Arrhythmic risk stratification in ischemic,non-ischemic and hypertrophic cardiomyopathy:A two-step multifactorial,electrophysiology study inclusive approach

Annual arrhythmic sudden cardiac death ranges from 0.6%to 4%in ischemic cardiomyopathy(ICM),1%to 2%in non-ischemic cardiomyopathy(NICM),and 1%in hypertrophic cardiomyopathy(HCM).Towards a more effective arrhythmic risk stratification(ARS)we hereby present a two-step ARS with the usage of seven non-invasive risk factors:Late potentials presence(≥2/3 positive criteria),premature ventricular contractions(≥30/h),non-sustained ventricular tachycardia(≥1episode/24 h),abnormal heart rate turbulence(onset≥0%and slope≤2.5 ms)and reduced deceleration capacity(≤4.5 ms),abnormal T wave alternans(≥65μV),decreased heart rate variability(SDNN<70ms),and prolonged QT_(c)interval(>440 ms in males and>450 ms in females)which reflect the arrhythmogenic mechanisms for the selection of the intermediate arrhythmic risk patients in the first step.In the second step,these intermediate-risk patients undergo a programmed ventricular stimulation(PVS)for the detection of inducible,truly high-risk ICM and NICM patients,who will benefit from an implantable cardioverter defibrillator.For HCM patients,we also suggest the incorporation of the PVS either for the low HCM Risk-score patients or for the patients with one traditional risk factor in order to improve the inadequate sensitivity of the former and the low specificity of the latter.

Magnetic resonance imaging and multi-detector computed tomography assessment of extracellular compartment in ischemic and non-ischemic myocardial pathologies

Myocardial pathologies are major causes of morbidity and mortality worldwide. Early detection of loss of cellular integrity and expansion in extracellular volume(ECV) in myocardium is critical to initiate effective treatment. The three compartments in healthy myocardium are: intravascular(approximately 10% of tissue volume), interstitium(approximately 15%) and intracellular(approximately 75%). Myocardial cells, fibroblasts and vascular endothelial/smooth muscle cells represent intracellular compartment and the main proteins in the interstitium are types Ⅰ/Ⅲ collagens. Microscopic studies have shown that expansion of ECV is an important feature of diffuse physiologic fibrosis(e.g., aging and obesity) and pathologic fibrosis [heart failure, aortic valve disease, hypertrophic cardiomyopathy, myocarditis, dilated cardiomyopathy, amyloidosis, congenital heart disease, aortic stenosis, restrictive cardiomyopathy(hypereosinophilic and idiopathic types), arrythmogenic right ventricular dysplasia and hypertension]. This review addresses recent advances in measuring of ECV in ischemic and non-ischemic myocardial pathologies. Magnetic resonance imaging(MRI) has the ability to characterize tissue proton relaxation times(T1, T2, and T2*). Proton relaxation times reflect the physical and chemical environments of water protons in myocardium. Delayed contrast enhanced-MRI(DE-MRI) and multi-detector computed tomography(DE-MDCT) demonstrated hyper-enhanced infarct, hypo-enhanced microvascular obstruction zone and moderately enhanced peri-infarct zone, but are limited for visualizing diffuse fibrosis and patchy microinfarct despite the increase in ECV. ECV can be measured on equilibrium contrast enhanced MRI/MDCT and MRI longitudinal relaxation time mapping. Equilibrium contrast enhanced MRI/MDCT and MRI T1 mapping is currently used, but at a lower scale, as an alternative to invasive sub-endomyocardial biopsies to eliminate the need for anesthesia, coronary catheterization and possibility of tissue sampling error. Similar to delayed contrast enhancement, equilibrium contrast enhanced MRI/MDCT and T1 mapping is completely noninvasive and may play a specialized role in diagnosis of subclinical and other myocardial pathologies. DE-MRI and when T1-mapping demonstrated sub-epicardium, sub-endocardial and patchy mid-myocardial enhancement in myocarditis, Behcet's disease and sarcoidosis, respectively. Furthermore, recent studies showed that the combined technique of cine, T2-weighted and DE-MRI technique has high diagnostic accuracy for detecting myocarditis. When the tomographic techniques are coupled with myocardial perfusion and left ventricular function they can provide valuable information on the progression of myocardial pathologies and effectiveness of new therapies.

Reduced cardiac output is associated with decreased mitochondrial efficiency in the non-ischemic ventricular wall of the acute myocardial-infarcted dog

Cardiogenic shock is the leading cause of death among patients hospitalized with acute myocardial infarction （MI）. Understanding the mechanisms for acute pump failure is therefore important. The aim of this study is to examine in an acute MI dog model whether mitochondrial bio-energetic function within non-ischemic wall regions are associated with pump failure. Anterior MI was produced in dogs via ligation of left anterior descending （LAD） coronary artery, that resulted in an infract size of about 30% of the left ventricular wall. Measurements ofhemodynamic status, mitochondrial function, free radical production and mitochondrial uncoupling protein 3 （UCP3） expression were determined over 24 h period. Hemodynamic measurements revealed a 〉 50% reduction in cardiac output at 24 h post infarction when compared to baseline. Biopsy samples were obtained from the posterior non-ischemic wall during acute infarction. ADP/O ratios for isolated mitochondria from non-ischemic myocardium at 6 h and 24 h were decreased when compared to the ADP/O ratios within the same samples with and without palmitic acid （PA）. GTP inhibition of （PA）-stimulated state 4 respiration in isolated mitochondria from the non-ischemic wall increased by 7% and 33% at 6 h and 24 h post-infarction respectively when compared to sham and pre-infarction samples. This would suggest that the mitochondria are uncoupled and this is supported by an associated increase in UCP3 expression observed on western blots from these same biopsy samples. Blood samples from the coronary sinus measured by electron paramagnetic resonance （EPR） methods showed an increase in reactive oxygen species （ROS） over baseline at 6 h and 24 h post-infarction. In conclusion, mitochondrial bio-energetic ADP/O ratios as a result of acute infarction are abnormal within the non-ischemic wall. Mitochondria appear to be energetically uncoupled and this is associated with declining pump function. Free radical production may be associated with the induction of uncoupling proteins in the mitochondria.

Clinical Study of Sulfotanshinone Sodium Injection in Treating Non-Ischemic Retinal Vein Occlusion

Objectives: To study the effect of sulfotanshinone sodium (SS) injection in the treatment of non-ischemic retinal vein occlusion (RVO). Methods: Sixty-two RVO patients treated in our hospital between Jan. 2013 and Oct. 2014 were randomly divided into Control Group (30 patients;Bendazol tablets) and Treatment Group (32 patients, Bendazol tablets + SS injections), each with a follow-up period of 6 months. Statistical analysis was then performed on changes in visual acuity, central retinal thickness (CRT) and retinal circulation time (RCT) before and after the treatment. Results: After treatment, both Control Group and Treatment Group witnessed an improvement on visual acuity (Control Group: t = 2.103, p = 0.044;Treatment Group: t = 8.021, p = 0.000). Visual acuity could be greatly improved in Treatment Group when compared with Control Group, with significant differences (p < 0.01). Macular edema could be greatly relieved in Treatment Group measured by CRT (t = 2.571, p = 0.007) while the difference was of no statistical significance in Control Group (t = 1.016, p = 0.070). RCT were remarkably shortened in both groups (Control Group: t = 43.83, p = 0.000;Treatment Group: t = 27.34, p = 0.000), and when compared with Control group, the changes in Treatment Group were more significant (p < 0.05). Conclusion: SS injection could effectively improve the therapeutic effect in patients with non-ischemic retinal vein occlusion.

Teneligliptin mitigates diabetic cardiomyopathy by inhibiting activation of the NLRP3 inflammasome

BACKGROUND Diabetic cardiomyopathy(DCM),which is a complication of diabetes,poses a great threat to public health.Recent studies have confirmed the role of NLRP3(NOD-like receptor protein 3)activation in DCM development through the inflammatory response.Teneligliptin is an oral hypoglycemic dipeptidyl peptidase-IV inhibitor used to treat diabetes.Teneligliptin has recently been reported to have anti-inflammatory and protective effects on myocardial cells.AIM To examine the therapeutic effects of teneligliptin on DCM in diabetic mice.METHODS Streptozotocin was administered to induce diabetes in mice,followed by treatment with 30 mg/kg teneligliptin.RESULTS Marked increases in cardiomyocyte area and cardiac hypertrophy indicator heart weight/tibia length reductions in fractional shortening,ejection fraction,and heart rate;increases in creatine kinase-MB(CK-MB),aspartate transaminase(AST),and lactate dehydrogenase(LDH)levels;and upregulated NADPH oxidase 4 were observed in diabetic mice,all of which were significantly reversed by teneligliptin.Moreover,NLRP3 inflammasome activation and increased release of interleukin-1βin diabetic mice were inhibited by teneligliptin.Primary mouse cardiomyocytes were treated with high glucose(30 mmol/L)with or without teneligliptin(2.5 or 5μM)for 24 h.NLRP3 inflammasome activation.Increases in CKMB,AST,and LDH levels in glucose-stimulated cardiomyocytes were markedly inhibited by teneligliptin,and AMP(p-adenosine 5‘-monophosphate)-p-AMPK(activated protein kinase)levels were increased.Furthermore,the beneficial effects of teneligliptin on hyperglycaemia-induced cardiomyocytes were abolished by the AMPK signaling inhibitor compound C.CONCLUSION Overall,teneligliptin mitigated DCM by mitigating activation of the NLRP3 inflammasome.

Effect of Trimetazidine on Functional Capacity in Patient with Ischaemic Cardiomyopathy (TOFCAPI)

Objective: This study aimed to evaluate the efficacy of trimetazidine on exercise capacity via a six-minute walk test in patients with ischaemic cardiomyopathy and also evaluate the effect of trimetazidine on left ventricular function via echocardiography in the same population. Methods: This prospective observational study, conducted at the National Institute of Cardiovascular Diseases in Dhaka, Bangladesh, enrolled 200 patients with ischaemic cardiomyopathy and a depressed left ventricular ejection fraction (LVEF Results: In this study (n = 200) of ischaemic cardiomyopathy patients, the mean age was 58 years, with 76% of the patients being male. All study subjects received GDMT (Guideline-Directed Medical Therapy) for angina and heart failure. Those who received the modified released form of trimetazidine developed lesions during the 1st and 2nd follow-ups, during which the LVEF, LVIDd, and six-minute walk distance significantly improved (p Conclusion: The findings of the present study demonstrated that the addition of modified-release trimetazidine to GDMT can improve exercise capacity and left ventricular function in patients with ischaemic cardiomyopathy.

Diabetic cardiomyopathy:Emerging therapeutic options

Diabetic cardiomyopathy(DbCM)is a common but underrecognized complication of patients with diabetes mellitus(DM).Although the pathobiology of other cardiac complications of diabetes such as ischemic heart disease and cardiac autonomic neuropathy are mostly known with reasonable therapeutic options,the mechanisms and management options for DbCM are still not fully understood.In its early stages,DbCM presents with diastolic dysfunction followed by heart failure(HF)with preserved ejection fraction that can progress to systolic dysfunction and HF with reduced ejection fraction in its advanced stages unless appropriately managed.Apart from prompt control of DM with lifestyle changes and antidiabetic medications,disease-modifying therapy for DbCM includes prompt control of hypertension and dyslipidemia inherent to patients with DM as in other forms of heart diseases and the use of treatments with proven efficacy in HF.A basic study by Zhang et al,in a recent issue of the World Journal of Diabetes elaborates the potential pathophysiological alterations and the therapeutic role of teneligliptin in diabetic mouse models with DbCM.Although this preliminary basic study might help to improve our understanding of DbCM and offer a potential new management option for patients with the disease,the positive results from such animal models might not always translate to clinical practice as the pathobiology of DbCM in humans could be different.However,such experimental studies can encourage more scientific efforts to find a better solution to treat patients with this enigmatic disease.

Isolated Hyperacute T-Waves in West Nile Encephalitis Indicating Atypical Variant of Stress-Induced Cardiomyopathy

Several cardiac outcomes have been reported with West Nile-encephalitis;however, the underlying pathophysiology remains complex. We present a 42-year-old female, with multiple sclerosis, whose neurological symptoms and respiratory decline were finally explained by the diagnosis of West Nile-encephalitis. During her admission, the isolated peaked T-waves indicated the underlying stress-induced cardiomyopathy. The absence of all other causes of hyperacute T-waves, their subsequent resolution with the resolution of infection and improvement in wall motion abnormalities, further supported the association. This case highlights the importance of considering hyperacute T-waves in an approach towards the diagnosis of WNV-encephalitis related atypical variant of stress-induced cardiomyopathy.

Atorvastatin ameliorated myocardial fibrosis by inhibiting oxidative stress and modulating macrophage polarization in diabetic cardiomyopathy

In this editorial,we commented on the article published in the recent issue of the World Journal of Diabetes.Diabetic cardiomyopathy(DCM)is characterized by myocardial fibrosis,ventricular hypertrophy and diastolic dysfunction in diabetic patients,which can cause heart failure and threaten the life of patients.The pathogenesis of DCM has not been fully clarified,and it may involve oxidative stress,inflammatory stimulation,apoptosis,and autophagy.There is lack of effective therapies for DCM in the clinical practice.Statins have been widely used in the clinical practice for years mainly to reduce cholesterol and stabilize arterial plaques,and exhibit definite cardiovascular protective effects.Studies have shown that statins also have anti-inflammatory and antioxidant effects.We were particularly concerned about the recent findings that atorvastatin alleviated myocardial fibrosis in db/db mice by regulating the antioxidant stress and antiinflammatory effects of macrophage polarization on diabetic myocardium,and thereby improving DCM.

Peripartum Cardiomyopathy Complicated by Ventricular Tachycardia during Labor: A Case Report and Literature Review

Background: Peripartum cardiomyopathy (PPCM) is a rare disease that typically affects young, healthy women. Because PPCM is associated with significant mortality, timely diagnosis and management are essential. Ventricular tachycardia (VT) is a major complication and contributor to sudden death. Available data on VT in patients with PPCM are limited. Aim: This case report demonstrates the clinical presentation, antenatal care, and management of labor and delivery in a patient with PPCM complicated by VT. Case report: 36-year old patient G4P3 presents at 27 weeks gestation to the emergency department complaining of chest tightness, palpitations, and profuse sweating. Peripartum cardiomyopathy was diagnosed after her last pregnancy a few years prior. Ventricular tachycardia was diagnosed at this visit and treated successfully. The remainder of the pregnancy was uneventful until she had another episode of ventricular tachycardia during labor. Treatment using antiarrhythmics (diltiazem, amiodarone, adenosine) highlights the importance of prompt intervention and the need for a range of therapeutic options. Results: This case demonstrated successful VT management during pregnancy and labor, emphasizing multidisciplinary collaboration, influencing maternal and fetal outcomes positively, providing insights into optimal care strategies. Conclusion: Peripartum cardiomyopathy complicated by ventricular tachycardia is a life-threatening combination. This case highlights the importance of timely diagnosis and management with combined care between cardiologists, maternal fetal medicine specialists and anesthesiologists to prevent morbidities and sudden maternal death.

Cardiac remodeling in patients with atrial fibrillation reversing bradycardia-induced cardiomyopathy:A case report

BACKGROUND Bradycardia-induced cardiomyopathy(BIC),which is a disease resulting from bradycardia,is characterized by cardiac chamber enlargement and diminished cardiac function.The correction of bradycardia can allow for significant improvements in both cardiac function and structure;however,this disease has been infrequently documented.In this case,we conducted a longitudinal followup of a patient who had been enduring BIC for more than 40 years to heighten awareness and prompt timely diagnosis and rational intervention.CASE SUMMARY A woman who presented with postactivity fatigue and dyspnea was diagnosed with bradycardia at the age of 7.Since she had no obvious symptoms,she did not receive any treatment to improve her bradycardia during the 42-year follow-up,except for the implantation of a temporary pacemaker during labor induction surgery.As time progressed,the patient's heart gradually expanded due to her low ventricular rate,and she was diagnosed with BIC.In 2014,the patient developed atrial fibrillation,her ventricular rate gradually increased,and her heart shape gradually returned to normal.This report describes the cardiac morphological changes caused by the heart rate changes in BIC patients older than 40 years,introduces another possible outcome of BIC,and emphasizes the importance of early intervention in treating BIC.CONCLUSION BIC can induce atrial fibrillation,causing an increased ventricular rate and leading to positive cardiac remodeling.

Potential mechanism of teneligliptin in the treatment of diabetic cardiomyopathy

Diabetic cardiomyopathy(DCM),a complication of diabetes,poses a significant threat to public health,both its diagnosis and treatment presents challenges.Teneligliptin has promising applications and research implications in the treat-ment of diabetes mellitus.Zhang et al observed the therapeutic effect of tenelig-liptin on cardiac function in mice with DCM.They validated that teneligliptin’s mechanism of action in treating DCM involves cardiomyocyte protection and inhibition of NLRP3 inflammasome activity.Given that the NLRP3 inflammasome plays a crucial role in the onset and progression of DCM,it presents a promising therapeutic target.Nevertheless,further clinical validation is required to ascertain the preventive and therapeutic efficacy of teneligliptin in DCM.

Bioinformatics Analysis of the Relationship between Dilated Cardiomyopathy and Chronic Heart Failure

Objective: To screen and analyze the differentially expressed genes between dilated cardiomyopathy (DCM) and chronic heart failure (CHF) based on bioinformatics methods. Methods: The Gene Expression Omnibus (GEO) database was used for data retrieval, and the chip data GSE3585 was downloaded, which was the original data of DCM and normal control group. At the same time, the chip data GSE76701 was downloaded, which was the original data of CHF and control group. Differentially expressed mRNAs (DEmRNAs) were screened by R language limma package, the data were standardized, and the common differentially expressed genes were screened. GO function and KEGG pathway enrichment analysis were performed on the common differentially expressed genes. String11.0 online tool was used for data analysis to obtain differentially expressed genes, and the results were imported into Cytoscape 3.9.1 software. The results were imported into Cytoscape 3.9.1 software, and the common expression gene module was obtained by MOCDE algorithm. Nine Hub genes were obtained by 10 algorithms such as MCC. Results: A total of 248 differentially expressed genes were screened. GO analysis showed that differentially expressed genes were mainly concentrated in 9 different physiological and pathological processes. KEGG analysis showed that the main signaling pathways involved in differentially expressed genes were 2, and 9 key differentially expressed genes were predicted: NPPB, NPPA, MYH6, FRZB, ASPN, SFRP4, RPS4Y1, DDX3Y. Conclusion: This study preliminarily explored the molecular mechanism of DCM and CHF, and obtained the common differentially expressed genes of the two diseases. Further experimental studies are needed to verify the correlation between gene expression and clinicopathological features. Provide new ideas for clinical drug treatment research.

Polyneuropathy, organomegaly, endocrinopathy, M-protein, skin changes syndrome with dilated cardiomyopathy: A case report

BACKGROUND Polyneuropathy,organomegaly,endocrinopathy,M-protein,skin changes(POEMS)syndrome is a rare paraneoplastic syndrome that encompass multiple systems.The most common clinical symptoms of POEMS syndrome are pro-gressive sensorimotor polyneuropathy,organ enlargement,endocrine disorders,darkening skin,a monoclonal plasma cell proliferative disorder,and lymph node hyperplasia.The organomegaly consists of hepatosplenomegaly and/or lym-phadenopathy;cases of cardiomyopathy are rare.Diagnoses are often delayed because of the atypical nature of the syndrome,exposing patients to possibly severe disability.Therefore,identifying atypical symptoms can improve the prognosis and quality of life among POEMS syndrome patients.lenalidomide and dexamethasone.CONCLUSION When patients with cardiomyopathy have systemic manifestations such as numb limbs and darkening skin,the POEMS syndrome is the most possible diagnosis.

Teneligliptin:A potential therapeutic approach for diabetic cardiomyopathy

In this editorial,we comment on the article by Zhang et al.Diabetes mellitus is a chronic disorder associated with several complications like cardiomyopathy,neuropathy,and retinopathy.Diabetes prevalence is increasing worldwide.Multiple diabetes medications are prescribed based on individual patients’needs.However,the exact mechanisms by which many of these drugs exert their protective effects remain unclear.Zhang et al elucidates molecular mechanisms undelaying cardioprotective effect of the dipeptidyl peptidase-IV inhibitor,teneligliptin.Briefly,teneligliptin alleviates the activation of NOD-like receptor protein 3 inflammasome,a multiprotein complex that plays a pivotal role in regulating the innate immune system and inflammatory signaling.Suppression of NOD-like receptor protein 3 inflammasome activity reduces the expression of cytokines,oxygen radicals and inflammation.These findings highlight teneligliptin as an anti-diabetic cardioprotective reagent.

Hypertrophic cardiomyopathy and left ventricular non-compaction:Distinct diseases or variant phenotypes of a single condition?

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.

Diabetic cardiomyopathy:Importance of direct evidence to support the roles of NOD-like receptor protein 3 inflammasome and pyroptosis

Recently,the roles of pyroptosis,a form of cell death induced by activated NODlike receptor protein 3(NLRP3)inflammasome,in the pathogenesis of diabetic cardiomyopathy(DCM)have been extensively investigated.However,most studies have focused mainly on whether diabetes increases the NLRP3 inflammasome and associated pyroptosis in the heart of type 1 or type 2 diabetic rodent models,and whether various medications and natural products prevent the development of DCM,associated with decreased levels of cardiac NLRP3 inflammasome and pyroptosis.The direct link of NLRP3 inflammasome and associated pyroptosis to the pathogenesis of DCM remains unclear based on the limited evidence derived from the available studies,with the approaches of NLRP3 gene silencing or pharmaceutical application of NLRP3 specific inhibitors.We thus emphasize the requirement for more systematic studies that are designed to provide direct evidence to support the link,given that several studies have provided both direct and indirect evidence under specific conditions.This editorial emphasizes that the current investigation should be circumspect in its conclusion,i.e.,not overemphasizing its role in the pathogenesis of DCM with the fact of only significantly increased expression or activation of NLRP3 inflammasome and pyroptosis in the heart of diabetic rodent models.Only clear-cut evidence-based causative roles of NLRP3 inflammasome and pyroptosis in the pathogenesis of DCM can help to develop effective and safe medications for the clinical management of DCM,targeting these biomarkers.

Macrophage modulation with dipeptidyl peptidase-4 inhibitors:A new frontier for treating diabetic cardiomyopathy?

This editorial introduces the potential of targeting macrophage function for diabetic cardiomyopathy(DCM)treatment by dipeptidyl peptidase-4(DPP-4)inhibitors.Zhang et al studied teneligliptin,a DPP-4 inhibitor used for diabetes management,and its potential cardioprotective effects in a diabetic mouse model.They suggested teneligliptin administration may reverse established markers of DCM,including cardiac hypertrophy and compromised function.It also inhibited the NLRP3 inflammasome and reduced inflammatory cytokine production in diabetic mice.Macrophages play crucial roles in DCM pathogenesis.Chronic hyperglycemia disturbs the balance between pro-inflammatory(M1)and antiinflammatory(M2)macrophages,favoring a pro-inflammatory state contributing to heart damage.Here,we highlight the potential of DPP-4 inhibitors to modulate macrophage function and promote an anti-inflammatory environment.These compounds may achieve this by elevating glucagon-like peptide-1 levels and potentially inhibiting the NLRP3 inflammasome.Further studies on teneligliptin in combination with other therapies targeting different aspects of DCM could be suggested for developing more effective treatment strategies to improve cardiovascular health in diabetic patients.

Identification of immune feature genes and intercellular profiles in diabetic cardiomyopathy

BACKGROUND Diabetic cardiomyopathy(DCM)is a multifaceted cardiovascular disorder in which immune dysregulation plays a pivotal role.The immunological molecular mechanisms underlying DCM are poorly understood.AIM To examine the immunological molecular mechanisms of DCM and construct diagnostic and prognostic models of DCM based on immune feature genes(IFGs).METHODS Weighted gene co-expression network analysis along with machine learning methods were employed to pinpoint IFGs within bulk RNA sequencing(RNA-seq)datasets.Single-sample gene set enrichment analysis(ssGSEA)facilitated the analysis of immune cell infiltration.Diagnostic and prognostic models for these IFGs were developed and assessed in a validation cohort.Gene expression in the DCM cell model was confirmed through real time-quantitative polymerase chain reaction and western blotting techniques.Additionally,single-cell RNA-seq data provided deeper insights into cellular profiles and interactions.RESULTS The overlap between 69 differentially expressed genes in the DCM-associated module and 2483 immune genes yielded 7 differentially expressed immune-related genes.Four IFGs showed good diagnostic and prognostic values in the validation cohort:Proenkephalin(Penk)and retinol binding protein 7(Rbp7),which were highly expressed,and glucagon receptor and inhibin subunit alpha,which were expressed at low levels in DCM patients(all area under the curves>0.9).SsGSEA revealed that IFG-related immune cell infiltration primarily involved type 2 T helper cells.High expression of Penk(P<0.0001)and Rbp7(P=0.001)was detected in cardiomyocytes and interstitial cells and further confirmed in a DCM cell model in vitro.Intercellular events and communication analysis revealed abnormal cellular phenotype transformation and signaling communication in DCM,especially between mesenchymal cells and macrophages.CONCLUSION The present study identified Penk and Rbp7 as potential DCM biomarkers,and aberrant mesenchymal-immune cell phenotype communication may be an important aspect of DCM pathogenesis.

Takotsubo Cardiomyopathy Triggered by Acute Pancreatitis: A Case Report

Takotsubo cardiomyopathy is a heart condition that is widely known to be caused by stress. It presents with symptoms that are similar to a myocardial infarction even though the coronary arteries are clear. This case report details the clinical characteristics, diagnostic assessment, and management plan of a 55-year-old male patient with a past medical history of alcoholism who arrived at the emergency department with the typical symptoms of acute pancreatitis. The case demonstrates the progression of Takotsubo cardiomyopathy, which was triggered by acute pancreatitis in the context of alcoholism, and underlines the significance of early detection and management to enhance the patient’s outcomes.