Non-compaction cardiomyopathy is a rare form of cardiomyopathy;its most common clinical manifestations are heart failure (HF), ventricular arrhythmia, thromboembolism, and sudden cardiac death. We report a rare case o...Non-compaction cardiomyopathy is a rare form of cardiomyopathy;its most common clinical manifestations are heart failure (HF), ventricular arrhythmia, thromboembolism, and sudden cardiac death. We report a rare case of a 63-year-old man with chest tightness, worsening lower leg edema, dyspnea, and decreased exercise tolerance. He had a medical history of gastric cancer treated with subtotal gastrectomy and post-operative chemotherapy with paclitaxel and fluorouracil three years ago. At that time, he was diagnosed with non-compaction cardiomyopathy, and the thickened and reticulated trabecular muscle was exclusively confined to left ventricular apex. Five months ago, he was admitted to our hospital with heart failure and treated for dilated cardiomyopathy, echocardiography revealed severe trabecular noncompact myocardium in both ventricles, which was confirmed by cardiac magnetic resonance imaging (CMR). It is generally accepted that non-compacted myocardium forms in the early embryonic stage, which raises a question in our case whether acquired factors, such as antineoplastic drugs, potentially accelerate the pathological progression of non-compaction cardiomyopathy. Considering there are disparities between current screening tools such as echocardiography and CMR regarding diagnostic criteria, multi-detector CT may be an alternative examination method that could provide a new perspective for diagnosis.展开更多
INTRODUCTION Isolated ventricular non-compaction is a rare congenital cardiomyopathy occurs due to arrest of normal myocardial development during embryogenesis. It is mainly diagnosed by echocar- diography through the...INTRODUCTION Isolated ventricular non-compaction is a rare congenital cardiomyopathy occurs due to arrest of normal myocardial development during embryogenesis. It is mainly diagnosed by echocar- diography through the appearance of characteristic prominent myocardial trabeculation and deep inter-trabecular spaces. Heart failore,展开更多
Left atrialmyxoma is a common primary cardiac tumor that is accompanied by organic heart diseases.But left atrial myxoma coexistent with left ventricular non-compaction(LVNC)is extremely rare.A young male patient with...Left atrialmyxoma is a common primary cardiac tumor that is accompanied by organic heart diseases.But left atrial myxoma coexistent with left ventricular non-compaction(LVNC)is extremely rare.A young male patient with left atrial myxoma and LVNC was reported in this study.A 25-year-old manpresented to the emergency department with sudden shortness of breath and syncope,accompanied by fever and cough.He had a history ofacute ischemic strokeone year before hospitalization.Echocardiography revealed that the endocardium of the left ventricle was not smooth with raised muscle trabeculae and deep recesses.There was an oval-shaped strong echo mass with a pedicle in the left atrium attached to the atrial septum.Tumor resection was operated during extracorporeal circulation.Pathological results confirmed left atrium myxoma.In this case report,the patient had heart failure and an ischemic stroke likely of cardiogenic origin.He underwenttumor resection and started on therapeutic anticoagulation.Left atrial myxoma and LVNC are associated with poor outcomes.Early diagnosis and prompt treatment are crucial.展开更多
Importance:Pathogenic variants in theRBM20 gene are associated with aggressive dilated cardiomyopathy(DCM).Recently,RBM20 was found to be associated with left ventricular non-compaction cardiomyopathy(LVNC).Thus far,o...Importance:Pathogenic variants in theRBM20 gene are associated with aggressive dilated cardiomyopathy(DCM).Recently,RBM20 was found to be associated with left ventricular non-compaction cardiomyopathy(LVNC).Thus far,only five families with LVNC have been reported to carry variants inRBM20.It remains unknown whether the variants inRBM20 associated with DCM can also cause LVNC.Objective:To elucidate the causativeRBM20 variant in two unrelated patients with both LVNC and DCM,and to identify the clinical characteristics associated with variants inRBM20.Methods:Trio whole-exome sequencing(WES)was performed.Variants were filtered and classified in accordance with the guidelines of the American College of Medical Genetics and Genomics(ACMG).Results:We identified two distinctde novo variants inRBM20(one per patient)in these two patients with LVNC.Both variants have been reported in patients with DCM,without the LVNC phenotype.Patient 1 was an 11-year-old girl who had DCM,LVNC,and heart failure;the ratio of noncompacted-to-compacted myocardium was 2.7:1.Ade novo heterozygous variant c.1907G>A(p.Arg636His)in exon 9 was identified in this patient.Patient 2 was a 13-year-old boy who had clinical phenotypes identical to those of Patient 1;the ratio of noncompacted-to-compacted myocardium was 3.2:1 in this patient.WES revealed ade novo heterozygous variant c.1909A>G(p.Ser637Gly)in exon 9.Both variants were previously characterized as pathogenic,and our study classified them as pathogenic variants based on the ACMG guidelines.Interpretation:We found that two patients with LVNC had variants inRBM20.Our results extended the clinical spectrum of the twoRBM20 variants and illustrated that the same variant inRBM20 can cause DCM,with or without the LVNC phenotype.展开更多
Cardiomyopathies are among the most prevalent causes of premature death in the Western world.A significant amount of cardiomyopathies has a genetic etiology.Currently,mutations in more than 170 genes associated with d...Cardiomyopathies are among the most prevalent causes of premature death in the Western world.A significant amount of cardiomyopathies has a genetic etiology.Currently,mutations in more than 170 genes associated with different cardiomyopathies,channelopathies,or syndromes with cardiac involvement are described.展开更多
Hypertrophic cardiomyopathy(HCM)is a genetically determined myocardial disease characterized by an increased thickness of the left ventricle(LV)wall that cannot be solely attributed to abnormal loading conditions.HCM ...Hypertrophic cardiomyopathy(HCM)is a genetically determined myocardial disease characterized by an increased thickness of the left ventricle(LV)wall that cannot be solely attributed to abnormal loading conditions.HCM may present with an intraventricular or LV outflow tract obstruction,diastolic dysfunction,myocardial fibrosis and/or ventricular arrhythmias.Differentiating HCM from other diseases associated with LV hypertrophy,such as hypertension,aortic stenosis,or LV non-compaction(LVNC),can at times be challenging.LVNC is defined by excessive LV trabeculation and deep recesses between trabeculae,often accompanied by increased LV myocardial mass.Previous studies indicate that the LVNC phenotype may be observed in up to 5%of the general population;however,in most cases,it is a benign finding with no impact on clinical outcomes.Nevertheless,LVNC can occasionally lead to LV systolic dysfunction,manifesting as a phenotype of dilated or non-dilated left ventricular cardiomyopathy,with an increased risk of thrombus formation and arterial embolism.In extreme cases,where LVNC is associated with a very thickened LV wall,it can even mimic HCM.There is growing evidence of an overlap between HCM and LVNC,including similar genetic mutations and clinical presentations.This raises the question of whether HCM and LVNC represent different phenotypes of the same disease or are,in fact,two distinct entities.展开更多
Hereditary cardiomyopathies and arrhythmias are major contributors to cardiovascular morbidity and mortality.The advent of next-generation sequencing(NGS)has made genetic testing more accessible,which is crucial for p...Hereditary cardiomyopathies and arrhythmias are major contributors to cardiovascular morbidity and mortality.The advent of next-generation sequencing(NGS)has made genetic testing more accessible,which is crucial for precise diagnosis and targeted therapeutic strategies.The aim of this study is to explore the landscape of genetic variants,the relationship between specific variants and clinical phenotypes,and the impact on clinical decision-making in China.A total of 1536 probands(median age,37 years;1025 males[66.7%])with suspected hereditary cardiomyopathy or arrhythmia(covering 15 clinical phenotypes)are recruited from 146 hospitals across 30 provinces and cities in China.Positive results are confirmed in 390 of 1536 probands,leading to a diagnostic yield of 25.4%.Forty-two and three-tenths percent(n=169)of family members carry the same variants as positive probands.Hypertrophic cardiomyopathy(HCM)and dilated cardiomyopathy(DCM)are the predominant phenotypes,with MYBPC3 variants having the highest frequency in HCM and TTN variants in DCM.In 76.9%of the positive probands,the identified variants are helpful in clinical management,family screening,and fertility.This large-scale study provides significant insights into the genetic landscape of hereditary cardiomyopathies and arrhythmias in China.展开更多
Human cardiac organoids have revolutionized the study of cardiac development,disease modeling, drug discovery, and regenerative therapies. This review systematically discusses strategies and progress in the constructi...Human cardiac organoids have revolutionized the study of cardiac development,disease modeling, drug discovery, and regenerative therapies. This review systematically discusses strategies and progress in the construction of cardiac organoids, categorizing them into three main types:cardiac spheroids, self-organizing/assembloid organoids, and organoid-on-a-chip systems. This review uniquely integrates the advances in vascularization, organ-on-chip design, and environmental cardiotoxicity modeling within cardiac organoid platforms, offering a critical synthesis that is absent in the literature. In the context of escalating environmental threats to cardiovascular health, there is an urgent need for physiologically relevant models to accurately identify cardiac toxicants and elucidate their underlying mechanisms of action. This review highlights advances in cardiac organoid applications for disease modeling-including congenital heart defects and acquired cardiovascular diseases-drug development, toxicity screening, and the study of environmentally induced cardiovascular pathogenesis. In addition, it critically examines ongoing challenges and underscores opportunities brought by bioengineering approaches. Finally, we propose future directions for developing standardized cardiac organoid platforms with clinical predictability, aiming to expand the utility of this technology across broader research applications.展开更多
A 39-year-old male with no known comorbidities presented with sudden onset right-sided weakness.On examination,blood pressure was 128/79 mmHg,National Institutes of Health Stroke Scale score was 4 and there were no si...A 39-year-old male with no known comorbidities presented with sudden onset right-sided weakness.On examination,blood pressure was 128/79 mmHg,National Institutes of Health Stroke Scale score was 4 and there were no signs of heart failure.Emergent computerized tomography demonstrated an ischemic infarct of the left middle cerebral artery distribution and brain magnetic resonance imaging later confirmed it(Figure 1).展开更多
Isolated left ventricular non-compaction is recently described as a rare form of cardiomyopathy that is associated with a heart failure, life threatening cardiac arrhythmia and thromboembolic complications. The diagno...Isolated left ventricular non-compaction is recently described as a rare form of cardiomyopathy that is associated with a heart failure, life threatening cardiac arrhythmia and thromboembolic complications. The diagnosis is based on echocardiography demonstration of spongy myocardium. Here we report a case of 74 years old female patient diagnosed as an isolated left ventricular non-compaction with congestive heart failure, intramural thrombus and hypertension. There is no specific treatment for LVNC;therapeutic measures are directed towards the patient’s symptom (heart failure, arrhythmia and thrombotic events) and consideration of an implantable cardioverter defibrillator and cardiac transplantation.展开更多
<div style="text-align:justify;"> <strong>Introduction</strong><span "=""><span>: Ventricular non-compaction, a cardiomyopathy recently described as likely to be ...<div style="text-align:justify;"> <strong>Introduction</strong><span "=""><span>: Ventricular non-compaction, a cardiomyopathy recently described as likely to be rare, belongs to the group of unclassified cardiomyopathy according to European Society of Cardiology. Few studies have been published on the ventricular non-compaction in sub-Saharan Africa. We aim to find out the various aspects, being diagnosis, therapeutic, in Togolese patients carrying the ventricular non-compaction. </span><b><span>Methodology</span></b><span>: This is a three</span></span><span>-</span><span>year</span><span> </span><span "=""><span>prospective and descriptive study conducted from January 2017 to December 2019 in the two University Hospital of Lomé. Patients having echocardiographic criteria of ventricular non-compaction were included in our study. </span><b><span>Results</span></b><span>: 10 patients (6 men and 4 women) were diagnosed for ventricular non-compaction during the study period. The mean age of patients was 32.3 years. The most frequent clinical manifestation was heart failure (7 patients). The main electrocardiogram anomaly was left ventricle hypertrophy (9 patients). The preferential segments were: apical (9 cases), apicolateral (8 cases), and septoapical (7 cases). The average ratio of non-compaction/compaction was 3.31. The main complication was thromboembolic event (4 patients). Angiotensin converting enzyme inhibitors and beta-blockers were essentially the medicines used. After a three (3) year follow-up, two (2) of the patients died. </span><b><span>Conclusion</span></b><span>: Tough ventricular non-compaction has been recently described</span></span><span>.</span><span> It is present in Togo. It displays many clinical manifestations and the prognosis is often guarded.</span> </div>展开更多
Ferroptosis is a new type of programmed cell death caused by the accumulation of iron-dependent lipid peroxides,and it plays a role in the occurrence and progression of diverse diseases.Diabetic cardiomyopathy(DCM),a ...Ferroptosis is a new type of programmed cell death caused by the accumulation of iron-dependent lipid peroxides,and it plays a role in the occurrence and progression of diverse diseases.Diabetic cardiomyopathy(DCM),a serious cardiovascular complication in patients with diabetes,eventually progresses to refractory heart failure(HF),which increases the risk of hospitalization for HF and cardiovascular death in patients with diabetes.Despite glycemic control,effective strategies to prevent DCM onset are currently lacking.Accumulating evidence suggests that ferroptosis is involved in oxidative stress,inflammation,and abnormal autophagy in diabetic myocardium,which plays an important role in myocardial apoptosis,hypertrophy,and cardiac fibrosis.The inhibition of ferroptosis can relieve DCM.Presently,ferroptosis inhibitors have been broadly suggested for the treatment of iron overload-related cardiomyopathy.This article reviewed relevant studies to offer a new therapeutic target for DCM.展开更多
Background Diabetic cardiomyopathy(DCM)represents a severe cardiovascular complication of diabetes mellitus,characterized by insidious onset,diagnostic challenges in early stages,and poor prognosis.Current diagnosis o...Background Diabetic cardiomyopathy(DCM)represents a severe cardiovascular complication of diabetes mellitus,characterized by insidious onset,diagnostic challenges in early stages,and poor prognosis.Current diagnosis of DCM primarily relies on imaging techniques,lacking convenient and effective early biomarkers.Method Using a case-control study design,we enrolled 50 DCM patients(DCM group)and 50 diabetes-only patients(control group)diagnosed at our hospital between January 2023 and January 2025.Demographic data were collected from all participants.Serum levels of hemoglobinA1c(HbAlc),interleukin-1β(IL-1β),and superoxide dismutase(SOD)were measured and compared between groups.Logistic regression analysis was performed to identify DCM risk factors,while receiver operating characteristic(ROC)curve analysis evaluated the diagnostic value of individual and combined biomarkers for DCM screening.Results The levels of HbAlc and IL-1βin the DCM group were higher than those in the control group,and the level of SOD was lower than that in the control group(P<0.05).Multivariate Logistic regression analysis showed that HbAlc,IL-1βand SOD were all independent risk factors for DCM.The results of the ROC curve showed that the areas under curve(AUC)of HbA1c,IL-1β,and SOD levels in diagnosing DCM patients were 0.673,0.783,and 0.728,respectively.The AUC predicted by the combination of the three was 0.836,which was higher than that detected by any above single index(P<0.05).Conclusions DCM patients exhibited significantly higher HbAlc and IL-1βlevels but lower SOD activity compared to the controls.Each biomarker demonstrated significant diagnostic value for DCM,and their combination yielded superior diagnostic performance compared to any single marker.展开更多
Arrhythmogenic right ventricular cardiomyopathy(ARVC)is a progressive disease characterized by adipose and fibrous replacement of the myocardium.While elevated testosterone levels have been implicated in the pathologi...Arrhythmogenic right ventricular cardiomyopathy(ARVC)is a progressive disease characterized by adipose and fibrous replacement of the myocardium.While elevated testosterone levels have been implicated in the pathological process of ARVC,its exact contribution to cardiac fibrosis in ARVC remains unclear.In this study,we analyzed the potential contribution of gender-based differences on the distribution of the low-voltage area in an ARVC cohort undergoing an electrophysiological study,which was indicated by feature selection.Additionally,we established engineered cardiac spheroid models in vitro using patient-specific induced pluripotent stem cell(iPSC)-derived cardiomyocytes(iPSC-CMs)and iPSC-derived cardiac fibroblasts(icFBs).We elucidated the pathogenicity of abnormal splicing in the plakophilin-2(PKP2)gene caused by an intronic mutation.Additionally,pathogenic validation of the desmoglein-2(DSG2)point mutation further confirms the reliability of the models.Moreover,testosterone exacerbated the DNA damage in the mutated cardiomyocytes and further activated myofibroblasts in a chain reaction.In conclusion,we designed and constructed an in vitro three-dimensionally-engineered cardiac spheroid model of ARVC based on clinical findings and provided direct evidence of the fibrotic role of testosterone in ARVC.展开更多
Objective Junctophilin-2(JPH2)is an essential structural protein that maintains junctional membrane complexes(JMCs)in cardiomyocytes by tethering the plasma membrane to the sarcoplasmic reticulum,thereby facilitating ...Objective Junctophilin-2(JPH2)is an essential structural protein that maintains junctional membrane complexes(JMCs)in cardiomyocytes by tethering the plasma membrane to the sarcoplasmic reticulum,thereby facilitating excitationcontraction(E-C)coupling.Mutations in JPH2 have been associated with hypertrophic cardiomyopathy(HCM),but the molecular mechanisms governing its membrane-binding properties and the functional relevance of its membrane occupation and recognition nexus(MORN)repeat motifs remain incompletely understood.This study aimed to elucidate the structural basis of JPH2 membrane association and its implications for HCM pathogenesis.Methods A recombinant N-terminal fragment of mouse JPH2(residues 1-440),encompassing the MORN repeats and an adjacent helical region,was purified under near-physiological buffer conditions.X-ray crystallography was employed to determine the structure of the JPH2 MORN-Helix domain.Sequence conservation analysis across species and junctophilin isoforms was performed to assess the evolutionary conservation of key structural features.Functional membrane-binding assays were conducted using liposome co-sedimentation and cell-based localization studies in COS7 and HeLa cells.In addition,site-directed mutagenesis targeting positively charged residues and known HCM-associated mutations,including R347C,was used to evaluate their effects on membrane interaction and subcellular localization.Results The crystal structure of the mouse JPH2 MORN-Helix domain was resolved at 2.6Å,revealing a compact,elongated architecture consisting of multiple tandem MORN motifs arranged in a curved configuration,forming a continuous hydrophobic core stabilized by alternating aromatic residues.A C-terminalα-helix further reinforced structural integrity.Conservation analysis identified the inner groove of the MORN array as a highly conserved surface,suggesting its role as a protein-binding interface.A flexible linker segment enriched in positively charged residues,located adjacent to the MORN motifs,was found to mediate direct electrostatic interactions with negatively charged phospholipid membranes.Functional assays demonstrated that mutation of these basic residues impaired membrane association,while the HCM-linked R347C mutation completely abolished membrane localization in cellular assays,despite preserving the overall MORN-Helix fold in structural modeling.Conclusion This study provides structural insight into the membrane-binding mechanism of the cardiomyocyte-specific protein JPH2,highlighting the dual roles of its MORN-Helix domain in membrane anchoring and protein interactions.The findings clarify the structural basis for membrane targeting via a positively charged linker and demonstrate that disruption of this interaction—such as that caused by the R347C mutation—likely contributes to HCM pathogenesis.These results not only enhance current understanding of JPH2 function in cardiac E-C coupling but also offer a structural framework for future investigations into the assembly and regulation of JMCs in both physiological and disease contexts.展开更多
Hypertrophic cardiomyopathy(HCM)is a primary myocardial disease characterized by myocardial hypertrophy,excluding other cardiovascular or systemic/metabolic causes of ventricular wall thickening.Apical hypertrophic ca...Hypertrophic cardiomyopathy(HCM)is a primary myocardial disease characterized by myocardial hypertrophy,excluding other cardiovascular or systemic/metabolic causes of ventricular wall thickening.Apical hypertrophic cardiomyopathy(ApHCM)represents a special form of ventricular hypertrophy predominantly affecting the left ventricular apex below the papillary muscles,typically without significant left ventricular outflow tract obstruction.[1,2]ApHCM often coexists with mild coronary artery abnormalities,[3]and reports of acute myocardial infarction with coronary artery stenosis in ApHCM or HCM patients are uncommon.展开更多
BACKGROUND Diabetes mellitus(DM)is a significant risk factor for cardiovascular diseases and can worsen the risk of cardiovascular events among patients with hypertrophic cardiomyopathy(HCM).However,strong evidence is...BACKGROUND Diabetes mellitus(DM)is a significant risk factor for cardiovascular diseases and can worsen the risk of cardiovascular events among patients with hypertrophic cardiomyopathy(HCM).However,strong evidence is needed to show the impact of DM on all-cause mortality(ACM)and atrial fibrillation(AF),which we explored in this systematic review and meta-analysis.AIM To determine the impact of DM on ACM and AF in patients with HCM.METHODS PubMed,Google Scholar,and EMBASE databases were searched for studies showing the effect of DM on ACM and AF in HCM.A binary random effects model with a 95%confidence interval(CI)was used to pool odds ratios(ORs)for ACM and AF outcomes.Study quality was assessed using the Joanna Briggs Institute’s critical appraisal tool and leave-one-out sensitivity analysis.P<0.05 was considered statistically significant.RESULTS Fourteen studies(n=106138)with a mean age of 61.76±19.84 years and 61.55%males were included in our systematic review;ten studies(n=102882)were eligible for meta-analysis.In the unadjusted analysis,DM was not significantly associated with ACM(OR=0.96;95%CI:0.43-2.15;P=0.93).However,after adjustment,DM showed a significant association with higher ACM risk(adjusted OR=1.37;95%CI:1.16-1.61;P<0.01).DM was significantly associated with AF in both unadjusted(OR=2.02;95%CI:1.14-3.58;P=0.04)and adjusted analyses(adjusted OR=2.68;95%CI:1.68-4.27;P=0.01).The Joanna Briggs Institute tool revealed a low risk of bias.Leaveone-out sensitivity analysis,performed by sequentially excluding each study,demonstrated no significant change in the overall effect estimates,indicating the robustness and stability of our results.CONCLUSION DM significantly increased the risk of ACM and AF,highlighting the importance of tighter glycemic control and cardiovascular risk factor modification among patients with HCM.展开更多
Hypertrophic cardiomyopathy(HCM)is an autosomal dominant inherited cardiomyopathy characterized by left ventricular hypertrophy.It is one of the chief causes of sudden cardiac death in younger people and athletes.Mole...Hypertrophic cardiomyopathy(HCM)is an autosomal dominant inherited cardiomyopathy characterized by left ventricular hypertrophy.It is one of the chief causes of sudden cardiac death in younger people and athletes.Molecular-genetic studies have confirmed that the vast majority of HCM is caused by mutations in genes encoding sarcomere proteins.HCM has a relatively wide phenotypic heterogeneity,varying from asymptomatic to sudden cardiac death,because of the many different mutations and pathogenic genes underlying it.Many studies have explored the clinical symptoms and prognosis of HCM,emphasizing the importance of genotype in evaluating patient prognosis and guiding the clinical management of HCM.To elaborate the main pathogenic genes and phenotypic prognosis in HCM to promote a better understanding of this genetic disease.Retrospective analysis of literature to evaluate the association between underlying gene mutations and clinical phenotypes in HCM patients.As sequencing technology advances,the pathogenic gene mutation spectrum and phenotypic characteristics of HCM are gradually becoming clearer.HCM is a widespread inherited disease with a highly variable clinical phenotype.The precise mechanisms linking known pathogenic gene mutations and the clinical course of this heterogeneous condition remain elusive.展开更多
Background:Diabetic cardiomyopathy(DCM)is a type of cardiomyopathy caused by long-term diabetes,characterized by abnormal myocardial structure and function,which can lead to heart failure.Berberine(BBR),a quaternary a...Background:Diabetic cardiomyopathy(DCM)is a type of cardiomyopathy caused by long-term diabetes,characterized by abnormal myocardial structure and function,which can lead to heart failure.Berberine(BBR),a quaternary ammonium alkaloid isolated from Coptidis Rhizoma,a traditional Chinese medicine,has superior anti-diabetic and heart-protective properties.The purpose of this study is to assess the impact of BBR on DCM.Methods:This study used a systems pharmacology approach to evaluate the related proteins and signalling pathways between BBR and DCM targets,combined with experimental validation using diabetic mouse heart sections.Microstructural and pathological changes were observed using Hematoxylin-eosin,Masson’s trichrome stain and wheat germ agglutinin staining.Immunofluorescence and western blot were used to determine protein expression.Results:The results indicate that BBR and DCM share 21 core relevant targets,with cross-targets predominantly located in mitochondrial,endoplasmic reticulum,and plasma membrane components.BBR exerts its main effects in improving DCM by maintaining mitochondrial integrity,particularly involving the PI3K-AKT-GSK3βand apoptosis signalling pathways.In addition,post-treatment changes in the key targets of BBR,including cysteine aspartate specific protease(Caspase)-3,phosphoinositide 3-kinase(PI3K)and mitochondria-related proteins,are suggestive of its efficacy.Conclusion:BBR crucially improves DCM by maintaining mitochondrial integrity,inhibiting apoptosis,and modulating PI3K-AKT-GSK3βsignaling.Further studies must address animal model limitations and validate clinical efficacy to understand BBR’s mechanisms fully and its potential clinical use.展开更多
BACKGROUND Hepatitis C virus(HCV)affects millions of individuals globally and is linked to dilated cardiomyopathy and hypertrophic cardiomyopathy via complex direct viral,immune,and metabolic mechanisms,often exacerba...BACKGROUND Hepatitis C virus(HCV)affects millions of individuals globally and is linked to dilated cardiomyopathy and hypertrophic cardiomyopathy via complex direct viral,immune,and metabolic mechanisms,often exacerbated by cirrhosis,increasing cardiovascular morbidity.AIM To review the pathogenesis of cardiomyopathy in patients infected with HCV and investigate its clinical implications.METHODS A narrative literature review(PubMed,Scopus,Google Scholar;1990–2024)focused on English-language studies examining the HCV–cardiomyopathy link,pathophysiology,and treatment.The findings were qualitatively synthesized.RESULTS HCV drives cardiomyopathy through direct viral toxicity,immune damage,genetic factors,and apoptosis.The associated cirrhosis contributes via cirrhotic cardiomyopathy mechanisms.Clinically,HCV increases cardiovascular events.Direct-acting antivirals(DAAs)generally improve cardiovascular outcomes by reducing adverse events and enhancing cardiac function.CONCLUSION HCV is a significant cardiomyopathy risk factor involving diverse pathways,including cirrhosis.DAA therapy offers cardiovascular benefits.Further research on the underlying mechanisms,biomarkers(e.g.,M2BPGi,Ang-2),and global DAA access is warranted.展开更多
文摘Non-compaction cardiomyopathy is a rare form of cardiomyopathy;its most common clinical manifestations are heart failure (HF), ventricular arrhythmia, thromboembolism, and sudden cardiac death. We report a rare case of a 63-year-old man with chest tightness, worsening lower leg edema, dyspnea, and decreased exercise tolerance. He had a medical history of gastric cancer treated with subtotal gastrectomy and post-operative chemotherapy with paclitaxel and fluorouracil three years ago. At that time, he was diagnosed with non-compaction cardiomyopathy, and the thickened and reticulated trabecular muscle was exclusively confined to left ventricular apex. Five months ago, he was admitted to our hospital with heart failure and treated for dilated cardiomyopathy, echocardiography revealed severe trabecular noncompact myocardium in both ventricles, which was confirmed by cardiac magnetic resonance imaging (CMR). It is generally accepted that non-compacted myocardium forms in the early embryonic stage, which raises a question in our case whether acquired factors, such as antineoplastic drugs, potentially accelerate the pathological progression of non-compaction cardiomyopathy. Considering there are disparities between current screening tools such as echocardiography and CMR regarding diagnostic criteria, multi-detector CT may be an alternative examination method that could provide a new perspective for diagnosis.
文摘INTRODUCTION Isolated ventricular non-compaction is a rare congenital cardiomyopathy occurs due to arrest of normal myocardial development during embryogenesis. It is mainly diagnosed by echocar- diography through the appearance of characteristic prominent myocardial trabeculation and deep inter-trabecular spaces. Heart failore,
基金supported by Research on Guangdong Provincial Science and Technology Innovation Strategy Special Project in 2022(Grant nos.Shantou Government Technology[2022]124-1)。
文摘Left atrialmyxoma is a common primary cardiac tumor that is accompanied by organic heart diseases.But left atrial myxoma coexistent with left ventricular non-compaction(LVNC)is extremely rare.A young male patient with left atrial myxoma and LVNC was reported in this study.A 25-year-old manpresented to the emergency department with sudden shortness of breath and syncope,accompanied by fever and cough.He had a history ofacute ischemic strokeone year before hospitalization.Echocardiography revealed that the endocardium of the left ventricle was not smooth with raised muscle trabeculae and deep recesses.There was an oval-shaped strong echo mass with a pedicle in the left atrium attached to the atrial septum.Tumor resection was operated during extracorporeal circulation.Pathological results confirmed left atrium myxoma.In this case report,the patient had heart failure and an ischemic stroke likely of cardiogenic origin.He underwenttumor resection and started on therapeutic anticoagulation.Left atrial myxoma and LVNC are associated with poor outcomes.Early diagnosis and prompt treatment are crucial.
文摘Importance:Pathogenic variants in theRBM20 gene are associated with aggressive dilated cardiomyopathy(DCM).Recently,RBM20 was found to be associated with left ventricular non-compaction cardiomyopathy(LVNC).Thus far,only five families with LVNC have been reported to carry variants inRBM20.It remains unknown whether the variants inRBM20 associated with DCM can also cause LVNC.Objective:To elucidate the causativeRBM20 variant in two unrelated patients with both LVNC and DCM,and to identify the clinical characteristics associated with variants inRBM20.Methods:Trio whole-exome sequencing(WES)was performed.Variants were filtered and classified in accordance with the guidelines of the American College of Medical Genetics and Genomics(ACMG).Results:We identified two distinctde novo variants inRBM20(one per patient)in these two patients with LVNC.Both variants have been reported in patients with DCM,without the LVNC phenotype.Patient 1 was an 11-year-old girl who had DCM,LVNC,and heart failure;the ratio of noncompacted-to-compacted myocardium was 2.7:1.Ade novo heterozygous variant c.1907G>A(p.Arg636His)in exon 9 was identified in this patient.Patient 2 was a 13-year-old boy who had clinical phenotypes identical to those of Patient 1;the ratio of noncompacted-to-compacted myocardium was 3.2:1 in this patient.WES revealed ade novo heterozygous variant c.1909A>G(p.Ser637Gly)in exon 9.Both variants were previously characterized as pathogenic,and our study classified them as pathogenic variants based on the ACMG guidelines.Interpretation:We found that two patients with LVNC had variants inRBM20.Our results extended the clinical spectrum of the twoRBM20 variants and illustrated that the same variant inRBM20 can cause DCM,with or without the LVNC phenotype.
文摘Cardiomyopathies are among the most prevalent causes of premature death in the Western world.A significant amount of cardiomyopathies has a genetic etiology.Currently,mutations in more than 170 genes associated with different cardiomyopathies,channelopathies,or syndromes with cardiac involvement are described.
基金Supported by The Department of Scientific Research and Structural Funds of Medical College,Jagiellonian University,No.N41/DBS/000594.
文摘Hypertrophic cardiomyopathy(HCM)is a genetically determined myocardial disease characterized by an increased thickness of the left ventricle(LV)wall that cannot be solely attributed to abnormal loading conditions.HCM may present with an intraventricular or LV outflow tract obstruction,diastolic dysfunction,myocardial fibrosis and/or ventricular arrhythmias.Differentiating HCM from other diseases associated with LV hypertrophy,such as hypertension,aortic stenosis,or LV non-compaction(LVNC),can at times be challenging.LVNC is defined by excessive LV trabeculation and deep recesses between trabeculae,often accompanied by increased LV myocardial mass.Previous studies indicate that the LVNC phenotype may be observed in up to 5%of the general population;however,in most cases,it is a benign finding with no impact on clinical outcomes.Nevertheless,LVNC can occasionally lead to LV systolic dysfunction,manifesting as a phenotype of dilated or non-dilated left ventricular cardiomyopathy,with an increased risk of thrombus formation and arterial embolism.In extreme cases,where LVNC is associated with a very thickened LV wall,it can even mimic HCM.There is growing evidence of an overlap between HCM and LVNC,including similar genetic mutations and clinical presentations.This raises the question of whether HCM and LVNC represent different phenotypes of the same disease or are,in fact,two distinct entities.
基金supported by Science,Technology&Innovation Project of Xiongan New Area(2023XAGG0069)National Key Research and Development Program of China(2022YFC2703100)+2 种基金National High Level Hospital Clinical Research Funding(2022-PUMCH-D-002)the National Natural Science Foundation of China(824B2011 to Z.W.)National High Level Hospital Clinical Research Funding(2023-PUMCH-E-012).
文摘Hereditary cardiomyopathies and arrhythmias are major contributors to cardiovascular morbidity and mortality.The advent of next-generation sequencing(NGS)has made genetic testing more accessible,which is crucial for precise diagnosis and targeted therapeutic strategies.The aim of this study is to explore the landscape of genetic variants,the relationship between specific variants and clinical phenotypes,and the impact on clinical decision-making in China.A total of 1536 probands(median age,37 years;1025 males[66.7%])with suspected hereditary cardiomyopathy or arrhythmia(covering 15 clinical phenotypes)are recruited from 146 hospitals across 30 provinces and cities in China.Positive results are confirmed in 390 of 1536 probands,leading to a diagnostic yield of 25.4%.Forty-two and three-tenths percent(n=169)of family members carry the same variants as positive probands.Hypertrophic cardiomyopathy(HCM)and dilated cardiomyopathy(DCM)are the predominant phenotypes,with MYBPC3 variants having the highest frequency in HCM and TTN variants in DCM.In 76.9%of the positive probands,the identified variants are helpful in clinical management,family screening,and fertility.This large-scale study provides significant insights into the genetic landscape of hereditary cardiomyopathies and arrhythmias in China.
基金supported by the Innovation Promotion Program of NHC and Shanghai Key Labs,SIBPT(grant number PT2025-01)。
文摘Human cardiac organoids have revolutionized the study of cardiac development,disease modeling, drug discovery, and regenerative therapies. This review systematically discusses strategies and progress in the construction of cardiac organoids, categorizing them into three main types:cardiac spheroids, self-organizing/assembloid organoids, and organoid-on-a-chip systems. This review uniquely integrates the advances in vascularization, organ-on-chip design, and environmental cardiotoxicity modeling within cardiac organoid platforms, offering a critical synthesis that is absent in the literature. In the context of escalating environmental threats to cardiovascular health, there is an urgent need for physiologically relevant models to accurately identify cardiac toxicants and elucidate their underlying mechanisms of action. This review highlights advances in cardiac organoid applications for disease modeling-including congenital heart defects and acquired cardiovascular diseases-drug development, toxicity screening, and the study of environmentally induced cardiovascular pathogenesis. In addition, it critically examines ongoing challenges and underscores opportunities brought by bioengineering approaches. Finally, we propose future directions for developing standardized cardiac organoid platforms with clinical predictability, aiming to expand the utility of this technology across broader research applications.
文摘A 39-year-old male with no known comorbidities presented with sudden onset right-sided weakness.On examination,blood pressure was 128/79 mmHg,National Institutes of Health Stroke Scale score was 4 and there were no signs of heart failure.Emergent computerized tomography demonstrated an ischemic infarct of the left middle cerebral artery distribution and brain magnetic resonance imaging later confirmed it(Figure 1).
文摘Isolated left ventricular non-compaction is recently described as a rare form of cardiomyopathy that is associated with a heart failure, life threatening cardiac arrhythmia and thromboembolic complications. The diagnosis is based on echocardiography demonstration of spongy myocardium. Here we report a case of 74 years old female patient diagnosed as an isolated left ventricular non-compaction with congestive heart failure, intramural thrombus and hypertension. There is no specific treatment for LVNC;therapeutic measures are directed towards the patient’s symptom (heart failure, arrhythmia and thrombotic events) and consideration of an implantable cardioverter defibrillator and cardiac transplantation.
文摘<div style="text-align:justify;"> <strong>Introduction</strong><span "=""><span>: Ventricular non-compaction, a cardiomyopathy recently described as likely to be rare, belongs to the group of unclassified cardiomyopathy according to European Society of Cardiology. Few studies have been published on the ventricular non-compaction in sub-Saharan Africa. We aim to find out the various aspects, being diagnosis, therapeutic, in Togolese patients carrying the ventricular non-compaction. </span><b><span>Methodology</span></b><span>: This is a three</span></span><span>-</span><span>year</span><span> </span><span "=""><span>prospective and descriptive study conducted from January 2017 to December 2019 in the two University Hospital of Lomé. Patients having echocardiographic criteria of ventricular non-compaction were included in our study. </span><b><span>Results</span></b><span>: 10 patients (6 men and 4 women) were diagnosed for ventricular non-compaction during the study period. The mean age of patients was 32.3 years. The most frequent clinical manifestation was heart failure (7 patients). The main electrocardiogram anomaly was left ventricle hypertrophy (9 patients). The preferential segments were: apical (9 cases), apicolateral (8 cases), and septoapical (7 cases). The average ratio of non-compaction/compaction was 3.31. The main complication was thromboembolic event (4 patients). Angiotensin converting enzyme inhibitors and beta-blockers were essentially the medicines used. After a three (3) year follow-up, two (2) of the patients died. </span><b><span>Conclusion</span></b><span>: Tough ventricular non-compaction has been recently described</span></span><span>.</span><span> It is present in Togo. It displays many clinical manifestations and the prognosis is often guarded.</span> </div>
文摘Ferroptosis is a new type of programmed cell death caused by the accumulation of iron-dependent lipid peroxides,and it plays a role in the occurrence and progression of diverse diseases.Diabetic cardiomyopathy(DCM),a serious cardiovascular complication in patients with diabetes,eventually progresses to refractory heart failure(HF),which increases the risk of hospitalization for HF and cardiovascular death in patients with diabetes.Despite glycemic control,effective strategies to prevent DCM onset are currently lacking.Accumulating evidence suggests that ferroptosis is involved in oxidative stress,inflammation,and abnormal autophagy in diabetic myocardium,which plays an important role in myocardial apoptosis,hypertrophy,and cardiac fibrosis.The inhibition of ferroptosis can relieve DCM.Presently,ferroptosis inhibitors have been broadly suggested for the treatment of iron overload-related cardiomyopathy.This article reviewed relevant studies to offer a new therapeutic target for DCM.
基金supported by Dongguan Social Development Science and Technology Program(No.202218009016172)。
文摘Background Diabetic cardiomyopathy(DCM)represents a severe cardiovascular complication of diabetes mellitus,characterized by insidious onset,diagnostic challenges in early stages,and poor prognosis.Current diagnosis of DCM primarily relies on imaging techniques,lacking convenient and effective early biomarkers.Method Using a case-control study design,we enrolled 50 DCM patients(DCM group)and 50 diabetes-only patients(control group)diagnosed at our hospital between January 2023 and January 2025.Demographic data were collected from all participants.Serum levels of hemoglobinA1c(HbAlc),interleukin-1β(IL-1β),and superoxide dismutase(SOD)were measured and compared between groups.Logistic regression analysis was performed to identify DCM risk factors,while receiver operating characteristic(ROC)curve analysis evaluated the diagnostic value of individual and combined biomarkers for DCM screening.Results The levels of HbAlc and IL-1βin the DCM group were higher than those in the control group,and the level of SOD was lower than that in the control group(P<0.05).Multivariate Logistic regression analysis showed that HbAlc,IL-1βand SOD were all independent risk factors for DCM.The results of the ROC curve showed that the areas under curve(AUC)of HbA1c,IL-1β,and SOD levels in diagnosing DCM patients were 0.673,0.783,and 0.728,respectively.The AUC predicted by the combination of the three was 0.836,which was higher than that detected by any above single index(P<0.05).Conclusions DCM patients exhibited significantly higher HbAlc and IL-1βlevels but lower SOD activity compared to the controls.Each biomarker demonstrated significant diagnostic value for DCM,and their combination yielded superior diagnostic performance compared to any single marker.
基金supported by the National Natural Science Foundation of China(Nos.82370322 to CC,82200352 to FZ,82300352 to YZ,22275034 to HX,and 82070343 to MLC)the Natural Science Foundation of Jiangsu Province of China(Nos.BK20220710 to FZ and BK20230733 to YZ)Postgraduate Research&Practice Innovation Program of Jiangsu Province(No.JX13414086 to HYC).
文摘Arrhythmogenic right ventricular cardiomyopathy(ARVC)is a progressive disease characterized by adipose and fibrous replacement of the myocardium.While elevated testosterone levels have been implicated in the pathological process of ARVC,its exact contribution to cardiac fibrosis in ARVC remains unclear.In this study,we analyzed the potential contribution of gender-based differences on the distribution of the low-voltage area in an ARVC cohort undergoing an electrophysiological study,which was indicated by feature selection.Additionally,we established engineered cardiac spheroid models in vitro using patient-specific induced pluripotent stem cell(iPSC)-derived cardiomyocytes(iPSC-CMs)and iPSC-derived cardiac fibroblasts(icFBs).We elucidated the pathogenicity of abnormal splicing in the plakophilin-2(PKP2)gene caused by an intronic mutation.Additionally,pathogenic validation of the desmoglein-2(DSG2)point mutation further confirms the reliability of the models.Moreover,testosterone exacerbated the DNA damage in the mutated cardiomyocytes and further activated myofibroblasts in a chain reaction.In conclusion,we designed and constructed an in vitro three-dimensionally-engineered cardiac spheroid model of ARVC based on clinical findings and provided direct evidence of the fibrotic role of testosterone in ARVC.
文摘Objective Junctophilin-2(JPH2)is an essential structural protein that maintains junctional membrane complexes(JMCs)in cardiomyocytes by tethering the plasma membrane to the sarcoplasmic reticulum,thereby facilitating excitationcontraction(E-C)coupling.Mutations in JPH2 have been associated with hypertrophic cardiomyopathy(HCM),but the molecular mechanisms governing its membrane-binding properties and the functional relevance of its membrane occupation and recognition nexus(MORN)repeat motifs remain incompletely understood.This study aimed to elucidate the structural basis of JPH2 membrane association and its implications for HCM pathogenesis.Methods A recombinant N-terminal fragment of mouse JPH2(residues 1-440),encompassing the MORN repeats and an adjacent helical region,was purified under near-physiological buffer conditions.X-ray crystallography was employed to determine the structure of the JPH2 MORN-Helix domain.Sequence conservation analysis across species and junctophilin isoforms was performed to assess the evolutionary conservation of key structural features.Functional membrane-binding assays were conducted using liposome co-sedimentation and cell-based localization studies in COS7 and HeLa cells.In addition,site-directed mutagenesis targeting positively charged residues and known HCM-associated mutations,including R347C,was used to evaluate their effects on membrane interaction and subcellular localization.Results The crystal structure of the mouse JPH2 MORN-Helix domain was resolved at 2.6Å,revealing a compact,elongated architecture consisting of multiple tandem MORN motifs arranged in a curved configuration,forming a continuous hydrophobic core stabilized by alternating aromatic residues.A C-terminalα-helix further reinforced structural integrity.Conservation analysis identified the inner groove of the MORN array as a highly conserved surface,suggesting its role as a protein-binding interface.A flexible linker segment enriched in positively charged residues,located adjacent to the MORN motifs,was found to mediate direct electrostatic interactions with negatively charged phospholipid membranes.Functional assays demonstrated that mutation of these basic residues impaired membrane association,while the HCM-linked R347C mutation completely abolished membrane localization in cellular assays,despite preserving the overall MORN-Helix fold in structural modeling.Conclusion This study provides structural insight into the membrane-binding mechanism of the cardiomyocyte-specific protein JPH2,highlighting the dual roles of its MORN-Helix domain in membrane anchoring and protein interactions.The findings clarify the structural basis for membrane targeting via a positively charged linker and demonstrate that disruption of this interaction—such as that caused by the R347C mutation—likely contributes to HCM pathogenesis.These results not only enhance current understanding of JPH2 function in cardiac E-C coupling but also offer a structural framework for future investigations into the assembly and regulation of JMCs in both physiological and disease contexts.
文摘Hypertrophic cardiomyopathy(HCM)is a primary myocardial disease characterized by myocardial hypertrophy,excluding other cardiovascular or systemic/metabolic causes of ventricular wall thickening.Apical hypertrophic cardiomyopathy(ApHCM)represents a special form of ventricular hypertrophy predominantly affecting the left ventricular apex below the papillary muscles,typically without significant left ventricular outflow tract obstruction.[1,2]ApHCM often coexists with mild coronary artery abnormalities,[3]and reports of acute myocardial infarction with coronary artery stenosis in ApHCM or HCM patients are uncommon.
文摘BACKGROUND Diabetes mellitus(DM)is a significant risk factor for cardiovascular diseases and can worsen the risk of cardiovascular events among patients with hypertrophic cardiomyopathy(HCM).However,strong evidence is needed to show the impact of DM on all-cause mortality(ACM)and atrial fibrillation(AF),which we explored in this systematic review and meta-analysis.AIM To determine the impact of DM on ACM and AF in patients with HCM.METHODS PubMed,Google Scholar,and EMBASE databases were searched for studies showing the effect of DM on ACM and AF in HCM.A binary random effects model with a 95%confidence interval(CI)was used to pool odds ratios(ORs)for ACM and AF outcomes.Study quality was assessed using the Joanna Briggs Institute’s critical appraisal tool and leave-one-out sensitivity analysis.P<0.05 was considered statistically significant.RESULTS Fourteen studies(n=106138)with a mean age of 61.76±19.84 years and 61.55%males were included in our systematic review;ten studies(n=102882)were eligible for meta-analysis.In the unadjusted analysis,DM was not significantly associated with ACM(OR=0.96;95%CI:0.43-2.15;P=0.93).However,after adjustment,DM showed a significant association with higher ACM risk(adjusted OR=1.37;95%CI:1.16-1.61;P<0.01).DM was significantly associated with AF in both unadjusted(OR=2.02;95%CI:1.14-3.58;P=0.04)and adjusted analyses(adjusted OR=2.68;95%CI:1.68-4.27;P=0.01).The Joanna Briggs Institute tool revealed a low risk of bias.Leaveone-out sensitivity analysis,performed by sequentially excluding each study,demonstrated no significant change in the overall effect estimates,indicating the robustness and stability of our results.CONCLUSION DM significantly increased the risk of ACM and AF,highlighting the importance of tighter glycemic control and cardiovascular risk factor modification among patients with HCM.
基金Supported by National Natural Science Foundation of China,No.81770379 and 81470521.
文摘Hypertrophic cardiomyopathy(HCM)is an autosomal dominant inherited cardiomyopathy characterized by left ventricular hypertrophy.It is one of the chief causes of sudden cardiac death in younger people and athletes.Molecular-genetic studies have confirmed that the vast majority of HCM is caused by mutations in genes encoding sarcomere proteins.HCM has a relatively wide phenotypic heterogeneity,varying from asymptomatic to sudden cardiac death,because of the many different mutations and pathogenic genes underlying it.Many studies have explored the clinical symptoms and prognosis of HCM,emphasizing the importance of genotype in evaluating patient prognosis and guiding the clinical management of HCM.To elaborate the main pathogenic genes and phenotypic prognosis in HCM to promote a better understanding of this genetic disease.Retrospective analysis of literature to evaluate the association between underlying gene mutations and clinical phenotypes in HCM patients.As sequencing technology advances,the pathogenic gene mutation spectrum and phenotypic characteristics of HCM are gradually becoming clearer.HCM is a widespread inherited disease with a highly variable clinical phenotype.The precise mechanisms linking known pathogenic gene mutations and the clinical course of this heterogeneous condition remain elusive.
基金supported by the National Natural Science Foundation of China(Grant No.82270892)Natural Science Foundation of Hubei Province(Grant No.2022CFB287)+2 种基金Xianning City Science and Technology Plan Project(Grant No.2022ZRKX052)School projects of Hubei University of Science and Technology(Grant No.2022T01,2021WG05,2021TNB01)Hubei University of Science and Technology School-level Fund(Grant No.BK202122).
文摘Background:Diabetic cardiomyopathy(DCM)is a type of cardiomyopathy caused by long-term diabetes,characterized by abnormal myocardial structure and function,which can lead to heart failure.Berberine(BBR),a quaternary ammonium alkaloid isolated from Coptidis Rhizoma,a traditional Chinese medicine,has superior anti-diabetic and heart-protective properties.The purpose of this study is to assess the impact of BBR on DCM.Methods:This study used a systems pharmacology approach to evaluate the related proteins and signalling pathways between BBR and DCM targets,combined with experimental validation using diabetic mouse heart sections.Microstructural and pathological changes were observed using Hematoxylin-eosin,Masson’s trichrome stain and wheat germ agglutinin staining.Immunofluorescence and western blot were used to determine protein expression.Results:The results indicate that BBR and DCM share 21 core relevant targets,with cross-targets predominantly located in mitochondrial,endoplasmic reticulum,and plasma membrane components.BBR exerts its main effects in improving DCM by maintaining mitochondrial integrity,particularly involving the PI3K-AKT-GSK3βand apoptosis signalling pathways.In addition,post-treatment changes in the key targets of BBR,including cysteine aspartate specific protease(Caspase)-3,phosphoinositide 3-kinase(PI3K)and mitochondria-related proteins,are suggestive of its efficacy.Conclusion:BBR crucially improves DCM by maintaining mitochondrial integrity,inhibiting apoptosis,and modulating PI3K-AKT-GSK3βsignaling.Further studies must address animal model limitations and validate clinical efficacy to understand BBR’s mechanisms fully and its potential clinical use.
文摘BACKGROUND Hepatitis C virus(HCV)affects millions of individuals globally and is linked to dilated cardiomyopathy and hypertrophic cardiomyopathy via complex direct viral,immune,and metabolic mechanisms,often exacerbated by cirrhosis,increasing cardiovascular morbidity.AIM To review the pathogenesis of cardiomyopathy in patients infected with HCV and investigate its clinical implications.METHODS A narrative literature review(PubMed,Scopus,Google Scholar;1990–2024)focused on English-language studies examining the HCV–cardiomyopathy link,pathophysiology,and treatment.The findings were qualitatively synthesized.RESULTS HCV drives cardiomyopathy through direct viral toxicity,immune damage,genetic factors,and apoptosis.The associated cirrhosis contributes via cirrhotic cardiomyopathy mechanisms.Clinically,HCV increases cardiovascular events.Direct-acting antivirals(DAAs)generally improve cardiovascular outcomes by reducing adverse events and enhancing cardiac function.CONCLUSION HCV is a significant cardiomyopathy risk factor involving diverse pathways,including cirrhosis.DAA therapy offers cardiovascular benefits.Further research on the underlying mechanisms,biomarkers(e.g.,M2BPGi,Ang-2),and global DAA access is warranted.
