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Electrocardiogram (ECG) is an important tool for the detection of acute ST-segment elevation myocardial infarction (STEMI). However, machine learning (ML) for the diagnosis of STEMI complicated with arrhythmia and infarct-related arteries is still underdeveloped based on real-world data. Therefore, we aimed to develop an ML model using the Least Absolute Shrinkage and Selection Operator (LASSO) to automatically diagnose acute STEMI based on ECG features. A total of 318 patients with STEMI and 502 control subjects were enrolled from Jan 2017 to Jun 2019. Coronary angiography was performed. A total of 180 automatic ECG features of 12-lead ECG were input into the model. The LASSO regression model was trained and validated by the internal training dataset and tested by the internal and external testing datasets. A comparative test was performed between the LASSO regression model and different levels of doctors. To identify the STEMI and non-STEMI, the LASSO model retained 14 variables with AUCs of 0.94 and 0.93 in the internal and external testing datasets, respectively. The performance of LASSO regression was similar to that of experienced cardiologists (AUC: 0.92) but superior (p < 0.05) to internal medicine residents, medical interns, and emergency physicians. Furthermore, in terms of identifying left anterior descending (LAD) or non-LAD, LASSO regression achieved AUCs of 0.92 and 0.98 in the internal and external testing datasets, respectively. This LASSO regression model can achieve high accuracy in diagnosing STEMI and LAD vessel disease, thus providing an assisting diagnostic tool based on ECG, which may improve the early diagnosis of STEMI. [ABSTRACT FROM AUTHOR]

This study aimed to investigate whether recombinant human brain natriuretic peptide (rhBNP) regulated hypoxia-induced injury in H9c2 cardiomyocytes through lncRNA EGOT. H9c2 cardiomyocytes were cultured under normoxia and hypoxia (21% and 3% O 2 ) conditions, and whether hypoxia induced injury by assessing cell viability, apoptosis and autophagy. H9c2 cells were then treated with different doses of exogenous rhBNP (200, 600 and 900 nmol/L, respectively) and the effects of rhBNP on hypoxia-induced injury in H9c2 cells as well as the expression of EGOT were studied. In addition, the regulatory relationships between rhBNP and EGOT as well as between rhBNP and PI3K/AKT/mTOR pathway in hypoxia-treated H9c2 cells were investigated. Hypoxia significantly induced injury in H9c2 cells (inhibited cell viability and promoted cell apoptosis and autophagy) and decreased the expression of EGOT. However, administration of rhBNP alleviated hypoxia-induced injury in H9c2 cells and elevated expression of EGOT. Suppression of EGOT significantly reversed the effects of rhBNP on hypoxia-induced injury in H9c2 cells. Further studies showed that the effects of EGOT on cell viability and apoptosis were by positively regulating the expression of Cyclin D1. Moreover, rhBNP alleviated hypoxia-induced cell injury by activating PI3K/AKT/mTOR pathway in H9c2 cells. Our results reveal that rhBNP may play a protective role in attenuating hypoxia-induced injury in H9c2 cardiomyocytes via regulating lncRNA EGOT/Cyclin D1/PI3K/AKT/mTOR pathway axis. The findings will provide a new strategy for the treatment of heart failure induced by hypoxia. [ABSTRACT FROM AUTHOR]

Vascular disease is one of the most significant threats to the lives of patients suffering from diabetes, and chronic exposure of vascular endothelial cells to high glucose has been shown to significantly contribute to the process of endothelial cell dysfunction, one of the earliest events in diabetes-associated vascular disease. Nucleotide oligomerization domain (NOD)-like receptor pyrin domain-containing 3 (NLRP3) inflammasome plays a key role in initiating the inflammatory process by facilitating the production of interleukin-1β (IL-1β) and IL-18. ASC and caspase 1 are also implicated in NLRP3 inflammasome-mediated chronic inflammation. While under normal conditions, a balance exists between oxidants and antioxidants, exposure to high glucose significantly increases the production of ROS, which is enhanced by NOX4 expression. In the present study, we explored the role of orexin A, an endogenous peptide produced in the hypothalamus, in high glucose-induced activation of the NLRP3 inflammasome, oxidative stress, and expression of several key cytokines. Our findings demonstrate that orexin A exerts potent antioxidant effects in human aortic endothelial cells exposed to high glucose by inhibiting mitochondrial ROS and expression of NOX4 at both the mRNA and protein levels as revealed by MitoSOX staining, real-time PCR, and Western blot analysis. We also show that orexin A inhibits high glucose-induced expression of TxNIP, which is crucial to the activation of the NLRP3 inflammasome, as well as that of HMGB1. We confirmed via real-time PCR and Western blot analysis that orexin A suppressed the production of the inflammatory cytokines IL-1β and IL-18. Additionally, through SIRT1 knockdown siRNA experimentation, we confirmed that SIRT1 knockdown abolishes the effects of orexin A described above, thereby indicating a critical role of SIRT in the capacity of orexin A to ameliorate high glucose-induced oxidative stress and activation of NLRP3 inflammasome. [ABSTRACT FROM AUTHOR]

Background: The relationship between remnant cholesterol (RC) and atrial fibrillation (AF) remains unclear., Objective: To comprehensively explore the association between RC characteristics and new-onset AF., Methods: Data from five follow-up visits of the ARIC study were analyzed. RC were multidimensionally evaluated in four characteristics, including baseline level, variability, cumulative exposure and trajectory. Baseline RC was obtained from the initial visit (V1), and new-onset AF was monitored in V2 to V5 (cohort 1, n=14450). RC variability, cumulative RC and RC trajectory were calculated by RC values gathered from V1 to V3, and new-onset AF was monitored in V4 and V5 (cohort 2, n=11012). Participants were divided into four groups based on quartiles or trajectories. Cox proportional hazards analyses were used to investigate the relationship between RC characteristics and AF., Results: Following a median follow-up of 22.39 years in cohort 1 and 16.71 years in cohort 2, a total of 1993 AF events in cohort 1 and 1571 in cohort 2 were identified. Participants with the highest quartile exhibited an elevated risk of new-onset AF, with the multivariable-adjusted HRs of 1.35 (P=0.009) for baseline RC and 1.26 (P=0.09) for RC variability. Although the highest quartile of cumulative RC (P=0.130) and the high-increasing trajectory (P=0.322) did not demonstrate a statistically significant association with AF occurrence, they indicate a trend towards a heightened risk., Conclusion: Our findings reveal that higher levels of RC, particularly at baseline and in variability, are associated with an increased risk of AF., (Copyright © 2024. Published by Elsevier Inc.)

Background: Deposition of adipose tissue may have a promoting role in the development of diabetic complications. This study is aimed at investigating the relationship between adipose tissue thickness and risk of contrast-induced nephropathy (CIN) in patients with Type 2 diabetes mellitus (T2DM). Methods: A total of 603 T2DM patients undergoing percutaneous coronary angiography or angioplasty with suspicious or confirmed stable coronary artery disease were enrolled in this study. The thicknesses of perirenal fat (PRF), subcutaneous fat (SCF), intraperitoneal fat (IPF), and epicardial fat (ECF) were measured by color Doppler ultrasound, respectively. The association of various adipose tissues with CIN was analyzed. Results: Seventy-seven patients (12.8%) developed CIN in this cohort. Patients who developed CIN had significantly thicker PRF (13.7 ± 4.0 mm vs. 8.9 ± 3.6 mm, p < 0.001), slightly thicker IPF ( p = 0.046), and similar thicknesses of SCF ( p = 0.782) and ECF ( p = 0.749) compared to those who did not develop CIN. Correlation analysis showed that only PRF was positively associated with postoperation maximal serum creatinine (sCr) ( r = 0.18, p = 0.012), maximal absolute change in sCr ( r = 0.33, p < 0.001), and maximal percentage of change in sCr ( r = 0.36, p < 0.001). In receiver operating characteristic (ROC) analysis, the area under the curve (AUC) of PRF (0.809) for CIN was significantly higher than those of SCF (0.490), IPF (0.594), and ECF (0.512). Multivariate logistic regression analysis further confirmed that thickness of PRF, rather than other adipose tissues, was independently associated with the development of CIN after adjusted for confounding factors (odds ratio (OR) = 1.53, 95% CI: 1.38-1.71, p < 0.001). Conclusions: PRF is independently associated with the development of CIN in T2DM patients undergoing coronary catheterization., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2024 Xixiang Tang et al.)

Introduction: Percutaneous coronary intervention (PCI)-related myocardial infarction (type 4a MI) and major periprocedural myocardial injury have been demonstrated leading to poor prognosis of patients with coronary heart disease (CHD) undergoing elective PCI and still remain high occurrence even after the therapy of dual antiplatelet agents and statins. Proprotein convertase subtilisin/kexin type 9 inhibitor alirocumab has been shown to be effectively in reducing the risk of acute MI (AMI). However, the effect of alirocumab on preventing PCI-related MI or major periprocedural myocardial injury in patients with CHD undergoing elective PCI remains uncertain., Methods and Analysis: Alirocumab effect on Preventing Periprocedural ischaemic Events in coronary heart diseAse patients undergoing coronary StEnting trial is a multicentre, open-label, randomised controlled trial aiming to determine whether alirocumab could reduce the incidence of type 4a MI or major periprocedural myocardial injury in patients with CHD undergoing elective PCI. In total, 422 non-AMI CHD patients planned to undergo elective PCI will be randomly assigned to receive standard pharmacotherapy of CHD (control group) or additional use of subcutaneous alirocumab 75 mg 1 day before procedure (alirocumab group). The primary outcome is type 4a MI or major periprocedural myocardial injury defined as high-sensitivity cardiac troponin elevating above 5×99 th percentile upper reference limit in 48 hours after PCI. Patients will continue receiving standard pharmacotherapy or additional biweekly subcutaneous alirocumab 75 mg for 3 months according to the initial randomisation group. We will follow up for 3 months and record all the major adverse cardiovascular events (MACEs). Incidence of PCI-related MI or major periprocedural myocardial injury, and MACE in 3 months after PCI will be compared between control group and alirocumab group., Ethics and Dissemination: Ethics approval has been obtained from the Medical Ethics Committee of the Third Affiliated Hospital of Sun Yat-sen University with approval number: (2022)02-140-01. The results of this study will be reported through peer-reviewed journals and conference presentations., Trial Registration Number: ChiCTR2200063191., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Hypoalbuminemia is common in congestive heart failure (CHF) patients. Serum albumin is associated with the prognosis of CHF patients. Impact of albumin infusion on prognosis of patients with CHF-hypoalbuminemia overlap remains unclear. We retrospectively investigated the impact of albumin infusion on prognosis of intensive care unit (ICU) patients with CHF-hypoalbuminemia overlap., Methods: We enrolled all patients whose diagnosis included CHF [ICD-9 (international classification of diseases 9) code =428.0] at first ICU admission from the MIMIC III (Medical Information Mart for Intensive Care III) database, and excluded those with missing serum albumin values, with serum albumin >3.4 g/dL or <18 years old. According to the exposure of albumin infusion during hospitalization, patients were stratified into non-albumin and albumin groups. Propensity-score matching (PSM) was performed (1:1 ratio) to control for baseline confounding. Outcome measures were in-hospital mortality as well as length of stay in the ICU (ICU LOS) and the hospital (hospital LOS)., Results: There were 3,190 eligible patients in the initial search. Patients with albumin infusion had markedly higher in-hospital mortality (36.42% vs. 21.81%, P<0.001), longer ICU LOS [median 6.93 (3.39-14.82) vs. 3.84 (1.96-8.00) days, P<0.001], and longer hospital LOS [median 17.46 (11.45-28.33) vs. 10.92 (6.81-18.00) days, P<0.001] than those without albumin infusion. The multivariate logistic regression analysis revealed that albumin infusion [odds ratio (OR), 1.509; 95% confidence interval (CI), 1.164-1.957; P=0.002] was significantly associated with increased risk of in-hospital mortality. After PSM, a cohort of 429 pairs of patients was included in the final analysis. Patients with albumin infusion had markedly higher in-hospital mortality (34.97% vs. 27.27%, P=0.015), longer ICU LOS [median 8.43 (4.33-16.28) vs. 6.43 (3.07-13.66) days, P<0.001], and longer hospital LOS [median 16.92 (11.27-28.06) vs. 13.33 (8.00-21.10) days, P<0.001] than those without albumin infusion. The multivariate logistic regression analysis revealed that albumin infusion (OR, 1.594; 95% CI, 1.143-2.223; P=0.006) was significantly associated with increased risk of in-hospital mortality., Conclusions: Albumin infusion increased in-hospital mortality, ICU LOS, and hospital LOS in ICU patients with CHF-hypoalbuminemia overlap., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-22-648/coif). The authors have no conflicts of interest to declare., (2022 Journal of Thoracic Disease. All rights reserved.)

Early diagnosis of acute ST-segment elevation myocardial infarction (STEMI) and early determination of the culprit vessel are associated with a better clinical outcome. We developed three deep learning (DL) models for detecting STEMIs and culprit vessels based on 12-lead electrocardiography (ECG) and compared them with conclusions of experienced doctors, including cardiologists, emergency physicians, and internists. After screening the coronary angiography (CAG) results, 883 cases (506 control and 377 STEMI) from internal and external datasets were enrolled for testing DL models. Convolutional neural network-long short-term memory (CNN-LSTM) (AUC: 0.99) performed better than CNN, LSTM, and doctors in detecting STEMI. Deep learning models (AUC: 0.96) performed similarly to experienced cardiologists and emergency physicians in discriminating the left anterior descending (LAD) artery. Regarding distinguishing RCA from LCX, DL models were comparable to doctors (AUC: 0.81). In summary, we developed ECG-based DL diagnosis systems to detect STEMI and predict culprit vessel occlusion, thus enhancing the accuracy and effectiveness of STEMI diagnosis., Competing Interests: 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 © 2022 Wu, Huang, Yu, Ye, Liu, Ling, Liu, Liu, Zhou, Liu, Zheng, Liang, Pu, He, Chen, Han and Qian.)

The impact of beta2-agonists (B2As) on heart failure (HF) remains controversial. This study aimed to investigate whether inhaled B2As increased in-hospital mortality in ICU patients with HF.The Multiparameter Intelligent Monitoring in Intensive Care III database was initially searched to identify adult patients (≥ 18 years old) with HF in ICU. Then, patients using or not using inhaled B2As were matched using propensity score matching on a 1:1 basis to control for baseline confounders. In-hospital mortality was compared between the two groups, and logistic regression analysis was performed to assess the association between B2As and in-hospital mortality.The initial search retrieved 2345 eligible patients with HF from the database. After propensity score matching, 705 pairs of patients were included in the final analysis. Patients using B2As had markedly higher in-hospital mortality than those not using B2As (4.68% versus 2.27%; P = 0.013). In the multivariate logistic regression analysis, B2A use (odd ratios (OR), 2.471; 95% confidence interval (CI), 1.289-4.734; P = 0.006), stroke (OR, 4.581; 95% CI, 1.621-12.948; P = 0.004), and simplified acute physiology score II (SAPS-II) scores (OR, 1.090; 95% CI, 1.064-1.116; P < 0.001) were significantly associated with increased risk of in-hospital mortality, whereas renin angiotensin system inhibitor use (OR, 0.396; 95% CI, 0.202-0.778; P = 0.007) was significantly associated with decreased risk of in-hospital mortality. Subgroup analysis further indicated that the association between B2A use and mortality was significant only in patients with HF without chronic pulmonary disease (OR, 2.427; 95% CI, 1.351-4.362; P = 0.003), but not in those with chronic pulmonary disease (OR, 2.094; 95% CI, 0.582-7.537; P = 0.258).In ICU patients with HF but without chronic pulmonary disease, the use of inhaled B2As is associated with increased in-hospital mortality.

Recent studies and guidelines have indicated that lipoprotein(a) [Lp(a)]was an independent risk factor of arteriosclerotic cardiovascular disease (ASCVD). This study aimed to determine the relationship between serum Lp(a) levels and the risk of periprocedural myocardial injury following percutaneous coronary intervention (PCI) in coronary heartdisease (CHD) patients. This study enrolled 528 nonacute myocardial infarction (AMI) coronary heart disease (CHD) patients who successfully underwent PCI. Fasting serum lipids including Lp(a) were tested before PCI. High-sensitivity cardiac troponin I (hs-cTnI) was tested before PCI and 24 h after PCI. Univariate and multivariate logistic regression analyses were used to determine the relationship between preprocedural Lp(a) levels and postprocedural cTnI elevation from 1 × upper limit of normal (ULN) to 70 × ULN. As a continuous variable, multivariate analyses adjusting for conventional covariates and other serum lipids revealed that increased Lp(a) levels were independently associated with the risk of elevated postprocedural cTnI values above 1 × ULN (odds ratio [OR] per log-unit higher: 1.31, 95% confidence interval [CI]: 1.02-1.68, P = 0.033], 5 × ULN (OR: 1.25, 95%CI: 1.02-1.53, P = 0.032), 10 × ULN (OR: 1.48, 95%CI: 1.18-1.86, P = 0.001) and 15 × ULN (OR: 1.28, 95%CI: 1.01-1.61, P = 0.038). As a categorical variable, Lp(a) > 300 mg/L was an independent risk factor of postproceduralc TnI≥1 × ULN (OR 2.17, 95%CI 1.12-4.21, P = 0.022), ≥5 × ULN (OR 1.82, 95%CI 1.12-2.97, P = 0.017) and ≥10 × ULN (OR 2.17, 95%CI 1.33-3.54, P = 0.002). Therefore, it could be concluded that elevated preprocedural Lp(a) levels were associated with the risk of PCI-related myocardial injury in non-AMI CHD patients., (© 2020 The Authors. Clinical Cardiology published by Wiley Periodicals LLC.)

This study aimed to investigate the effects and mechanisms of long noncoding RNA SRA1 on regulating hypoxia-induced injury in H9c2 cardiomyocytes. The H9c2 cardiomyocytes were cultured under hypoxic (3% O 2 ) conditions and whether hypoxia induced injury was assessed by detecting cell viability, apoptosis and autophagy. Then, SRA1 was overexpressed and suppressed in H9c2 cardiomyocytes by transfection with pc-SRA1 and sh-SRA1, and the effects of SRA1 dysregulation on cell viability, apoptosis, and autophagy of H9c2 cardiomyocytes under hypoxia condition were detected. Furthermore, the regulatory relationship between SRA1 and PPARγ was explored, as well as the association between SRA1 and NF-κB signaling. Hypoxia induced injury to H9c2 cardiomyocytes, such as inhibiting cell viability, and promoting cell apoptosis and autophagy. Moreover, hypoxia resulted in a decreased expression of SRA1 in H9c2 cardiomyocytes, and overexpression of SRA1 alleviated hypoxia-induced injury, while suppression of SRA1 indicated the contrary results. Further studies showed that SRA1 positively regulated PPARγ. Overexpression of SRA1 alleviated hypoxia injury by activating PPARγ. Besides, suppression of SRA1 activated NF-κB pathway in hypoxia-treated H9c2 cardiomyocytes, which were significantly reversed after suppression of SRA1 and overexpression of PPARγ at the same time. Our findings indicated that suppression of SRA1 may aggravate hypoxia-induced injury to H9c2 cardiomyocytes by positive regulation of PPARγ and activation of NF-κB pathway. SRA1 may serve as a promising perspective for the therapy of heart failure induced by hypoxia., Competing Interests: None., (IJCEP Copyright © 2018.)

Free fatty acids (FFAs) increase in visceral fat and are inferred to be one of the underlying inducers of adipose tissue inflammation. In our previous study, it was demonstrated that ginsenoside Rb1 stimulates endothelial nitric oxide synthase (eNOS) and Sirtuin 1 to protect against endothelial cell senescence. In the present study, 3T3‑L1 adipocytes were exposed to 0.5 mM FFAs with or without Rb1 (10‑40 µM). Monocyte chemotactic protein‑1 (MCP‑1) and interleukin‑6 (IL‑6) secretion was measured using ELISA. Tumor necrosis factor‑α (TNF‑α) expression and nuclear factor‑κB (NF‑κB) p65 phosphorylation were detected using western blot analysis. Oxidative stress was determined via measuring intracellular reactive oxygen species (ROS) and nitric oxide (NO) production. The results demonstrated that MCP‑1 and IL‑6 secretion, as well as TNF‑α expression, were significantly increased following FFA treatment, which was attenuated by Rb1 in a dose‑dependent manner. Furthermore, Rb1 attenuated FFA‑induced NF‑κB phosphorylation, suggesting that the inhibitory effect of Rb1 on inflammatory cytokines was partially mediated through blockade of NF‑κB phosphorylation. Further experiments demonstrated that Rb1 ameliorated FFA‑induced ROS generation and NO reduction through upregulation of superoxide dismutase 2 and eNOS expression. Taken together, these results demonstrate proinflammatory and pro‑oxidant effects of FFA on 3T3‑L1 adipocytes, which are effectively ameliorated by Rb1. Suppression of inflammatory responses and oxidative stress may be a novel mechanism for attenuating the effect of Rb1 on adipocyte dysfunction.