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Fully restoring the lost population of cardiomyocytes and heart function remains the greatest challenge in cardiac repair post myocardial infarction. In this study, a pioneered highly ROS-eliminating hydrogel was designed to enhance miR-19a/b induced cardiomyocyte proliferation by lowering the oxidative stress and continuously releasing miR-19a/b in infarcted myocardium in situ. In vivo lineage tracing revealed that ∼20.47 % of adult cardiomyocytes at the injected sites underwent cell division in MI mice. In MI pig the infarcted size was significantly reduced from 40 % to 18 %, and thereby marked improvement of cardiac function and increased muscle mass. Most importantly, our treatment solved the challenge of animal death--all the treated pigs managed to live until their hearts were harvested at day 50. Therefore, our strategy provides clinical conversion advantages and safety for healing damaged hearts and restoring heart function post MI, which will be a powerful tool to battle cardiovascular diseases in patients.

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Acute Myocardial Infarction (AMI) has seen rising cases, particularly in younger people, leading to public health concerns. Standard treatments, like coronary artery recanalization, often don't fully repair the heart's microvasculature, risking heart failure. Advances show that Mesenchymal Stromal Cells (MSCs) transplantation improves cardiac function after AMI, but the harsh microenvironment post-AMI impacts cell survival and therapeutic results. MSCs aid heart repair via their membrane proteins and paracrine extracellular vesicles that carry microRNA-125b, which regulates multiple targets, preventing cardiomyocyte death, limiting fibroblast growth, and combating myocardial remodeling after AMI. This study introduces ultrasound-responsive phase-change bionic nanoparticles, leveraging MSCs' natural properties. These particles contain MSC membrane and microRNA-125b, with added macrophage membrane for stability. Using Ultrasound Targeted Microbubble Destruction (UTMD), this method targets the delivery of MSC membrane proteins and microRNA-125b to AMI's inflamed areas. This aims to enhance cardiac function recovery and provide precise, targeted AMI therapy.

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BACKGROUND AND AIMS: Recurrent events after myocardial infarction (MI) are common and often originate from native non-culprit (NC) lesions that are non-flow limiting. These lesions consequently pose as targets to improve long-term outcome. It is, however, largely unknown whether these lesions differ between sexes. The aim of this study was to assess such potential differences. METHODS: From the PECTUS-obs study, we assessed sex-related differences in plaque characteristics of fractional flow reserve (FFR)-negative intermediate NC lesions in 420 MI-patients. RESULTS: Among the included patients, 80 (19.1 %) were female and 340 (80.9 %) male. Women were older and more frequently had hypertension and diabetes. In total, 494 NC lesions were analyzed. After adjustment for clinical characteristics and accounting for within-patients clustering, lesion length was longer in female patients (20.8 ± 10.0 vs 18.3 ± 8.5 mm, p = 0.048) and minimum lumen area (2.30 ± 1.42 vs 2.78 ± 1.54 mm2, p < 0.001) and minimum lumen diameter (1.39 ± 0.45 vs 1.54 ± 0.44 mm, p < 0.001) were smaller. The minimum fibrous cap thickness was smaller among females (96 ± 53 vs 112 ± 72 µm, p = 0.025), with more lesions harboring a thin cap fibroatheroma (39.3 % vs 24.9 %, p < 0.001). Major adverse cardiovascular events at two years occurred in 6.3 % of female patients and 11.8 % of male patients (p = 0.15). CONCLUSIONS: FFR-negative NC lesions after MI harbored more high-risk plaque features in female patients. Although this did not translate into an excess of recurrent events in female patients in this modestly sized cohort, it remains to be investigated whether this difference affects clinical outcome.

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Sleep apnea involves almost one billion individuals throughout the world, including 40 million Americans. Of major medical concern is the fact that the prevalence of sleep apnea is significantly increasing due to the epidemic of obesity, physical inactivity, and diabetes mellitus which are important risk factors for the development and persistence of sleep apnea in individuals. Sleep apnea is characterized by multiple episodes of apnea or hypopnea during sleep, which cause nocturnal arousals, gasping for breath during the night, daytime sleepiness, irritability, forgetfulness, fatigue and recurrent headaches. Obstructive sleep apnea occurs when upper airway obstruction occurs in an individual during sleep with absent or markedly reduced airflow in the presence of continued activity of inspiratory thoracic and diaphragmatic muscles. Central sleep apnea is defined as the absence or the significant reduction of naso-oral airflow due to the withdrawal during sleep of ponto-medullary respiratory center stimulation of the nerves of the inspiratory thoracic and diaphragmatic muscles and absence of contraction of these muscles during apnea. Complex sleep apnea occurs when an individual exhibits characteristics of both obstructive and central sleep apnea. The severity of sleep apnea is measured by polysomnography and the apnea hypopnea index (AHI), which is the average number of apneas and hypopneas per hour of sleep measured by polysomnography. Sleep apnea is mild if the AHI is 5-14/hour with no or mild symptoms, moderate if the AHI is 15 to 30/hour with occasional daytime sleepiness, and severe if the AHI is >30/hour with frequent daytime sleepiness that interferes with the normal activities of daily life. Chronic sleep apneas and hypopneas followed by compensatory hyperpneas are associated with significant adverse cardiovascular consequences including: 1) recurrent hypoxemia and hypercarbia; 2) Increased sympathetic nerve activity and decreased parasympathetic nerve activity; 3) oxidative stress and vascular endothelial dysfunction; and 4) cardiac remodeling and cardiovascular disease. Moderate or severe sleep apnea significantly increases the risk of coronary artery disease, congestive heart failure, cerebral vascular events (strokes), and cardiac dysrhythmias, and also increase the morbidity and mortality of these diseases. Nevertheless, sleep apnea is currently underdiagnosed and untreated in many individuals due to the challenges in the prediction and detection of sleep apnea and a lack of well-defined optimal treatment guidelines. Chronic continuous positive airway pressure for ≥4 hours/night for >70% of nights is beneficial in the treatment of patients with sleep apnea. CPAP Improves sleep quality, reduces the AHI, augments cardiac output and increases oxygen delivery to brain and heart, reduces resistant hypertension, decreases cardiac dysrhythmias, and reduces daytime sleepiness. The present article discusses the diagnosis of obstructive sleep apnea, central sleep apnea, and complex apnea. Thereafter the important pathophysiologic mechanisms in sleep apnea and the relationship of these pathophysiologic mechanics to atherosclerotic vascular disease are reviewed. Guidelines are then provided for the treatment of mild, moderate and severe sleep apnea In order to reduce the cardiovascular morbidity and mortality caused by sleep apnea and facilitate the diagnosis and the long-term, effective treatment of sleep apnea in patients, the close cooperation is necessary of cardiovascular specialists, pulmonary specialists, and respiratory therapy/ rehabilitation specialists.

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Acute myocardial infarction (AMI) is a heart lesion, that endangers the life safety of patients. This study focused on exploring the clinical effect of miR-542-3p on AMI and no-reflow after percutaneous coronary intervention (PCI). Serum samples were collected from 100 AMI emergency inpatients. The expression of miR-542-3p was quantified by qPCR. The predictive role of miR-542-3p was disclosed by plotting ROC curve. In addition, AMI subjects were cataloged into a group of no-reflow and normal reflow group. The risk factors of no-reflow were estimated by logistic regression analysis. In the serum samples of AMI patients, the level of miR-542-3p showed a pattern of decreasing. MiR-542-3p expression represented a high sensitivity and specificity of the prediction of AMI. A decrease of miR-542-3p content was revealed in AMI patients without reflow after PCI. Logistic regression results reflected that miR-542-3p was an independent biomarker for no-reflow. The declined miR-542-3p expression was a predictive marker for AMI and no-reflow in AMI patients.

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BACKGROUND: There are limited data on volume-outcome relationships in acute myocardial infarction (AMI) with cardiogenic shock (CS). OBJECTIVES: In this study, the authors sought to evaluate the association between hospital percutaneous coronary intervention (PCI) volume and readmission after AMI-CS. METHODS: Adult AMI-CS patients were identified from the Nationwide Readmissions Database for 2016-2019 and were categorized into hospital quartiles (Q1 lowest volume to Q4 highest) based on annual inpatient PCI volume. Outcomes of interest included 30-day all-cause, cardiac, noncardiac, and heart-failure (HF) readmissions. RESULTS: There were 49,558 AMI-CS admissions at 3,954 PCI-performing hospitals. Median annual PCI volume was 174 (Q1-Q3: 70-316). Patients treated at Q1 hospitals were on average older, female, and with higher comorbidity burden. Patients at Q4 hospitals had higher rates of noncardiac organ dysfunction, complications, and use of cardiac support therapies. Overall, 30-day readmission rate was 18.5% (n = 9,179), of which cardiac, noncardiac, and HF readmissions constituted 56.2%, 43.8%, and 25.8%, respectively. From Q1 to Q4, there were no differences in 30-day all-cause (17.6%, 18.4%, 18.2%, 18.7%; P = 0.55), cardiac (10.9%, 11.0%, 10.6%, 10.2%; P = 0.29), and HF (5.0%, 4.8%, 4.8%, 4.8%; P = 0.99) readmissions. Noncardiac readmissions were noted more commonly in higher quartiles (6.7%, 7.4%, 7.7%, 8.5%; P = 0.001) but was not significant after multivariable adjustment. No relationship was noted between hospital PCI volume as a continuous variable and readmissions. CONCLUSIONS: In AMI-CS, there was no association between hospital annual PCI volume and 30-day readmissions despite higher acuity in the higher volume PCI centers suggestive of better care pathways for CS at higher volume centers.

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Background: Interleukin-6-receptor inhibition with tocilizumab improves myocardial salvage in patients with ST-segment elevation myocardial infarction (STEMI). Reduced levels of neutrophil extracellular traps (NETs), which consist of nuclear material studded with proteins released upon neutrophil activation, might contribute to this effect. Objectives: The purpose of this study was to evaluate the effect of tocilizumab on NETs and investigate the association between NETs and myocardial injury in patients with STEMI. Methods: In the ASSAIL-MI study, 199 patients with STEMI were randomized to tocilizumab or placebo during percutaneous coronary intervention. In this substudy, we analyzed blood levels of the NET markers double-stranded deoxyribonucleic acid (dsDNA), myeloperoxidase-DNA, and citrullinated histone 3 (H3Cit) at admission and after 24 hours and 3 to 7 days. In a subgroup of patients, we assessed regulation of transcripts related to the formation of NETs. We also investigated associations between NET markers and the myocardial salvage index (MSI). Results: All NET markers were lower in the tocilizumab group than in the placebo group at 3 to 7 days (all P < 0.04). Several NET-related pathways were downregulated in the tocilizumab group. The beneficial effect of tocilizumab on the MSI seemed to be partly dependent on reduction of NETs (structural equation modeling: 0.05, P = 0.001 [dsDNA] and 0.02, P = 0.055 [H3Cit]). Patients with NETs in the 3 lowest quartiles had higher MSI than patients in quartile 4 (10.9 [95% CI: 4.0-15.0] [dsDNA] and 8.9 [95% CI: 2.0-15.9] [H3Cit], both P = 0.01). Conclusions: NETs were reduced by tocilizumab and associated with myocardial injury. The effect of tocilizumab on MSI might be mediated through reduced NETs. (ASSessing the Effect of Anti-IL-6 Treatment in Myocardial Infarction: The ASSAIL-MI Trial [ASSAIL-MI]; NCT03004703).

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Objective: Evaluate the effects of sodium-glucose cotransporter 2 inhibitor (SGLT2i) on cardiovascular and cerebrovascular diseases. Methods: Articles of SGLT2i on cardiovascular and cerebrovascular diseases were searched. Two authors independently screened the literature, extracted the data, assessed the quality of the study and performed statistical analyses using Review Manager 5.4. Results: Random-effect model was used to merge the OR values, and the pooled effect showed that SGLT2i had significant preventive effects on cardiovascular death (OR=0.76, 95%CI 0.64 to 0.89), myocardial infarction (OR=0.90, 95%CI 0.84 to 0.96), heart failure (OR=0.69, 95%CI 0.64 to 0.74) and all-cause mortality (OR=0.65, 95%CI 0.58 to 0.73). Empagliflozin, dapagliflozin and canagliflozin all reduced the incidence of heart failure (OR=0.72, 95%CI 0.64 to 0.82; OR=0.56, 95%CI 0.39 to 0.80; OR=0.62, 95%CI 0.53 to 0.73), but only dapagliflozin displayed a favorable effect on inhibiting stroke (OR=0.78, 95%CI 0.63 to 0.98). SGLT2i could prevent stroke (OR=0.86, 95%CI 0.75 to 0.99), heart failure (OR=0.63, 95%CI 0.56 to 0.70) and all-cause mortality (OR=0.64, 95%CI 0.57 to 0.72) compared to DPP-4i. Furthermore, SGLT2i could reduce the incidence of heart failure (OR=0.72, 95%CI 0.67 to 0.77) and cardiovascular death (OR=0.72, 95%CI 0.54 to 0.95) in patients with high-risk factors. Conclusions: SGLT2i affects cardiovascular death, myocardial infarction, heart failure and all-cause mortality. Only dapagliflozin displayed a favorable effect on inhibiting stroke. SGLT2i could prevent stroke, heart failure and all-cause mortality compared to DPP-4i. In addition, SGLT2i significantly reduced the development of heart failure and cardiovascular death in patients with high-risk factors. Systematic review registration: https://www.crd.york.ac.uk/prospero, identifier CRD42024532783.

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BACKGROUND: The contemporary healthcare resource utilization following an acute myocardial infarction (MI) is not well known. METHODS: All patients admitted due to MI between 01/2015 and 12/2021 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. RESULTS: Of 6804 patients admitted due to MI, 6556 were discharged alive. Median age was 69 years, 60% were male, and 77% had non-ST elevation MI (NSTEMI); 17% (1090) 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%), 1372 (21%) and 2306 (35%), respectively, with a higher readmission rate in patients with NSTEMI, prior heart failure (HF), new-onset HF, and left ventricular ejection fraction (LVEF) ≤40%. ED visits at 12 months for any cause were 2401 (37%) of which 1321 (55%) were for any CV cause, with a higher incidence in patients with prior HF. Of the 6556 patients, 4102 (63%) had at least one primary care visit in the past year, 5009 (76%) had CV specialty visits, and 3860 (59%) had non-CV visits, with a similar distribution across subgroups. CONCLUSIONS: Patients hospitalized with an MI had a high risk of subsequent hospital readmissions, and ED and outpatient visits, especially amongst those with a prior HF diagnosis and those discharged with both an MI and HF diagnosis.

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Promoting angiogenesis and modulating the inflammatory microenvironment are promising strategies for treating acute myocardial infarction (MI). Macrophages are crucial in regulating inflammation and influencing angiogenesis through interactions with endothelial cells. However, current therapies lack a comprehensive assessment of pathological and physiological subtleties, resulting in limited myocardial recovery. In this study, legumain-guided ferulate-peptide nanofibers (LFPN) are developed to facilitate the interaction between macrophages and endothelial cells in the MI lesion and modulate their functions. LFPN exhibits enhanced ferulic acid (FA) aggregation and release, promoting angiogenesis and alleviating inflammation. The multifunctional role of LFPN is validated in cells and an MI mouse model, where it modulated macrophage polarization, attenuated inflammatory responses, and induces endothelial cell neovascularization compare to FA alone. LFPN supports the preservation of border zone cardiomyocytes by regulating inflammatory infiltration in the ischemic core, leading to significant functional recovery of the left ventricle. These findings suggest that synergistic therapy exploiting multicellular interaction and enzyme guidance may enhance the clinical translation potential of smart-responsive drug delivery systems to treat MI. This work emphasizes macrophage-endothelial cell partnerships as a novel paradigm to enhance cell interactions, control inflammation, and promote therapeutic angiogenesis.

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BACKGROUND: Cardiac troponin (cTn) is key in diagnosing myocardial infarction (MI). After MI, the clinically observed half-life of cTn has been reported to be 7 to 20 hours, but this estimate reflects the combined elimination and simultaneous release of cTn from cardiomyocytes. More precise timing of myocardial injuries necessitates separation of these 2 components. We used a novel method for determination of isolated cTn elimination kinetics in humans. METHODS: Patients with MI were included within 24 hours after revascularization and underwent plasmapheresis to obtain plasma with a high cTn concentration. After at least 3 weeks, patients returned for an autologous plasma retransfusion followed by blood sampling for 8 hours. cTn was measured with 5 different high-sensitivity cTn assays. RESULTS: Of 25 included patients, 20 participants (mean age, 64.5 years; SD, 8.2 years; 4 women [20%]) received a retransfusion after a median of 5.8 weeks (interquartile range, 5.0-6.9 weeks) after MI. After retransfusion of a median of 620 mL (range, 180-679 mL) autologous plasma, the concentration of cTn in participants' blood increased 4 to 445 times above the upper reference level of the 5 high-sensitivity cTn assays. The median elimination half-life ranged from 134.1 minutes (95% CI, 117.8-168.0) for the Elecsys high-sensitivity cTnT assay to 239.7 minutes (95% CI, 153.7-295.1) for the Vitros high-sensitivity cTnI assay. The median clearance of cTnI ranged from 40.3 mL/min (95% CI, 32.0-44.9) to 52.7 mL/min (95% CI, 42.2-57.8). The clearance of cTnT was 77.0 mL/min (95% CI, 45.2-95.0). CONCLUSIONS: This novel method showed that the elimination half-life of cTnI and cTnT was 5 to 16 hours shorter than previously reported. This indicates a considerably longer duration of cardiomyocyte cTn release after MI than previously thought. Improved knowledge of timing of myocardial injury may call for changes in the management of MI and other disorders with myocardial injury.

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BACKGROUND: National-level differences in myocardial infarction (MI) quality of care among Asian patients in the United States are unclear. We assessed the quality of MI care in the 6 largest US Asian ethnic groups. METHODS: Patients aged ≥18 years with ST-segment-elevation MI or non-ST-segment-elevation MI in the Get With The Guidelines-Coronary Artery Disease registry (711 US hospitals, 2015-2021) were assessed. The odds of MI-related quality of care and process outcomes were evaluated in Asian Indian, Chinese, Filipino, Japanese, Korean, Vietnamese, and other Asian adults compared with non-Hispanic White adults. Sex-stratified logistic regression models were adjusted for age and clinical characteristics. RESULTS: There were 5691 Asian patients (1520 Asian Indian, 422 Chinese, 430 Filipino, 114 Japanese, 283 Korean, 553 Vietnamese, and 2369 other Asian) and 141 271 non-Hispanic White patients, overall 30% female, and mean age of 66.5 years. Relative to non-Hispanic White adults, among patients with ST-segment-elevation MI, door-to-ECG time ≤10 minutes was less likely in Asian Indian (adjusted odds ratio [aOR], 0.64 [95% CI, 0.50-0.82]), Chinese (aOR, 0.65 [95% CI, 0.46-0.93]), and Korean (aOR, 0.57 [95% CI, 0.33-0.97]) men and in other Asian women (aOR, 0.61 [95% CI, 0.41-0.90]). Door-to-balloon time ≤90 minutes was less likely in Asian Indian men (aOR, 0.71 [95% CI, 0.56-0.90]) and Filipina women (aOR, 0.48 [95% CI, 0.24-0.98]). In patients with ST-segment-elevation MI or non-ST-segment-elevation MI, optimal medical therapy for MI was less likely in Korean men (aOR, 0.65 [95% CI, 0.47-0.90]) and more likely in Asian Indian men (aOR, 1.22 [95% CI, 1.06-1.40]) and women (aOR, 1.32 [95% CI, 1.04-1.67]) and Filipina women (aOR, 1.84 [95% CI, 1.27-2.67]). CONCLUSIONS: MI quality of care varies among US Asian patients with ST-segment-elevation MI and non-ST-segment-elevation MI. Quality improvement programs must identify and address the factors that result in suboptimal MI quality of care among US Asian patients.

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BACKGROUND: Little is known about the underlying factors contributing to unfavourable clinical outcomes in patients with diabetes mellitus (DM) complicated by new-onset acute myocardial infarction (AMI). The aim of this study was to investigate the impact of DM on the pathophysiologic features and prognosis of patients with new-onset AMI following successful revascularization by utilizing cardiac magnetic resonance (CMR). METHODS: Consecutive patients diagnosed with new-onset AMI between June 2022 and January 2024 were included. All patients underwent culprit vessel revascularization upon admission and CMR imaging 3-7 days later. The primary clinical endpoint of this study was the occurrence of major adverse cardiac and cerebrovascular events (MACCEs), for which the average follow-up was 10 months. RESULTS: A total of 72 patients were divided into a DM group (n = 23) and a non-DM group (n = 49). Multivariate logistic regression analysis revealed that DM was an independent risk factor for the occurrence of microvascular obstruction. Multivariate linear regression analysis found that DM was the influencing factor of global radial strain (B = -4.107, t = -2.328, p = 0.023), while fasting blood glucose influenced infarct segment myocardial radial strain (B = -0.622, t = -2.032, p = 0.046). DM independently contributed to the risk of MACCEs following successful revascularization in patients with AMI (p < 0.05). CONCLUSION: Comprehensive phenotypic characterization of myocardial injury and microcirculatory status could enable reliable identification of high-risk MACCEs in DM patients with new-onset AMI following successful revascularization.

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The management of cardiogenic shock is an ongoing challenge. Despite all efforts and tremendous use of resources, mortality remains high. Whilst reversing the underlying cause, restoring/maintaining organ perfusion and function are cornerstones of management. The presence of comorbidities and preexisting organ dysfunction increases management complexity, aiming to integrate the needs of vital organs in each individual patient. This review provides a comprehensive overview of contemporary literature regarding the definition and classification of cardiogenic shock, its pathophysiology, diagnosis, laboratory evaluation, and monitoring. Further, we distill the latest evidence in pharmacologic therapy and the use of mechanical circulatory support including recently published randomized-controlled trials as well as future directions of research, integrating this within an international group of authors to provide a global perspective. Finally, we explore the need for individualization, especially in the face of neutral randomized trials which may be related to a dilution of a potential benefit of an intervention (i.e., average effect) in this heterogeneous clinical syndrome, including the use of novel biomarkers, artificial intelligence, and machine learning approaches to identify specific endotypes of cardiogenic shock (i.e., subclasses with distinct underlying biological/molecular mechanisms) to support a more personalized medicine beyond the syndromic approach of cardiogenic shock.

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Ferroptosis is principally initiated by dysregulation of iron metabolism and excessive accumulation of ROS, which exacerbates myocardial injury during acute myocardial infarction (AMI). Previous studies have indeed demonstrated the significant involvement of long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) exerts its pleiotropic effects in the pathophysiology of myocardial infarction, heart failure and atherosclerosis by modulating inflammation, apoptosis, and oxidative stress. However, whether and how NEAT1 mediates myocardial ferroptosis remain unknown. In this study, we found that NEAT1 expression was significantly elevated in hypoxic HL-1 cells and AMI mice, while silencing of NEAT1 alleviated lipid peroxidation and myocardial ferroptosis both in vitro and in vivo. Mechanistically, NEAT1 directly sponged miR-450b-5p and negatively regulated its expression. In addition, miR-450b-5p directly targeted Acyl-CoA synthase long-chain family member 4 (ACSL4). Notably, inhibition of miR-450b-5p reversed the role of NEAT1 in AMI mice. Collectively, these findings newly illustrated that NEAT1 acts as a competitive endogenous RNA (ceRNA) of miR-450-5p in AMI. Especially, silencing of NEAT1 effectively ameliorated myocardium ischemia by suppression of ferroptosis via miR-450-5p/ACSL4 pathway, which providing a brand-new therapeutic strategy for myocardial ischemia injury.

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Precise quantification of myocardial infarction is crucial for evaluating the therapeutic strategies. We developed a robust, color-based semi-automatic algorithm capable of infarct region detection, isolation and quantification with four different histological staining techniques, and the isolation and quantification of diffuse fibrosis in the heart. Our method is developed based on the color difference in the infarct and non-infarct regions after histological staining. Mouse cardiac tissues stained with Masson's trichrome (MTS), hematoxylin and eosin (H&E), 2,3,5-Triphenyltetrazolium chloride and picrosirius red were included to demonstrate the performance of our method. We demonstrate that our algorithm can effectively identify and produce a clear visualization of infarct tissue for the four staining techniques. Notably, the infarct region on a H&E-stained tissue section can be clearly visualized after processing. The MATLAB-based program we developed holds promise in the infarct quantification. Additionally, our program can isolate and quantify the diffuse fibrotic elements from an MTS-stained cardiac section, which suggested the algorithm's potential for evaluating pathological cardiac fibrosis in diseased cardiac tissues. In conclusion, we demonstrate that this color-based algorithm is capable of accurately identifying, isolating and quantifying cardiac infarct regions with different staining techniques, as well as the diffuse and patchy fibrosis in MTS-stained cardiac tissues.

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We report a case of a 53-year-old male with inferolateral myocardial infarction, presenting an atypical Aslanger pattern on electrocardiogram (ECG). The ECG showed ST elevation in leads III, aVR, aVF, and posterior leads, with ST depression in II and V2-V6 with terminal positive T waves. Coronary angiography revealed total occlusion of the left circumflex artery (LCx) with significant stenosis of the left anterior descending (LAD) and right coronary artery (RCA). The LCx was successfully revascularized. This case highlights the importance of recognizing atypical Aslanger patterns, which may indicate multivessel coronary artery disease.