review: Cardiomyopathy is a disorder of the myocardium, in which structural and functional abnormalities of the heart muscle result in mechanical and/or electrical cardiac dysfunction. Aging increases susceptibility to molecular damage and related risks of cardiomyopathy, often in combination with other chronic diseases and geriatric syndromes (e.g., frailty, sarcopenia). With the rapidly growing population of older adults, awareness of the most prevalent cardiomyopathies in this population provides important insight to optimize prevention and treatment.
Recent findings: Hypertrophic, restrictive and dilated cardiomyopathies are highly prevalent in older adults. Furthermore, coronary artery disease, hypertension and valve disease increase with aging, and often lead to myocardial abnormalities that have many similar features to cardiomyopathy that are important to clarify. This review provides important age-related perspectives regarding pathophysiology, diagnosis, management and prevention. Aging is associated with inflammation and oxidative stress that can lead to molecular damage and vulnerability to many chronic diseases, including various cardiomyopathies. However, development is not inevitable. Prevention via lifestyle modification is paramount, with novel gerotherapeutic options targeting biologic hallmarks of aging under investigation. This increases the potential to improve the lifespan and healthspan of older adults.
{"title":"Cardiomyopathy in Older Adults.","authors":"Deirdre E O'Neill, Daniel E Forman","doi":"10.1007/s11886-025-02306-8","DOIUrl":"10.1007/s11886-025-02306-8","url":null,"abstract":"<p><strong>Purpose of review: </strong>Cardiomyopathy is a disorder of the myocardium, in which structural and functional abnormalities of the heart muscle result in mechanical and/or electrical cardiac dysfunction. Aging increases susceptibility to molecular damage and related risks of cardiomyopathy, often in combination with other chronic diseases and geriatric syndromes (e.g., frailty, sarcopenia). With the rapidly growing population of older adults, awareness of the most prevalent cardiomyopathies in this population provides important insight to optimize prevention and treatment.</p><p><strong>Recent findings: </strong>Hypertrophic, restrictive and dilated cardiomyopathies are highly prevalent in older adults. Furthermore, coronary artery disease, hypertension and valve disease increase with aging, and often lead to myocardial abnormalities that have many similar features to cardiomyopathy that are important to clarify. This review provides important age-related perspectives regarding pathophysiology, diagnosis, management and prevention. Aging is associated with inflammation and oxidative stress that can lead to molecular damage and vulnerability to many chronic diseases, including various cardiomyopathies. However, development is not inevitable. Prevention via lifestyle modification is paramount, with novel gerotherapeutic options targeting biologic hallmarks of aging under investigation. This increases the potential to improve the lifespan and healthspan of older adults.</p>","PeriodicalId":10829,"journal":{"name":"Current Cardiology Reports","volume":"27 1","pages":"139"},"PeriodicalIF":3.3,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145250114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-09DOI: 10.1007/s11886-025-02292-x
Tomoyo Hamana, Alyssa Grogan, Rika Kawakami, Renu Virmani, Aloke V Finn
Purpose of review: Calcified nodules (CNs) account for ~ 5% of acute coronary syndrome cases. Although the progression of calcification generally leads to plaque stability, CNs ─ an advanced form of calcified plaques ─ can trigger coronary thrombosis and sudden cardiac death.
Recent findings: CNs are histologically defined as lesions with fibrous cap disruption and luminal thrombus, associated with dense, eruptive calcific nodules protruding into the lumen. They are linked to poor prognosis both post percutaneous coronary intervention and in non-culprit lesions. Interventionalists are exploring various treatment strategies using debulking devices and drug-coated balloons; however, no effective treatment has been established. While histological classifications can be inferred from optical coherence tomography findings, accurately predicting CNs from intravascular imaging remains challenging. This review discusses the pathological features, etiology, clinical outcomes, and current treatment strategies for CNs, offering valuable insights into the correlation and discrepancies between histological findings and optical coherence tomography.
{"title":"Calcified Nodules: Pathology, Mechanisms, and Clinical Challenges.","authors":"Tomoyo Hamana, Alyssa Grogan, Rika Kawakami, Renu Virmani, Aloke V Finn","doi":"10.1007/s11886-025-02292-x","DOIUrl":"10.1007/s11886-025-02292-x","url":null,"abstract":"<p><strong>Purpose of review: </strong>Calcified nodules (CNs) account for ~ 5% of acute coronary syndrome cases. Although the progression of calcification generally leads to plaque stability, CNs ─ an advanced form of calcified plaques ─ can trigger coronary thrombosis and sudden cardiac death.</p><p><strong>Recent findings: </strong>CNs are histologically defined as lesions with fibrous cap disruption and luminal thrombus, associated with dense, eruptive calcific nodules protruding into the lumen. They are linked to poor prognosis both post percutaneous coronary intervention and in non-culprit lesions. Interventionalists are exploring various treatment strategies using debulking devices and drug-coated balloons; however, no effective treatment has been established. While histological classifications can be inferred from optical coherence tomography findings, accurately predicting CNs from intravascular imaging remains challenging. This review discusses the pathological features, etiology, clinical outcomes, and current treatment strategies for CNs, offering valuable insights into the correlation and discrepancies between histological findings and optical coherence tomography.</p>","PeriodicalId":10829,"journal":{"name":"Current Cardiology Reports","volume":"27 1","pages":"140"},"PeriodicalIF":3.3,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145250184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-09DOI: 10.1007/s11886-025-02298-5
Astrid B M Heymans, Lorenzo Bianchi, Paul G A Volders, Saskia N van der Crabben, Job A J Verdonschot
Purpose of review: Although SCN5A variants are an established cause of arrhythmia and conduction disease, their association with dilated cardiomyopathy (DCM) is less studied. This review summarizes recent insights into SCN5A-related cardiomyopathy, focusing on genotype-phenotype correlations, overlap with arrhythmia, and implications for management.
Recent findings: Both gain- and loss-of-function SCN5A variants are associated with cardiomyopathy, found in 0.5-0.9% of DCM cases. Presentation ranges from isolated DCM to overlap phenotypes, in both pediatric and adult patients. High variability and intrafamilial heterogeneity suggest pleiotropic effects and variable penetrance. High prevalence of arrhythmias and conduction disease suggests the DCM phenotype may be mediated by electrical disturbances. However, functional studies and cases without prior arrhythmia suggest SCN5A variants may directly contribute to structural myocardial changes. SCN5A-related cardiomyopathy is a rare disorder at the intersection of structural and electrical heart disease. Genotype-informed strategies, including arrhythmia management, and early cascade genetic screening are clinically relevant. Further research should address SCN5A-specific risk management in DCM patients.
{"title":"SCN5A Cardiomyopathy: from Ion Channel Dysfunction To Clinical Disease.","authors":"Astrid B M Heymans, Lorenzo Bianchi, Paul G A Volders, Saskia N van der Crabben, Job A J Verdonschot","doi":"10.1007/s11886-025-02298-5","DOIUrl":"10.1007/s11886-025-02298-5","url":null,"abstract":"<p><strong>Purpose of review: </strong>Although SCN5A variants are an established cause of arrhythmia and conduction disease, their association with dilated cardiomyopathy (DCM) is less studied. This review summarizes recent insights into SCN5A-related cardiomyopathy, focusing on genotype-phenotype correlations, overlap with arrhythmia, and implications for management.</p><p><strong>Recent findings: </strong>Both gain- and loss-of-function SCN5A variants are associated with cardiomyopathy, found in 0.5-0.9% of DCM cases. Presentation ranges from isolated DCM to overlap phenotypes, in both pediatric and adult patients. High variability and intrafamilial heterogeneity suggest pleiotropic effects and variable penetrance. High prevalence of arrhythmias and conduction disease suggests the DCM phenotype may be mediated by electrical disturbances. However, functional studies and cases without prior arrhythmia suggest SCN5A variants may directly contribute to structural myocardial changes. SCN5A-related cardiomyopathy is a rare disorder at the intersection of structural and electrical heart disease. Genotype-informed strategies, including arrhythmia management, and early cascade genetic screening are clinically relevant. Further research should address SCN5A-specific risk management in DCM patients.</p>","PeriodicalId":10829,"journal":{"name":"Current Cardiology Reports","volume":"27 1","pages":"138"},"PeriodicalIF":3.3,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511166/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145250162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-09DOI: 10.1007/s11886-025-02297-6
Xander Jacquemyn, Jef Van den Eynde, Sruti Rao, Shelby Kutty
Purpose of review: Explore the clinical progression, diagnostic challenges, and evolving treatments of systemic right ventricular (SRV) failure, highlighting key gaps and advances.
Recent findings: Recent evidence highlights the distinct pathophysiology of SRV failure and limited efficacy of conventional heart failure (HF) treatments. Emerging drugs like SGLT2 inhibitors are being studied for modulating ventricular remodeling and fibrosis. Echocardiography, enhanced by speckle-tracking and 3D imaging, is first-line, while cardiac MRI remains the gold standard for volumetric, functional, and tissue characterization. SRV-specific machine learning models improve prognostication and personalized care. Advances in transcatheter tricuspid valve interventions offer less invasive options for high-risk patients. In end-stage SRV failure, ventricular assist devices effectively unload the ventricle, enhance transplant candidacy, may be combined with tricuspid procedures, and are increasingly used as long-term destination therapy. SRV failure is a unique condition requiring personalized, multidisciplinary management, with advances in risk stratification and treatments shaping future care.
{"title":"Evidence-based Management of Heart Failure in the Systemic Right Ventricle.","authors":"Xander Jacquemyn, Jef Van den Eynde, Sruti Rao, Shelby Kutty","doi":"10.1007/s11886-025-02297-6","DOIUrl":"10.1007/s11886-025-02297-6","url":null,"abstract":"<p><strong>Purpose of review: </strong>Explore the clinical progression, diagnostic challenges, and evolving treatments of systemic right ventricular (SRV) failure, highlighting key gaps and advances.</p><p><strong>Recent findings: </strong>Recent evidence highlights the distinct pathophysiology of SRV failure and limited efficacy of conventional heart failure (HF) treatments. Emerging drugs like SGLT2 inhibitors are being studied for modulating ventricular remodeling and fibrosis. Echocardiography, enhanced by speckle-tracking and 3D imaging, is first-line, while cardiac MRI remains the gold standard for volumetric, functional, and tissue characterization. SRV-specific machine learning models improve prognostication and personalized care. Advances in transcatheter tricuspid valve interventions offer less invasive options for high-risk patients. In end-stage SRV failure, ventricular assist devices effectively unload the ventricle, enhance transplant candidacy, may be combined with tricuspid procedures, and are increasingly used as long-term destination therapy. SRV failure is a unique condition requiring personalized, multidisciplinary management, with advances in risk stratification and treatments shaping future care.</p>","PeriodicalId":10829,"journal":{"name":"Current Cardiology Reports","volume":"27 1","pages":"137"},"PeriodicalIF":3.3,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145250194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-07DOI: 10.1007/s11886-025-02300-0
Shakira F Suglia
Purpose of review: To review the current state of the science relating adverse childhood experiences (ACEs) and cardiovascular health and disease.
Recent findings: Recent work has demonstrated associations between ACEs and development of cardiovascular disease (CVD) and has additionally shed a light on potential mechanistic pathways noting associations between ACEs and genomics, vascular health and cardiac structure. Existing work has advanced our understanding of the mechanisms by which ACEs are associated with CVD, yet much work remains particularly as we strive to understand how to ameliorate the impact of ACEs on CVD. Future research on interventions that promote cardiovascular health and integrate ACEs and emotional wellbeing are needed. A multilevel framework that understands how sociopolitical, neighborhood and family level factors contribute to childhood experiences is necessary to address the root causes of ACEs.
{"title":"Childhood Adversity and Cardiovascular Disease; Current Knowledge and Future Directions.","authors":"Shakira F Suglia","doi":"10.1007/s11886-025-02300-0","DOIUrl":"10.1007/s11886-025-02300-0","url":null,"abstract":"<p><strong>Purpose of review: </strong>To review the current state of the science relating adverse childhood experiences (ACEs) and cardiovascular health and disease.</p><p><strong>Recent findings: </strong>Recent work has demonstrated associations between ACEs and development of cardiovascular disease (CVD) and has additionally shed a light on potential mechanistic pathways noting associations between ACEs and genomics, vascular health and cardiac structure. Existing work has advanced our understanding of the mechanisms by which ACEs are associated with CVD, yet much work remains particularly as we strive to understand how to ameliorate the impact of ACEs on CVD. Future research on interventions that promote cardiovascular health and integrate ACEs and emotional wellbeing are needed. A multilevel framework that understands how sociopolitical, neighborhood and family level factors contribute to childhood experiences is necessary to address the root causes of ACEs.</p>","PeriodicalId":10829,"journal":{"name":"Current Cardiology Reports","volume":"27 1","pages":"136"},"PeriodicalIF":3.3,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}