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Purpose: To examine whether patient-level disease diagnoses, drug treatments, and dental clinical factors are correlates of early implant failure. Materials and Methods: This historical, nested case-control study used electronic medical records to retrieve patient-level data on individuals with implant failure occurring up to 6 months after implantation, including demographics, clinical information (number, location, and complicated status of implants), underlying diseases (osteoporosis, diabetes, hypertension, inflammatory bowel disease [IBD], myocardial infarction [MI]), and drug purchases (chemotherapy, bisphosphonates, selective serotonin inhibitors, antihypertensive medications, proton pump inhibitors [PPIs], disease-modifying antirheumatic drugs, corticosteroids, and nonsteroidal anti-inflammatory drugs) among adult members of a large, state-mandated health provider in Israel between 2015 and 2020. Individuals with implant extraction occurring up to 6 months after implantation were matched 1:1 to controls. Univariate and adjusted multivariate conditional logistic regression models were used to examine the odds ratios (ORs) of all dental implant risk factors among the patients. Results: A total of 585 individuals with implant failure (mean age, 53 years [42,62], 51.3% females and 49.7% males) were identified among 29,378 eligible patients. Compared to controls, patients who experienced implant failure (ie, cases) were more likely to have smoked in their lifetime (18% vs 11.5%, P = .009), experienced IBD (1.5% vs 0.02%, P = .059), and consumed PPIs within 6 months of the implant surgery (40.0% vs 32.5%, P = .028). Clinical factors, including the number of implants per person (individuals with two implants, OR = 1.53; individuals with at least four implants, OR = 3.33; P < .01), location of implant (maxilla; OR = 1.59; 95% CI: 1.2-2.04), and smoking (OR = 1.57; 95% CI: 1.09-2.26) were significant correlates of early implant failure among the included cases. Crohn's disease, MI, and osteoporosis were found to be borderline significant correlates of early dental implant failure. Conclusions: Among the factors examined, the number of implants, the location of implants, and smoking history were significant correlates of early implant failure, while Crohn's disease, MI, and osteoporosis were found to not be significant. Larger patient-level studies are needed to examine the individual and combined effects of diseases, medications, and clinical factors on early implant failure. [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI) is a leading cause of heart failure, disability and mortality worldwide. In this study, the effects of intramyocardial injection of human platelet lysate (HPL), bone marrow mesenchymal stem cells pretreated with HPL (PMSCs), and PMSC lysate (lys), alone and in combination were investigated on MI-induced by LAD ligation in male Wistar rats. The experiment was carried out on sham, vehicle (Veh), HPL, PMSCs, PMSC lysate (PMSC lys), HPL + PMSCs, and HPL + PMSC lys groups. SBP, DBP, and ± dp/dt max were monitored by the PowerLab physiograph. The MSC characteristics and CD31, NKX2.5, and cardiac troponin I (cTnI) contents were determined by flow cytometry, immunohistochemistry, and immunofluorescence, respectively. SBP, DBP, and ± dp/dt max that decreased in the MI group were recovered by HPL, PMSC, PMSC lys, HPL + PMSC, and HPL + PMSC lys treatments. CD31 density was higher in all treated groups compared to the Veh group. CD31 density in the HPL + PMSCs and HPL + PMSC lys groups was higher than in the PMSCs group. The number of Dil+/NKX2.5 + and Dil+/cTnI + cells was higher in the HPL + PMSCs group compared to the PMSCs group. The HPL and PMSCs mitigates heart injuries and cardiac dysfunction after MI. HPL provides an appropriate environment for cardiomyocyte differentiation from PMSCs. [ABSTRACT FROM AUTHOR]

Background: Myocardial Infarction still persists as the most prevalent cardiovascular disease and is a top cause of morbidity and mortality in doxorubicin treated cancer patients. This study evaluated the prophylactic effect of the ethanol root bark extract of Cleistopholis patens (ERBECP) against doxorubicin-induced myocardial infarction in wistar rats. Extraction, preliminary phytochemical analysis, acute toxicity study and body weight (b.w.) of ERBECP were achieved using standard methods. Phyto-constituents in ERBECP were indentified using Gas Chromatography-Mass Spectrometry (GC–MS) technique. Thirty (30) male albino Wistar rats of average b.w. ranging between 100 and 130 g were divided into six groups of five rats each. Groups I, II and III served as normal, doxorubicin (DOX) and standard (Vasoprin 150 mg/kg b.w) controls respectively, while groups IV, V and VI were orally pre-treated with the extract (200, 400 and 600 mg/kgb.w) for two weeks prior to intraperitoneal induction of cardiotoxicity with DOX (20 mg/kg bw) on day 14. Results: Disturbances in serum cardiac function bio-markers such as; Cardiac Troponin-I (CTnI), Creatine Kinase (CK), Lactate Dehydrogenase (LDH), Aspartate aminotransferase (AST), Alanine aminotransferase (ALT). Lipid profile markers such as; Total cholesterol (TC), Triacylglycerol (TAG), Low Density Lipoprotein (LDL), High Density Lipoprotein (HDL). Oxidative stress markers such as; Malondialdehyde (MDA), Superoxide Dismutase (SOD), Catalase (CAT), Glutathione (GSH) confirmed the induction of myocardial infarction. Histological assessment of heart tissues was performed to validate biochemical results. The GC–MS analysis of ERBECP identified a total of 69 compounds. Safety profile of the aqueous extract was safe for the animals up to the highest dose of 5000 mg/kg b.w. Pre-treatment of DOX group with ERBECP could significantly increase the b.w. compared to the DOX-treated group during the experimental period of 2 weeks. There were significant (p < 0.05) alterations in the levels of CTnI, CK, LDH, AST, ALT and lipid profile indices in the DOX control rats. Also, significant (p < 0.05) increase was observed in MDA and decrease in SOD, CAT and GSH in the DOX control rats. However, administration of the extract significantly (p < 0.05) normalized these alterations and reversed the architectural changes in the heart. The 69 compounds were screened against the target protein (CBR1); we identified seven hits based on the docking score and interactions with the active site residues. All the C. patens constituents had MW (g/mol) less than 500, HBA < 10 and HBD not more than 5. Apart, 9-Octadecenoic acid (Z)-, 2,3-dihydroxy propyl ester and Estra-1,3,5(10)-trien-17. beta. -ol, all the constituents had LD50 lower than 2000 mg/kg. Conclusions: The findings reveals ERBECP demonstrated promising potential and can be exploited in the development novel cardiac therapeutic agents. [ABSTRACT FROM AUTHOR]

This study focused on examining the protection of QiShenYiQi dripping pills (QSYQ) against myocardial infarction (MI) and investigating its potential mechanisms. Ultra high performance liquid chromatography-q exactive-orbitrap high resolution mass spectrometry (UHPLC-Q-Orbitrap HRMS) was employed to analyze potential active compounds of QSYQ. The targets of these compounds were predicted using an integrated in silico method and cross-referenced with relevant databases to identify associated pathways. Experimental validation was then conducted to confirm the accuracy of the systems pharmacology findings. In the end, network analysis combined with UHPLC screened 13 potential active compounds and obtained 99 targets for the intersection of potential active compounds and diseases. The enrichment analysis results indicated that the cyclic guanosine monophosphate-protein kinase G (cGMP-PKG) signaling pathway might be the mechanism of action of QSYQ in the treatment of MI. Experimental verification demonstrated that QSYQ could alleviate oxidative stress, promote vasodilation, and activate proteins related to the mitochondrial ATP-sensitive potassium channel (KATP) and nitric oxide (NO)-cGMP-PKG signaling pathway. This study provides insights into both the pathogenic mechanisms underlying MI and the molecular mechanisms through which QSYQ may confer protection. Given the role of PKG in regulating myocardial stiffness, it emerges as a promising therapeutic target for myocardial remodeling. We propose that the NO-cGMP-PKG and mitochondrial KATP pathways may serve as candidate therapeutic targets for the development of new interventions for MI. [ABSTRACT FROM AUTHOR]

Background and aims Few population-based cohort studies, including both men and women, have explored circulating proteins associated with incident myocardial infarction (MI). This study investigated the relationships between circulating cardiometabolic-related proteins and MI risk using cohort-based and Mendelian randomization (MR) analyses and explored potential sex-specific differences. Methods The discovery cohort included 11 751 Swedish adults (55–93 years). Data on 259 proteins assessed with Olink proximity extension assays, biochemical, and questionnaire-based information were used. Participants were followed up for incident MI and death over 8 years through linkage to Swedish registers. Replication analyses were conducted on the UK Biobank sample (n = 51 613). In MR analyses, index cis -genetic variants strongly related to the proteins were used as instrumental variables. Genetic association summary statistic data for MI were obtained from the CARDIoGRAMplusC4D consortium and FinnGen. Results Forty-five proteins were associated with incident MI in discovery and replication samples following adjustment for potential confounders and multiple testing. In the secondary analysis, 13 of the protein associations were sex-specific, with most associations identified among women. In MR analysis, genetically predicted higher levels of renin, follistatin, and retinoic acid receptor responder protein 2 were linked to an increased risk of MI. Tissue factor pathway inhibitor, tumor necrosis factor receptors 1 and 2, placenta growth factor had an inverse association with MI. Conclusions This study identified both new and confirmed previously established associations between circulating proteins and incident MI and, for the first time, suggested sex-specific patterns in multiple protein-MI associations. [ABSTRACT FROM AUTHOR]

Background and Aims Risk stratification of sudden cardiac death after myocardial infarction and prevention by defibrillator rely on left ventricular ejection fraction (LVEF). Improved risk stratification across the whole LVEF range is required for decision-making on defibrillator implantation. Methods The analysis pooled 20 data sets with 140 204 post-myocardial infarction patients containing information on demographics, medical history, clinical characteristics, biomarkers, electrocardiography, echocardiography, and cardiac magnetic resonance imaging. Separate analyses were performed in patients (i) carrying a primary prevention cardioverter-defibrillator with LVEF ≤ 35% [implantable cardioverter-defibrillator (ICD) patients], (ii) without cardioverter-defibrillator with LVEF ≤ 35% (non-ICD patients ≤ 35%), and (iii) without cardioverter-defibrillator with LVEF > 35% (non-ICD patients >35%). Primary outcome was sudden cardiac death or, in defibrillator carriers, appropriate defibrillator therapy. Using a competing risk framework and systematic internal–external cross-validation, a model using LVEF only, a multivariable flexible parametric survival model, and a multivariable random forest survival model were developed and externally validated. Predictive performance was assessed by random effect meta-analysis. Results There were 1326 primary outcomes in 7543 ICD patients, 1193 in 25 058 non-ICD patients ≤35%, and 1567 in 107 603 non-ICD patients >35% during mean follow-up of 30.0, 46.5, and 57.6 months, respectively. In these three subgroups, LVEF poorly predicted sudden cardiac death (c -statistics between 0.50 and 0.56). Considering additional parameters did not improve calibration and discrimination, and model generalizability was poor. Conclusions More accurate risk stratification for sudden cardiac death and identification of low-risk individuals with severely reduced LVEF or of high-risk individuals with preserved LVEF was not feasible, neither using LVEF nor using other predictors. [ABSTRACT FROM AUTHOR]

Introduction and Purpose: The COVID-19 pandemic has posed significant challenges to healthcare systems worldwide, particularly impacting the management of critical non-COVID conditions such as myocardial infarction (MI). This review aims to explore the alterations in the management of MI during the pandemic and assess how these changes have influenced patient outcomes. State of Knowledge: Numerous studies have reported delays in MI treatment during the pandemic due to healthcare resource reallocation towards COVID-19 care and patient hesitance in seeking timely medical help. Innovations such as telemedicine have been integrated into patient care to overcome barriers. However, these changes have varied impacts on clinical outcomes, including increased mortality and complication rates among MI patients during the pandemic. This review consolidates findings from recent studies focusing on altered treatment protocols, patient care strategies, and overall health system response during this period. Summary: The management of myocardial infarction during the COVID-19 pandemic has witnessed substantial shifts, leading to both challenges and innovations in cardiac care. While some adjustments have provided temporary solutions, the overall impact on MI outcomes has highlighted the need for more resilient healthcare strategies that ensure the continuity of care for acute cardiac events during global health emergencies. [ABSTRACT FROM AUTHOR]

Cardiovascular disease such as myocardial infarction is one of the chief reasons for death universally. An extensive variety of natural and synthetic biodegradable polymers have been studied lately for cardiac tissue engineering applications. Cardiac tissue regeneration is a substitute approach for in situ cellular cardiomyoplasties, which is considered to renovate infarcted myocardium utilizing cells, scaffold, and growth factors. Polymer-based scaffolds including graphene and carbon nanotubes can be employed for heart tissue engineering. In this review, we consider the literature in terms of cardiac tissue engineering and discuss the most recent developments in terms of scaffold-based polymers for cardiac tissue regeneration. [ABSTRACT FROM AUTHOR]

Background: Previous literature has explored the relationship between television viewing and cardiovascular disease (CVD) in adults; however, there remains a paucity of longitudinal data describing how young adult television viewing relates to premature CVD events. Objective: To ascertain the relationship between level and annualized changes in television viewing from young adulthood to middle age and the incidence of premature CVD events before age 60. Design: The Coronary Artery Risk Development in Young Adults (CARDIA) study, a prospective community-based cohort with over 30 years of follow-up (1985–present). Participants: Black and White men and women who were 18–30 years old at baseline (1985–1986). Main Measures: Independent variables: Individualized television viewing trajectories were developed using linear mixed models. Dependent variables: Fatal and nonfatal coronary heart disease (CHD), heart failure, and stroke outcomes were analyzed separately and as a combined CVD event outcome. Key Results: Among 4318 included participants, every 1-h increase in daily hours of television viewing at age 23 was associated with higher odds of incident CHD (adjusted odds ratio [AOR] 1.26, 95% confidence interval [CI] 1.06–1.49) and incident CVD events (AOR 1.16, 95% CI 1.03–1.32). Each additional hour of daily television viewing annually was associated with higher annual odds of CHD incidence (AOR 1.55, 95% CI 1.06–2.25), stroke incidence (AOR 1.58, 95% CI 1.02–2.46), and CVD incidence (AOR 1.32, 95% CI 1.03–1.69). Race and sex modified the association between television viewing level at age 23 and CHD, heart failure, and stroke, with White men most consistently having significant associations. Conclusions: In this prospective cohort study, greater television viewing in young adulthood and annual increases in television viewing across midlife were associated with incident premature CVD events, particularly CHD. Young adulthood as well as behaviors across midlife may be important periods to promote healthy television viewing behavior patterns. [ABSTRACT FROM AUTHOR]

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Background and objective: Retinal vein occlusion (RVO) and acute myocardial infarction (MI) are significant vascular events that impact patient health and mortality. Both conditions share common risk factors, such as hypertension, diabetes, and atherosclerosis. This study investigated the potential connection between RVO and MI, particularly among younger individuals, to improve preventive measures and management protocols. Method: A systematic review and meta-analysis were conducted, adhering to the PRISMA and MOOSE guidelines. Multiple databases, including PubMed, Scopus, MEDLINE, ScienceDirect, and ClinicalTrials.gov, were exhaustively searched until August 24, 2024. Studies were selected based on their reports of the association between RVO and MI risk. Quality assessment was performed using the Newcastle-Ottawa Quality Assessment Scale, and data were pooled using a random-effects model with hazard ratios and 95% confidence intervals. Result: Twelve studies comprising 371,817 participants were included. Meta-analysis revealed a pooled hazard ratio of 1.324 (95% CI, 1.238–1.415), indicating a significant association between RVO and increased MI risk (p = 0.0001). Subgroup analysis for central retinal vein occlusion (CRVO) showed a hazard ratio of 1.691 (95% confidence interval [CI] 1.142, 2.502, p = 0.009) with moderate heterogeneity (I2 = 36%), whereas branch retinal vein occlusion (BRVO) yielded a non-significant hazard ratio of 1.167 (95% CI 0.843, 2.106, p = 0.444; I2 = 33%). Publication bias was identified (Egger's test, p = 0.036) and addressed through trim-and-fill adjustment, maintaining statistical significance. Conclusion: Our meta-analysis shows a strong association between CRVO and a 69.1% increased risk of MI, while BRVO shows no significant correlation. Overall, RVO is linked to a 32.4% elevated risk of MI. Despite slight publication bias, adjusted analyses confirm reliability, indicating that improved cardiovascular monitoring for RVO patients, especially those with CRVO, is essential to mitigate MI risk. Clinical trial number: Not applicable. [ABSTRACT FROM AUTHOR]

Background: Although stem cell transplantation is a promising approach for the treatment of myocardial infarction (MI), there are still some problems faced such as the low survival rate of stem cells. Here, we investigated the role of Notoginsenoside R1 (NGR1) pretreatment in improving the effects of neonatal rat bone marrow mesenchymal stem cell (MSC) transplantation for treatment of MI. Methods: Cardiac functions were detected by echocardiography and the myocardial infarct size was determined by Masson's trichrome staining in a rat model of MI. The cardioprotective effects of NGR1/LY294002 co-pretreated MSCs was evaluated to explore the underlying mechanism. The angiogenesis was determined by vWF and α-SMA immunofluorescence staining and cell apoptosis was detected by TUNEL. In vitro, the effects of NGR1 on stem cell proliferation was examined by CCK-8 and levels of P-Akt, P-CREB, P-FoxO1 were detected by western blot. Apoptosis, ROS content, and cytokine levels were examined by DAPI and TUNEL staining, a ROS assay kit, and ELISA, respectively. Results: NGR1 elevated the therapeutic effect of MSC transplantation on infarction by preserving cardiac function, increasing angiogenesis and expressions of IGF-1, VEGF, and SDF-1, and reducing cell apoptosis, whereas the addition of LY294002 prior to NGR1 treatment significantly counteracted the foregoing effects of NGR1. NGR1 pretreatment and SC79 pretreatment were similar in that both significantly increased P-Akt and P-FoxO1 levels in MSC and did not affect P-CREB levels. Besides, both NGR1 and SC79 promoted VEGF, SCF and bFGF levels in MSC cultures, and significantly reduced ROS accumulation and the attenuated cell apoptosis in MSC triggered by H2O2. Similarly, addition of LY294002 before NGR1 treatment significantly counteracted the aforementioned effects of NGR1 in vitro. Conclusions: NGR1 pretreatment enhances the effect of MSC transplantation for treatment of MI through paracrine signaling, and the mechanism underlying this effect may be associated with PI3K/Akt/FoxO1 signaling pathways. [ABSTRACT FROM AUTHOR]

Background: The efficiency of mesenchymal stem cells (MSCs) in treating myocardial infarction (MI) remains inconsistent, which limits their therapeutic applications. Therefore, exploring the mechanism for the inconsistent efficacy of MSCs and identification the criteria for screening MSCs are important for improving the efficiency of MSCs. Methods: Mouse model after MI was utilized to test the role of MSCs from different donors and the functional subpopulation in improving cardiac function. Heterogeneity of MSCs was identified using single-cell RNA sequencing (scRNA-seq) of MSC-GY. GSEA and Scissor analyses were used to find the functional subpopulations of MSCs that promote angiogenesis. The role of functional subpopulations in promoting angiogenesis was verified by detecting the secretory proteins, the ratio of N-CADHERIN+/CD168− subpopulations in MSCs, and the tube formation, migration, and proliferation of HUVECs after treatment with conditional medium (CM) derived from different MSCs. Results: We found that umbilical cord-derived MSCs (UC-MSCs) from different donors have varied therapeutic efficacy in MI mice and UC-MSCs with higher therapeutic effectiveness exhibited the most potent pro-angiogenic effects by secreting elevated levels of angiogenesis-related proteins, such as MYDGF, VEGFA, and FGF2. ScRNA-seq of 10,463 UC-MSCs revealed that the N-CADHERIN+/CD168− subpopulation was closely associated with pro-angiogenic effects, and the ratio of this cell subpopulation was positively correlated with the angiogenic potential of MSCs. We also found that the N-CADHERIN+/CD168− subpopulation was the functional subpopulation of MSCs in improving cardiac function of MI mice. Conclusions: Our study identified that the N-CADHERIN+/CD168− subpopulation was the functional subpopulation of MSCs in treating MI, which was essential for the development and utilization of MSCs in MI treatment. [ABSTRACT FROM AUTHOR]

Background: Circular RNAs (circRNAs) are differentially expressed in various cardiovascular diseases, including myocardial infarction (MI) injury. However, their functional role in necroptosis-induced loss of cardiomyocytes remains unclear. We identified a cardiac necroptosis-associated circRNA transcribed from the Cacna1c gene (circCacna1c) to investigate the involvement of circRNAs in cardiomyocyte necroptosis. Methods: To investigate the role of circCacna1c during oxidative stress, H9c2 cells and neonatal rat cardiomyocytes were treated with hydrogen peroxide (H2O2) to induce reactive oxygen species (ROS)-induced cardiomyocyte death. The N6-methyladenosine (m6A) modification level of circCacna1c was determined by methylated RNA immunoprecipitation quantitative polymerase chain reaction (MeRIP–qPCR) analysis. Additionally, an RNA pull-down assay was performed to identify interacting proteins of circCacna1c in cardiomyocytes, and the regulatory role of circCacna1c in target protein expression was tested using a western blotting assay. Furthermore, the MI mouse model was constructed to analyze the effect of circCacna1c on heart function and cardiomyocyte necroptosis. Results: The expression of circCacna1c was found to be reduced in cardiomyocytes exposed to oxidative stress and in mouse hearts injured by MI. Overexpression of circCacna1c inhibited necroptosis of cardiomyocytes induced by hydrogen peroxide and MI injury, resulting in a significant reduction in myocardial infarction size and improved cardiac function. Mechanistically, circCacna1c directly interacts with heterogeneous nuclear ribonucleoprotein F (Hnrnpf) in the cytoplasm, preventing its nuclear translocation and leading to reduced Hnrnpf levels within the nucleus. This subsequently suppresses Hnrnpf-dependent receptor-interacting protein kinase 1 (RIPK1) expression. Furthermore, fat mass and obesity-associated protein (FTO) mediates demethylation of m6A modification on circCacna1c during necrosis and facilitates degradation of circCacna1c. Conclusion: Our study demonstrates that circCacna1c can improve cardiac function following MI-induced heart injury by inhibiting the Hnrnpf/RIPK1-mediated cardiomyocyte necroptosis. Therefore, the FTO/circCacna1c/Hnrnpf/RIPK1 axis holds great potential as an effective target for attenuating cardiac injury caused by necroptosis in ischemic heart disease. [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI) is a leading cause of heart failure, disability and mortality worldwide. In this study, the effects of intramyocardial injection of human platelet lysate (HPL), bone marrow mesenchymal stem cells pretreated with HPL (PMSCs), and PMSC lysate (lys), alone and in combination were investigated on MI-induced by LAD ligation in male Wistar rats. The experiment was carried out on sham, vehicle (Veh), HPL, PMSCs, PMSC lysate (PMSC lys), HPL + PMSCs, and HPL + PMSC lys groups. SBP, DBP, and ± dp/dt max were monitored by the PowerLab physiograph. The MSC characteristics and CD31, NKX2.5, and cardiac troponin I (cTnI) contents were determined by flow cytometry, immunohistochemistry, and immunofluorescence, respectively. SBP, DBP, and ± dp/dt max that decreased in the MI group were recovered by HPL, PMSC, PMSC lys, HPL + PMSC, and HPL + PMSC lys treatments. CD31 density was higher in all treated groups compared to the Veh group. CD31 density in the HPL + PMSCs and HPL + PMSC lys groups was higher than in the PMSCs group. The number of Dil+/NKX2.5 + and Dil+/cTnI + cells was higher in the HPL + PMSCs group compared to the PMSCs group. The HPL and PMSCs mitigates heart injuries and cardiac dysfunction after MI. HPL provides an appropriate environment for cardiomyocyte differentiation from PMSCs. [ABSTRACT FROM AUTHOR]

Background: The clinical application of mesenchymal stem cells (MSCs) in myocardial infarction (MI) is severely hampered by their poor survival. Pretreatment is a key strategy that has been adopted to promote their therapeutic efficacy. This study aimed to investigate the benefit of growth differentiation factor 15-pretreated MSCs (GDF15-MSCs) in enhancing cardiac repair following MI and to determine the underlying mechanisms. Methods: MSCs with or without GDF15 pretreatment were exposed to serum deprivation and hypoxia (SD/H) challenge. Apoptosis of MSCs was assessed by TUNEL staining. The conditioned media (CM) of MSCs and GDF15-MSCs was collected by centrifugation. MSCs and GDF15-MSCs were transplanted into the peri-infarct region in a mouse model of MI. Cardiac function, fibrosis and MSC survival were examined 4 weeks after MSC transplantation. Results: Pretreatment with GDF15 greatly reduced SD/H-induced apoptosis of MSCs via inhibition of reactive oxygen species (ROS) generation by attenuating mitochondrial fission. Mechanistically, GDF15 pretreatment ameliorated mitochondrial fission of MSCs under SD/H challenge by activating the AMPK pathway. These effects were partially abrogated by AMPK inhibitor. Pretreatment with GDF15 also promoted paracrine effects of MSCs in vitro, evidenced by improving tube formation of HUVECs, and inhibited the apoptosis of cardiomyocytes induced by SD/H. At 4 weeks after transplantation, compared with MSCs, GDF15 pretreatment strongly promoted the survival of MSCs in the ischemic heart with consequent enhanced cardiac function, reduced cardiac fibrosis and increased angiogenesis. Conclusions: Our study showed that pretreatment with GDF15 promoted the cardioprotective effects of MSCs in MI via regulation of pro-survival signaling and paracrine actions. GDF15 pretreatment is an effective approach to enhance the therapeutic efficacy of MSCs in ischemic heart disease. [ABSTRACT FROM AUTHOR]

Background: Progranulin is a secreted glycoprotein that regulates inflammation and wound healing. However, plasma progranulin levels in the acute phase and their clinical significance in patients with acute myocardial infarction (AMI) remain to be elucidated. Objective: We aimed to investigate the relationship between the increase in plasma progranulin levels in the acute phase and the recovery of left ventricular function in the chronic phase in AMI patients. Method and result: Eighteen AMI patients were followed up for 6 months. Blood samples were collected from the antecubital vein on day 0 (on admission) and day 7 in the acute phase. The control group consisted of patients without significant coronary artery stenosis, as assessed by cardiac catheterization (n = 16). Plasma progranulin levels were measured by enzyme-linked immunosorbent assay. Echocardiography was performed in the acute (within 7 days) and chronic (6 months) phases of AMI to evaluate left ventricular ejection fraction using the modified Simpson's method. Plasma progranulin levels in the AMI group on day 0 (69.5 ± 24.6 ng/mL) were similar to those in the control group (84.2 ± 47.1 ng/mL). There was a significant increase in progranulin levels in the AMI group on day 7 (104.2 ± 52.0 ng/mL) compared with day 0. The increase in plasma progranulin levels in the acute phase was positively correlated with the increase in left ventricular ejection fraction between the acute and chronic phases. Among various factors, only plasma progranulin levels were favorably correlated with left ventricular functional recovery in the chronic phase. Conclusion: The increase in plasma progranulin levels in the acute phase may serve as a predictive biomarker and a contributer for the recovery of left ventricular function in the chronic phase in patients with AMI. [ABSTRACT FROM AUTHOR]

Background: In older adults with hypertension, hip fractures accompanied by preoperative acute heart failure significantly elevate surgical risks and adverse outcomes, necessitating timely identification and management to improve patient outcomes. Research objective: This study aims to enhance the early recognition of acute heart failure in older hypertensive adults prior to hip fracture surgery by developing a predictive model using logistic regression (LR) and machine learning methods, optimizing preoperative assessment and management. Methods: Employing a retrospective study design, we analyzed hypertensive older adults who underwent hip fracture surgery at Hebei Medical University Third Hospital from January 2018 to December 2022. Predictive models were constructed using LASSO regression and multivariable logistic regression, evaluated via nomogram charts. Five additional machine learning methods were utilized, with variable importance assessed using SHAP values and the impact of key variables evaluated through multivariate correlation analysis and interaction effects. Results: The study included 1,370 patients. LASSO regression selected 18 key variables, including sex, age, coronary heart disease, pulmonary infection, ventricular arrhythmias, acute myocardial infarction, and anemia. The logistic regression model demonstrated robust performance with an AUC of 0.753. Although other models outperformed it in sensitivity and F1 score, logistic regression's discriminative ability was significant for clinical decision-making. The Gradient Boosting Machine model, notable for a sensitivity of 95.2%, indicated substantial capability in identifying patients at risk, crucial for reducing missed diagnoses. Conclusion: We developed and compared efficacy of predictive models using logistic regression and machine learning, interpreting them with SHAP values and analyzing key variable interactions. This offers a scientific basis for assessing preoperative heart failure risk in older adults with hypertension and hip fractures, providing significant guidance for individualized treatment strategies and underscoring the value of applying machine learning in clinical settings. [ABSTRACT FROM AUTHOR]

Cardiac cell damage frequently occurs as a consequence of acute myocardial infarction (AMI), a critical complication of coronary atherosclerotic heart disease. There is an escalating recognition of the association between COX2 and myocardial damage induced by ischemia. The objective of this study is to investigate the inhibitory effect of the COX2 on cardiomyocyte damage in the context of AMI. To create an AMI model, mice with the genetic background of wild-type C57BL6/J (WT) and COX2-/- mice were utilized. The left anterior descending (LAD) coronary artery in their hearts was obstructed, and subsequent assessment of hemodynamic parameters and heart function was conducted. Notably, increased levels of COX2 were observed in AMI mice. Through correlational analysis between COX2 expression and cardiac function following AMI, it was revealed that COX2 knockout mice had smaller infarct sizes, better cardiac performance, and suppressed levels of reactive oxygen species (ROS) compared to WT mice. Additionally, we discovered that COX2 knockout mice exhibited significantly higher mRNA levels of smooth muscle actin, collagen I, and collagen III than normal mice with AMI. Conversely, the levels of superoxide dismutase (SOD), malondialdehyde (MDA) were higher but iron content was decreased in COX2 knockout mice compared to normal mice with AMI.In summary, our research demonstrates that the downregulation of COX2 enhances cardiac tissue recovery in the context of AMI. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases are a cause of death making it crucial to accurately diagnose them. Electrocardiography plays a role in detecting heart issues such as heart attacks, bundle branch blocks and irregular heart rhythms. Manual analysis of ECGs is prone to mistakes and time consuming, underscoring the importance of automated methods. This study uses AI models like AlexNet and a dual branch model for categorizing ECG signals from the PTB Diagnostic ECG Database. AlexNet achieved a validation accuracy of 98.64% and a test set accuracy of 99% while the dual branch fusion network model achieved a test set accuracy of 99%. Data preprocessing involved standardizing, balancing and reshaping ECG signals. These models exhibited precision, sensitivity and specificity. In comparison to state of the arts' models such as Hybrid AlexNet SVM and DCNN LSTM our proposed models displayed performance. The high accuracy rates of 99% underscore their potential for ECG classification. These results validate the advantages of incorporating learning models into setups for automated ECG analysis providing adaptable solutions for various healthcare settings including rural areas. [ABSTRACT FROM AUTHOR]

Background and Aims The question of when and how to treat truly asymptomatic patients with severe aortic stenosis (AS) and normal left ventricular (LV) systolic function is still subject to debate and ongoing research. Here, the results of extended follow-up of the AVATAR trial are reported (NCT02436655, ClinicalTrials.gov). Methods The AVATAR trial randomly assigned patients with severe, asymptomatic AS and LV ejection fraction ≥ 50% to undergo either early surgical aortic valve replacement (AVR) or conservative treatment with watchful waiting strategy. All patients had negative exercise stress testing. The primary hypothesis was that early AVR will reduce a primary composite endpoint comprising all-cause death, acute myocardial infarction, stroke, or unplanned hospitalization for heart failure (HF), as compared with conservative treatment strategy. Results A total of 157 low-risk patients (mean age 67 years, 57% men, mean Society of Thoracic Surgeons score 1.7%) were randomly allocated to either the early AVR group (n = 78) or the conservative treatment group (n = 79). In an intention-to-treat analysis, after a median follow-up of 63 months, the primary composite endpoint outcome event occurred in 18/78 patients (23.1%) in the early surgery group and in 37/79 patients (46.8%) in the conservative treatment group [hazard ratio (HR) early surgery vs. conservative treatment 0.42; 95% confidence interval (CI) 0.24–0.73, P =.002]. The Kaplan–Meier estimates for individual endpoints of all-cause death and HF hospitalization were significantly lower in the early surgery compared with the conservative group (HR 0.44; 95% CI 0.23–0.85, P =.012, for all-cause death and HR 0.21; 95% CI 0.06–0.73, P =.007, for HF hospitalizations). Conclusions The extended follow-up of the AVATAR trial demonstrates better clinical outcomes with early surgical AVR in truly asymptomatic patients with severe AS and normal LV ejection fraction compared with patients treated with conservative management on watchful waiting. [ABSTRACT FROM AUTHOR]

Despite the widespread adoption of emergency coronary reperfusion therapy, reperfusion‐induced myocardial injury remains a challenging issue in clinical practice. Following myocardial reperfusion, S100A8/A9 molecules are considered pivotal in initiating and regulating tissue inflammatory damage. Effectively reducing the S100A8/A9 level in ischemic myocardial tissue holds significant therapeutic value in salvaging damaged myocardium. In this study, HA (hemagglutinin)‐ and RAGE (receptor for advanced glycation end products)‐ comodified macrophage membrane‐coated siRNA nanoparticles (MMM/RNA NPs) with siRNA targeting S100A9 (S100A9‐siRNA) are successfully prepared. This nanocarrier system is able to target effectively the injured myocardium in an inflammatory environment while evading digestive damage by lysosomes. In vivo, migration of MMM/RNA NPs to myocardial injury lesions is confirmed in a myocardial ischemia‐reperfusion injury (MIRI) mouse model. Intravenous injection of MMM/RNA NPs significantly reduced S100A9 levels in serum and myocardial tissues, further decreasing myocardial infarction area and improving cardiac function. Targeted reduction of S100A8/A9 by genetically modified macrophage membrane‐coated nanoparticles may represent a new therapeutic intervention for MIRI. [ABSTRACT FROM AUTHOR]

18F-GP1 is a novel highly specific radiotracer that binds to activated platelets and thrombus. We aimed to establish the observer repeatability of coronary, carotid and cerebral 18F-GP1 uptake in patients presenting with acute myocardial infarction or ischaemic stroke. Forty-three patients presenting with acute myocardial infarction or ischaemic stroke underwent hybrid positron emission tomography (PET) and computed tomography (CT) angiography. Qualitative and quantitative assessment of 18F-GP1 uptake was performed on coronary arteries, carotid arteries and brain parenchyma. Qualitative uptake of 18F-GP1 had excellent intraobserver and interobserver agreement, with complete agreement for the presence or absence of visual 18F-GP1 uptake. For quantitative analysis, there were excellent intraclass correlation coefficients for intraobserver repeatability for coronary artery, carotid artery and brain parenchymal SUVmax and TBRmax measurements (all ≥ 0.92). Coronary artery and brain parenchymal analyses showed the strongest agreement in SUVmax values with mean biases of − 0.04 (limits of agreement − 0.21 to 0.20) and 0.02 (limits of agreement − 0.29 to 0.32) respectively. There was good interclass correlation coefficients for interobserver repeatability for coronary artery, carotid artery and brain parenchymal SUVmax and TBRmax measurements (all ≥ 0.89). The strongest interobserver agreement was seen with brain parenchymal SUVmax (mean SUVmax 1.95 ± 0.94) and TBRmax (mean TBRmax 9.55 ± 6.56) with mean biases of − 0.05 (limits of agreement − 0.37 to 0.27) and 0.04 (limits of agreement − 0.59 to 0.52) respectively. Visual qualitative and quantitative 18F-GP1 PET-CT image analyses provide robust and repeatable measurements of activated platelets and thrombi within the coronary arteries, carotid arteries and brain parenchyma. [ABSTRACT FROM AUTHOR]

Cardiac troponin I (cTnI) is the most resorted biomarker for the detection of cardiovascular disease (CVD). The means of rapid quantification of cTnI levels in the blood can substantially minimize the risk of acute myocardial infarction and heart failure. A sensor for the non‐enzymatic evaluation of cardiac troponin‐I has been developed using fluorescent iron nanoclusters via a one‐pot synthesis employing (BSA) as the template and reducing agent, and hydrogen peroxide as the additive. The fluorescence of Iron Nanocluster is quenched with graphene oxide (GO) via fluorescence resonance energy transfer (FRET) between conjugate iron nanoclusters and graphene oxide. The sensor shows a low detection limit of 0.011 ng/mL. The benefits of utilizing a non‐enzymatic probe for detecting cardiac troponin I is that it avoids the need for enzymes and hence is economical, stable, and less impacted by environmental conditions such as temperature and pH. Non‐enzymatic probes are more useful for clinical use since they are more stable and have a longer shelf life. The developed non‐enzymatic probes are also highly selective and sensitive to the target analyte, making them suitable for the direct detection of cardiac troponin I in actual biological samples. [ABSTRACT FROM AUTHOR]

Myocardial ischemia-reperfusion injury (MIRI) is a significant factor in the development of cardiac dysfunction following a myocardial infarction. Ferroptosis, a type of regulated cell death driven by iron and marked by lipid peroxidation, has garnered growing interest for its crucial involvement in the pathogenesis of MIRI.This review comprehensively examines the mechanisms of ferroptosis, focusing on its regulation through iron metabolism, lipid peroxidation, VDAC signaling, and antioxidant system dysregulation. We also compare ferroptosis with other forms of cell death to highlight its distinct characteristics. Furthermore, the involvement of ferroptosis in MIRI is examined with a focus on recent discoveries concerning ROS generation, mitochondrial impairment, autophagic processes, ER stress, and non-coding RNA regulation. Lastly, emerging therapeutic strategies that inhibit ferroptosis to mitigate MIRI are reviewed, providing new insights into potential clinical applications. [ABSTRACT FROM AUTHOR]

Objectives: Coronary artery bypass grafting (CABG) is essential for treating coronary artery disease, with postoperative aspirin crucial to prevent graft restenosis. However, its gastrointestinal side effects may limit tolerability in some patients. Indobufen presents a potential alternative, but its safety and efficacy need further validation. This study aimed to compare the efficacy and safety of indobufen versus aspirin in patients' post-CABG. Methods: This retrospective observational study included 39 patients who underwent CABG at two centers from January to December 2023. Patients were retrospectively assigned to two groups based on the antiplatelet therapy they received: the indobufen group (n = 19) and the aspirin group (n = 20). The primary endpoint was a composite of non-fatal myocardial infarction, stroke, and revascularization due to acute coronary syndrome in the intention-to-treat population. Postoperative data on platelet count, hemoglobin, D-dimer, activated partial thromboplastin time (APTT), and hospital stay length were collected. Transfusion rate, bleeding, thrombotic events, and gastrointestinal adverse reactions were compared between the two groups. Results: Over the 8-to-18-month follow-up period, 5 patients (25%) in the aspirin group reached the primary endpoint, while none in the indobufen group did, a difference that was statistically significant (p = 0.02). Although the rates of non-fatal myocardial infarction, revascularization, stroke, and thrombotic events were higher in the aspirin group, these differences did not reach statistical significance. Importantly, the total bleeding events were markedly lower in the indobufen group (15.79% vs. 55%, p = 0.011), with major bleeding events also significantly reduced in the indobufen group (0% vs. 20%, p = 0.04). Both groups showed no significant differences were observed in postoperative hospital stay, hemoglobin, and D-dimer levels between the groups. However, the indobufen group demonstrated significantly lower platelet count and APTT. The average daily cost of indobufen was 27.8 times higher than that of aspirin. Conclusion: Indobufen demonstrates a comparable antiplatelet effect to aspirin and offers significant advantages in reducing gastrointestinal adverse reactions and bleeding risk. It can be considered a preferable alternative for patients who cannot tolerate or have contraindications to aspirin. Further large-scale clinical trials are needed to confirm its potential as the first-choice antiplatelet therapy post-CABG. [ABSTRACT FROM AUTHOR]

Introduction: Myocardial infarction (MI), a leading cause of heart failure, is characterized by the loss of cardiomyocytes, which severely limits the heart's regenerative capacity. The Hippo pathway, which regulates cell proliferation and apoptosis, presents a therapeutic target for cardiac regeneration. This study explores the efficacy of Lats-IN-1, a LATS1/2 kinase inhibitor targeting the Hippo pathway, as a novel treatment for MI. Methods: Using male C57BL/6 mice subjected to surgically induced MI, we administered Lats-IN-1 and evaluated the effects on cardiac function, infarct size, cardiomyocyte proliferation, and apoptosis through various assays and echocardiographic assessments. Results: Our results demonstrate that Lats-IN-1 significantly improves cardiac function, as evidenced by enhanced ejection fraction and reduced ventricular dimensions. Additionally, Lats-IN-1 decreased infarct size and apoptosis rates while promoting cardiomyocyte proliferation. These findings suggest that Lats-IN-1 promotes cardiac repair and regeneration. Discussion: By modulating the Hippo pathway and reducing apoptosis markers, Lats-IN-1 represents a promising therapeutic strategy for improving outcomes in heart diseases characterized by cardiomyocyte loss. This study highlights the critical role of the Hippo pathway in facilitating cardiac regeneration. [ABSTRACT FROM AUTHOR]

Introduction: Myocardial ischemia/reperfusion (I/R) injury remains a major obstacle in cardiovascular therapies. Hydrogen sulfide (H2S) shows promise for mitigating I/R injury, but conventional delivery methods, such as NaHS injections or adenovirus-mediated CSE gene therapy, face low efficiency and systemic side effects. This study explores the use of angiotensin 1 (AT1) peptide-conjugated CdSe/ZnS quantum dots (QDs) for targeted delivery of cystathionine-γ-lyase (CSE) plasmids to the myocardium, aiming to boost local H2S production and minimize I/R injury. Methods: CdSe/ZnS QDs were conjugated with AT1 peptides to create a nanocarrier system capable of delivering the CSE plasmid specifically to the myocardium. In vivo fluorescence imaging confirmed heart-specific accumulation. Myocardial infarct size, cardiac function, cell death, and oxidative stress were evaluated. Endoplasmic reticulum stress and mitophagy markers, including CHOP/GRP78/eIF2α, were analyzed, and the CHOP gene's role was further assessed using an adenovirus vector. Results: The AT1-conjugated nanocarriers significantly increased CSE expression in the myocardium, as confirmed by fluorescence imaging, without affecting other organs. This localized delivery reduced myocardial infarct size, improved cardiac function, and decreased oxidative stress and cell death. Importantly, a reduction in endoplasmic reticulum stress and mitophagy markers was observed, suggesting that cardioprotection was mediated via the CHOP/GRP78/eIF2α signaling pathway. Reintroduction of CHOP using an adenovirus vector reversed these protective effects, confirming the pathway's involvement. Discussion: This study demonstrates that AT1 peptide-conjugated QDs can effectively deliver CSE plasmids to the heart, providing significant protection against I/R injury through enhanced localized H2S production. This approach offers a promising, targeted, and side-effect-free therapy for myocardial I/R injury, with potential for clinical translation. [ABSTRACT FROM AUTHOR]

Background: Inflammation and neurohormonal activation play a significant role in the adverse outcome seen in acute myocardial infarction (AMI) and the development of cardiogenic shock (CS), which is associated with a mortality rate up to 50%. Treatment with anti-inflammatory drugs such as tocilizumab, an interleukin-6 receptor antagonist, has been shown to reduce troponin release and reduce the myocardial infarct size in AMI patients and it may therefore have cardioprotective properties. Methods: This is a double-blind, placebo-controlled, single-center randomized clinical trial, including adult AMI patients without CS at hospital arrival, undergoing percutaneous coronary intervention (PCI) within 24 h from symptom onset, and at intermediate to high risk of developing CS (ORBI risk score ≥ 10). A total of 100 participants will be randomized to receive a single intravenous dose of tocilizumab (280 mg) or placebo (normal saline). The primary outcome is peak plasma pro-B-type natriuretic peptide (proBNP) within 48 h, assessed using serial measurements at intervals: before infusion, 12, 24, 36, and 48 h after infusion. Secondary endpoints include the following: (1) cardiac magnetic resonance imaging (CMR) during 24–48 h after admission and at follow-up after 3 months with assessment of left ventricular area at risk, final infarct size, and the derived salvage index and (2) biochemical markers of inflammation (C-reactive protein and leukocyte counts) and cardiac injury (troponin T and creatinine kinase MB). Discussion: Modulation of interleukin-6-mediated inflammation in patients with AMI, treated with acute PCI, and at intermediate to high risk of in-hospital CS may lead to increased hemodynamic stability and reduced left ventricular infarct size, which will be assessed using blood biomarkers with proBNP as the primary outcome and inflammatory markers, troponin T, and CMR with myocardial salvage index as the secondary endpoints. Trial registration: Registered with the Regional Ethics Committee (H-21045751), EudraCT (2021–002028-19), ClinicalTrials.gov (NCT05350592). Study registration date: 2022-03-08, Universal Trial Number U1111-1277–8523. [ABSTRACT FROM AUTHOR]

Background: Multivessel disease(MVD) is linked to a poorer prognosis, increased complications, longer hospital stays, and higher in-hospital mortality when compared to single-vessel disease(SVD).The purpose of this study is to explore the clinically relevant predictors of acute cornary syndrome (ACS) combined with MVD. Methods: This multicenter retrospective study included 68,378 ACS patients from 240 hospitals.The clinical data were retrospectively analyzed with univariate and multivariate analyses to identify the predictive factors for MVD. Results: When compared to SVD group, the MVD group showed a higher incidence of Major Adverse Cardiovascular Events(MACCEs), including all-cause death, myocardial infarction, stent thrombosis, and ischemic stroke during hospitalization, These differences were found to be statistically significant (P < 0.05).The multivariate analysis revealed that age over 75 years (OR: 1.246, 95% CI: 1.176, 1.319), LDL/HDL ratio > 1.98 (OR: 1.245, 95% CI: 1.192, 1.302), history of heart failure (OR: 1.446, 95% CI: 1.143, 1.829), hypertension (OR: 1.274, 95% CI: 1.225, 1.325), diabetes (OR: 1.341, 95% CI: 1.278, 1.406), eGFRs < 60 ml/min·1.73m2 (OR: 1.179, 95% CI: 1.112, 1.249), family history of CAD (OR: 1.236, 95% CI: 1.108, 1.379), and high homocysteine levels (OR: 1.209, 95% CI: 1.029, 1.420) are independent predictors of MVD. The incidence of multivessel disease increased from 37.7 to 58.6% with an increase in the number of predictive factors, while the incidence of single vessel disease decreased from 62.3 to 41.4%. This trend was statistically significant (P trend < 0.001). Conclusions: MVD is strongly correlated with a range of risk factors including diabetes, hypertension, LDL/HDL ratio greater than 1.98, hyperhomocysteinemia, family history of CAD, reduced glomerular filtration rate (< 60 ml/(min·1.73m2), age over 75 years, and a history of heart failure. Furthermore, as the number of predictive factors increases, the odds ratio (OR) for patients with MVD also increases, reaching 2.344 times the OR for patients without any predictive factors. [ABSTRACT FROM AUTHOR]

The study's goals are to fabricate PLGA nanoparticles (PNPs) loaded with apigenin (AP) and adenosine (AD) using a microfluidic preparation method to a standard emulsification method and investigate the possible heart-protective effects of AP-AD PNPs made using the emulsification method. Compared to microfluidics, the emulsification method fabricated small-size nanoparticles, which are better at encapsulating drugs, retaining more drugs, and having a low viscosity for the myocardial infarction (MI) injection. TheMI model was developed using SD rats injected under the skin with 85 mg/kg doxorubicin (DOX) for 2 days. The metabolic results showed that our AP-AD PNPs accelerated the blood flow in rats with MI, which increased the amounts of AP and AD in the circulatory system. This led to significant improvements in the cardiac index and lower amounts of AST, LDH, and CK in the blood. A histopathological study using Hematoxylin&eosin, and TUNEL staining showed that cardiac function had improved and apoptosis had decreased. Moreover, tests that checked the amounts of IL-6, TNF-α, NO, GSH, MDA, and SOD showed that AP-AD PNPs may help treat MI by reducing oxidative stress and inflammation, making it a potentially useful therapeutic approach. [ABSTRACT FROM AUTHOR]

A novel immunoassay platform is presented utilizing a cardiac troponin T antibody (Ab-cTnT) labelled with 5-carboxyfluorescein (5-FAM) integrated into a two-dimensional (2D) manganese dioxide nanosheet (MnO2 NS) matrix. This strategy enables a turn-on response towards cTnT antigen within a mere 10-min incubation period, boasting an impressive lower detection limit of 0.038 ng/mL. Crucially, our probe demonstrates exceptional selectivity amidst the presence of coexisting biomolecules and ions, ensuring precise detection of cTnT. Moreover, the developed platform showcases promising utility in sensing cTnT from spiked human serum samples, yielding satisfactory recovery percentages ranging from 82 to 105%. Additionally, we introduce and easy-to-use and cost-effective test strip for point-of-care detection of cTnT, further enhancing accessibility to critical cardiovascular diagnostics. [ABSTRACT FROM AUTHOR]

Cardiac fibrosis is featured cardiac fibroblast activation and extracellular matrix accumulation. Ac4C acetylation is an important epigenetic regulation of RNAs that has been recently discovered, and it is solely carried out by NAT10, the exclusive enzyme used for the modification. However, the potential regulatory mechanisms of ac4C acetylation in myocardial fibrosis following myocardial infarction remain poorly understood. In our study, we activated fibroblasts in vitro using TGF‐β1 (20 ng/mL), followed by establishing a myocardial infarction mouse model to evaluate the impact of NAT10 on collagen synthesis and cardiac fibroblast proliferation. We utilized a NAT10 inhibitor, Remodelin, to attenuate the acetylation capacity of NAT10. In the cardiac fibrosis tissues of chronic myocardial infarction mice and cultured cardiac fibroblasts (CFs) in response to TGF‐β1 treatment, there was an elevation in the levels of NAT10 expression. This increase facilitated proliferation, the accumulation of collagens, as well as fibroblast‐to‐myofibroblast transition. Through the administration of Remodelin, we effectively reduced cardiac fibrosis in myocardial infarction mice by inhibiting NAT10's ability to acetylate mRNA. Inhibition of NAT10 resulted in changes in collagen‐related gene expression and ac4C acetylation levels. Mechanistically, we found that NAT10 upregulates the acetylation modification of BCL‐XL mRNA and enhances the stability of BCL‐XL mRNA, thereby upregulating its protein expression, inhibiting the activation of Caspase3 and blocking the apoptosis of CFs. Therefore, the crucial involvement of NAT10‐mediated ac4C acetylation is significant in the cardiac fibrosis progression, affording promising molecular targets for the treatment of fibrosis and relevant cardiac diseases. [ABSTRACT FROM AUTHOR]

Although observational studies have linked primary aldosteronism (PA) with cardiovascular diseases (CVDs), the causality remains uncertain. In this study, we aimed to investigate whether PA is causally associated with CVD risk and cardiac magnetic resonance (CMR) parameters using the Mendelian randomization (MR) method. Independent and genome‐wide significant single nucleotide polymorphisms for PA were extracted from genome‐wide association study (GWAS) summary statistics. Genetic associations with the CVDs and CMR parameters were obtained from recent large‐scale GWASs or genetic consortia. Inverse‐variance weighted (IVW) method was utilized for the preliminary estimates, and multiple sensitivity analyses (including weighted median, Cochran's Q test, MR‐Egger, MR‐PRESSO, and leave‐one‐out analysis) were conducted to verify the robustness of the results. The MR analyses using the IVW method showed that genetically predicated PA was significantly associated with atrial fibrillation (OR = 1.046, 95% CI: 1.029–1.062, padj < 0.001), myocardial infarction (OR = 1.029, 95% CI: 1.005–1.053, padj = 0.027), heart failure (OR = 1.023, 95% CI: 1.004–1.042, padj = 0.027), any stroke (OR = 1.062, 95% CI: 1.031–1.095, padj < 0.001), any ischemic stroke (OR = 1.058, 95% CI: 1.022–1.095, padj = 0.004), and small vessel stroke (OR = 1.116, 95% CI: 1.041–1.196, padj = 0.004). Notably, PA also had a causal effect on adverse cardiac remodeling, including larger ventricular and atrial volumes, higher ventricular stroke volume, and reduced left atrial emptying fraction. Our findings support a causal role of PA in higher cardiovascular disease risk and adverse cardiac remodeling. Given the diagnostic delay and disease burden in PA, more attention should be paid to the screening and treatment of PA to reduce the incidence of cardiovascular outcomes. [ABSTRACT FROM AUTHOR]

Heart failure (HF) remains prevalent in patients who survived myocardial infarction (MI). Despite the accessibility of the primary percutaneous coronary intervention and medications that alleviate ventricular remodeling with functional improvement, there is an urgent need for clinicians and basic scientists to further reveal the mechanisms behind post‐MI HF as well as investigate earlier and more efficient treatment after MI. Growing numbers of studies have highlighted the crucial role of macrophages in cardiac repair and remodeling following MI, and timely intervention targeting the immune response via macrophages may represent a promising therapeutic avenue. Recently, technology such as single‐cell sequencing has provided us with an updated and in‐depth understanding of the role of macrophages in MI. Meanwhile, the development of biomaterials has made it possible for macrophage‐targeted therapy. Thus, an overall and thorough understanding of the role of macrophages in post‐MI HF and the current development status of macrophage‐based therapy will assist in the further study and development of macrophage‐targeted treatment for post‐infarction cardiac remodeling. This review synthesizes the spatiotemporal dynamics, function, mechanism and signaling of macrophages in the process of HF after MI, as well as discusses the emerging bio‐materials and possible therapeutic agents targeting macrophages for post‐MI HF. [ABSTRACT FROM AUTHOR]

We examined the prospective associations of social isolation and loneliness with incident cardiovascular disease (CVD) among aging nonveteran and veteran women, and effect modification by veteran status. Participants with no history of myocardial infarction (MI), stroke, coronary heart disease (CHD), or coronary heart failure from the Women's Health Initiative Extension Study II self-reported social isolation, loneliness, health behaviors, health status, and veteran status. CVD and CVD subevents were physician adjudicated. Hazard ratios (HR) and 95% confidence intervals (CI) for the Interquartile Range (IQR) in social isolation (IQR = 1) and loneliness (IQR=.33) were calculated using Cox proportional hazard models adjusting for sociodemographic, health behavior, and health status characteristics. Veteran status was tested as an effect modifier. Among 52,442 women (Mean age = 79 ± 6.1; veterans n = 1023; 89.2% non-Hispanic White), 3579 major CVD events occurred over an average 5.8 follow-up years. Compared to nonveterans, veteran women reported higher levels of social isolation (p <.01) and loneliness (p <.01). The CVD HR was 1.07 (95% CI, 1.04–1.10) for the IQR in social isolation and 1.03 (95% CI, 1.10–1.06) for the IQR in loneliness. The HR for the IQR in both social isolation and loneliness was 1.10 (95% CI, 1.05–1.15). Social isolation was associated with CHD (HR = 1.12; 95% CI, 1.03–1.21). The CHD HR for the IQR in social isolation was 1.12 (95% CI, 1.03–1.21). Associations did not differ by veteran status (all p-interactions > 0.08). Findings suggest that the adverse associations of social isolation and loneliness with CVD are similar among veteran and nonveteran women. [ABSTRACT FROM AUTHOR]

This study evaluated the role of the mesenchymal stem cells derived from adipose tissue (MSCs) in provoked ventricular arrhythmias (VAs) in animals with myocardial infarction (MI). The experimental groups were: sham, subjected to sham surgery and intramyocardial saline injection; MIV, infarcted rats subjected to intramyocardial saline injection; MI + MSCs, infarcted rats subjected to intramyocardial MSCs injection. Injections were performed two days after infarction and the arrhythmogenic inducibility experiment was performed the next day. Only 35% of the MI + MSCs group developed VAs, while the one in the MIV group was 65%. The proportion of nonsustained ventricular tachycardia, sustained tachycardia, and ventricular fibrillation was similar between the infarcted groups, but MSCs animals had shorter duration of nonsustained ventricular tachycardia. However, MSCs increased connexin 43 content in the remote area, even above the levels found in the sham group. MSCs prevented the increase of IL-1β in the different areas of the myocardium. There was higher carbonylation and content of 4-hydroxynonenal (4-HNE, a marker of lipoperoxidation) in the myocardium of infarcted rats, but MSCs attenuated the increase of 4-HNE in the infarcted area. In conclusion, MSCs have a protective effect against the development of arrhythmias, but do not imply a significant benefit for animals that have developed VAs. It is possible to think that the cardioprotection of MSCs involves anti-inflammatory/oxidative actions and improvement in the formation of communicating junctions. Graphical abstract [ABSTRACT FROM AUTHOR]

Introduction: Chronic myeloid leukemia (CML) is a hematological malignancy with an excellent prognostic outcome. After the advancements in CML treatment and the introduction of different tyrosine kinase inhibitors (TKIs), the life expectancy of CML patients has become equivalent to that of the general population. As a result, coronary artery disease is anticipated to be the leading cause of death among CML patients. Moreover, TKI use is associated with a risk of endothelial dysfunction, thrombosis, and cardiovascular events, including myocardial infarction. In this study, we compare the outcomes of percutaneous coronary intervention (PCI) in patients with CML to their matched non-CML counterparts. Method: This is a retrospective cohort study using the Nationwide Readmission Database from January 2016 to December 2020. Adults with or without CML hospitalized for acute myocardial infarction and underwent PCI were included. The patients were identified using ICD-10 codes. The primary outcomes were in-hospital mortality and 30-day readmission rates. The secondary outcomes were PCI complications rates. Results: Out of 2,727,619 patients with myocardial infarction, 2,124 CML patients were identified. A total of 888 CML patients underwent PCI. CML patients were significantly older (mean age: 68.34 ± 11.14 vs. 64.40 ± 12.61 years, p < 0.001) than non-CML patients without a difference in sex distribution. Hypertension (85.45% vs. 78.64%), diabetes (45.48% vs. 37.29), stroke (11.84% vs. 7.78) at baseline were significantly higher in the CML group. Prior myocardial infarction events (20.51% vs. 15.17%) and prior PCI procedure (24.47% vs. 16.89%) were significantly higher in the CML group. CML patients had a significantly longer hospital stay (4.66 ± 4.40 vs. 3.75 ± 4.62 days, p = 0.001). The primary outcomes did not differ between the comparison groups. The risk of post-PCI complications did not differ between the comparison groups in the propensity matched analysis except for coronary artery dissection (odds ratio [OR]: 0.10; 95% confidence interval [CI]: 0.02–0.65, p = 0.016) and ischemic stroke (OR: 0.35; 95% CI: 0.14–0.93, p = 0.034) which were lower in the CML group. Conclusion: This analysis showed no statistically significant difference in mortality, 30-day readmission, and post PCI complications rates between CML and non-CML patients. However, interestingly, CML patients may experience lower coronary artery dissection and ischemic stroke events than those without CML diagnosis. [ABSTRACT FROM AUTHOR]

Background/Objectives: The impact of alcohol consumption and its restriction on clinical outcomes in patients undergoing percutaneous coronary intervention (PCI) remains elusive. We aimed to investigate the clinical outcomes in drinkers undergoing PCI. Methods: We included 77,409 patients who underwent PCI and a health check-up within one year of the PCI using a nationwide prospective database from the Korean National Health Insurance System. Primary outcomes were major adverse cardiovascular and cerebrovascular events (MACCE), a composite of all-cause mortality, myocardial infarction, coronary revascularization, and stroke. Patients were classified as non-drinkers, within-the-guideline (≤1 standard drink in women and ≤2 in men), and above-the-guideline drinkers based on drinking status at the first health check-up after PCI. Results: During a 4.0-year follow-up duration, MACCE incidence was 19.7% (n = 15,214) (4689 [6.1%] deaths, 1916 [2.5%] MI, 2033 [2.6%] strokes, and 10,086 [13.0%] revascularizations). Both within-the-guideline- (aHR [95%CI], 0.843 [0.773–0.919]) and above-the-guideline drinkers (0.829 [0.784–0.876]) had a lower MACCE risk than the non-drinkers. A characteristic J-curve relationship was observed between the frequency or body weight-adjusted alcohol consumption and MACCE risk, with the lowest risk in the once-per-week and a mild amount per body weight (≤0.33 g/kg/week) group. Drinking habits after PCI were associated with a lower risk of adverse cardiovascular outcomes; those who continued to drink before and after PCI had the lowest risk. Conclusions: Alcohol consumption was associated with a lower risk of adverse outcomes in patients undergoing PCI. Further studies with longer-term follow-up are warranted. [ABSTRACT FROM AUTHOR]

Dual antiplatelet therapy (DAPT), which is essential in AMI management, combines aspirin with a P2Y12 receptor antagonist. This study compared the effectiveness of potent P2Y12 inhibitors versus clopidogrel in AMI patients treated with percutaneous coronary intervention (PCI). Methods: 65,986 AMI patients included in a nationwide prospective registry who underwent PCI and received DAPT were studied. In total, 9,014 patients received potent P2Y12 inhibitors, and 56,074 received clopidogrel. This study focused on mortality, recurrent myocardial infarction, stroke, repeat revascularization, and major adverse cardiovascular events (MACE) over seven years. The analysis utilized unadjusted models and inverse probability of treatment weighting (IPTW) to compare prognosis, and decision curve analyses were constructed to aid clinical decision making. Results: Potent P2Y12 inhibitors significantly reduced mortality risk (unadjusted hazard ratio (HR): 0.58; IPTW HR: 0.68) and MACE (unadjusted HR: 0.66; IPTW HR: 0.78). Diabetic patients showed greater benefits (HR:0.45). In patients at high bleeding risk, the mortality rate was 13% (HR: 0.87, p = 0.08). For patients aged 75–79, the HR for mortality was 0.82, whereas for those aged >80 years, it was 0.79, indicating significant mortality risk reduction. Similar trends were observed for MACE. Conclusion: This study demonstrated that potent P2Y12 inhibitors are more effective than clopidogrel in reducing mortality and MACE in patients with AMI and underscored their potential role in improving outcomes across diverse patient subgroups. The trend was consistent even during the COVID-19 pandemic. These findings highlight the need for personalized DAPT strategies, particularly for high-bleeding-risk patients, and challenge current guidelines favoring clopidogrel use in older patients. [ABSTRACT FROM AUTHOR]

Background/Objectives: In recent decades, the number of patients with chronic cardiovascular diseases (CVDs) has increased, and CVD survivors are more likely to be old and frail and to have multiple comorbidities. A better understanding of geriatric conditions and their prevalence would help improve the management of older patients with CVDs. The main objective of this study is to estimate the association of myocardial infarction (MI) history with geriatric syndromes (GSs) in people 65 years of age and older. Methods: The cross-sectional study EVKALIPT included patients who were 65 years of age and older. All patients underwent a comprehensive geriatric assessment. The presence of MI history was assessed by medical records. Results: A total of 4295 participants were included. The prevalence of MI history was 12.6%. According to univariate regression analysis, MI history was associated with an increase in the odds of 12 GSs by 1.3–2.4 times. Multivariate regression analysis showed that male sex and four GSs (impairment in basic and instrumental activities of daily living, depression, falls) were independently associated with a history of MI, with the odds ratio ranging from 1.28 to 1.86. Conclusions: This study showed the association between MI history and GSs. [ABSTRACT FROM AUTHOR]

The document discusses the association between high red cell mass (RCM) and high plasma volume with thrombotic risk in polycythemia vera (PV) patients. The study included 211 PV patients from Serbia and Croatia and found that patients with both high RCM and high plasma volume had the highest risk of thrombotic events. The findings suggest that RCM and plasma volume measurements may be important for prognostic purposes in PV, highlighting the need for further research and validation of these results in larger datasets and different populations. [Extracted from the article]

Mesenchymal stem cell (MSC) therapy aids cardiac repair and regeneration, but the low rate of MSC survival and engulfment in the infarcted heart remains a major obstacle for routine clinical application. Here, an injectable suspension of human acellular amniotic membrane (HAAM) that may serve as synergistic cell delivery vehicle for the treatment of myocardial infarction (MI) by improving MSC homing and survival is developed. The results demonstrate that compared with MSC transplantation alone, HAAM‐loaded MSCs have higher survival and engraftment rates in infarcted tissue, alleviated hypoxia‐induced myocardial damage, achieved higher improvements in cardiac function, promoted angiogenesis, and reduced myocardial fibrosis. In addition, HAAM‐loaded MSCs increase N‐cadherin levels and thereby enhance the efficacy of MSCs in treating MI. This study provides a new approach for MSC‐based cardiac repair and regeneration. [ABSTRACT FROM AUTHOR]

Mesenchymal stem cell (MSC)‐derived extracellular vesicles (EVs) are a promising treatment for myocardial infarction (MI), but their therapeutic efficacy is limited by inefficient accumulation at the target site. A minimally invasive MSC EV therapy that enhances EV accumulation at the disease site and extends EV retention could significantly improve post‐infarct cardiac regeneration. Here, we show that EVs decorated with the next‐generation of high‐affinity (HiA) heterodimerizing leucine zippers, termed HiA Zippersomes, amplify targetable surface areas through in situ crosslinking and exhibited ~7‐fold enhanced accumulation within the infarcted myocardium in mice after 3 days and continued to be retained up to Day 21, surpassing the performance of unmodified EVs. After MI in mice, HiA Zippersomes increase the ejection fraction by 53% and 100% compared with unmodified EVs and phosphate‐buffered saline (PBS), respectively. This notable improvement in cardiac function played a crucial role in restoring healthy heart performance. HiA Zippersomes also robustly decrease infarct size by 52% and 60% compared with unmodified EVs and PBS, respectively, thus representing a promising platform for minimally invasive vesicle delivery to the infarcted heart compared to intramyocardial injections. [ABSTRACT FROM AUTHOR]

Background: The risk of life‐threatening major cardiovascular outcomes among patients with bullous pemphigoid (BP) is inconsistent in the current literature. Objective: To evaluate the risk and prognostic outcomes of myocardial infarction (MI), cerebrovascular accident (CVA), peripheral vascular disease (PVD) and pulmonary embolism (PE) in patients with BP. We additionally aimed to explore the influence of different therapeutic approaches on the risk of these outcomes. Methods: A population‐based retrospective cohort study was conducted to compare BP patients (n = 3924) with age‐, gender‐ and ethnicity‐matched control subjects (n = 19,280) with regard to incident cases of MI, CVA, PVD and PE. Adjusted hazard ratio (HR) and 95% confidence intervals (CI) were estimated by multivariate Cox regression analysis. Data were retrieved from Clalit Health Services' computerized database. Results: Relative to their matched controls, patients with BP were at an elevated risk of MI (fully‐adjusted HR: 1.44; 95% CI: 1.14–1.81; p = 0.002), CVA (fully‐adjusted HR: 1.24; 95% CI: 1.06–1.45; p = 0.007), PVD (fully‐adjusted HR: 1.60; 95% CI: 1.27–2.03; p = 0.003) and PE (fully‐adjusted HR: 1.72; 95% CI: 1.28–2.32; p < 0.008). Patients with BP experienced heightened risk of all‐cause mortality in the presence of comorbid MI (fully‐adjusted HR: 1.61; 95% CI: 1.44–1.81; p < 0.001), CVA (fully‐adjusted HR: 1.70; 95% CI: 1.52–1.89; p < 0.001), PVD (fully‐adjusted HR: 1.38; 95% CI: 1.20–1.58; p < 0.001) and PE (fully‐adjusted HR: 1.44; 95% CI: 1.10–1.88; p = 0.007). The therapeutic approach utilized to manage BP did not significantly influence the risk of cardiovascular outcomes. Conclusions: BP is associated with an elevated risk of MI, CVA, PVD, PE and cardiovascular mortality. Primary, secondary and tertiary cardiovascular prevention measures should be implemented among patients with BP. [ABSTRACT FROM AUTHOR]

Recent progress in developing cardiac patches for regenerating the myocardium has opened a new hope after myocardial infarction (MI). Herein, we introduce a novel bilayer nanofiber cardiac patch composed of polycaprolactone (PCL), poly(xylitol sebacate) (PXS), and multi-walled carbon nanotubes (MWCNTs). First, we electrospun different monolayer scaffolds, including PCL, PCL/MWCNT, PCL/PXS, and PCL/PXS/MWCNTs, and characterized their physical, mechanical, and biological performance to determine the interaction effects of different material compositions on their scaffold properties. In vitro examinations confirmed the cooperative effect of PXS and MWCNT in blending with PCL to fabricate conductive and well-organized nanofibers with good biocompatibility. Subsequently, a bilayer nanofiber scaffold composed of PCL/PXS/MWCNT nanofibers electrospun over a PCL fibrous layer was fabricated to achieve an efficient structure capable of providing the desirable characteristics of a cardiac patch. The bilayer nature increased the mechanical performance of the PCL/PXS/MWCNT monolayer while preserving its appropriate wettability and acceptable conductivity. Excellent viability and proliferation of H9c2 cells on the bilayer scaffolds were observed in the live/dead assay. Moreover, cell-matrix interaction confirmed that bilayer nanofibers decrease myofibroblast differentiation of seeded NIH3T3 cells, which may be beneficial for cardiac repair post-MI. After transplantation of the bilayer nanofiber onto the infarcted heart of the MI rats for 4 weeks, the ischemic zone decreased, cardiac function significantly improved and very slightly activated macrophages were observed. These findings suggested a potentially durable nanofiber cardiac patch containing PXS for myocardial repair post-MI. [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI) is a critical global health issue and a leading cause of heart failure. Indeed, while neonatal mammals can regenerate cardiac tissue mainly through cardiomyocyte proliferation, this ability is lost shortly after birth, resulting in the adult heart's inability to regenerate after injury effectively. In adult mammals, the adverse cardiac remodelling, which compensates for the loss of cardiac cells, impairs cardiac function due to the non-contractile nature of fibrotic tissue. Moreover, the neovascularisation after MI is inadequate to restore blood flow to the infarcted myocardium. This review aims to synthesise the most recent insights into the molecular and cellular players involved in endogenous myocardial and vascular regeneration, facilitating the identification of mechanisms that could be targeted to trigger cardiac regeneration, reduce fibrosis, and improve functional recovery post-MI. Reprogramming adult cardiomyocytes to regain their proliferative potential, along with the modulation of target cells responsible for neovascularisation, represents promising therapeutic strategies. An updated overview of endogenous mechanisms that regulate both myocardial and coronary vasculature regeneration—including stem and progenitor cells, growth factors, cell cycle regulators, and key signalling pathways—could help identify new critical intervention points for therapeutic applications. [ABSTRACT FROM AUTHOR]

The structure of aspirated coronary thrombus in ST-segment elevation myocardial infarction (STEMI) is still being studied. Our aims were to characterize coronary thrombi of different ages, focusing on the appearance of activated protein C (APC/PC) and its relation to the elements of neutrophil extracellular traps (NETs), and the factors closely related to fibrin as factor XIII (FXIII) and α2 plasmin inhibitor (α2-PI). The thrombi of n = 24 male patients with atherosclerotic coronary plaque rupture related to native coronary artery occlusion were selected for histopathology analysis. Thrombus age was distinguished as fresh, lytic, and organized, and then analyzed by immunofluorescent staining and confocal microscopy. FXIII was present at a high level and showed a high degree of co-localization with fibrin in all stages of thrombus evolution. The amount of α2-PI was low in the fresh thrombi, which increased significantly to the lytic phase. It was evenly distributed and consistently associated with fibrin. APC/PC appeared in the fresh thrombus and remained constant during its evolution. The presence of NET marker and CD66b was most dominant in the lytic phase. APC/PC co-localization with the elements of NET formation shows its role in NET degradation. These observations suggest the importance of searching for further targeted therapeutic strategies in STEMI patients. [ABSTRACT FROM AUTHOR]

Background The utilization of postdilatation in primary percutaneous coronary intervention (PCI) is feared to induce suboptimal coronary blood flow and compromise the outcome of the patients. This meta-analysis sought to verify whether postdilatation during primary PCI is associated with worse angiographic or long-term clinical outcomes. Methods Systematic literature searches were conducted on PubMed, The Cochrane Library, ClinicalTrials.gov , EBSCO, and Europe PMC on 10 March 2024. Eligible studies reporting the outcomes of postdilatation among ST-segment elevation myocardial infarction patients were included. The primary outcome was no-reflow condition during primary PCI based on angiographic finding. The secondary clinical outcome was major adverse cardiovascular events (MACEs) comprising all-cause death, myocardial infarction, target vessel revascularization (TVR), and stent thrombosis. Results Ten studies were finally included in this meta-analysis encompassing 3280 patients, which was predominantly male (76.6%). Postdilatation was performed in 40.7% cases. Postdilatation was associated with increased risk of no-reflow during primary PCI [Odd Ratio (OR) = 1.33, 95% Confidence Interval (CI): 1.12–1.58; P =.001)]. Conversely, postdilatation had a tendency to reduce MACE (OR = 0.70, 95% CI: 0.51–0.97; P =.03) specifically in terms of TVR (OR = 0.41, 95% CI: 0.22–0.74; P =.003). No significant differences between both groups in relation to mortality (OR = 0.58, 95% CI: 0.32–1.05; P =.07) and myocardial infarction (OR = 1.5, 95% CI: 0.78–2.89; P =.22). Conclusions Postdilatation after stent deployment during primary PCI appears to be associated with an increased risk of no-reflow phenomenon after the procedure. Nevertheless, postdilatation strategy has demonstrated a significant reduction in MACE over the course of long-term follow-up. Specifically, postdilatation significantly decreased the occurrence of TVR. Key messages: What is already known on this topic? Optimizing stent deployment by performing postdilatation during percutaneous coronary intervention (PCI) is essential for long-term clinical outcomes. However, its application during primary PCI is controversial due to the fact that it may provoke distal embolization and worsen coronary blood flow. What this study adds? In this systematic review and meta-analysis of 10 studies, we confirm that postdilatation during primary PCI is associated with worse coronary blood flow immediately following the procedure. On the contrary, this intervention proves advantageous in improving long-term clinical outcomes, particularly in reducing target vessel revascularization. How this study might affect research, practice, or policy? Given the mixed impact of postdilatation during primary PCI, this strategy should only be applied selectively. Future research should focus on identifying patients who may benefit from such strategy. [ABSTRACT FROM AUTHOR]