Incidence,prognosis,and risk factors of sepsis-induced cardiomyopathy

BACKGROUND At present,large-scale studies on the clinical characteristics of sepsis-induced cardiomyopathy(SIC)are lacking.AIM To investigate the clinical characteristics of SIC.METHODS Based on the analysis of the MIMIC-III public database,we performed a largescale retrospective study involving sepsis patients who were admitted to the intensive care unit(ICU)and had no concomitant cardiac disease.We used propensity score matching analysis and multivariate logistic regression to ensure the robustness of the results.The primary outcome was hospital mortality,and the secondary outcomes included the number of patients who received mechanical ventilation or renal replacement therapy during their hospital stay,the number of patients administered with vasopressors,the length of ICU stay,and the length of hospital stay.RESULTS In the present study,after screening 38605 patients,3530 patients with sepsis were included.A total of 997 patients met the SIC diagnostic criteria,and the incidence of SIC was 28.20%(95%confidence interval[CI]:26.80%-29.70%).Compared to patients in the non-SIC group,patients in the SIC group were of older age and had a higher Simplified Acute Physiology Score(SAPS)-Ⅰ score,SAPS-Ⅱ score,and Elixhauser comorbidity index(ECI).A total of 367(36.8%)of 997 patients in the SIC group and 818(32.3%)of 2533 patients in the non-SIC group died in the hospital,which resulted in a significant between-group difference(odds ratios=1.22,95%CI:1.05-1.42;P=0.011).For the secondary outcomes,more patients in the SIC group received mechanical ventilation and vasopressors.Multivariate logistic regression analysis showed that age,male sex,ECI,hemoglobin level,diabetes,and mechanical ventilation use on the first day of ICU admission were risk factors for SIC.CONCLUSION Compared with non-SIC patients,hospital mortality is higher in SIC patients.

The Role of GPER in Sepsis-Induced Myocardial Cell Damage and 28-Day Mortality Risk

Purpose: The role of GPER in sepsis-induced myocardial cell injury and its potential impact on the risk of death within 28 days in sepsis. Methods: An in vitro experiment was conducted to establish a sepsis-induced myocardial cell model. H9C2 myocardial cells were treated with 10 μg/ml lipopolysaccharide (LPS) for 24 hours. The effects of different concentrations of the GPER agonist G1 (1, 3, and 10 μmol/L) on cell viability, expression of inflammatory markers, cell apoptosis, and the NF-κB pathway were evaluated. A Mendelian randomization analysis was conducted using Single Nucleotide Polymorphism (SNPs) related to the GPER gene as instrumental variables to investigate the causal relationship between the GPER gene variations and sepsis (28-day death). Results: The results indicate that the group treated with LPS showed a significant decrease in myocardial cell viability, an increase in concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), higher apoptosis rates, and increased phosphorylation levels of NF-κB p65 (p-P65/P65) and IκB-α (p-IκB-α/IκB-α) compared to the control group (P κB pathway. However, genetic evidence did not show a causal relationship between GPER gene variations and sepsis (28-day death) (P κB pathway. However, genetic evidence did not show a causal relationship between GPER gene variations and sepsis (28-day death).

Comparison between sepsis-induced coagulopathy and sepsis-associated coagulopathy criteria in identifying sepsis-associated disseminated intravascular coagulation

BACKGROUND:Disseminated intravascular coagulation(DIC)is associated with increased mortality in sepsis patients.In this study,we aimed to assess the clinical ability of sepsis-induced coagulopathy(SIC)and sepsis-associated coagulopathy(SAC)criteria in identifying overt-DIC and preDIC status in sepsis patients.METHODS:Data from 419 sepsis patients were retrospectively collected from July 2018 to December 2022.The performances of the SIC and SAC were assessed to identify overt-DIC on days 1,3,7,or 14.The SIC status or SIC score on day 1,the SAC status or SAC score on day 1,and the sum of the SIC or SAC scores on days 1 and 3 were compared in terms of their ability to identify pre-DIC.The SIC or SAC status on day 1 was evaluated as a pre-DIC indicator for anticoagulant initiation.RESULTS:On day 1,the incidences of coagulopathy according to overt-DIC,SIC and SAC criteria were 11.7%,22.0%and 31.5%,respectively.The specificity of SIC for identifying overt-DIC was significantly higher than that of the SAC criteria from day 1 to day 14(P<0.05).On day 1,the SIC score with a cut-off value>3 had a significantly higher sensitivity(72.00%)and area under the curve(AUC)(0.69)in identifying pre-DIC than did the SIC or SAC status(sensitivity:SIC status 44.00%,SAC status 52.00%;AUC:SIC status 0.62,SAC status 0.61).The sum of the SIC scores on days 1 and 3 had a higher AUC value for identifying the pre-DIC state than that of SAC(0.79 vs.0.69,P<0.001).Favorable effects of anticoagulant therapy were observed in SIC(adjusted hazard ratio[HR]=0.216,95%confidence interval[95%CI]:0.060–0.783,P=0.018)and SAC(adjusted HR=0.146,95%CI:0.041–0.513,P=0.003).CONCLUSION:The SIC and SAC seem to be valuable for predicting overt-DIC.The sum of SIC scores on days 1 and 3 has the potential to help identify pre-DIC.

Induction and deduction in sepsis-induced cardiomyopathy: five typical categories

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection.The heart is one of the most important oxygen delivery organs,and dysfunction significantly increases the mortality of the body.Hence,the heart has been studied in sepsis for over half a century.However,the definition of sepsis-induced cardiomyopathy is not unified yet,and the conventional conception seems outdated:left ventricular systolic dysfunction(LVSD)along with enlargement of the left ventricle,recovering in 7 to 10 days.With the application of echocardiography in intensive care units,not only LVSD but also left ventricular diastolic dysfunction,right ventricular dysfunction,and even diffuse ventricular dysfunction have been seen.The recognition of sepsis-induced cardiomyopathy is gradually becoming complete,although our understanding of it is not deep,which has made the diagnosis and treatment stagnate.In this review,we summarize the research on sepsis-induced cardiomyopathy.Women and young people with septic cardiomyopathy are more likely to have LVSD,which may have the same mechanism as stress cardiomyopathy.Elderly people with ischemic cardiomyopathy and hypertension tend to have left ventricular diastolic dysfunction.Patients with mechanical ventilation,acute respiratory distress syndrome or other complications of increased right ventricular afterload mostly have right ventricular dysfunction.Diffuse cardiac dysfunction has also been shown in some studies;patients with mixed or co-existing cardiac dysfunction are more common,theoretically.Thus,understanding the pathophysiology of sepsis-induced cardiomyopathy from the perspective of critical care echocardiography is essential.

HSP70 alleviates sepsis-induced cardiomyopathy by attenuating mitochondrial dysfunction-initiated NLRP3 inflammasome-mediated pyroptosis in cardiomyocytes

Background:Sepsis-induced cardiomyopathy(SIC)is an identified serious complication of sepsis that is associated with adverse outcomes and high mortality.Heat shock proteins(HSPs)have been implicated in suppressing septic inflammation.The aim of this study was to investigate whether HSP70 can attenuate cellular mitochondrial dysfunction,exuberated inflammation and inflammasome-mediated pyroptosis for SIC intervention.Methods:Mice with cecal ligation plus perforation(CLP)and lipopolysaccharide(LPS)-treated H9C2 cardiomyocytes were used as models of SIC.The mouse survival rate,gross profile,cardiac function,pathological changes and mitochondrial function were observed by photography,echocardiography,hematoxylin-eosin staining and transmission electron microscopy.In addition,cell proliferation and the levels of cardiac troponin I(cTnI),interleukin-1β(IL-1β)and tumor necrosis factor-α(TNF-α)were determined by Cell Counting Kit-8,crystal violet staining and enzyme-linked immunosorbent assay.Moreover,mitochondrial membrane potential was assessed by immunofluorescence staining,and dynamin-related protein 1 and pyroptosis-related molecules[nucleotide-binding domain,leucine-rich-repeat containing family pyrin domain-containing 3(NLRP3),caspase-1,gasdermin-D(GSDMD),gasdermin-D N-terminal(GSDMD-N)]were measured by western blotting,immunoprecipitation and immunoblotting.Finally,hsp70.1 knockout mice with CLP were used to verify the effects of HSP70 on SIC and the underlying mechanism.Results:Models of SIC were successfully established,as reduced consciousness and activity with liparotrichia in CLP mice were observed,and the survival rate and cardiac ejection fraction(EF)were decreased;conversely,the levels of cTnI,TNF-αand IL-1βand myocardial tissue damage were increased in CLP mice.In addition,LPS stimulation resulted in a reduction in cell viability,mitochondrial destabilization and activation of NLRP3-mediated pyroptosis molecules in vitro.HSP70 treatment improved myocardial tissue damage,survival rate and cardiac dysfunction caused by CLP.Additionally,HSP70 intervention reversed LPS-induced mitochondrial destabiliza-tion,inhibited activation of the NLRP3 inflammasome,caspase-1,GSDMD and GSDMD-N,and decreased pyroptosis.Finally,knockout of hsp70.1 mice with CLP aggravated cardiac dysfunction and upregulated NLRP3 inflammasome activity,and exogenous HSP70 significantly rescued these changes.It was further confirmed that HSP70 plays a protective role in SIC by attenuating mitochondrial dysfunction and inactivating pyroptotic molecules.Conclusions:Our study demonstrated that mitochondrial destabilization and NLRP3 inflammasome activation-mediated pyroptosis are attributed to SIC.Interestingly,HSP70 ameliorates sepsis-induced myocardial dysfunction by improving mitochondrial dysfunction and inhibiting the acti-vation of NLRP3 inflammasome-mediated pyroptosis,and such a result may provide approaches for novel therapies for SIC.

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.

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.

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.

Effects of 8-OHdG,H-FABP and CRP on the Development of Ischemic Cardiomyopathy

[Objectives]To analyze the relationship between serum 8-hydroxydeoxyguanosine(8-OHdG),heart fatty acid-binding protein(H-FABP),C-reactive protein(CRP)levels and clinical efficacy and short-term prognosis in patients with ischemic cardiomyopathy.[Methods]The clinical data of 100 patients with ischemic cardiomyopathy from October 2021 to November 2022 were retrospectively analyzed,and the serum levels of 8-OHdG,H-FABP and CRP were compared before and one week after treatment.The patients were followed up for 12 months after discharge,and the incidence of major adverse cardiovascular events(MACE)was counted during the follow-up period.Univariate and multivariate Logistic regression analysis were used to analyze the prognostic factors of patients with ischemic cardiomyopathy in the near future,and the predictive value of serum 8-OHdG,H-FABP and CRP levels for the prognosis of patients was evaluated by ROC curve.[Results]After 1 week of treatment,the serum levels of 8-OHdG,H-FABP and CRP in patients with ischemic cardiomyopathy were significantly lower than those before treatment(P<0.05).During the follow-up period,34 patients developed MACE;the serum levels of 8-OHdG,H-FABP and CRP in the MACE group were higher than those in the non-MACE group,and the differences were statistically significant(P<0.05).Multivariate Logistic regression analysis showed that 8-OHdG,H-FABP and CRP were the risk factors of MACE in patients with ischemic cardiomyopathy(P<0.05).ROC curve analysis showed that the combined prediction of 8-OHdG,H-FABP and CRP for MACE in patients with ischemic cardiomyopathy was higher than that of CRP,H-FABP and 8-OHdG alone(P<0.05).[Conclusions]8-OHdG,H-FABP and CRP are closely related to the clinical efficacy and short-term prognosis of patients with ischemic cardiomyopathy,and the detection of serum 8-OHdG,H-FABP and CRP levels can help to evaluate the clinical efficacy and short-term prognosis of patients with ischemic cardiomyopathy.