Improvement In Cardiac Function Research Articles

(155) - Defining Optimal Criteria for LVAD Weaning in HF Patients with an Improvement in Cardiac Structure and Function: A VAD Wean Registry Analysis

(155) - Defining Optimal Criteria for LVAD Weaning in HF Patients with an Improvement in Cardiac Structure and Function: A VAD Wean Registry Analysis

Semaglutide attenuates doxorubicin-induced cardiotoxicity by ameliorating BNIP3-Mediated mitochondrial dysfunction

AimsDoxorubicin is a powerful chemotherapeutic agent for cancer, whose use is limited due to its potential cardiotoxicity. Semaglutide (SEMA), a novel analog of glucagon-like peptide-1 (GLP-1), has received widespread attention for the treatment of diabetes. However, increasing evidence has highlighted its potential therapeutic benefits on cardiac function. Therefore, the objective of this study was to examine the efficacy of semaglutide in ameliorating doxorubicin-induced cardiotoxicity. Methods and resultsDoxorubicin-induced cardiotoxicity is an established model to study cardiac function. Cardiac function was studied by transthoracic echocardiography and invasive hemodynamic monitoring. The results showed that semaglutide significantly ameliorated doxorubicin-induced cardiac dysfunction. RNA sequencing suggested that Bnip3 is the candidate gene that impaired the protective effect of semaglutide in doxorubicin-induced cardiotoxicity. To determine the role of BNIP3 on the effect of semaglutide in doxorubicin-induced cardiotoxicity, BNIP3 with adeno-associated virus serotype 9 (AAV9) expressing cardiac troponin T (cTnT) promoter was injected into tail vein of C57/BL6J mice to overexpress BNIP3, specifically in the heart. Overexpression of BNIP3 prevented the improvement in cardiac function caused by semaglutide. In vitro experiments showed that semaglutide, via PI3K/AKT pathway, reduced BNIP3 expression in the mitochondria, improving mitochondrial function. ConclusionSemaglutide ameliorates doxorubicin-induced mitochondrial and cardiac dysfunction via PI3K/AKT pathway, by reducing BNIP3 expression in mitochondria. The improvement in mitochondrial function reduces doxorubicin-mediated cardiac injury and improves cardiac function. Therefore, semaglutide is a potential therapy to reduce doxorubicin-induced acute cardiotoxicity.

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 follow-up 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.

Efficacy of physical exercise on the physical ability, cardiac function and cardiopulmonary fitness of patients with atrial fibrillation: a systematic review and meta-analysis.

It is advised that patients engage in physical activity to enhance their quality of life and achieve better results. The purpose of the current study was to measure the efficacy of exercise on the physical ability, cardiac function and cardiopulmonary fitness of patients with AF. A comprehensive systematic literature search was performed in PubMed, Embase, and Web of Science from 1991 to 2023 for RCTs comparing physical exercise combined with AF routine treatments to routine treatments alone. The meta-analysis was conducted following PRISMA guidelines. Our main outcomes were physical ability (measured by the 6-min walk test, 6MWT), cardiac function (measured by left ventricular ejection fraction, LVEF) and cardiopulmonary fitness (measured by peak oxygen uptake and resting heart rate). Quality assessments were conducted using the Cochrane Collaboration tool. Thirteen trials involving 672 patients met the criteria for analysis. The results showed that physical exercise increased physical ability by improving the 6MWT (m) performance (MD = 96.99, 95% CI: 25.55-168.43; Z = 2.66; p = 0.008); and enhanced peak VO2 (ml/kg per min) (MD = 4.85, 95% CI: 1.55-8.14; Z = 2.89; p = 0.004) while reducing resting heart rate (beats per minute, bpm) (MD = -6.14, 95% CI: -11.30 to -0.98; Z = 2.33; p = 0.02). However, the results showed that regular exercise could improve LVEF (%) inpatients clinically, which had no statistic difference between experimental and control group (MD = 1.49, 95% CI: -0.25-3.24; Z = 1.68; p = 0.09). Our meta-analysis shows that physical exercise is an effective intervention to improve the exercise ability and cardiopulmonary fitness for AF patients. Meanwhile, we also do not exclude the positive effect of exercise on the improvement of cardiac function (LVEF) in patients with AF. To this end, doctors should consider the positive impact of exercise on patients and give advice on exercise limits in practical clinical practice.

CircPAN3/miR-221/PTEN axis and apoptosis in myocardial Infarction: Quercetin's regulatory effects

The circular RNA/microRNA/mRNA axis is a new layer of non-coding RNA(ncRNA)-based regulatory gene expression networks upstream of numerous cell signaling pathways. Circular RNAPAN3 (circPAN3) is involved in autophagy, fibrosis and apoptosis which are responsible for the reduction incardiac functional capacityfollowingmyocardial infarction(MI). However, the molecular mechanism of circPAN3 association with apoptosis is unknown. In addition, the relationship between quercetin as a cardioprotective factor in MI and circular RNA-dependent regulatory pathways has not yet been elucidated. MI was induced in Wistar rats using the left anterior descending artery (LAD) ligation method. One day after surgery, quercetin (30 mg/kg) was injected intraperitoneal (IP) every other day for two weeks. The expression of circPAN3 was increased in the MI group (P < 0.05). The increase in circPAN3 was accompanied by a decrease in miR-221 (P < 0.0001), an increase in PTEN (P < 0.0001), and cleaved caspase 3 (P < 0.001). Quercetin effectively reduced the expression of circPAN3 (P < 0.05), PTEN (P < 0.0001), and cleaved caspase 3 (P < 0.001), and increased the expression of miR-221 (P < 0.0001) and the ratio of p-AKT to p-PI3K (P < 0.001). The circPAN3/miR-221/PTEN pathway is an ncRNA-dependent apoptotic pathway in MI cardiac tissue. Quercetin effectively modulated this pathway, resulting in a reduction of cardiac tissue death and improvement in cardiac function after MI. This suggests that the circPAN3/miR-221 axis plays a role in apoptosis in MI, and quercetin can act as a protective candidate by modulating this pathway.

A fibrin patch loaded with mesenchymal stem cells-derived exosomes improves cardiac functions after myocardial infarction

Myocardial infarction (MI) is a typical cardiovascular disease, causing disability and death worldwide. Exosomes secreted by mesenchymal stem cells (MSCs) showed remarkable therapeutic effects in MI by restoring cardiac function. However, the application of exosomes remains a challenge because of their low residence rate in the infarcted myocardium. Herein, a fibrin-based cardiac patch was prepared to deliver MSCs-derived exosomes to the infarcted heart using an MI mouse model, aiming at improvement of cardiac functions. The fibrin patch was optimized for size to minimize the mouse mortality rate. The composite patch showed sustained release of exosomes in vitro and could improve the retention of exosomes in the infarcted heart, inhibiting fibrosis and improving cardiac functions in vivo. Therefore, this combination of natural biomaterial-based cardiac patch and MSCs-derived exosomes may have a promising clinical translational potential for the MI treatment.

Early postoperative constrictive pericarditis in China: a single-center retrospective observational study.

The diagnosis, treatment, and prognosis of early postoperative constrictive pericarditis (EPCP) have not been discussed in depth. The objective of this study was to devise and propose a management strategy for EPCP. In this study, constrictive pericarditis (CP) within 6 months after cardiac surgery was defined as EPCP, and patients were divided into two groups based on intraoperative findings: a parietal thickening group and a visceral thickening group. A total of 20 patients were included in this study, and the incidence rate of recurrent pericardiectomy was 0.32% among all patients undergoing cardiovascular surgery. EPCP after valve surgery occurred in 85.0% of patients. Pleural effusion was the most common preoperative symptom, occurring in 90% of patients. Pericardial thickening occurred in the visceral layer in seven cases and in the parietal layer in 13 cases. There were no differences in comorbidities, C-reactive protein (CRP) level, or erythrocyte sedimentation rate (ESR) between the two groups. Most patients with visceral thickening (83.3%) needed cardiopulmonary bypass (CPB) assistance during surgery and had a longer hospital stay than those with parietal thickening (52.8±21.8 vs. 34.9±13.8 days, P=0.049). Central venous pressure (CVP) was decreased in all patients after pericardiectomy (24.9±6.96 vs. 8.9±2.92 cmH2O, P<0.001), and the cardiac function improved significantly in patients with parietal thickening [New York Heart Association (NYHA) grade ≥ III accounted for 28.6% of patients]. The long-term survival rate of patients with parietal thickening was 92.3% and that of patients with visceral thickening was 57.1%, and there was no significant difference between them (P=0.056). Recurrent episodes of chest tightness, pleural effusion, and elevated CVP within 6 months after cardiac surgery should be considered highly suggestive of EPCP. There are few points of difference between pericarditis with thickening of the parietal and visceral layers. After failure of conservative medical treatment, pericardiectomy results in significant improvements in cardiac function and quality of life, especially in patients with thickening of the parietal layer.

Proteomic Analysis and Sex-Specific Changes in Chronically Ischemic Swine Myocardium Treated with Sodium-Glucose Cotransporter-2 Inhibitor Canagliflozin.

Although sodium-glucose cotransporter-2 inhibitors have been shown to improve cardiovascular outcomes in general, little is presently known about any sex-specific changes that may result from this therapy. We sought to investigate and quantify potential sex-specific changes seen with the sodium-glucose cotransporter-2 inhibitor canagliflozin (CAN) in a swine model of chronic myocardial ischemia. Eighteen Yorkshire swine underwent left thoracotomy with placement of an ameroid constrictor. Two weeks postop, swine were assigned to receive either control (F = 5 and M = 5) or CAN 300 mg daily (F = 4 and M = 4). After 5 weeks of therapy, swine underwent myocardial functional measurements, and myocardial tissue was sent for proteomic analysis. Functional measurements showed increased cardiac output, stroke volume, ejection fraction, and ischemic myocardial flow at rest in male swine treated with CAN compared with control male swine (all p < 0.05). The female swine treated with CAN had no change in cardiac function as compared with control female swine. Proteomic analysis demonstrated 6 upregulated and 97 downregulated proteins in the CAN female group compared with the control female group. Pathway analysis showed decreases in proteins in the tricarboxylic acidic cycle. The CAN male group had 639 upregulated and 172 downregulated proteins compared with control male group. Pathway analysis showed increases in pathways related to cellular metabolism and decreases in pathways relevant to the development of cardiomyopathy and to oxidative phosphorylation. Male swine treated with CAN had significant improvements in cardiac function that were not observed in female swine treated with CAN. Moreover, CAN treatment in male swine was associated with significantly more changes in protein expression than in female swine treated with CAN. The increased proteomic changes seen in the CAN male group likely contributed to the more robust changes in cardiac function seen in male swine treated with CAN.

The evaluation of bariatric surgery effect on cardiac structure and function using transthoracic echocardiography: a cohort study

BackgroundObesity is a pathology and a leading cause of death worldwide. Obesity can harm multiple organs, including the heart. In this study, we aim to investigate the effect of bariatric surgery and following weight loss on cardiac structure and functions using echocardiography parameters in patients with morbid obesity.MethodsIn this cohort study, 30 patients older than 18 with BMI > 40 or BMI > 35 and comorbidity between March 2020 to March 2021 were studied. The patients underwent transthoracic echocardiography before and after six months of the bariatric surgery.ResultsIn total, 30 patients (28 women, 93.3%) with a mean age of 38.70 ± 9.19 were studied. Nine (30%) were diabetic, and 9 (30%) had hypertension. After six months of bariatric surgery, all physical measurements, including weight, Body mass index, and Body surface area, decreased significantly (p < 0.001). After bariatric surgery, all parameters regarding left ventricular morphology, including left ventricular mass, interventricular septal thickness, left ventricular posterior wall thickness, left ventricular end-systolic diameter, and left ventricular end-diastolic diameter, improved significantly (p < 0.001). Also, LVEF rose post-bariatric surgery (p < 0.001). TAPSE parameter indicating right ventricular function also improved (p < 0.001). Right ventricular diameter, left atrium volume, and mitral inflow E/e’ decreased significantly (p < 0.001).ConclusionSystolic and diastolic parameters refine significantly after bariatric surgery in patients with obesity. Bariatric surgery lead to significant cardiac structure and function improvement.

MiR-873-5p Suppression Reinvigorates Aging Mesenchymal Stem Cells and Improves Cardiac Repair after Myocardial Infarction.

Aging poses obstacles to the functionality of human mesenchymal stem cells (MSCs), resulting in a notable decline in their valuable contribution to myocardial infarction (MI). MicroRNAs (miRNAs) play a pivotal role in governing MSC aging; nonetheless, the specific mechanisms remain puzzling. This research delved into the value of miR-873-5p in the management of MSC aging and investigated whether the restraint of miR-873-5p could regenerate aged MSCs (AMSCs), thereby enhancing their healing success for MI. In this study, MSCs were isolated from both young donors (referred to as YMSCs) and aged donors (referred to as AMSCs). The senescence status of these MSCs was evaluated through the application of age-related β-galactosidase (SA-β-gal) staining. Following this assessment, the MSCs, including those treated with anti-miR-873-5p-AMSCs, were then transplanted into the hearts of Sprague-Dawley rats experiencing acute myocardial infarction. Increasing miR-873-5p levels in YMSCs resulted in elevated cellular aging, whereas reducing miR-873-5p expression decreased aging in AMSCs. Mechanistically, miR-873-5p inhibited autophagy in MSCs through the AMPK signaling pathway, leading to cellular aging by suppressing the Cab39 expression. Partial alleviation of these effects was achieved by the administration of the autophagy inhibitor 3-methyladenine. Grafting of anti-miR-873-5p-AMSCs, by enhancing angiogenesis and bolstering cell survival, led to an improvement in cardiac function in the rat model, unlike the transplantation of AMSCs. miR-873-5p which serves as a pivotal element in mediating MSC aging through its regulation of the Cab39/AMPK signaling pathway. It represents an innovative target for revitalizing AMSCs and enhancing their heart-protective abilities.

Flaxseed oil fraction reverses cardiac remodeling at a molecular level: improves cardiac function, decreases apoptosis, and suppresses miRNA-29b and miRNA 1 gene expression.

Flaxseed is an ancient commercial oil that historically has been used as a functional food to lower cholesterol levels. However, despite its longstanding treatment, there is currently a lack of scientific evidence to support its role in the management of cardiac remodeling. This study aimed to address this gap in knowledge by examining the molecular mechanism of standardized flaxseed oil in restoring cardiac remodeling in the heart toxicity vivo model. The oil fraction was purified, and the major components were standardized by qualitative and quantitative analysis. In vivo experimental design was conducted using isoproterenol ISO (85mg/kg) twice subcutaneously within 24h between each dose. The rats were treated with flaxseed oil fraction (100mg/kg orally) and the same dose was used for omega 3 supplement as a positive control group. The GC-MS analysis revealed that α-linolenic acid (24.6%), oleic acid (10.5%), glycerol oleate (9.0%) and 2,3-dihydroxypropyl elaidate (7%) are the major components of oil fraction. Physicochemical analysis indicated that the acidity percentage, saponification, peroxide, and iodine values were 0.43, 188.57, 1.22, and 122.34 respectively. As compared with healthy control, ISO group-induced changes in functional cardiac parameters. After 28-day pretreatment with flaxseed oil, the results indicated an improvement in cardiac function, a decrease in apoptosis, and simultaneous prevention of myocardial fibrosis. The plasma levels of BNP, NT-pro-BNP, endothelin-1, Lp-PLA2, and MMP2, and cTnI and cTn were significantly diminished, while a higher plasma level of Topo 2B was observed. Additionally, miRNA - 1 and 29b were significantly downregulated. These findings provide novel insight into the mechanism of flaxseed oil in restoring cardiac remodeling and support its future application as a cardioprotective against heart diseases.

Effect of short-term cardiac function changes after cardiac resynchronization therapy on long-term prognosis in heart failure patients with and without diabetes.

The relationship between short-term cardiac function changes and long-term outcomes in heart failure (HF) patients undergoing cardiac resynchronization therapy (CRT) remains uncertain, especially when stratified by diabetes status. This study aims to assess the association between short-term cardiac function changes and outcomes such as all-cause mortality and HF hospitalization in patients undergoing CRT, stratified by diabetes status. This is a cohort longitudinal retrospective study. A total of 666 HF patients, treated with CRT between March 2007 and March 2019, were included in this study. Among them, 166 patients (24.9%) were diagnosed with diabetes. Cardiac function was assessed at baseline and again at 6 months, incorporating evaluations of left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), left atrial diameter (LAD), N-terminal prohormone of brain natriuretic peptide (NT-proBNP), and QRS duration. The QRS duration represents the time required for a stimulus to spread through the ventricles (ventricular depolarization). The primary endpoints of the study were all-cause mortality and HF-related hospitalization. During a median follow-up of 2.51 years, 172 (25.8%) patients died and 197 (29.6%) were hospitalized for HF. Changes in LVEF, LVEDD, and LAD within 6 months had similar effects on adverse outcomes in both diabetic and nondiabetic patients. However, the presence of diabetes significantly modified the association between changes in NT-proBNP and QRS duration and adverse outcomes. Short-term changes in NT-proBNP and QRS duration were positively associated with all-cause mortality and HF hospitalization in patients without diabetes. However, the relationship between short-term changes in NT-proBNP and QRS duration and adverse outcomes was non-linear in diabetic patients. Improvement of cardiac function after CRT implantation can reduce long-term risk of all-cause mortality and HF hospitalization in HF patients. However, the presence of diabetes may affect the association between short-term changes in NT-proBNP and QRS duration and adverse outcomes.

Puerarin attenuates myocardial ischemic injury and endoplasmic reticulum stress by upregulating the Mzb1 signal pathway.

This study investigated the role of Mzb1 in puerarin protection against heart injury and dysfunction in acute myocardial infarction (AMI) mice. C57BL/6 mice were pretreated with and without puerarin at doses of 50mg/kg and 100mg/kg for 14days before establishing the AMI model. An AMI model was induced by ligating the left descending anterior coronary artery, and AC16 cardiomyocytes were treated with H2O2 in vitro. Echocardiography was performed to measure cardiac function. DHE staining, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase assay, and DCFH-DA oxidative fluorescence staining were used to determine reactive oxygen species (ROS) production in vivo and in vitro. Bioinformatics analysis was used to predict potential upstream transcription factors of Mzb1. Puerarin dose-dependently reduced myocardial infarction area and injury, accompanied by the improvement of cardiac function in AMI mice. AMI mice manifested an increase in myocardial oxidative stress, endoplasmic reticulum (ER) stress, apoptosis, and mitochondrial biogenesis dysfunction, which were inhibited by pretreatment with puerarin. Puerarin also prevented Mzb1 downregulation in the hearts of AMI mice or H2O2-treated AC16 cells. Consistent with the in vivo findings, puerarin inhibited H2O2-induced cardiomyocyte apoptosis, ER stress, and mitochondrial dysfunction, which were attenuated by siRNA Mzb1. Furthermore, the JASPAR website predicted that KLF4 may be a transcription factor for Mzb1. The expression of KLF4 was partially reversed by puerarin in the cardiomyocyte injury model, and KLF4 inhibitor (kenpaullone) inhibited Mzb1 expression and affected its function. These results suggest that puerarin can protect against cardiac injury by attenuating oxidative stress and endoplasmic reticulum stress through upregulating the KLF4/Mzb1 pathway and that puerarin may expand our armamentarium for the prevention and treatment of ischemic heart diseases.

Simultaneous initiation of quadruple therapy for heart failure with reduced ejection fraction: initial experience in Afro Caribbean Jamaican population

Background: Among Afro Caribbean Jamaican patients with heart failure with reduced ejection fraction (HFrEF), improvements in cardiac function associated with simultaneous initiation of quadruple therapy, have not been previously reported and we aimed to assess this special population. Methods: Combined quadruple therapy (angiotensin-receptor neprilysin inhibitor, beta-blocker, mineralocorticoid receptor antagonist, and Sodium-glucose cotransporter-2 inhibitors) was simultaneously initiated in 120 Afro Jamaican patients with HFrEF from the Heart Institute of the Caribbean. Patient data was consecutively recorded in our electronic medical records. Changes in Ejection fraction (EF) and N-terminal pro b-type natriuretic peptide (NT-ProBNP) levels, were evaluated after 90 days and statistically analysed during this two-year study. Results: Patient mean age was 63 ± 12.7 years old, 68% male, with mean Body Mass index (BMI) 32.2±6.7 Kg/m2. Hypertension was observed in 62.5 %, T2Diabetes Mellitus in 31.7%, and history of old myocardial infarction in 15.7 %. Atrial fibrillation was present in 7.8% and left bundle branch block in 16.5 %. Other cardiomyopathies (idiopathic, peripartum and non-compaction) were noted in 16.6 %. After the quadruple therapy for a median follow-up period of 90 days, significant improvements of cardiac function were achieved. The mean NT pro-BNP level was significantly decreased from a Baseline of 3111.21 pg/mL ± 4535 to 1806.6 ± 2265.3 pg/ml. A mean change in NT Pro BNP of 1305 pg/mL ± 5069 (p &lt; 0.001). The mean left ventricle ejection fraction (LVEF) improved from a baseline of 33.4 % ± 7.8 to 44.4 % ± 10.9. A mean change in LVEF of 11.3% ± 9.1 (p &lt;0.001). Notably, an improvement of &gt;10% in the LVEF was observed in 41.5% of the total population. In a separate analysis, the subgroup with T2 Diabetes mellitus showed more pronounced (mean change in EF 9.1% ± 11.0) improvement in LVEF than the non-diabetic (mean change in EF 7.7% ± 11.7) but no significant differences in the change of the NT pro-BNP levels were noted between both subgroups. The most frequent therapy adverse effect was hypotension (13.63%) followed by cough (6.81%) and kidney dysfunction (2.27%) but none of the patients presented Angioedema. Conclusion: Among Afro Caribbean Jamaican patients with heart failure and reduced ejection fraction, simultaneous initiation of the quadruple therapy was demonstrated to be feasible, well tolerated and associated with significant functional improvement.

Dilated cardiomyopathy in patients with hypoparathyroidism: A narrative review.

Hypoparathyroidism is a rare endocrine disorder characterized by low blood calcium levels, elevated phosphorus levels, and insufficient parathyroid hormone production. It can lead to dilated cardiomyopathy (DCM), a cardiac condition characterized by enlarged ventricles and reduced heart function. This review aims to explore the relationship between hypoparathyroidism and DCM, the impact of calcium on cardiac function, and the potential for DCM reversal with calcium supplementation. A comprehensive literature search was conducted using PubMed, Google Scholar, and relevant keywords and Mesh terms. Case reports evaluating dilated cardiomyopathy in patients with Hypoparathyroidism were included in the study. Additionally, references cited in each study were carefully examined to identify relevant reports. The cases included in the review were analyzed, and common cardiac manifestations, diagnostic approaches, and management were identified. DCM in hypoparathyroidism presents with symptoms of heart failure, reduced ejection fraction, and impaired left ventricular function. Laboratory tests show low serum calcium levels and elevated phosphate levels. Prompt diagnosis and treatment with calcium and vitamin D supplementation can lead to improvements in cardiac function. Hypoparathyroidism-induced DCM is reversible with timely calcium and vitamin D supplementation. Patient compliance with prescribed medications and supplements is crucial to prevent and manage cardiac complications. Regular follow-up check-ups and monitoring of calcium levels can aid in early detection and improve patient outcomes. Educating patients about the importance of treatment adherence can significantly reduce the risk of developing DCM and other cardiac symptoms associated with hypoparathyroidism. Routine follow-up of DCM among patients with endocrine disorders is recommended.

A Biomimetic Nanocarrier Strategy Targets Ferroptosis and Efferocytosis During Myocardial Infarction.

Myocardial infarction (MI) is characterized by irreversible cardiomyocyte death resulting from an inadequate supply of oxygenated blood to the myocardium. Recent studies have indicated that ferroptosis, a form of regulated cell death, exacerbates myocardial injury during MI. Concurrently, the upregulation of CD47 on the surface of damaged myocardium following MI impairs the clearance of dead cells by macrophages, thereby hindering efferocytosis. In this context, simultaneously inhibiting ferroptosis and enhancing efferocytosis may represent a promising strategy to mitigate myocardial damage post-MI. In this study, we engineered platelet membrane-coated hollow mesoporous silicon nanoparticles (HMSN) to serve as a drug delivery system, encapsulating ferroptosis inhibitor, Ferrostatin-1, along with an anti-CD47 antibody. We aimed to assess the potential of these nanoparticles (designated as Fer-aCD47@PHMSN) to specifically target the site of MI and evaluate their efficacy in reducing cardiomyocyte death and inflammation. The platelet membrane coating on the nanoparticles significantly enhanced their ability to successfully target the site of myocardial infarction (MI). Our findings demonstrate that treatment with Fer-aCD47@PHMSN resulted in a 38.5% reduction in cardiomyocyte ferroptosis under hypoxia, indicated by decreased lipid peroxidation and increased in vitro. Additionally, Fer-aCD47@PHMSN improved cardiomyocyte efferocytosis by approximately 15% in vitro. In MI mice treated with Fer-aCD47@PHMSN, we observed a substantial reduction in cardiomyocyte death (nearly 30%), decreased inflammation, and significant improvement in cardiac function. Our results demonstrated that the cooperation between the two agents induced anti-ferroptosis effects and enhanced dead cardiomyocyte clearance by macrophage as well as anti-inflammation effects. Thus, our nanoparticle Fer-aCD47@PHMSN provides a new therapeutic strategy for targeted therapy of MI.

Daphnetin ameliorates diabetic cardiomyopathy by regulating inflammation and endoplasmic reticulum stress-induced apoptosis.

Daphnetin has been demonstrated to exert beneficial effects on diabetes mellitus and renal complications. However, the role and molecular mechanism of daphnetin in diabetic cardiomyopathy (DCM) remain unclear. In this study, rats were injected with streptozotocin (STZ) to induce diabetes. The diabetic rats were then administered daphnetin (1 and 4 mg/kg) or dimethyl sulfoxide (DMSO) daily for 12 weeks. The results demonstrated that the diabetic rats exhibited elevated blood glucose levels, which were dose-dependently ameliorated by daphnetin. At 13 weeks following STZ injection, the rats exhibited typical diabetic signs, cardiac dysfunction, and evident pathological alterations in myocardial tissues. The administration of daphnetin to diabetic rats resulted in improvement in cardiac function, reductions in myocardial injury biomarkers, and the inhibition of myocardial fibrosis. Furthermore, daphnetin treatment suppressed inflammation and endoplasmic reticulum stress-induced apoptosis in a dose-dependent manner. Additionally, daphnetin exhibited partial blockade of the activation of mitogen-activated protein kinase pathways induced by diabetes. These findings indicate that daphnetin may be a promising therapeutic agent for the treatment of DCM.

Comparison of cardiac function and structure after left atrial appendage occlusion without versus with ablation in patients with non-valvular atrial fibrillation: a retrospective study.

The Aim of this study was to investigate the long-term impact of left atrial appendage occlusion (LAAO) on cardiac function and structure in patients with non-valvular atrial fibrillation (NVAF). 157 patients with NVAF who underwent LAAO or combined with ablation were included and divided into simple LAAO group or combined group. Long term impact of LAAO on cardiac function and structure were evaluated. Results showed that the procedures were performed successfully with 6.4% complications. During follow-up, there was a significant decrease of left atrial anteroposterior diameter (LAAD) at 6 months and a significant increase of left ventricular end-diastolic dimension (LVEDD) at 12 months after LAAO. A significant decrease in plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) was noted at 3 months, 6 months and 12 months after procedure. There was a significant decrease of LAAD, LVEDD, left ventricular end-systolic dimension (LVESD) and NT-proBNP levels in combined group at 3 months, 6 months and 12 months post- procedure, while an increase of left ventricular ejection fraction (LVEF). Meanwhile, no significant change of LAAD, LVEDD, LVESD, NT-proBNP and LVEF was seen in simple LAAO group at 3 months follow-up, but a decrease of NT-proBNP during 6 months and 12 months follow-up. Compared with simple LAAO group, combined group was associated with a significant increase of residual flow. In conclusion, LAAO has no significant effect on cardiac structure and function but can significantly reduce NT-proBNP. The improvement of cardiac structure and function in combined therapy comes from the result of ablation, not LAAO.

A potential research target for cardiac rehabilitation: brain-derived neurotrophic factor.

Cardiovascular diseases pose a major threat to human life, functional activity, and quality of life. Once the disease is present, patients can experience varying degrees of problems or limitations on three levels: physical, psychological, and social. Patients with cardiovascular disease are always at risk for adverse cardiac events, decreased physical activity, psychoemotional disturbances, and limited social participation due to their varying pathologies. Therefore, personalized cardiac rehabilitation is of great significance in improving patients' physical and mental functions, controlling disease progression, and preventing deterioration. There is a consensus on the benefits of cardiac rehabilitation in improving patients' quality of life, enhancing functional activity, and reducing mortality. As an important part of cardiac rehabilitation, Exercise plays an irreplaceable role. Aerobic exercise, resistance training, flexibility training, and other forms of exercise are recommended by many experts. Improvements in exercise tolerance, lipid metabolism, cardiac function, and psychological aspects of the patients were evident with appropriate exercise interventions based on a comprehensive assessment. Further studies have found that brain-derived neurotrophic factor may be an important mediator of exercise's ability to improve cardiovascular health. Brain-derived neurotrophic factor exerts multiple biological effects on the cardiovascular system. This article provides another perspective on the cardiac effects of exercise and further looks at the prospects for the use of brain-derived neurotrophic factor in cardiac rehabilitation. Meanwhile, the new idea that brain-derived neurotrophic factor is a key mediator connecting the brain-cardiac axis is proposed in light of the current research progress, to provide new ideas for clinical rehabilitation and scientific research.

Evaluating the Efficacy of Interventional Approaches for Cardiac Arrhythmias in Acute Myocardial Infarction

Objective: To assess the effectiveness of interventional treatments for cardiac arrhythmias in acute myocardial infarction (AMI). Methods: Eighty AMI patients admitted between August 2022 and August 2023 were selected and randomly assigned into groups using the random number table method. The control group (n = 40) received conventional thrombolytic treatment, while the observation group (n = 40) underwent percutaneous coronary intervention (PCI). Clinical effects were compared between the two groups. Results: Before treatment, there were no significant differences in heart rate indicators, cardiac function indicators, and physiological indicators between the two groups (P &gt; 0.05). After treatment, the observation group showed significantly improved heart rate indicators, cardiac function indicators, and physiological indicators compared to the control group (P &lt; 0.05). The adverse reaction rates in the observation group were lower than in the control group (P &lt; 0.05). Conclusion: PCI treatment demonstrated significant improvements in heart rate, cardiac function, and physiological indicators among AMI patients, leading to a reduced incidence of adverse reactions such as arrhythmia. The overall effect is deemed significant.