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Reducing the price of expensive medical products through centralized procurement is generally considered an effective way to save public medical resources. Against this background, this paper presents an analysis of the impact of centralized procurement in China by comparing the treatment costs and patterns for acute myocardial infarction (AMI) patients before and after the introduction of this method of purchasing, with specific reference to the use of coronary stents. We found that, after the implementation of centralized procurement for coronary stents, the total expenditure of AMI cases receiving percutaneous coronary interventions with stent implantation (PCI with stents) dropped by 23.4%. The use rate of PCI with stents decreased by 32.5%, with the most significant decrease being evident in cases in which two stents were used simultaneously (32.9%). Meanwhile, percutaneous coronary interventions with balloon implantation (PCI with balloons) increased by 31.5% and coronary artery bypass grafting (CABG) increased by 80.3%. Based on these patterns, it can be observed that the use of centralized procurement significantly reduced the profits of the relevant medical manufacturers, forcing them to decrease their marketing investments, weakening their influence on providers, and ultimately resulting in a more principled use of coronary stents. We therefore conclude that, with reference to the data cited, the centralized procurement program led not only to a reduction in procurement prices but also to decreased overuse of these expensive medical products.

Exosomes derived from bone marrow mesenchymal stem cells (BMSCs) exhibit considerable therapeutic potential for myocardial regeneration. In our investigation, we delved into their impact on various aspects of myocardial infarction (MI), including cardiac function, tissue damage, inflammation, and macrophage polarization in a murine model. We meticulously isolated the exosomes from TNF-α-treated BMSCs and evaluated their therapeutic efficacy in a mouse MI model induced by coronary artery ligation surgery. Our comprehensive analysis, incorporating ultrasound, serum assessment, Western blot, and qRT-PCR, revealed that exosomes from TNF-α-treated BMSCs demonstrated significant therapeutic potential in reducing MI-induced injury. Treatment with these exosomes resulted in improved cardiac function, reduced infarct area, and increased left ventricular wall thickness in MI mice. On a mechanistic level, exosome treatment fostered M2 macrophage polarization while concurrently suppressing M1 polarization. Hence, exosomes derived from TNF-α-treated BMSCs emerge as a promising therapeutic strategy for alleviating MI injury in a mouse model.

Cardiac fibrosis is associated with myocardial remodeling following myocardial infarction (MI), which can lead to heart failure, arrhythmias, and even death. This study aimed to determine the effects of tubuloside A (TA) on cardiac fibrosis after MI and elucidate their underlying molecular mechanisms. Rats were divided into the following groups: sham (fake surgery), MI, MI + 1 mg/kg TA, and MI + 3 mg/kg TA. Compared with MI, the addition of TA significantly reduced mortality, improved cardiac function, decreased infarct size, and inhibited myocardial injury and fibrosis. To verify the direct targets of TA, we used cellular thermal shift assay and drug affinity responsive target stability to analyze drug-protein interactions and discovered that TA can bind directly to TGM2 and inhibit its enzymatic activity. Furthermore, to investigate whether TA can inhibit the TGF-β1-mediated activation of cardiac fibroblasts (CFs) through TGM2, we overexpressed TGM2 in CF cells and treated them with TA. We found that TA inhibited the activity of TGM2 in CF cells and reduced α-SMA, collagen-I, and collagen-III levels, thereby inhibiting the progression of fibrosis. Similarly, we found that TA could exert anti-inflammatory and antiapoptotic effects by inhibiting TGM2. Overall, we demonstrated that TA is a potential candidate drug for inhibiting the impacts of myocardial infarction and cardiac fibrosis, reducing postinfarction fibrosis by inhibiting the NF-κB signaling pathway and suppressing mitochondrial pathway-mediated apoptosis. Therefore, focusing on drug discovery strategies for TA may provide a promising therapeutic approach for MI., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Elderly patients are often under-represented in studies about coronary revascularization in acute coronary syndromes (ACS) and undertreated in clinical practice. We sought to evaluate differences in outcomes between an initial invasive or conservative strategy in this subset of patients, METHODS: The analysis was performed following PRISMA guidelines. Randomized controlled trials (RCTs) and adjusted observational studies comparing an invasive and conservative strategy in old patients with ACS were systematically identified. Random or fixed effect model was used accordingly to heterogeneity testing results. Short-term mortality was the primary outcome. 30-day and longer-term re-infarction, MACE and all-cause mortality were secondary endpoints. Sensitivity analysis including RCTs only were performed for the primary endpoint and 1 year mortality and another analysis, stratifying NSTEMI and STEMI studies, was performed for short-term mortality., Results: Invasive management was associated with lower short and long-term mortality (30 days OR 0.64, 95 % CI 0.54-0.76, p < 0.001; 1 year HR 0.60, 95 % CI 0.52-0.78, p < 0.001; Long-term HR 0.62, 95 % CI 0.55-0.71, p < 0.001) compared to a conservative strategy. In the short-term follow-up, the benefit was preserved when differentiating for NSTEMI or STEMI studies but not when considering only RCTs. Major bleedings were more frequent in the invasive group (30 days OR 1.61, 95 % CI 1.39-1.87, p < 0.001). The mean difference in length of stay was not significantly different between the two strategies (mean difference in days 0.14, 95 % CI -0.79 to 1.06, p = 0.77)., Conclusion: An initial invasive strategy might lead to reduced short and long-term mortality in elderly patients presenting with acute coronary syndrome but it is associated with increased bleeding events rate. No difference in hospital stay length was observed. Results were mainly driven by non-randomized studies., Competing Interests: Declaration of competing interest The authors declare no conflict of interest., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Given the global prevalence of myocardial infarction (MI) as the leading cause of mortality, there is an urgent need to devise novel strategies that target reducing infarct size, accelerating cardiac tissue repair, and preventing detrimental left ventricular (LV) remodeling. Macrophages, as a predominant type of innate immune cells, undergo metabolic reprogramming following MI, resulting in alterations in function and phenotype that significantly impact the progression of MI size and LV remodeling. This article aimed to delineate the characteristics of macrophage metabolites during reprogramming in MI and elucidate their targets and functions in cardioprotection. Furthermore, we summarize the currently proposed regulatory mechanisms of macrophage metabolic reprogramming and identify the regulators derived from endogenous products and natural small molecules. Finally, we discussed the challenges of macrophage metabolic reprogramming in the treatment of MI, with the goal of inspiring further fundamental and clinical research into reprogramming macrophage metabolism and validating its potential therapeutic targets for MI., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)

Objective: To investigate the most common causes of death and trends in cause-specific long-term mortality in patients hospitalized for acute myocardial infarction (AMI)., Methods: This analysis was based on 10,718 patients, aged 25-74 years, recorded by the population-based Myocardial Infarction Registry Augsburg between 2000 and 2017. All hospitalized cases of AMI occurring in the study region during this period were included. If a patient died during follow-up (median: 6.6 years, IQR: 2.8-11.2) the death certificate was obtained and coded using the ICD-10 to determine the main cause of death. Cause-specific mortality was calculated for three 6-year periods. Multivariable adjusted Cox regression models stratified by time interval were calculated., Results: The most common cause of death was cardiovascular disease (CVD), more precisely ischemic-heart disease (IHD), followed by cancer. The proportions of CVD deaths and IHD deaths were stable over time. An increasing trend was observed in cancer mortality in post-AMI patients. In male patients, the hazard ratio for cancer mortality was 44.4% higher in 2012-2017 compared to 2000-2005, in female patients, it was more than twice as high in 2006-2012 compared to 2000-2005., Conclusion: This study revealed consistent CVD and IHD long-term mortality and increasing trends in long-term cancer mortality in patients post-AMI. Thus, post-AMI patients should emphasize tertiary prevention of CVD by minimizing risk factors. Furthermore, patients should regularly undergo cancer screening programs. The reasons for the unfavorable development in terms of increasing cancer mortality should be investigated in further studies.

Purpose: Lifestyle advice for cardiac patients with overweight/obesity includes weight management, yet few achieve significant weight loss. People with heart disease may require different support to the general population. We synthesized evidence that reported cardiac patients' weight management experiences to identify barriers and facilitators to weight loss., Methods: Our realist review identified five manuscripts reporting four studies of weight management experiences of people with heart disease. The capability, opportunity, motivation behaviour change model (COM-B) provided the framework for thematic synthesis., Results: The studies included qualitative data from 117 participants and revealed factors favouring or impeding effective weight management during cardiac rehabilitation (CR) and in participants' daily lives. We identified four major themes illustrating participants' wish to change harmful health behaviours, adopting exercise and psychological strategies to facilitate change, social and professional support, and regaining control after a cardiac event. These themes broadly aligned with the COM-B categories of capability, opportunity, and motivation., Conclusions: Most cardiac patients with overweight/obesity express a desire to lose weight. Participants preferred personalized services that could adapt to meet their individual needs, but struggled to make sustainable changes for interconnecting psychological, social, cultural, and financial reasons. Consideration of these complexities when designing programmes may help to support successful weight management.

Purpose: Cardiovascular diseases (CVDs) are a leading cause of morbidity and mortality worldwide. Ischemic heart diseases, particularly acute myocardial infarction (MI), represent the most common cause of death. MI is influenced by multiple factors, including the release of inflammatory mediators. A significant percentage of individuals with CVD experience psychological effects, such as anxiety and depression, which are linked to an increased risk of coronary heart disease. Certain anti-anxiety medications have demonstrated immunomodulatory and anti-inflammatory effects. Tofisopam, a 2,3-benzodiazepine with anxiolytic properties, has been shown to exert in vitro anti-inflammatory and immunomodulatory effects. The present study investigates the potential of tofisopam as a protective adjuvant against isoprenaline-induced MI in rats and explores the possible underlying mechanisms., Methods: The study included four groups: a control group, a group pretreated with tofisopam, an isoprenaline toxic group, and an isoprenaline toxic group pretreated with tofisopam., Results: The findings demonstrated that isoprenaline significantly increased cardiac enzyme levels, as well as elevated oxidative and inflammatory stress parameters, along with evident apoptosis in cardiac cells. In contrast, the tofisopam-pretreated group showed a significant reversal of the cardiac damage induced by isoprenaline., Conclusions: Tofisopam protects against isoprenaline-induced MI through its antioxidant, anti-inflammatory, and anti-apoptotic properties.

Aim: To explore the association of hyperhomocysteinaemia (HHcy) and diabetes synergies with cardiovascular events in the adult population of northern China., Methods: Data were collected from the Asymptomatic Polyvascular Abnomalities Community study for 2010 to 2019. Serum homocysteine (Hcy) levels were determined by enzyme-linked immunosorbent assay. The participants were categorized into four groups based on their Hcy levels and diabetes status: non-diabetes/non-HHcy, non-diabetes/HHcy, diabetes/non-HHcy and diabetes/HHcy. The composite endpoint consisted of the occurrence of first-ever stroke, myocardial infraction (MI) or all-cause mortality. Cox regression analyses were performed to evaluate the associations of diabetes and HHcy with cardiovascular disease (CVD) events., Results: In total, 5278 participants were eligible (average age 55.1 years, 60% male). Over a follow-up of 9.1 years, 618 events were identified, 202 stroke, 52 MI and 406 all-cause deaths. Compared with the non-diabetes/non-HHcy group, hazard ratios with 95% confidence intervals in the diabetes/HHcy group for stroke, MI, major adverse cardiovascular event (MACE), all-cause death and composite endpoint were 1.85 (1.12-3.04), 1.33 (0.42-4.23), 1.78 (1.13-2.80), 2.24 (1.56-3.23) and 1.97 (1.47-2.65), respectively. Significant interactions between HHcy and diabetes status were found for stroke, MI and MACE (P for interaction = .002, .027 and .044, respectively). In addition, the association of diabetes/HHcy with stroke was modified by age (< 60 and ≥ 60 years; P for interaction = .016)., Conclusions: The findings highlight the synergistic impact of diabetes and HHcy on CVD. Joint assessments of diabetes and Hcy levels should be emphasized for risk stratification and primary prevention of CVD., (© 2024 The Author(s). Diabetes, Obesity and Metabolism published by John Wiley & Sons Ltd.)

Background: The aim of the current study is to identify the possible protective effect of bupropion (BUP) on liver injury in rat model of myocardial infarction (MI). BUP was administered in the presence and absence of MI., Materials and Methods: Thirty-two Wistar adult male rats were randomly arranged into four groups: control, BUP (30 mg/kg/day, intraperitoneal) for 28 days, isoproterenol (ISO) was injected subcutaneous (85 mg/kg) in the 26th and 27th days and BUP/ISO groups. Cardiac and hepatic enzymes were measured, also Hepatic oxidative stress indicators, as well as inflammatory and apoptotic biomarkers, were evaluated. Cardiac and hepatic histopathological examination and hepatic nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) immunohistochemical study were also detected., Results: ISO significantly increased cardiac and hepatic enzymes, hepatic oxidative stress, inflammatory, apoptotic, with a histopathological picture of cardiac and hepatic damage and high hepatic NF-κB immunoexpression were detected. BUP significantly normalized the upraised oxidative, inflammatory, and apoptotic parameters, with an impressive improvement in the histopathological picture and a reduction in hepatic NF-κB immunoexpression., Conclusion: BUP protects against liver injury on top of MI in rat model via modulation of Sirtuin type 1 (Sirt1)/Nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/tumor necrosis factor α (TNFα); Toll-like receptor 4 (TLR4)/Hepatic myeloid differentiation primary response 88(Myd88)/NF-κB signaling pathways.

Endothelial dysfunction is an early consequence of vascular inflammation and a driver of coronary atherosclerotic disease leading to myocardial infarction. The red blood cells (RBCs) mediate endothelial dysfunction in patients at cardiovascular risk, but their role in patients with acute myocardial infarction is unknown. This study aimed to investigate if RBCs from patients with ST-elevation myocardial infarction (STEMI) induced endothelial dysfunction and the role of systemic inflammation in this effect. RBCs from patients with STEMI and aged-matched healthy controls were coincubated with rat aortic segments for 18 h followed by evaluation of endothelium-dependent (EDR) and endothelium-independent relaxation (EIDR). RBCs and aortic segments were also analyzed for arginase and oxidative stress. The patients were divided into groups depending on C-reactive protein (CRP) levels at admission. RBCs from patients with STEMI and CRP levels ≥2 mg/L induced impairment of EDR, but not EIDR, compared with RBCs from STEMI and CRP <2 mg/L and healthy controls. Aortic expression of arginase 1 was increased following incubation with RBCs from patients with STEMI and CRP ≥2, and arginase inhibition prevented the RBC-induced endothelial dysfunction. RBCs from patients with STEMI and CRP ≥2 had increased reactive oxygen species compared with RBCs from patients with CRP <2 and healthy controls. Vascular inhibition of NADPH oxidases and increased dismutation of superoxide improved EDR. RBCs from patients with STEMI and low-grade inflammation induce endothelial dysfunction through a mechanism involving arginase 1 as well as increased RBC and vascular superoxide by NADPH oxidases. NEW & NOTEWORTHY Red blood cells from patients with STEMI and systemic inflammation induce endothelial dysfunction ex vivo. The RBC-induced endothelial dysfunction is mediated through increased arginase 1 and a shift in the redox balance toward oxidative stress. Inhibition of arginase or free radicals attenuates the impairment of endothelial function. The study suggests that red blood cells deserve attention as a key player in systemic inflammation and STEMI.

Myocardial infarction (MI) is a lethal cardiovascular disease worldwide. Emerging evidence has revealed the critical role of gut dysbiosis and impaired gut-brain axis in the pathological progression of MI. Tanshinone IIA (Tan IIA), a traditional Chinese medicine, has been demonstrated to exert therapeutic effects for MI. However, the effects of Tan IIA on gut-brain communication and its potential mechanisms post-MI are still unclear. In this study, we initially found that Tan IIA significantly reduced myocardial inflammation, apoptosis and fibrosis, therefore alleviating hypertrophy and improving cardiac function following MI, suggesting the cardioprotective effect of Tan IIA against MI. Additionally, we observed that Tan IIA improved the gut microbiota as evidenced by changing the α-diversity and β-diversity, and reduced histopathological impairments by decreasing inflammation and permeability in the intestinal tissues, indicating the substantial improvement of Tan IIA in gut function post-MI. Lastly, Tan IIA notably reduced lipopolysaccharides (LPS) level in serum, inflammation responses in paraventricular nucleus (PVN) and sympathetic hyperexcitability following MI, suggesting that restoration of Tan IIA on MI-induced brain alterations. Collectively, these results indicated that the cardioprotective effects of Tan IIA against MI might be associated with improvement in gut-brain axis, and LPS might be the critical factor linking gut and brain. Mechanically, Tan IIA-induced decreased intestinal damage reduced LPS release into serum, and reduced serum LPS contributes to decreased neuroinflammation with PVN and sympathetic inactivation, therefore protecting the myocardium against MI-induced injury., Competing Interests: Declarations Conflict of interest The authors declare that they have no known competing financial interest or personal relationships that could have appeared to influence the work reported in this paper. Ethical Approval All the animal experiments were approved by Xi’an Jiaotong University Laboratory Animal Administration Committee and were carried out strictly in accordance with Xi’an Jiaotong University Guidelines for Animal Experimentation. Consent to Participate Authors give full consent to participate. Consent for Publication Authors give full consent for publication., (© 2024. The Author(s).)

Background: Our prior research determined that USP7 exacerbates myocardial injury. Additionally, existing studies indicate a strong connection between USP7 and ferroptosis. However, the influence of USP7 on ferroptosis-mediated myocardial infarction (MI) remains unclear. Given these findings, we are particularly interested in USP7's regulatory role in ferroptosis-mediated MI and its underlying mechanisms., Methods: In this study, we established MI models and lentivirus-transfected groups to inhibit USP7 expression both in vivo and in vitro. Cardiac function was detected with Echocardiography. TTC and HE staining were employed to assess myocardial alterations. The expression of ferroptosis markers (PTGS2, ACSL4, GPX4) were analyzed by RT-qPCR and Western blotting. Flow cytometry and ELISA were used for measuring Fe 2+ , lipid ROS, GSH, and GSSG levels. TEM and Prussian blue staining were used to observe mitochondrial alterations and iron deposition. RT-qPCR, Western blotting, and immunofluorescence were conducted to analyze Keap1, Nrf2, and nuclear Nrf2 expression in vitro and in vivo., Results: In the MI model group, USP7 expression significantly increased, worsening ferroptosis-mediated MI. Conversely, in the USP7-inhibited group, activation of the Keap1-Nrf2 signaling pathway improved ferroptosis-mediated MI outcomes. In vitro, the MI model exhibited a marked decline in cardiomyocyte viability and notable mitochondrial damage. However, these issues improved in the USP7-inhibited groups. In vivo, USP7 intensified MI and iron deposition within the MI model group, with decreased values of LVEF, LVFS, SV, LVAWd, and LVPWs, all of which showed improvement in the USP7-inhibited group, except for LVPWd and LVPWs, which showed no significant variation. Importantly, both the in vitro and in vivo experiments revealed analogous results: a reduction in Keap1 expression and an increase in both Nrf2 and nuclear Nrf2 post USP7 inhibition. Additionally, GPX4 expression decreased while PTGS2 and ACSL4 expressions increased. Notably, concentrations of Fe 2+ , lipid ROS, GSH, and GSSG significantly decreased., Conclusion: In vitro and in vivo studies have found that inhibition of USP7 attenuates iron deposition and suppresses oxidative stress, resulting in amelioration of ferroptosis-induced MI., Competing Interests: Declaration of competing interest The authors have declared that they have no conflicts of interest., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Whether physiology-guided complete revascularization of nonculprit lesions is superior to culprit lesion-only percutaneous coronary intervention (PCI) in patients with myocardial infarction (MI) and multivessel disease remains debated. Online databases were searched for randomized controlled trials comparing physiology-guided complete revascularization and culprit lesion-only PCI in patients with MI. The outcomes of interest were all-cause death, cardiovascular (CV) death, repeat revascularization, MI, stent thrombosis, and contrast-associated nephropathy/acute kidney injury. Pooled odds ratios, along with 95% confidence intervals (CI) were calculated. A total of 4,849 patients (n = 2,288 physiology-guided complete revascularization, n = 2,561 culprit lesion-only PCI) were included. The mean age was 66 years and 76% were men. At a mean follow-up of 2.5 years, physiology-guided complete revascularization was associated with significant reductions in CV death (odds ratio 0.72, 95% CI 0.54 to 0.97, p = 0.03) and repeat revascularizations (0.50, 95% CI 0.38 to 0.66, p <0.00001) compared with culprit lesion-only PCI. There were no differences between the 2 approaches in all-cause death (0.91, 95% CI 0.69 to 1.19, p = 0.50), MI (0.85, 95% CI 0.59 to 1.21, p = 0.36), stent thrombosis (1.24, 95% CI 0.58 to 2.69, p = 0.58), and contrast-associated nephropathy/acute kidney injury (1.07, 95% CI 0.88 to 1.31, p = 0.50). In conclusion, among patients with MI and multivessel disease, physiology-guided complete revascularization was associated with significant reductions in CV death and revascularizations compared with culprit lesion-only PCI., Competing Interests: Declaration of competing interest J. Dawn Abbott - research (Boston Scientific, Shockwave, Med Alliance), consulting (Medtronic, Recor, Abbott, Penumbra). Aakash Garg - speaker for edwards Lifesciences. All other authors have no competing interests to declare., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Persistent post-COVID conditions (PCCs) have become inevitable challenges for individuals who have survived COVID. The National Research Plan on Long COVID-19 underscores the priority of addressing post-COVID conditions (PCCs) within specific subgroups of the United States (US) population. This study aimed to investigate the prevalence and factors associated with PCCs among stroke survivors in the US., Method: In this retrospective cross-sectional study, we utilized the Behavioral Risk Factor Surveillance System (BRFSS) 2022 dataset. First, we identified respondents with a positive history of both COVID-19 and stroke. Subsequently, we categorized these respondents based on whether they experienced PCCs and conducted a comparative analysis of their characteristics. Additionally, our study included a comparison of our findings with those among individuals who have survived myocardial infarction (MI) and cancer., Results: A total of 3999 stroke, 5406 MI, and 10551 cancer survivors were included. The estimated prevalence of PCCs among stroke survivors was 30.6 %, compared to 22.4 %, 29.2 %, and 24.6 % among non-stroke (p < 0.001), MI, and cancer survivors, respectively. Fatigue, dyspnea, and taste/smell loss were the most common primary symptoms. In multivariate regression analysis, female sex (adjusted odds ratio (aOR):1.62, 95 %CI:[1.17-2.24]), stroke-belt residence (aOR:1.67, 95 %CI: [1.13-2.46]), pulmonary disease (aOR:2.12, 95 %CI:[1.53-2.92]), and depression (aOR:1.55, 95 %CI: [1.1-2.2]) were independent factors associated with higher odds of PCCs among stroke survivors. Additionally, age above 64 years was associated with lower odds of PCCs (aOR:0.6, 95 %CI: [0.41-0.86])., Conclusion: Our study highlights a considerable prevalence of PCCs among stroke survivors, particularly among younger women and individuals with other chronic conditions., Competing Interests: Declaration of competing interest None., (Copyright © 2024. Published by Elsevier Inc.)

Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Left ventricular (LV) thrombus formation remains a post-acute myocardial infarction (AMI) complication even in the modern era of early reperfusion. The optimal anticoagulation regimen in this clinical scenario is poorly defined. The present meta-analysis sought to investigate the efficacy and safety profile of direct oral anticoagulants (DOACs) compared with vitamin K antagonists (VKAs) for the management of LV thrombus after AMI. A systematic literature review was conducted in electronic databases to identify studies reporting efficacy and safety outcome data regarding the use of DOACs versus VKAs for patients with LV thrombus after AMI. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated, and random-effects meta-analyses were conducted to synthesize pooled ORs. Eight studies comprising a total of 605 patients were included. DOACs were associated with an almost twofold higher likelihood of thrombus resolution compared with VKAs (pooled OR 1.95 [1.25 to 3.04], p = 0.003, I 2 = 0%), and decreased the risk of systemic embolism by 70% (pooled OR 0.30 [0.12 to 0.75]; p = 0.01, I 2 = 0%). The use of DOACs was associated with a 54% lower risk of bleeding compared with VKAs (pooled OR 0.46 [0.26 to 0.84], p = 0.01, I 2 = 0%). Overall, patients receiving DOACs had a 63% lower risk of reaching the composite outcome of safety and efficacy compared with patients using VKAs (pooled OR 0.37 [0.23 to 0.60], p <0.0001, I 2 = 0%). In conclusion, DOACs appear to have a more favorable efficacy and safety profile compared with VKAs for the management of LV thrombus related to AMI., Competing Interests: Declaration of competing interest The authors have no competing interests to declare., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Beta-blocker therapy, a treatment burdened by side effects including fatigue, erectile dysfunction and depression, was shown to reduce mortality and cardiovascular events after acute coronary syndromes (ACS) in the pre-coronary reperfusion era. Potential mechanisms include protection from ventricular arrhythmias, increased ischaemia threshold and prevention of left ventricular (LV) adverse remodelling. With the advent of early mechanical reperfusion and contemporary pharmacologic secondary prevention, the benefit of beta-blockers after ACS in the absence of LV dysfunction has been challenged., Methods: The present narrative review discusses the contemporary evidence based on searching the PubMed database and references in identified articles., Results: Recently, the REDUCE-AMI trial-the first adequately powered randomized trial in the reperfusion era to test beta-blocker therapy after myocardial infarction with preserved left ventricular ejection fraction (LVEF)-showed no benefit on the composite of all-cause death or myocardial infarction over a median 3.5-year follow-up. While the benefit of beta-blockers in patients with reduced LVEF remains undisputed, their value in post-ACS patients with mildly reduced systolic function (LVEF 41%-49%) has not been studied in contemporary randomized trials; in this setting, observational studies have suggested a reduction in cardiovascular events with these agents. The adequate duration of beta-blocker therapy remains unknown, but observational data suggests that any mortality benefit may be lost beyond 1-12 months after ACS in patients with LVEF >40%., Conclusion: We believe that there is sufficient evidence to abandon routine beta-blocker prescription in post-ACS patients with preserved LV systolic function., (© 2024 The Author(s). European Journal of Clinical Investigation published by John Wiley & Sons Ltd on behalf of Stichting European Society for Clinical Investigation Journal Foundation.)

The contemporary health care resource utilization after an acute myocardial infarction (MI) is not well-known. All patients admitted because of MI between January 2015 and December 2021 across 28 hospitals in the Baylor Scott & White Health system were studied. Patient characteristics and outcomes, including all-cause and cardiovascular (CV) rehospitalizations, emergency department (ED) visits, and outpatient visits were evaluated. Of 6,804 patients admitted because of MI, 6,556 were discharged alive. The median age was 69 years, 60% were men, and 77% had non-ST-elevation MI; 17% (1,090) had multivessel disease. The number of patients with first all-cause readmissions within 30 days, 3 months, and 12 months of discharge were 844 (13%), 1,372 (21%), and 2,306 (35%), respectively, with a higher readmission rate in patients with non-ST-elevation MI, previous heart failure (HF), new-onset HF, and left ventricular ejection fraction ≤40%. ED visits at 12 months for any cause were 2,401 (37%), of which 1,321 (55%) were for any CV cause, with a higher incidence in patients with previous HF. Of the 6,556 patients, 4,102 (63%) had at least 1 primary care visit in the past year, 5,009 (76%) had CV specialty visits, and 3,860 (59%) had non-CV visits, with a similar distribution across subgroups. Patients hospitalized with an MI had a high risk of subsequent hospital readmissions and ED and outpatient visits, especially those with a previous HF diagnosis and those discharged with an MI and HF diagnosis., Competing Interests: Declaration of competing interest Dr. Butler reports financial support was provided by Boehringer Ingelheim & Eli Lilly and Company Diabetes Alliance. Dr. Afzal reports a relationship with AstraZeneca that includes: speaking and lecture fees. Dr. Alhamdow reports a relationship with Boehringer Ingelheim GmbH that includes: employment. Dr. Hartgers-Gubbels reports a relationship with Boehringer Ingelheim GmbH that includes: employment. Dr. Martinez-Traba reports a relationship with Boehringer Ingelheim GmbH that includes: employment. Dr. Butler reports a relationship with Abbott that includes: consulting or advisory. Dr. Butler reports a relationship with American Regent Inc that includes: consulting or advisory. Dr. Butler reports a relationship with Amgen Inc that includes: consulting or advisory. Dr. Butler reports a relationship with Applied Therapeutics Inc that includes: consulting or advisory. Dr. Butler reports a relationship with AskBio that includes: consulting or advisory. Dr. Butler reports a relationship with Astellas that includes: consulting or advisory. Dr. Butler reports a relationship with AstraZeneca that includes: consulting or advisory and speaking and lecture fees. Dr. Butler reports a relationship with Bayer that includes: consulting or advisory. Dr. Butler reports a relationship with Boehringer Ingelheim that includes: consulting or advisory and speaking and lecture fees. Dr. Butler reports a relationship with Boston Scientific Corporation that includes: consulting or advisory. Dr. Butler reports a relationship with Bristol Myers Squibb Co that includes: consulting or advisory. Dr. Butler reports a relationship with Cardiac Dimensions Inc that includes: consulting or advisory. Dr. Butler reports a relationship with Cardiocell that includes: consulting or advisory. Dr. Butler reports a relationship with Cardior that includes: consulting or advisory. Dr. Butler reports a relationship with Cardiorem that includes: consulting or advisory. Dr. Butler reports a relationship with CSL Behring that includes: consulting or advisory. Dr. Butler reports a relationship with CVRx Inc that includes: consulting or advisory. Dr. Butler reports a relationship with Cytokinetics Inc that includes: consulting or advisory. 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Dr. Butler reports a relationship with Novo Nordisk Inc that includes: consulting or advisory. Dr. Butler reports a relationship with Pfizer that includes: consulting or advisory. Dr. Butler reports a relationship with Pharmacosmos that includes: consulting or advisory. Dr. Butler reports a relationship with PharmaIN that includes: consulting or advisory. Dr. Butler reports a relationship with Prolaio that includes: consulting or advisory. Dr. Butler reports a relationship with Regeneron that includes: consulting or advisory. Dr. Butler reports a relationship with Renibus Therapeutics, Inc. that includes: consulting or advisory. Dr. Butler reports a relationship with Roche that includes: consulting or advisory. Dr. Butler reports a relationship with Salamandra that includes: consulting or advisory. Dr. Butler reports a relationship with Sanofi that includes: consulting or advisory. Dr. Butler reports a relationship with SC Pharma that includes: consulting or advisory. Dr. Butler reports a relationship with Secretome that includes: consulting or advisory. Dr. Butler reports a relationship with Sequana that includes: consulting or advisory. Dr. Butler reports a relationship with SQ Innovation that includes: consulting or advisory. Dr. Butler reports a relationship with Tenex that includes: consulting or advisory. Dr. Butler reports a relationship with Tricog that includes: consulting or advisory. Dr. Butler reports a relationship with Ultromics that includes: consulting or advisory. Dr. Butler reports a relationship with Vifor that includes: consulting or advisory. Dr. Butler reports a relationship with ZOLL that includes: consulting or advisory. Dr. Gottlieb reports a relationship with Alnylam Pharmaceuticals Inc that includes: consulting or advisory, funding grants, and speaking and lecture fees. Dr. Gottlieb reports a relationship with AstraZeneca that includes: consulting or advisory and funding grants. Dr. Gottlieb reports a relationship with Eli Lilly and Company that includes: consulting or advisory and funding grants. Dr. Gottlieb reports a relationship with Pfizer that includes: funding grants and speaking and lecture fees. Dr. Gottlieb reports a relationship with Johnson & Johnson that includes: funding grants. Dr. Priest reports a relationship with AstraZeneca that includes: funding grants. Dr. Priest reports a relationship with Owkin Inc that includes: funding grants. The remaining authors have no competing interests to declare., (Copyright © 2024. Published by Elsevier Inc.)

Aim . Chronic kidney disease (CKD) and diabetes mellitus (DM) contribute significantly to cardiovascular disease (CVD) and mortality, with prevalence increasing. The evolving demographic of myocardial infarction (MI) patients, influenced by sedentary lifestyles and advanced medical care, lacks understanding regarding the interplay of CKD, DM, age, and post-MI mortality. This study aims to address this gap by evaluating the long-term impact of CKD and DM on post-MI mortality across age groups. Methods . A retrospective cohort study utilized data from the Estonian Myocardial Infarction Registry (EMIR), Estonian Population Register (EPR), and six major hospitals in Estonia, covering AMI hospitalizations from 2012 to 2019. Statistical analyses included Cox proportional hazards regression models and Kaplan-Meier's curves. Results . Analysis of 17,085 MI patients revealed age-dependent associations between renal function and mortality. In patients <65 years, even minor decreases in renal function increased both short-term (HR 2.79, 95% CI 1.71-4.55) and long-term (HR 1.24, 95% CI 1.05-1.47) mortality. Mortality significantly increased in patients >80 years only below an estimated glomerular filtration rate (eGFR) of 44 ml/min/1.73 m 2 . Newly diagnosed DM patients exhibited higher mortality rates (average HR 1.53, 95% CI 1.45-1.62), while pre-DM did not significantly differ from non-DM patients across all age groups. The DM-renal failure interaction did not significantly influence mortality. Conclusions . An age-dependent association between eGFR and post-MI outcomes emphasizes the need for personalized therapeutic approaches considering age-specific eGFR thresholds and comorbidities to optimize patient management.

Objectives: To investigate whether normal body mass index (BMI) shortly after percutaneous coronary intervention (PCI) for myocardial infarction is associated with increased risk of long-term major cardiovascular events (MACE), and to explore potential clinical determinants of long-term weight loss (WL) after PCI. Methods: Single-center cohort study with 5-year follow-up of patients treated with PCI for myocardial infarction between 2016 and 2018. Categorical WL was defined as > 0 kg body weight reduction from baseline to end of follow-up. Results: Of 236 patients (24% women), mean age was 64.9 ± 10.2 years and mean BMI within 4 days after PCI was 27.1 ± 4.3 kg/m 2 . Seventy-five patients (32%) had at least one MACE, equally distributed between those with normal weight (31%), overweight (32%), and obesity (31%). Patients with overweight or obesity had a lower crude mortality rate than their normal weight counterparts (7.4% vs 16.4%, p  = 0.049), but the relative hazard of death did not differ from those with normal weight, HR 0.50, 95% CI 0.22-1.15. Patients with either a long-term WL ( n  = 112) or no WL ( n  = 95) had a comparable incidence of non-fatal MACE (27% vs 22%, p  = 0.518). The proportion of patients reporting unintentional weight loss was significantly higher in the normal weight group (82%) compared with those with overweight (41%) or obesity (28%), p  < 0.001. Conclusion: Our results did not confirm any association between normal BMI after PCI and long-term MACE. However, patients with normal BMI at baseline had a higher incidence of unintentional WL than those with elevated BMI. Trial registration: Current research information system in Norway (CRISTIN): ID 542528.

This meta-analysis and systematic review compiles comparative data from 2004 to 2024, investigating the safety and efficacy of mesenchymal stem/stromal cells (MSCs) derived from various tissues for the treatment of ischemic cardiomyopathy (ICM) and associated heart failure. In addition, this review highlights the limitations of these interventions and provides valuable insights for future therapeutic approaches. Relevant articles were retrieved from the PubMed® database using targeted keywords. Our inclusion criteria included clinical trials with patients over 18 years of age, case reports and pilot studies. Animal experiments, in vitro studies, correlational and longitudinal studies, and study designs and protocols were excluded. Forty-nine original articles resulted in follow-up reports of 45 trials. MSCs from bone marrow, umbilical cord and adipose tissue were moderately well tolerated. Of the 1408 participants who received MSCs, 33 trials (67.3%) reported the occurrence of death or serious adverse events. These events resulted in 80 deaths (52% of reported cases) following MSC administration. Importantly, 41.3% of these deaths (n = 33) were not considered to be related to the intervention itself, while 40% of these deaths had no reported cause. As the primary outcome, the mean increase in left ventricular ejection fraction (LVEF) from baseline was 5.75% (95% CI: 3.38% -8.11%, p < 0.0001, I 2 = 90,9%) in the randomized controlled trials only (n = 24) within the treatment groups and 3.19% (95% CI: 1.63% to 4.75%, p < 0.0001, I 2 = 74,17%) in the control groups after the intervention. When the above results were compared using the standardized mean difference (SDM), a significance in favor of the treatment group was also found (SDM = 0.41; 95% CI: 0.19-0.64, p < 0.001, I 2 = 71%). Although improvements were also seen in the control groups, 33.3% (n = 15) of the studies showed no significant difference between the control and treatment groups. The 6-minute walking test (6MWT) and New York Heart Association (NYHA) class scores, used for assessing exercise tolerance and quality of life (QoL), respectively, further supported the improvements in the treatment group. These improvements were noted as 62.5% (n = 10) for the 6MWT and 54.5% (n = 12) for the NYHA class scores. According to the risk of bias analysis, 4 trials were of good quality (11.8%), 15 were of fair quality (44.1%), and 15 were of poor quality (44.1%). Major limitations of these studies included small sample size, diagnostic challenges/lack, uncertain cell dosage and potential bias in patient selection. Despite the ongoing debate surrounding cell administration for ICM, there are supporting signs of improved clinical and laboratory outcomes, as well as improved QoL in the MSC-treated groups. However, it is important to recognize the limitations of each study, highlighting the need for larger, controlled trials to validate these findings., Competing Interests: Declaration of competing interest The authors have no commercial, proprietary, or financial interest in the products or companies described in this article., (Copyright © 2024 International Society for Cell & Gene Therapy. Published by Elsevier Inc. All rights reserved.)

Background: This study evaluates the relationship between global longitudinal strain (GLS) and late major adverse cardiovascular events (MACEs) in patients after acute myocardial infarction (AMI)., Methods: Data of newly diagnosed AMI patients between March 2010 and July 2014 were retrospectively evaluated. The patients underwent serial echocardiography at admission and at third and sixth months post-admission. We calculated GLS by averaging the strain from all myocardial segments using speckle-tracking echocardiography (STE). We used multivariate Cox regression analysis and receiver operating characteristic (ROC) curve analyses to assess the relationship between GLS at admission and late MACEs., Results: Eighty-nine newly diagnosed AMI patients were enrolled. The average age at diagnosis was 61 ± 12.5 years, and approximately 89.9% of the patients were men. The average level of GLS was -17.5 ± 3.9%. The overall prevalence of MACEs was 23.6% (21/89), compared with 44% (11/25) in the group with GLS≥-15% and 17.9% (5/28) in the group with GLS<-20%. GLS was positively linked with MACEs in the fully adjusted Cox proportional hazard model (hazard ratio [HR], 1.19; 95% confidence interval [CI], 1.04-1.37; P=0.014) after adjusting potential confounders. The ROC curve analysis for one year MACEs between GLS at admission, with the most significant area under the curve(AUC) 78.1% (95% CI, 63.8% - 92.6%)., Conclusions: Myocardial dysfunction, characterized by impaired GLS, is often observed in AMI patients, and a decrease in GLS levels at admission were associated with an increased risk of long-term MACEs in post-myocardial infarction patients., Competing Interests: Declaration of competing interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Acute myocardial infarction (MI) leads to a loss of cardiac function which, following adverse ventricular remodeling (AVR), can ultimately result in heart failure. Tissue-engineered contractile patches placed over the infarct offer potential for restoring cardiac function and reducing AVR. In this computational study, we investigate how improvement of pump function depends on the orientation of the cardiac patch and the fibers therein relative to the left ventricle (LV). Additionally, we examine how model outcome depends on the choice of material properties for healthy and infarct tissue. In a finite element model of LV mechanics, an infarction was induced by eliminating active stress generation and increasing passive tissue stiffness in a region comprising 15% of the LV wall volume. The cardiac patch was modeled as a rectangular piece of healthy myocardium with a volume of 25% of the infarcted tissue. The orientation of the patch was varied from 0 to 150 ∘ relative to the circumferential plane. The infarct reduced stroke work by 34% compared to the healthy heart. Optimal patch support was achieved when the patch was oriented parallel to the subepicardial fiber direction, restoring 9% of lost functionality. Typically, about one-third of the total recovery was attributed to the patch, while the remainder resulted from restored functionality in native myocardium adjacent to the infarct. The patch contributes to cardiac function through two mechanisms. A contribution of tissue in the patch and an increased contribution of native tissue, due to favorable changes in mechanical boundary conditions., Competing Interests: Declarations Conflict of interest The authors declare no Conflict of interest, (© 2024. The Author(s).)

Robinin is one of the glycosyloxyflavones that has been less explored for its therapeutic application, especially in the field of CVD. Herein, we explored the cardioprotective efficacy of Robinin by using H 2 O 2 and Doxorubicin (DOX) - treated H9c2 cells as an in vitro model. H 2 O 2 and DOX treatment resulted in severe cellular damage to the cardiomyocytes, which was followed by apoptosis. Apoptosis and nuclear morphology were analysed through Hoechst 33342 and AO/EB staining. qPCR was employed to detect the expression of apoptosis as well as ERS-related markers. Reactive oxygen species (ROS) generation was observed using DCFH-DA staining and FACS analysis. Signaling pathways involved were analysed using Western blot. Robinin pre-treatment considerably decreased the apoptotic rate by boosting the endogenous anti-oxidative activity and lowering the activity of Malonaldehyde and Lactate dehydrogenase enzyme. Robinin also inhibited the generation of ROS. Robinin reduced the expression of ERS-associated genes and proteins, thereby decreasing apoptosis-related proteins. Upon comparing the cardioprotective effect of Robinin with a known cardioprotective agent Dexrazoxane (DEX) it was revealed that DEX has more cardioprotective effect against DOX than H 2 O 2 -induced stress, while Robinin showed a significant protective effect against both H 2 O 2 and DOX induced stress., Competing Interests: Compliance with ethical standards Conflict of interest The authors declare no competing interests., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Objectives . The prevalence of patients with prior stroke is increasing globally. Accordingly, there is a need for up-to-date evidence of patient-related prognostic factors for stroke recurrence, post stroke myocardial infarction (MI) and death based on long-term follow-up of stroke survivors. For this purpose, the RIALTO study was established in 2004. Design. A prospective cohort study in which patients diagnosed with ischemic stroke (IS) or transient ischemic attack (TIA) in three Copenhagen hospitals were included. Data were collected from medical records and by structured interview. Data on first stroke recurrence, first MI and all-cause death were extracted from the Danish National Patient Registry and the Danish Civil Registration System. Results . We included 1215 patients discharged after IS or TIA who were followed up by register data from April 2004 to end of 2018 giving a median follow-up of 3.5-6.9 years depending on the outcome. At the end of follow-up 406 (33%) patients had been admitted with a recurrent stroke, 100 (8%) had a MI and 822 (68%) had died. Long-term prognostic predictors included body mass index, diabetes, antihypertensive and lipid lowering treatment, smoking, a sedentary lifestyle as well as poor self-rated health and psychosocial problems. Conclusions . Long-term risk of recurrent stroke and MI remain high in patients discharged with IS or TIA despite substantial improvements in tertiary preventive care in recent decades. Continued attention to the patient risk profile among patients surviving the early phase of stroke, including comorbidities, lifestyle, and psychosocial challenges, is warranted.

Currently, the standard treatment for patients who have undergone percutaneous coronary intervention (PCI) following acute myocardial infarction (MI) involves dual antiplatelet therapy (DAPT) with a combination of aspirin and a potent P2Y12 receptor inhibitor. However, the potential benefits of aspirin were partially constrained by the intolerance of some patients. The safety and efficacy of indobufen, an alternative antiplatelet agents to aspirin, in patients with AMI after PCI are yet to be thoroughly investigated.This retrospective study was conducted at a single center and utilized propensity score matching. The enrollment spanned from January 2019 to June 2022, incorporating patients with AMI after PCI. The participants were categorized into two groups based on discharged prescriptions: the aspirin DAPT group and the indobufen DAPT group. The primary endpoint focused on net adverse clinical event (NACE), defined as a composite outcome, including cardiac death, recurrence of MI, definite or probable stent thrombosis (ST), target lesion revascularization (TLR), ischemic stroke and Bleeding Academic Research Consortium (BARC) criteria type 2, 3, or 5. All the patients underwent a one-year follow-up period.A total of 1451 patients were enrolled in this study, with 258 assigned to the indobufen DAPT group and 1193 to the aspirin DAPT group. Following 1:1 propensity score matching, 224 patients were retained in each group. In the indobufen DAPT group, 58 individuals (25.9%) experienced the primary endpoint within one year, compared to 52 individuals (23.2%) in the aspirin DAPT group (HR 1.128, 95% CI 0.776-1.639, p  = .527). Specifically, no significant differences were observed in either the efficacy endpoint (MACCE, 20.1% vs. 14.7%, HR 1.392, 95% CI 0.893-2.170, p  = .146) or the safety endpoint (BARC 2,3 or 5, 8.04% vs. 10.30%, HR 0.779, p  = .427). These findings remained consistent at 1, 3, or 6 months. Additionally, the incidence of gastrointestinal symptoms were significantly lower in indobufen DAPT group compared to the aspirin DAPT group (7.1% vs. 14.3%, p  = .022).Our research reveals that the efficacy and safety of indobufen are comparable to aspirin in Chinese patients with AMI following PCI. Given the potential advantages of indobufen in alleviating gastrointestinal symptoms, we propose it as a viable alternative for individuals intolerant to aspirin.

Aim: Left ventricular remodeling (LVR) after myocardial infarction (MI) can lead to heart failure, arrhythmia, and death. We aim to describe adverse LVR patterns at 6 months post-MI and their relationships with subsequent outcomes and to determine baseline., Methods and Results: A multicenter cohort of 410 patients (median age 57 years, 87% male) with reperfused MI and at least 3 akinetic LV segments on admission was analyzed. All patients had transthoracic echocardiography performed 4 days and 6 months post-MI, and 214 also had cardiac magnetic resonance imaging performed on day 4. To predict LVR, machine learning methods were employed in order to handle many variables, some of which may have complex interactions. Six months post-MI, echocardiographic increases in LV end-diastolic volume (LVEDV), LV end-systolic volume (LVESV), and LV ejection fraction (LVEF) were 14.1% [interquartile range 0.0, 32.0], 5.0% [- 14.0, 25.8], and 8.7% [0.0, 19.4], respectively. At 6 months, ≥ 15% or 20% increases in LVEDV were observed in 49% and 42% of patients, respectively, and 37% had an LVEF < 50%. The rate of death or new-onset HF at the end of 5-year follow-up was 8.8%. Baseline variables associated with adverse LVR were determined best by random forest analysis and included stroke volume, stroke work, necrosis size, LVEDV, LVEF, and LV afterload, the latter assessed by Ea or Ea/Ees. In contrast, baseline clinical and biological characteristics were poorly predictive of LVR. After adjustment for predictive baseline variables, LV dilation > 20% and 6-month LVEF < 50% were significantly associated with the risk of death and/or heart failure: hazard ratio (HR) 2.12 (95% confidence interval (CI) 1.05-4.43; p = 0.04) and HR 2.68 (95% CI 1.20-6.00; p = 0.016) respectively., Conclusion: Despite early reperfusion and cardioprotective therapy, adverse LVR remains frequent after acute MI and is associated with a risk of death and HF. A machine learning approach identified and prioritized early variables that are associated with adverse LVR and which were mainly hemodynamic, combining LV volumes, estimates of systolic function, and afterload., Competing Interests: Declarations. Conflict of interest: The authors state that they have no conflict of interest to declare., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.)

Objective: To study cumulative incidence and predictors of myocardial infarction (MI) in two random general population samples consisting of middle-aged Swedish men born 30 years apart., Method: Results from the "Study of Men Born In 1913" and the "Study of Men Born In 1943", two longitudinal cohort studies performed in the same geographic area and using the same methodology were compared. Both cohorts were followed prospectively from 50 to 70 years of age. MI was defined as first myocardial infarction, fatal or non-fatal., Results: Men born in 1943 had a 34% lower cumulative risk of first MI [HR 0.66 (0.50-0.88), p = 0.0051] during follow-up as compared to men born in 1913. Interaction analysis showed that hypertension had a significantly higher impact on risk of MI in cohort 1943 than in cohort 1913 [HR 2.33 (95% CI 1.41-3.83)] and [HR 1.10 (0.74-1.62)], p = 0.0009 respectively. The population attributable risk for hypertension was 2.5-fold higher in the cohort of men born in 1943 as compared to men born in 1913, and diabetes mellitus and sedentary lifestyle attributed more to MI risk in cohort 1943 than in cohort 1913. On the contrary, smoking and total cholesterol have less attributable risk to MI in cohort 1943 than in cohort 1913., Conclusion: Despite declining incident MI and improved cardiovascular prevention in general, hypertension remains an increasingly important attributable risk factor to MI together with diabetes mellitus and sedentary lifestyle over time., Competing Interests: Declarations. Competing interests: None declared. Ethics approval: The study complies with the Helsinki Declaration. Written informed consent was obtained from all participants, except for the screening examination in 1963 where only oral informed consent was given (standard procedure at the time). The Research Ethics Board in Gothenburg, later the National Research Ethics Authority, approved the study protocol on several occasions (DNR 157–93, 0067–03, and DNR 649–13). Patient and public involvement: Patient and/or public were not involved in the design, conduct, reporting, or dissemination plans of this research. Patient consent for publication: Not applicable. Provenance and peer review: Not commissioned, externally peer reviewed., (© 2023. The Author(s).)

Purpose: Myocardial T 1ρ mapping techniques commonly acquire multiple images in one breathhold to calculate a single-slice T 1ρ map. Recently, non-selective adiabatic pulses have been used for robust spin-lock preparation (T 1ρ,adiab ). The objective of this study was to develop a fast multi-slice myocardial T 1ρ,adiab mapping approach., Methods: The proposed-sequence reduces the number of breathholds required for whole-heart 2D T 1ρ,adiab mapping by acquiring multiple interleaved slices in each breathhold using slice-selective T 1ρ,adiab preparation pulses. The proposed-sequence was implemented with two interleaved slices per breathhold scan and was quantitatively evaluated in phantom experiments and 10 healthy-volunteers against a single-slice T 1ρ,adiab mapping sequence. The sequence was demonstrated in two patients with myocardial scar., Results: The phantom experiments showed the proposed-sequence had slice-to-slice variation of 1.62% ± 1.05% and precision of 4.51 ± 0.68 ms. The healthy volunteer cohort subject-wise mean relaxation time was lower for the proposed-sequence than the single-slice sequence (137.7 ± 5.3 ms vs. 148.4 ± 8.3 ms, p < 0.001), and spatial-standard-deviation was better (18.7 ± 1.8 ms vs. 21.8 ± 3.4 ms, p < 0.018). The mean within-subject, coefficient of variation was 5.93% ± 1.57% for the proposed-sequence and 6.31% ± 1.92% for the single-slice sequence (p = 0.35) and the effect of slice variation (0.81 ± 4.87 ms) was not significantly different to zero (p = 0.61). In both patient examples increased T 1ρ,adiab (maximum American Heart Association-segment mean = 174 and 197 ms) was measured within the myocardial scar., Conclusion: The proposed sequence provides a twofold acceleration for myocardial T 1ρ,adiab mapping using a multi-slice approach. It has no significant difference in within-subject variability, and significantly better precision, compared to a 2D T 1ρ,adiab mapping sequence based on non-selective adiabatic spin-lock preparations., (© 2024 The Author(s). Magnetic Resonance in Medicine published by Wiley Periodicals LLC on behalf of International Society for Magnetic Resonance in Medicine.)

Background: Anemia and chronic kidney disease (CKD) adversely affect prognosis following acute myocardial infarction (AMI). We aimed to assess their interaction regarding long-term survival post-AMI., Methods: This is a single-center, retrospective analysis of consecutive AMI survivors. Stratified by admission-time anemia status and CKD grade, as determined by hemoglobin and creatinine levels, the cohort was evaluated for all-cause mortality at 10 years after hospital discharge., Results: A total of 11,395 patients (69.1% males, mean age 65.8 ± 13.9 years, 49.6% with ST elevation MI) were included, of whom 29.9% had anemia and 15.9% - grade 3b or higher CKD. CKD was more advanced among anemic patients and the prevalence of anemia rose as CKD grade increased (p for trend < 0.001). At 10 years, 47.8% of patients died. Notwithstanding differences in baseline characteristics, presentation, and treatment between those with various anemia status and CKD grades, anemia presence (HR 1.40, 95% CI 1.32-1.49, p < 0.001) and increasing CKD grade (HR 1.10, 95% CI 1.02-1.20, p for trend < 0.001) were independently associated with a higher mortality risk. The incremental hazard imposed by either anemia or more advanced CKD was limited to patients with normal renal function and up to grade 3a (in the total cohort and the conservative treatment subgroup) or 4 (in the invasive revascularization subgroup) CKD. The added risk associated with increasing CKD grade also affected non-anemic individuals irrespective of the specific CKD grade., Conclusion: Anemia and more advanced CKD are associated with reduced long-term survival post-AMI, inflicting higher risk when conjoined in lower-grade CKD., Competing Interests: Declarations. Ethics approval: This project conformed to the Declaration of Helsinki and was approved by Soroka’s Institutional Review Board (approval number SOR-0319–16), which waived the need for informed consent in view of the investigation’s retrospective nature. Conflict of interest: The authors declare no competing interests., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.)

Background: While Cardiac Rehabilitation (CR) programs have shown effectiveness in improving cardiac outcomes, there is limited understanding of how patients perceive and adapt to these interventions. Furthermore, alternative modes of delivering CR that have received positive evaluations from participants remain underexplored, yet they have the potential to enhance CR uptake., Objectives: To explore the patient experience in CR programmes following Acute Myocardial Infarction (AMI) and describe their adaptive processing., Patients and Methods: This qualitative study was conducted at a nationally certified centre in China between July 2021 and September 2022, encompassing three stages: in-hospital, centre-based, and home-based CR programs. Purposive sampling was used to select eligible AMI patients for in-depth semi-structured interviews. The interview outline and analytical framework were aligned with the key concepts derived from the middle-range theory of adaptation to chronic illness and the normalization process theory. The findings were reported following the Consolidated Criteria for Reporting Qualitative Research checklist., Results: Forty AMI patients were recruited. Four main themes describing the process of AMI patients normalizing CR intervention were identified, including (1) experiencing CR service driving by role's responsibilities, (2) engaging in collaborative relationship based on interpersonal trust, (3) exploring a personalized rehabilitation plan by complex integration, and (4) expecting a promised outcome to shape decision-making., Conclusion: Integrated care interventions for AMI patients could benefit from a collaborative co-designed approach to ensure that CR interventions are normalized and fit into patients' daily lives. Organizational-level CR services should align with the rehabilitation needs and expectations of patients.

Introduction: Coronary artery disease (CAD) is a main cause of morbidity and mortality. The effectiveness of coronary revascularization in chronic coronary syndromes (CCS) is still debated. Our recent study showed the superiority of coronary revascularization over optimal medical therapy (OMT) in reducing cardiovascular (CV) mortality and myocardial infarction (MI). The recent publication of the ORBITA-2 trial suggested superiority of percutaneous coronary revascularization (PCI) in reducing angina and improving quality of life. Therefore, we aimed to provide an updated meta-analysis evaluating the impact of PCI on both clinical outcomes and angina in CCS., Methods: Relevant studies were screened in PubMed/Medline until 08/01/2024. Randomized controlled trials (RCTs) comparing PCI to OMT in CCS were selected. The primary outcome was CV death. Secondary outcomes were MI, all-cause mortality, stroke, major bleeding and angina severity., Results: Nineteen RCTs involving 8616 patients were included. Median follow-up duration was 3.3 years. Revascularization significantly reduced CV death (4.2% vs. 5.5%; OR = .77; 95% CI .62-.96, p = .02). Subgroup analyses favoured revascularization in patients without chronic total occlusions (CTOs) (p = .052) and those aged <65 years (p = .02). Finally, a follow-up duration beyond 3 years showed increased benefit of coronary revascularization (p = .04). Secondary outcomes analyses showed no significant differences, except for a lower angina severity in the revascularization group according to the Seattle Angina Questionnaire (SAQ) (p = .04) and to the Canadian Cardiovascular Society (CCS) classification (p = .005)., Conclusions: PCI compared to OMT significantly reduces CV mortality and angina severity, improving quality of life in CCS patients. This benefit was larger without CTOs, in patients aged <65 years and with follow-up duration beyond 3 years., (© 2024 The Author(s). European Journal of Clinical Investigation published by John Wiley & Sons Ltd on behalf of Stichting European Society for Clinical Investigation Journal Foundation.)

Background: We sought to evaluate the associations of chest pain and dyspnea with the long-term risk of cardiovascular disease including coronary disease, heart failure, atrial fibrillation, and stroke., Methods: In 13,200 participants without cardiovascular disease in the Atherosclerosis Risk in Communities study (1987-1989), chest pain was categorized into definite angina, possible angina, non-anginal chest pain, and no chest pain using the Rose questionnaire. Dyspnea was categorized into grades 3-4, 2, 1, and 0 by the modified Medical Research Council scale. The associations of chest pain and dyspnea with incident myocardial infarction, heart failure, atrial fibrillation, and stroke over a median follow-up of ∼27 years were quantified with multivariable Cox models., Results: Definite angina and possible angina were associated with myocardial infarction (adjusted hazard ratios [HR] 1.80 [95%CI 1.45-2.13] and 1.65 [1.27-2.15]). Although lesser magnitude than myocardial infarction, both definite and possible angina were associated with heart failure. For atrial fibrillation, possible angina showed higher HR than definite angina. Dyspnea showed similar HRs for myocardial infarction and heart failure in grades 3-4 (2.00 [1.61-2.49] and 1.94 [1.62-2.32]). Stroke was least associated with chest symptoms. Chest pain and dyspnea significantly improved the discrimination of cardiovascular disease except stroke, beyond traditional risk factors., Conclusions: In individuals without cardiovascular disease, chest pain and dyspnea were independently associated with incident cardiovascular disease for about 3 decades, suggesting the need for evaluating chest pain from a broader perspective of cardiovascular disease beyond coronary disease and the importance of dyspnea for cardiovascular risk assessment including myocardial infarction., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Myocardial fibrosis (MF) is characterized by the excessive deposition of extracellular matrix within the heart, often following a cardiovascular insult. SHARPIN, a protein implicated in fibrosis, has emerged as a potential therapeutic target. This study aimed to elucidate the molecular mechanisms of SHARPIN in MF and to investigate the influence of its single nucleotide polymorphism (SNP), rs117299156, on myocardial infarction (MI) patients. A mouse model of Angiotensin II (AngII)-induced MF was established in SHARPIN heterozygous (SHARPIN+/-) and wild-type mice. Adult mouse cardiac fibroblasts (CFs) were isolated and subjected to adenovirus-encapsulated SHARPIN short hairpin RNA (shRNA) infection. Transcriptomic analysis was performed on CFs from SHARPIN+/- and wild-type (WT) mice, complemented by single-cell sequencing data from human cardiac tissues. Additionally, the association between the rs117299156 mutation and cardiovascular events in MI patients was assessed. Our findings indicate that SHARPIN is predominantly expressed in CFs and is upregulated in fibrotic myocardium. Partial knockdown of SHARPIN in murine hearts mitigated AngII-induced cardiac dysfunction and MF. Furthermore, reduced SHARPIN expression in CFs attenuated TGF-β1-induced collagen synthesis, cell proliferation, and myofibroblast transformation. Notably, MI patients carrying the rs117299156&#95;C allele exhibited a reduced incidence of stroke events compared to those without the mutation., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Following an acute myocardial infarction (AMI), patients remain at risk for subsequent cardiovascular (CV) events. In the AEGIS-II trial, CSL112, a human apolipoprotein A-I derived from plasma that enhances cholesterol efflux, did not significantly reduce the first occurrence of CV death, myocardial infarction (MI), or stroke through 90 days compared with placebo. However, an analysis involving only the first event may not capture the totality of the clinical impact of an intervention because patients may experience multiple events., Objectives: This prespecified exploratory analysis examines the effect of CSL112 on total burden of nonfatal ischemic events (ie, recurrent MI and stroke) and CV death., Methods: A total of 18,219 patients with AMI, multivessel coronary artery disease, and additional CV risk factors were randomized to either 4 weekly infusions of 6 g CSL112 (n = 9,112) or matching placebo (n = 9,107). A negative binomial regression model was applied to estimate the effect of CSL112 compared with placebo on the rate ratio (RR) of ischemic events., Results: For CV death, MI, and stroke, there were numerically fewer total events at 90 days (503 vs 545 events; rate ratio [RR]: 0.88; 95% CI: 0.76-1.03, P = 0.11), and nominally significantly fewer total events at 180 days (745 vs 821 events, RR: 0.87; 95% CI: 0.77-0.99; P = 0.04) and 365 days (1,120 vs 1,211 events; RR: 0.89; 95% CI: 0.80-0.99; P = 0.04). Subsequent events constituted 13% of events at 90 days, 17% at 180 days, and 22% at 1 year. Similar findings were seen with the total occurrence of nonfatal MI and CV death. When type II MIs, unlikely to be modified by enhancing cholesterol efflux, were excluded, there were nominally significant reductions in the total occurrence of nonfatal MI (excluding type 2) and CV death at all time points (90 days: RR: 0.81; 95% CI: 0.68-0.97; P = 0.02; 180 days: RR: 0.82; 95% CI: 0.71-0.95; P < 0.01; 365 days: RR: 0.86; 95% CI: 0.76-0.98; P = 0.02)., Conclusions: In this prespecified exploratory analysis of the AEGIS-II trial, 4 weekly infusions of CSL112 among high-risk patients after AMI significantly reduced the total burden of nonfatal ischemic events and CV death at 180 and 365 days compared with placebo. (AEGIS-II [Study to Investigate CSL112 in Subjects With Acute Coronary Syndrome]; NCT03473223)., Competing Interests: Funding Support and Author Disclosures The study was sponsored by CSL Behring. CSL Behring was involved in the study design, data collection, data analysis, data interpretation, and the preparation, review, and approval of the manuscript. The decision to submit the manuscript for publication was made by the academic leadership of the steering committee. Dr Gibson has received research funding from CSL Behring, Janssen Pharmaceuticals, Johnson and Johnson Corporation, and SCAD Alliance; has been a consultant for Angel/Avertix Medical Corporation, AstraZeneca, Bayer Corporation, Beren Therapeutics, Boehringer Ingelheim, Boston Clinical Research Institute, Boston Scientific, Bristol Myers Squibb, Cardiovascular Research Foundation, CeleCor Therapeutics, CSL Behring, DCRI, Esperion, EXCITE International ($0 received), Fortress Biotech, Gilead Sciences Inc., Janssen, Pharmaceuticals, Johnson & Johnson Corporation, MashUp MD, MD Magazine, Microport, MJHealth, Novartis, Novo Nordisk, Pfizer, PHRI, PLxPharma, SCAI, Solstic Health/New Amsterdam Pharma, Somahlution/Marizyme, Vectura, Web MD, and Women as One; has equity in nference, Dyad Medical, Absolutys, and Fortress Biotech; and has received royalties as a contributor to UpToDate. Dr Chi has received research grant support paid to the Beth Israel Deaconess Medical Center, Harvard Medical School from Bayer, CSL Behring, Janssen Scientific Affairs, and SCAD Alliance. Dr Duffy has received salary as an employee of CSL Behring. Dr Bahit has received honoraria from MSD, Pfizer, Bristol Myers Squibb, CSL Behring, Janssen, Boehringer Ingelheim, and Anthos Therapeutics. Dr White has received grant support to institution from Sanofi, Regeneron Pharmaceuticals, Eli Lilly, Omthera Pharmaceuticals, American Regent, Eisai Inc, DalCor Pharma UK Inc., CSL Behring, NHI, Sanofi-Aventis Australia Pty Ltd, Esperion Therapeutics Inc, and National Institutes of Health; has received fees for serving on Steering Committees of the ODYSSEY trial from Sanofi and Regeneron Pharmaceuticals, the ISCHEMIA and the MINT studies from the National Institutes of Health, the STRENGTH trial from Omthera Pharmaceuticals, the HEART-FID study from American Regent, the DAL-GENE study from DalCor Pharma UK Inc., the AEGIS-II study from CSL Behring, the SCORED trial and the SOLOIST-WHF trial from Sanofi Australia Pty Ltd, and the CLEAR OUTCOMES study from Esperion Therapeutics. Dr Korjian has received research grant support paid to the Beth Israel Deaconess Medical Center, Harvard Medical School from CSL Behring. Dr Alexander has received research grants through Duke University from Artivion/CryoLife, Bayer, Bristol Myers Squibb, CSL Behring, Ferring, the U.S. FDA, Humacyte, and the U.S. NIH; has served as advisory board member or received honoraria or consulting payments from AbbVie, Artivion/CryoLife, AtriCure, Bayer, Bristol Myers Squibb, Curis, Eli Lilly, Ferring, GlaxoSmithKline, Janssen, Novostia, Pfizer, Portola, Theravance, and Veralox. Dr Lincoff has received research funding from Esperion, Eli Lilly, Novartis, AstraZeneca, AbbVie; and has been a consultant for Novo Nordisk, Eli Lilly, Glaxo, Akebia, Endologix, Fibrogen, Provention, Becton Dickson, Brainstorm Cell, Intarcia, Medtronic, and Recor. Dr Anschuetz has received a salary as an employee of CSL Behring. Dr Girgis has received a salary as an employee of CSL Behring. Dr Nicolau has received a scholarship from the National Council of Scientific and Technological Development (CNPq) #303448/2021-0; has received research grants from Amgen, AstraZeneca, Bayer, CSL Behring, Daiichi-Sankyo, Dalcor, Esperion, Ionis, Janssen, Novartis, Novo Nordisk, Sanofi, and Vifor; and has received consulting fees from Libbs. Dr Lopes has received grant support from Amgen, Bristol Myers Squibb, GlaxoSmithKline, Medtronic, Pfizer, and Sanofi; has been a consultant for AstraZeneca, Bayer, Boehringer, Bristol Myers Squibb, and Novo Nordisk; and has participated in educational activities for Daiichi-Sankyo, AstraZeneca, Novo Nordisk, and Pfizer. Dr Bainey has received research support from CSL Behring. Dr Libby has served on a scientific advisory board for Amgen, Kowa Pharmaceuticals, Novo Nordisk, Caristo, CSL Behring, DalCor, Dewpoint, Euclid Bioimaging, Xbiotech, Olatec, Medimmune, PlaqueTec, Polygon Therapeutics, TenSixteen Bio, Soley Therapeutics; and has been a consultant for Amgen, Baim Institute Beren, Esperion, Genentech, Kancera, Kowa Pharmaceuticals, Novo Nordisk, Novartis, and Sanofi-Regeneron. Dr Sacks has received support from CSL Behring. Dr Ridker has received institutional research grant support from Kowa, Novartis, Amarin, Pfizer, Esperion, Novo Nordisk, and the NHLBI; has served as a consultant to numerous companies including Novartis, Flame, Agepha, Ardelyx, Arrowhead, AstraZeneca, CSL Behring, Janssen, Civi Biopharm, GlaxoSmithKline, SOCAR, Novo Nordisk, Health Outlook, Montai Health, Eli Lilly, New Amsterdam, Boehringer Ingelheim, RTI, Zomagen, Cytokinetics, Horizon Therapeutics, and Cardio Therapeutics; holds minority shareholder equity positions in Uppton, Bitteroot Bio, and Angiowave; and receives compensation for service on the Peter Munk Advisory Board (University of Toronto), the Leducq Foundation (Paris, FR), and the Baim Institute (Boston, Massachusetts). Dr Goodman has received research grant support (eg, steering committee or data and safety monitoring committee) and/or speaker/consulting honoraria (eg, advisory boards) from Alnylam, Amgen, Anthos Therapeutics, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, CSL Behring, CYTE Ltd., Daiichi-Sankyo/American Regent, Eli Lilly, Esperion, Ferring Pharmaceuticals, HLS Therapeutics, Idorsia, JAMP Pharma, Merck, Novartis, Novo Nordisk A/C, Pendopharm/Pharmascience, Pfizer, Regeneron, Roche, Sanofi, Servier, Tolmar Pharmaceuticals, Valeo Pharma; has received salary support/honoraria from the Canadian Heart Failure Society, Canadian Heart Research Centre and MD Primer, Canadian VIGOUR Centre, Cleveland Clinic Coordinating Centre for Clinical Research, Duke Clinical Research Institute, Jewish General Hospital∖CIUSSS Centre-Ouest-de-l'Ile-de-Montreal, New York University Clinical Coordinating Centre, PERFUSE Research Institute, Peter Munk Cardiac Centre Clinical Trials and Translation Unit, Ted Rogers Centre for Heart Research, and TIMI Study Group (Brigham Health). Dr Mahaffey has received grants from AHA, Apple Inc, Bayer, California Institute Regenerative Medicine, CSL Behring, Eidos, Ferring, Gilead, Google (Verily), Idorsia, Johnson & Johnson, Luitpold, Novartis, PAC-12, Precordior, Sanifit; has received consulting fees from applied Therapeutics, Bayer, BMS, BridgeBio, CSL Behring, Elsevier, Fosun Pharma, Human, Johnson & Johnson, Moderna, Myokardia, Novartis, Novo Nordisk, Otsuka, Phasebio, Portola, Quidel, Theravance; has received payment or honoraria from CSL Behring; and has stock or stock options in Human, Medeloop, Precordior, and Regencor. Dr Nicholls has received research support from AstraZeneca, Amgen, Anthera, CSL Behring, Cerenis, Eli Lilly, Esperion, Resverlogix, Novartis, InfraReDx, and Sanofi-Regeneron; and has been a consultant for Amgen, Akcea, AstraZeneca, Boehringer Ingelheim, CSL Behring, Daiichi-Sankyo, Eli Lilly, Esperion, Kowa, Merck, Takeda, Pfizer, Sanofi-Regeneron, Novo Nordisk, CSL Sequiris, and Vaxxinity. Dr Pocock has been a consultant to CSL Behring. Dr Mehran has received institutional research payments from Abbott, Affluent Medical, Alleviant Medical, Amgen, AstraZeneca, BAIM, Beth Israel Deaconess Medical Center, Boston Scientific, Bristol Myers Squibb, CardiaWave, CERC, Chiesi, Concept Medical, Daiichi-Sankyo, Duke, Faraday, Idorsia, Janssen, MedAlliance, Medscape, Mediasphere, Medtelligence, Medtronic, Novartis, OrbusNeich, Pi-Cardia, Protembis, RM Global Bioaccess Fund Management, and Sanofi; has received personal fees from Affluent Medical, Boehringer Ingelheim, Chiesi USA, Cordis, Daiichi-Sankyo, Esperion Science/Innovative Biopharma, Gaffney Events, Educational Trust, Global Clinical Trial Partners, Ltd., IQVIA, Medscape/WebMD Global, Novo Nordisk, PeerView Institute for Medical Education, TERUMO Europe N.V., and Radcliffe; has held equity <1% in Elixir Medical, Stel, ControlRad (spouse); has received an honorarium from AMA; is associate editor of JAMA Cardiology; and is a BOT Member, SC Member CTR Program of ACC. Dr Harrington has research relationships with Baim Institute, CSL, Janssen, NHLBI, PCORI, and DCRI; has consulting relationships with Atropos Health, Bitterroot Bio, BMS, BridgeBio, Element Science, Edwards Lifesciences, Foresite Labs, Medscape/WebMD; and serves on boards of directors for the American Heart Association, College of the Holy Cross, and Cytokinetics. Dr Cornel has reported that he has no relationships relevant to the contents of this paper to disclose., (Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

People who experience incarceration have a heightened risk for cardiovascular disease (CVD) mediated by both traditional and incarceration-specific risk factors related to their environment. In this Viewpoint, we summarize what is known about the epidemiology and management of acute CV events, specifically acute myocardial infarction (AMI), congestive heart failure exacerbation (CHFe), and stroke, among people who are incarcerated. We also highlight gaps in available evidence. Our literature review found no studies that provided population-based rates (e.g., events per 1,000 incarcerated persons per year) of AMI, CHFe, or stroke in people who are incarcerated. Similarly, we did not identify any empirical studies that systematically described the treatment of AMI, CHFe, or stroke in this population. We outline a series of research studies that should be conducted to inform future interventions and guide quality improvement efforts.

Aims: Given the extremely limited regeneration potential of the heart, one of the most effective strategies to reduce the prevalence and mortality of coronary artery disease is prevention. Short-chain fatty acids (SCFAs), which are by-products of beneficial probiotics, have been reported to possess cardioprotective effects. Despite their beneficial roles, delivering SCFAs and maintaining their effective concentration in plasma present major challenges. Therefore, in the present study, we aimed to devise a strategy to prevent coronary heart disease effectively by using engineered probiotics to continuously release SCFAs in vivo., Methods and Results: We engineered a novel probiotic cocktail, namely EcN&#95;TL, from the commercially available Escherichia coli Nissle 1917 (EcN) strain to continuously secrete SCFAs by introducing the propionate and butyrate biosynthetic pathways. Oral administration of EcN&#95;TL enhanced and maintained an effective concentration of SCFAs in the plasma. As a preventative strategy, we observed that daily intake of EcN&#95;TL for 14 days prior to ischaemia-reperfusion injury significantly reduced myocardial injury and improved cardiac performance compared with EcN administration. We uncovered that EcN&#95;TL's protective mechanisms included reducing neutrophil infiltration into the infarct site and promoting the polarization of wound healing macrophages. We further revealed that SCFAs at plasma concentration protected cardiomyocytes from inflammation by suppressing the NF-κB activation pathway., Conclusion: These data provide strong evidence to support the use of SCFA-secreting probiotics to prevent coronary heart disease. Since SCFAs also play a key role in other metabolic diseases, EcN&#95;TL can potentially be used to treat a variety of other diseases., Competing Interests: Conflict of interest: none declared., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Ventricular fibrillation (VF)-induced cardiac arrest frequently complicates ST-segment elevation myocardial infarction (STEMI). Although larger infarct sizes (IS) correlate with a higher risk of VF, the influence of VF itself on IS has remained poorly investigated. To address this knowledge gap, we analyzed the effect of VF on IS in patients and two experimental models. From a prospective cohort, 30 STEMI patients with VF were matched 1:2 with STEMI patients without VF on the common determinants of IS. The primary endpoint was IS, assessed using the 48-h area under the curve (AUC) for troponin. We also compared IS in pigs with/without spontaneous VF during STEMI (n = 15/group), and in an isolated rat heart model of myocardial infarction with/without electrically induced VF (n = 7/group). After matching, the patient characteristics, including the area at risk (AR), were similar. IS was 33% lower in the VF group compared to the control group (troponin AUC 1.6 [0.5-3.3] 10 6 arbitrary units vs. 2.4 [0.9-4.1] 10 6 arbitrary units; p < 0.05), but infarct scar size (assessed using MRI and ECG) did not differ between the groups at 1 and 6 months. In both experimental models, IS, expressed as a percentage of AR, was lower (p < 0.05) in the VF group than in the control group. When common determinants of IS are comparable, VF occurring prior to myocardial infarction reperfusion appears to be associated with smaller IS. Nevertheless, this finding, observed under specific experimental conditions and in a highly selected group of patients, was not associated with reduced infarct scar size.Registration (HIBISCUS-STEMI cohort): ClinicalTrials.gov NCT05794022., Competing Interests: Declarations. Conflict of interests: The authors reports that they have no relationships relevant to the contents of this paper to disclose., (© 2024. The Author(s).)

Atrial infarction is often undiagnosed in patients with underlying ischemic heart disease and is identified only later, upon autopsy. One of the main challenges in diagnosing the condition is its localization within the affected atria. Treatment of atrial infarction focuses on acute reperfusion therapy, long-term management of cardiovascular disease risk factors, consideration of antiarrhythmia medications, and anticoagulation therapy. This review covers the anatomy of the atrial vasculature, complications associated with atrial infarction, diagnostic criteria for use of electrocardiography and other imaging modalities, and overall prognosis and management., Competing Interests: Conflict of Interest Disclosure: The authors were not compensated or funded in any way for the preparation of this manuscript. This study has not been submitted elsewhere. We understand and agree that if the manuscript is accepted for publication, copyright in the article, including the right to reproduce the article in all forms and media, shall be assigned to the publisher., (© 2024 The Authors. Published by The Texas Heart Institute®.)

Rationale and Objectives: The aim of the present retrospective study was to evaluate the prognostic role of the extracellular volume fraction (ECV) in patients with myocardial infarction (MI) and myocardial infarction with nonobstructive coronary arteries (MINOCA). The present study hypothesized that ECV is associated with major adverse cardiovascular events (MACEs) in MI and MINOCA patients., Materials and Methods: Cardiac magnetic resonance (CMR) imaging was performed on 351 consecutive patients (mean age: 58 ± 12 years; 252 [71.8%] males) who were diagnosed with MI between October 2015 and November 2023. From CMR imaging, the extent of late gadolinium enhancement (LGE), native T1 and ECV were derived. Patients were categorized into groups according to the degree of coronary artery stenosis, namely, patients with MINOCA and patients with obstructive MI. Follow-up was performed to assess MACEs., Results: The final cohort consisted of 61 MINOCA patients and 290 obstructive MI patients. During a mean follow-up of 27 ± 16 months, there was no statistically significant difference in the incidence of MACEs between patients with MINOCA and those with obstructive MI, and the two groups of patients had similar ECVs (32.2 ± 3.6 vs. 32.3 ± 6.0, p = 0.864). According to the multivariate Cox regression, ECV was an independent predictor of MACEs (HR: 1.13; p < 0.001) and significantly improved the prognostic value of the baseline multivariate models (C-statistic improvement: 0.816-0.864, p = 0.001). Similarly, ECV maintained an independent association with MACEs in the MINOCA (HR: 1.35; p < 0.001) and obstructive MI (HR: 1.13; p < 0.001) groups., Conclusion: In MI and MINOCA patients, ECV is an independent predictor of MACEs. MINOCA is not a benign disease, and its long-term prognosis is as poor as that of patients with obstructive MI., Competing Interests: Declaration of Competing Interest None declared., (Copyright © 2024 The Association of University Radiologists. Published by Elsevier Inc. All rights reserved.)

Background: Aberrant alternative splicing (AS) events, triggered by the alterations in serine/arginine splicing factor 1 (SRSF1), a member of the SR protein family, have been implicated in various pathological processes. However, the function and mechanism of SRSF1 in cardiovascular diseases remain unclear., Results: In this study, we found that the expression of SRSF1 was significantly down-regulated in the hearts of mice with acute myocardial infarction (AMI) and H9C2 cells exposed to H 2 O 2 . Moreover, in vivo experiments utilizing adeno-associated virus serotype 9-mediated SRSF1 overexpression improved cardiac function and reduced infarct size in AMI mice. Mechanistically, we employed RNA-seq assay to identify AS aberrations associated with altered SRSF1 level in cardiomyocytes, and found that SRSF1 regulates the splice switching of Bcl2L12. Further study showed that silencing SRSF1 inhibits the inclusion of exon7 in Bcl2L12. Importantly, the truncated Bcl2L12 lacked the necessary structural elements and failed to interact with p53, thus compromising its ability to suppress apoptosis., Conclusions: Our study unraveled the role of SRSF1 as a splicing factor involved in the regulation of Bcl2L12 splice switching, thereby exerting an anti-apoptotic effect through the p53 pathway, which provides new insights into potential approaches targeting cardiomyocyte apoptosis in cardiovascular diseases., Competing Interests: Declarations. Ethics approval and consent to participate: The use of laboratory animals was approved by the Ethics Committee of Shenzhen University (No. IACUC-202300046) and followed the Guidelines for the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (publication No. 85 − 23; revised, 1996). Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2024. The Author(s).)

Background: Electrolyte imbalances are commonly observed in individuals diagnosed with myocardial infarction (MI). The levels of serum sodium have been linked to unfavorable outcomes in relation to MI. Additionally, there exists a correlation between serum sodium and serum chloride, although the combined influence of these electrolytes on the prognosis of MI patients has not been extensively studied. Consequently, our study aimed to examine whether an autonomous association exists between the sodium-to-chloride (Na/Cl) ratio and mortality rates during hospitalization among patients admitted to intensive care unit (ICU) with MI., Methods: A retrospective cohort study analysis was conducted on the Na/Cl ratio within the ICU from 2008 to 2019. Patients diagnosed with MI were divided into two groups based on a predetermined cutoff value for the Na/Cl ratio. Various statistical models, including the Cox proportional hazard model, generalized additive model, and two-piecewise linear regression model, were employed to assess the relationship between the initial Na/Cl ratio upon admission and the likelihood of in-hospital mortality while accounting for other relevant covariates., Results: After adjusting for all other factors, the study revealed that the Na/Cl ratio exhibited an independent association with in-hospital mortality (HR = 1.28; 95% CI: 1.11-1.47, P < 0.001). Further analysis indicated a nonlinear relationship between the Na/Cl ratio and in-hospital mortality among patients with MI, with a threshold at approximately 1.37. Specifically, if the Na/Cl ratio exceeded 1.37, there was a significant and progressively increasing likelihood of mortality during hospitalization (HR = 1.46; 95% CI: 1.20-1.77)., Conclusion: The in-hospital mortality of patients admitted to ICU with MI is predicted independently by the ratio of sodium to chloride (Na/Cl). A curvilinear correlation was observed between the Na/Cl ratio and in-hospital mortality, with a statistically significant threshold identified at 1.37., Competing Interests: Declarations. Ethics approval and consent to participate: The studies involving human participants were reviewed and approved by the Institutional Review Boards of Massachusetts Institute of Technology (Cambridge, MA, USA) and Beth Israel Deaconess Medical Center (Boston, MA, USA). Written informed consent for participation was not required for this study in accordance with the national legislation and the institutional requirements. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2024. The Author(s).)

Purpose: To investigate the effect of first 24-hour (24-h) urine output (UO) on in-hospital and 1-year mortality in patients admitted to intensive care units due to acute myocardial infarction., Methods: This was a retrospective cohort study based on the medical information mart for intensive care IV database involving patients admitted to intensive care units due to acute myocardial infarction. Patients were classified as low UO (LUO), high UO (HUO), and middle UO with a first 24-h UO below 800 ml, over 2500 ml, or in between, respectively. The primary outcome was in-hospital mortality and the secondary outcome was 1-year mortality., Results: A total of 4337 patients were involved. Taking middle UO group as reference, after adjusting for confounders including age, gender, height, weight, comorbidity, occurrence of cardiogenic shock, revascularization, blood pressure, creatinine, N-terminal pro-brain natriuretic peptide, and use of loop diuretics, LUO was independently associated with higher in-hospital mortality [odds ratio 4.05, 95% confidence interval (CI): 3.12-5.26], while HUO was an independent protective factor (odds ratio 0.52, 95% CI: 0.35-0.77). In the multivariant Cox regression model, LUO was an independent risk factor for 1-year mortality (hazard ratio 2.65, 95% CI: 2.16-3.26), while HUO did not show significant association., Conclusion: In patients admitted to intensive care units due to acute myocardial infarction, first 24-h UO <800 ml was a strong predictor for higher in-hospital and 1-year mortality, while first 24-h UO over 2500 ml was associated with lower in-hospital mortality but not long-term mortality., (© The Author(s) 2024. Published by Oxford University Press on behalf of Fellowship of Postgraduate Medicine. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Ethnopharmacological Relevance: Cardiac apoptosis has been reported to be involved in the development of Heart failure (HF) after Myocardial infarction (MI). As a traditional Chinese medicine with cardioprotective properties, Gualou Xiebai Banxia Decoction (GXBD) is therapeutically effective in treating MI. However, whether GXBD regulates cardiac apoptosis in HF after MI remains unknown, and the underlying mechanisms still unclear., Aim of the Study: This study aimed to explore the effects and potential mechanisms of GXBD on cardiac apoptosis after MI., Materials and Methods: The MI model was constructed by ligating the left anterior descending coronary artery (LAD) in mice. The cardioprotective effects of GXBD were determined by echocardiography, masson staining, and hematoxylin and eosin (HE) staining. Bioinformatics analysis and network Pharmacology were used to explore the underlying molecular mechanisms of GXBD in MI. The effects of GXBD on apoptosis as well as the ALDH2 were examined by TUNEL staining, Immunohistochemistry (IHC), and Western blot (WB). Additionally, the effects of GXBD on oxidative stress, apoptosis and the ALDH2 in cardiomyocytes (H9c2) were investigated using reactive oxygen species (ROS) detection, Hoechst33342/PI stainingand and WB. Moreover, the effects of suppressing and overexpressing ALDH2 in H9c2 cells were further examined., Results: Target prediction analysis showed that ALDH2 was a key target of GXBD which could ameliorate myocardial infarction. GXBD dose-dependently reduced cardiomyocyte apoptosis and ventricular dysfunction. In vivo experiments, GXBD activated ALDH2 enzymatic activity and inhibited the expression levels of Bax, Bcl-2, Cleaved Caspase 3, and Caspase 9. In vitro experiments, GXBD inhibited apoptosis in H9c2 cells. ALDH2 activation enhanced these inhibitory effects of GXBD while silencing of ALDH2 significantly reversed these inhibitory effects of GXBD., Conclusion: GXBD exerts inhibitory effects on oxidative stress and cardiomyocyte apoptosis in mice after MI, suppresses H9c2 oxidative stress and apoptosis through activation of the enzyme activity of ALDH2., Competing Interests: Declaration of Competing Interest ☒ The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)

Aims: The aim of this study was determine the incidence of major adverse cardiac events within 30 and 365-days among patients discharged from emergency departments (EDs), following a single high-sensitivity cardiac troponin I test result below or close to the limits of detection (LoD)., Methods and Results: Patients ≥20 years old who presented to four EDs from mid-2014 to end-2015, underwent a single high-sensitivity troponin test and were discharged were included. Data from ED presentations, hospital admissions, mortality records, and pathology laboratories were linked and harmonized. High-sensitivity troponin levels were categorized as below (<2 ng/L) or close to (<5 ng/L) the LoD. The primary outcome was cardiovascular death and myocardial infarction (MI), identified using ICD-10-AM codes. In a cohort of 6633 patients, 49% had high-sensitivity troponin levels below the LoD (<2 ng/L), and 79% had levels <5 ng/L. There were no primary outcome events at 30-day follow-up among patients with high-sensitivity troponin results below 2 or 5 ng/L. At 365-days, there were 5 (0.15%) and 11 (0.21%) primary outcome events for patients with high-sensitivity troponin results below 2 and 5 ng/L, indicating negative predictive values of 99.85% and 99.79%., Conclusion: These findings confirm that patients with a single very low level of high-sensitivity troponin on presentation to EDs are at low risk of MI and cardiovascular death at 30 and 365 days, supporting the safety of a triage strategy incorporating a single high-sensitivity troponin result below the LoD to identify patients at low-risk, who may be suitable for expedited discharge., Competing Interests: Conflict of interest: Derek Chew has received research support from Roche Diagnostics and Siemens Healthineers. All other authors have no competing interests to declare., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Background: Despite increasing evidence on the benefits of statin therapy for acute myocardial infarction (AMI), differential outcomes in accordance with statin intensity have not been evaluated in patients with AMI and low-density lipoprotein cholesterol (LDL-C) levels < 55 mg/dL. Therefore, this study aimed to compare the clinical outcomes of high- and moderate-intensity statin therapy in this population., Methods: A total of 752 participants with AMI and LDL-C levels < 55 mg/dL from a Korean nationwide multicenter observational cohort (2016-2020) were included and categorized into two groups: high-intensity statin group (n = 384) and moderate-intensity statin group (n = 368). The primary outcome was 1-year major adverse cardiac and cerebrovascular events (MACCEs). Propensity score matching (PSM) and Cox models were used to determine whether statin intensity independently influenced the primary outcome., Results: Compared to the moderate-intensity statin group, the high-intensity statin group had a comparable risk of MACCE in all Cox models and PSM-adjusted analyses. The cumulative incidence of MACCE was comparable between the two groups., Conclusions: Statin intensity appeared to have no significant impact on clinical outcomes in AMI patients with LDL-C levels < 55 mg/dL. These results underscore the need for further investigations aimed at refining treatment strategies for this specific patient cohort, potentially reducing treatment-related burdens without compromising clinical effectiveness.