Cardiology discovery最新文献

{"title":"The Heart's Hidden Influencer: Epicardial Adipose Tissue in the Pathogenesis of Heart Failure.","authors":"Aobo Li, Avilash Mondal, Jianli Zhao, John Zhang, Xinliang Ma, Yajing Wang","doi":"10.1097/CD9.0000000000000184","DOIUrl":"10.1097/CD9.0000000000000184","url":null,"abstract":"<p><p>Heart failure (HF) is a complex, multifactorial clinical syndrome with diverse etiologies and phenotypic manifestations, affecting millions of people globally. HF is broadly classified into 3 subtypes: HF with reduced ejection fraction, HF with mildly reduced ejection fraction, and HF with preserved ejection fraction. Each subtype exhibits distinct pathophysiological mechanisms, clinical trajectories, and therapeutic responses, posing significant challenges in terms of diagnosis and management. Epicardial adipose tissue (EAT), a metabolically active visceral fat depot situated in close proximity to the myocardium, plays a dual role in physiological and pathological states, offering potential utility as a biomarker and therapeutic target. Despite its unique anatomical and functional characteristics, the EAT has been largely overlooked in both clinical practice and basic research. This review aims to elucidate the mechanisms by which dysfunctional EAT contributes to HF progression, particularly through the promotion of proinflammatory and profibrotic phenotypes. Specific attention is given to the effects of EAT-derived extracellular vesicles, altered adipokine secretion, and immune modulation on myocardial metabolism, endothelial function, and immune cell activity. These pathways contribute to cardiomyocyte injury, myocardial fibrosis, and adverse remodeling, which are hallmarks of HF pathogenesis. Furthermore, the review highlights the distinct and potentially divergent roles of EAT across HF subtypes, including HF with reduced ejection fraction, HF with preserved ejection fraction, and the intermediate phenotype HF with mildly reduced ejection fraction, with special attention to the emerging evidence of EAT involvement in the transitional pathophysiological characteristics of HF with mildly reduced ejection fraction. Finally, this review synthesizes current insights into the pathogenic role of EAT in HF and evaluates its potential as a biomarker for disease severity and progression, as well as a target for novel therapeutic interventions. Advances in imaging modalities and molecular profiling techniques may enhance the precision of EAT characterization and facilitate the development of personalized strategies for the diagnosis, risk stratification, and management of HF in the future.</p>","PeriodicalId":72524,"journal":{"name":"Cardiology discovery","volume":"6 3","pages":"201-209"},"PeriodicalIF":0.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13592825/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149018836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Commentary: Unveiling a Metabolic-Lymphatic Axis in the Pathogenesis of Heart Failure With Preserved Ejection Fraction.","authors":"John Zhang, Dhrubo Ahmad, Taslima Akter Shila, Kayleigh Wyatt, Bo Wang, Yuhui Yang, Huilan Tan, Yanwen Liu, Jianli Zhao, Yajing Wang","doi":"10.1097/CD9.0000000000000197","DOIUrl":"10.1097/CD9.0000000000000197","url":null,"abstract":"","PeriodicalId":72524,"journal":{"name":"Cardiology discovery","volume":"6 3","pages":"171-174"},"PeriodicalIF":0.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13592827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149018902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Worldwide Epidemiology of Pulmonary Hypertension Associated With Left Heart Disease.","authors":"Suela Vani, Filippo Novarese, Matteo Toma, Italo Porto, Pietro Ameri","doi":"10.1097/CD9.0000000000000191","DOIUrl":"10.1097/CD9.0000000000000191","url":null,"abstract":"<p><p>Globally, around 1 in 2 patients with left heart disease (LHD) has pulmonary hypertension (PH). The prevalence of PH associated with heart failure, mitral regurgitation, aortic valve disease, hypertrophic cardiomyopathy, and cardiac amyloidosis has mainly been investigated in high-income countries, especially the United States and Europe, by transthoracic echocardiography without right heart catheterization confirmation. It is estimated that around 80% of patients with hypertrophic cardiomyopathy or cardiac amyloidosis, around 65% of patients with heart failure or mitral regurgitation, and around 40% of patients with aortic valve disease have PH. In contrast, data about PH associated with mitral stenosis and rheumatic heart disease are primarily from low-income countries. The prevalence is around 80% in mitral stenosis-as determined by right heart catheterization in candidates for surgery or balloon valvuloplasty-and around 45% in rheumatic heart disease based on transthoracic echocardiography screening. PH associated with LHD (PH-LHD) clinical trials have focused on PH secondary to heart failure and have most often been performed in the United States and Europe (sites from these countries in 53.3% and 43.3% of the trials, respectively). The heterogeneous epidemiology of PH-LHD may reflect actual differences in the frequency of the underlying types of LHD, but it may also be the consequence of detection and reporting biases. Regional health authority choices, diagnostic capacity, and socio-economic factors likely influence the selection of the sites of PH-LHD trials. Efforts are needed to better characterize the worldwide burden of PH-LHD and to conduct truly global clinical trials.</p>","PeriodicalId":72524,"journal":{"name":"Cardiology discovery","volume":"6 2","pages":"117-132"},"PeriodicalIF":0.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13293000/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148335108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endocytic Adaptor Proteins in Vascular Diseases: Critical Role of Intracellular Trafficking in Regulating Pathobiology of Vascular Disorders.","authors":"Jianing Gao, Bo Zhu, Beibei Wang, Bandana Singh, Shahram Eisa-Beygi, Hao Wu, Kui Cui, Kulandai Samy Arulsamy, Wendong Huang, Wenyi Wei, Prasad Vg Katakam, Hong Chen","doi":"10.1097/CD9.0000000000000188","DOIUrl":"10.1097/CD9.0000000000000188","url":null,"abstract":"<p><p>Endocytic adaptor proteins are essential regulators of intracellular trafficking, coupling receptor internalization with downstream signaling. Recent discoveries have deepened our understanding of how endocytic adaptor proteins contribute to both physiological and pathological processes in the vascular system. This review summarizes the emerging roles of key adaptor proteins-such as epsins, disabled-2, and adaptor protein 2-across multiple vascular cell types, including endothelial cells, vascular smooth muscle cells, and macrophages. These adaptors have diverse but essential functions, ranging from regulating angiogenic signaling and maintaining endothelial barrier integrity to modulating inflammatory responses, vascular smooth muscle cells phenotypic switching, lipid uptake, and structural remodeling of blood vessels. We also highlight advances in therapeutic strategies, such as nanomedicine, viral expression vectors, DNA nanostructures, and small molecule inhibitors that target endocytic adaptors and their function. Understanding the diverse and cell-specific roles of endocytic adaptor proteins is important for gaining insights into vascular disease mechanisms and uncovering novel targets for therapeutic interventions.</p>","PeriodicalId":72524,"journal":{"name":"Cardiology discovery","volume":"6 1","pages":"26-41"},"PeriodicalIF":0.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13003415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147500913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Heart-Brain Axis: Key Concepts in Neurocardiology.","authors":"Fang Qin Goh, Benjamin Y Q Tan, Leonard L L Yeo, Ching-Hui Sia","doi":"10.1097/CD9.0000000000000156","DOIUrl":"10.1097/CD9.0000000000000156","url":null,"abstract":"<p><p>The heart-brain axis involves complex interactions between the cardiovascular and nervous systems via a network of cortical and subcortical structures working with the autonomic nervous system and intracardiac nervous system. Heart-brain interactions may be divided into 2 broad categories: cardiac effects of neurological disease and neurological effects of cardiac disease. The pathogenesis of neurogenic cardiac effects is thought to involve a neurogenic cascade where sudden shifts in autonomic balance lead to an exaggerated catecholamine release. This can occur in acute neurological conditions such as ischemic stroke, intracranial hemorrhage, and epilepsy. Cardiovascular complications include the stroke-heart syndrome, neurogenic pulmonary edema and cardiomyopathy, Takotsubo syndrome, arrhythmias, and even sudden cardiac death. Certain areas of the brain, such as the insular cortex, play key roles in cardiac autonomic regulation, and disorders affecting these areas have greater effects on the heart. On the other hand, cardiac conditions can also adversely impact the neurological system. Atrial fibrillation and left ventricular thrombus can cause cardioembolic strokes, whereas heart failure and severe aortic stenosis have been linked to the development of cognitive impairment. This review aims to provide a broad overview of key topics in neurocardiology as well as delve into the evidence and pathophysiology behind these conditions.</p>","PeriodicalId":72524,"journal":{"name":"Cardiology discovery","volume":"5 2","pages":"162-177"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12173172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144327897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Challenges and Opportunities for Atrial Fibrillation Management.","authors":"Minsi Cai, Jordi Heijman","doi":"10.1097/CD9.0000000000000155","DOIUrl":"10.1097/CD9.0000000000000155","url":null,"abstract":"<p><p>Atrial fibrillation (AF) is the most common sustained arrhythmia worldwide and is associated with poor clinical outcomes and a huge economic burden on healthcare systems. Optimized anticoagulation, better symptom control via rhythm or rate control, and comprehensive comorbidity/risk factor management are 3 essential pillars of current AF management, where much progress has been made during the past decades. However, numerous challenges in AF management remain at the disease, patient, and population levels, including an incomplete understanding of basic mechanisms that can be clinically targeted; heterogenous progressive natural history; poor correlation between rhythm and symptoms/outcomes; as well as suboptimal detection methods and treatment options. Recent advances in disease perception in combination with modern monitoring devices, state-of-the art computational models, and novel antiarrhythmic drugs and ablation strategies can contribute to addressing these issues, ultimately leading to a paradigm shift in AF diagnosis, classification, and treatment. This narrative review summarizes these key challenges and future opportunities in the field of AF management.</p>","PeriodicalId":72524,"journal":{"name":"Cardiology discovery","volume":"5 2","pages":"149-161"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12173171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144327896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Association Between Clonal Hematopoiesis of Indeterminate Potential and Cardiovascular Outcomes in Patients With Acute Coronary Syndrome Who Have Quit Smoking: Study Design of a Prospective Cohort Study.","authors":"Jing Li, Zizhao Qi, Ying Xu, Yinan Cao, Yi Li, Yaling Han","doi":"10.1097/CD9.0000000000000151","DOIUrl":"10.1097/CD9.0000000000000151","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1097/CD9.0000000000000139.].</p>","PeriodicalId":72524,"journal":{"name":"Cardiology discovery","volume":"5 1","pages":"94"},"PeriodicalIF":0.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11925343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143694603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiac Functional Assessment by Magnetic Resonance Imaging.","authors":"Mengdi Jiang, Minjie Lu, Shihua Zhao","doi":"10.1097/CD9.0000000000000141","DOIUrl":"10.1097/CD9.0000000000000141","url":null,"abstract":"<p><p>The assessment of cardiac function using echocardiography has gained a strong foothold in clinical practice. Cardiac magnetic resonance (CMR) imaging harbors distinct advantages over echocardiography, as it is not affected by limitations of acoustic windows and operator dependence. CMR is also designed to non-invasively assess cardiac morphology, ventricular geometry, myocardial wall motion, and intra-cardiac flow quantification without the use of ionizing radiation. These inherent features make CMR appropriate for diagnosing cardiovascular diseases, monitoring patients after treatment, and providing longitudinal follow-up. In this paper, the state-of-the-art work that has demonstrated the aspects of cardiac function by CMR is reviewed, and acquisition techniques and clinical applications are covered.</p>","PeriodicalId":72524,"journal":{"name":"Cardiology discovery","volume":"4 4","pages":"284-299"},"PeriodicalIF":0.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637579/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142831124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Novel Long QT Syndrome Type 2-associated F129I Mutation in the KCNH2 Gene Significantly Affects I Kr Through the hERG1 Homomeric and Heteromeric Potassium Channels","authors":"Li Feng, Kejuan Ma, Xin Li, Nian Liu, Deyong Long, Changsheng Ma","doi":"10.1097/cd9.0000000000000125","DOIUrl":"https://doi.org/10.1097/cd9.0000000000000125","url":null,"abstract":"\u0000 \u0000 The long QT syndrome type 2 is caused by the loss-of-function mutations in the KCNH2 gene, which encodes hERG1, the voltage-gated potassium channel. The hERG1 channels conduct rapid delayed rectifier K+ currents (I\u0000 Kr) in the human cardiac tissue. KCNH2 encodes 2 main isoforms—hERG1a and hERG1b, which assemble to form the homomeric or heteromeric hERG1 channels. However, the functional characteristics of the heteromeric hERG1 channels in long QT syndrome type 2 are not clear. In this study, a novel mutation in the N-terminus of hERG1a (F129I) was identified in a proband of long QT syndrome type 2. The purpose of this study was to identify the electrophysiological change of homomeric and heteromeric hERG1 channels with the F129I-hERG1a.\u0000 \u0000 \u0000 \u0000 Candidate genes were screened by direct sequencing. F129I-hERG1a was cloned in the pcDNA3.1 vector by site-directed mutagenesis. Then, the wild-type (WT) hERG1a and/or F129I-hERG1a were transiently expressed in the HEK293 cells with or without hERG1b co-expression. The expression levels of the transgenes, cellular distribution of hERG1a and hERG1b, and the electrophysiological features of the homomeric and the heteromeric hERG1 channels with the WT-hERG1a or F129I-hERG1a were analyzed using whole-cell patch-clamp electrophysiology, western blotting, and immunofluorescence techniques.\u0000 \u0000 \u0000 \u0000 The proband was clinically diagnosed with long QT syndrome type 2 and carried a heterozygous mutation c.385T>A (F129I) in the KCNH2 gene. Electrophysiology study proved that the F129I substitution in hERG1a significantly decreased I\u0000 Kr in both the homomeric and heteromeric hERG1channels by 86% and 70%, respectively (WT-hERG1a (54.88 ± 18.74) pA/pF vs. F129I-hERG1a (7.34 ± 1.90) pA/pF, P < 0.001; WT-hERG1a/hERG1b (89.92 ± 24.51) pA/pF vs. F129I-hERG1a/hERG1b (26.54 ± 9.83) pA/pF, P < 0.001). The voltage dependence of IKr activation (V½ and k) was not affected by the mutation in both the homomeric and heteromeric hERG1 channels. The peak current densities and the kinetic characteristics of IKr were comparable for both WT/F129I-hERG1a and WT-hERG1a. The channel inactivation and deactivation analysis showed that F129I substitution did not affect deactivation of the homomeric hERG1a channel, but significantly accelerated the deactivation and recovery from inactivation of the heteromeric hERG1a/hERG1b channel based on the time constants of fast and slow recovery from deactivation F129I-hERG1a/hERG1b vs. WT-hERG1a/hERG1b (P < 0.05). Western blotting and immunofluorescence labeling experiments showed that maturation and intracellular trafficking of the F129I-hERG1a protein was impaired and potentially increased the ratio of hERG1b to hERG1a in the F129I-hERG1a/hERG1b tetramer channel, thereby resulting in electrophysiological changes characteristic of the long QT syndrome type 2 pathology.\u0000 \u0000 \u0000 \u0000 \u0000 I\u0000 Kr was significantly reduced in the homomeric and heteromeric hERG1 channels with F129I-hERG1a. The F129I mutation significa","PeriodicalId":72524,"journal":{"name":"Cardiology discovery","volume":"7 12","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141100511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fulminant Myocarditis Complicated by Stiff-person Syndrome: A Case Report","authors":"Peng Chen, Nana Tang, Huilan Zhang, Dao Wen Wang","doi":"10.1097/cd9.0000000000000117","DOIUrl":"https://doi.org/10.1097/cd9.0000000000000117","url":null,"abstract":"This case report described a 61-year-old woman who presented with dizziness, headache, muscle ache, diplopia, and vomiting who lost consciousness. Upon hospital admission, the levels of high-sensitivity cardiac troponin I and partial pressure of carbon dioxide were increased markedly. Loss of consciousness occurred twice after removal of invasive ventilator support. Coronary angiography demonstrated no stenosis in coronary arteries. Ultrasonography revealed inactivity of respiratory muscles. Oculomotor disturbance and autonomic-nerve dysfunctions were observed. Serum antibody against glutamic acid decarboxylase was positive. The rare phenotypes of persistent stiffness of muscles in the neck, face, bilateral upper and lower limbs were observed. The patient was diagnosed with fulminant myocarditis complicated by Stiff-person syndrome. Immunomodulatory treatment (glucocorticoids and immunoglobulins) elicited satisfactory therapeutic effects. In this case report, it was found that fulminant myocarditis and Stiff-person syndrome shared a common pathogenesis: “cytokine storm”. Such patients may benefit from early treatment with immunomodulatory agents.","PeriodicalId":72524,"journal":{"name":"Cardiology discovery","volume":"36 11","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140373985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}