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At present, the incidence rate of acute myocardial infarction is increasing year by year. Patients with acute myocardial infarction may experience myocardial ischemia-reperfusion injury (MIRI) after reperfusion of coronary blood flow, which further exacerbates the injury and leads to a decrease in the patient' s quality of life. Therefore, reducing MIRI has become one of the urgent issues that need to be addressed in the treatment of cardiovascular diseases. Traditional Chinese medicine has the advantages of multiple pathways and targets in the treatment of MIRI, which can provide new ideas for alleviating MIRI. The Wnt signaling pathway is closely related to the occurrence and development of MIRI, and it can improve MIRI by regulating inflammatory response, cell apoptosis, oxidative stress, autophagy, and other factors. The article reviews the research progress of traditional Chinese medicine in alleviating MIRI by regulating the Wnt signaling pathway, in order to provide a theoretical basis for the treatment of MIRI. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of PCSK9 inhibitors on the level of inflammation and ventricular remodeling after PCI in ST-elevation acute myocardial infarction. Methods A total of 220 patients with acute ST-segment elevation myocardial infarction who received percutaneous coronary artery intervention in the Emergency Center of Qingdao Central Hospital from April 2021 to July 2023 were randomly divided into two groups, 110 patients in the control group were treated with conventional treatment, and 110 patients in the PCSK9i group were treated with PCSK9 inhibitors on the basis of conventional treatment. Compared before and after treatment left ventricular endsystolic diameter (LVESD) and left ventricular ejection fraction (LVEF) and triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC). C-reactive protein (CRP), interleukin 6 (IL-6), tumor necrosis factor α (TNF- α). The incidence of major adverse cardiovascular events (MACE) (including myocardial infarction, recurrence of heart failure, malignant arrhythmia, and cardiovascular death) was compared. Results After 6 months of treatment and follow-up, LVEDD (mm), LVESD(mm), TG(mmol/L), TC(mmol/L), LDL-C(mmol/L), CRP(mg/L), TNF-α(pg/mL) and JL-6 (ng/mL) after PCSK9i treatment were significantly lower than those in the control group, and the difference was statistically significant [(51.32 ± 5.84) vs. (54.43 ± 2.91);(34.88 ± 2.69) vs. (36.96 ± 3.19);(1.41 ± 0.61) vs. (2.13 ± 1.26);(3.53 ± 1.06) vs. (3.98 ± 0.93);(0.95 ± 0.36) vs. (1.79 ± 0.27);(5.18 ± 1.92) vs. (7.69 ± 2.61);(36.43 ± 9.41) vs. (57.79 ± 14.43);(17.4 ± 0.68) vs. (28.55 ± 8.92),All P < 0.01], and the LVEF (%)and HDL-C(mmol/L)in the PCSK9i group were higher than patients in the control group, and the difference was statistically significant [(46.69 ± 3.63) vs. (41.34 ± 3.42),P < 0.05,(1.35 ± 0.29) vs. (1.29 ± 0.27),P < 0.01]. The incidence of MACE events in the PCSK9i group was obviously lower than patients in the control group (5.2% vs. 13.6%, P < 0.05). Conclusion The application of PCSK9 inhibitors after PCI in patients with ST-segment elevation acute myocardial infarction can better reduce blood lipids, stabilize coronary plaque, reduce local and circulatory inflammatory responses after myocardial infarction, improve ventricular adverse remodeling after myocardial infarction, inhibit ventricular remodeling, and reduce the total incidence of MACE, worthing promoting use. [ABSTRACT FROM AUTHOR]

Acute myocardial infarction (AMI) is a severe disease caused by the persistent coronary artery obstruction, posing a great threat to people's health. In recent years, Toll-like receptor 4 (TLR4), an important pattern recognition receptor, has been widely studied and found to play a crucial role in AMI. This review introduces the recent progress of TLR4 in regulating the progression and prognosis of AMI, and summarizes recent TLR4-targeted therapies using clinical drugs, TLR4 inhibitors, mesenchymal stem cells, and natural bioactive molecules, providing valuable insights for addressing myocardial damage caused by AMI and improving prognosis. [ABSTRACT FROM AUTHOR]

Aim To investigate the inhibition role and mechanism of adipose derived mesenchymal stem cell (ADMSC) exosomes (Exo) on adverse ventricular remodeling after myocardial infarction (MI). Methods The changes of autophagy and inflammasomes phenotype of cardiac fibroblasts after H2O2 treatment were observed. MI rats were injected with an equal volume of normal saline, adipose derived mesenchymal stem cell exosomes (MSC-Exo) or fibroblast exosomes (MEF-Exo) via a tail vein. The expression of autophagy related 16 like protein 1 (ATG16L1), autophagy related protein 7 (ATG7) and NOD-like receptor protein 3 (NLRP3), inflammatory response, the degree of myocardial fibrosis, and the cardiac function were observed in different groups. Results After treatment with H2O2 on cardiac fibroblasts, the expressions of ATG16L1 and ATG7 were significantly decreased (P<0. 001), NLRP3 was significantly increased ( P < 0. 001 ), and the levels of inflammatory cytokines interleukin-1β ( IL-1β) and IL-18 were significantly elevated (P < 0. 001 ). After MI rats were intervened with MSC-Exo, the expressions of autophagy related proteins ATG16L1 and ATG7 were significantly up-regulated (P<0. 001), NLRP3 was significantly down-regulated (P<0. 001), serum IL-1β and IL-18 levels were significantly decreased (P<0. 001), fibrosis-related proteins collagen Ⅰ and Ⅲ were significantly reduced (P<0. 001), myocardial fibrosis was significantly relieved (P<0. 001), and cardiac function was significantly improved (P<0. 001). Conclusion Adipose derived MSC-Exo play a role in inhibiting adverse ventricular remodeling after MI by regulating the balance of autophagy and NLRP3 inflammasomes. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of hyperbaric oxygen combined with ulinastatin on choline acetyltransferase (ChAT), malondialdehyde (MDA), and myocardial function in rats with acute organophosphorus pesticide poisoning. Methods 50 specific-pathogen-free (SPF) male SD rats were randomly divided into five groups of ten each: normal group (N), model group (M), hyperbaric oxygen group (H), and ulinastatin group (U), and hyperbaric oxygen combined ulinastatin (O) group. The model of acute organophosphorus pesticide poisoning was established in the M, H, U, and O groups via cumulative subcutaneous injections on the neck back, and the N group did not set up the model. After the success of the modeling, the H group was treated with hyperbaric oxygen therapy, and the U group was intraperitoneally injected with ulinastatin at a dose of 100 000 U/kg.The O group received a combination of hyperbaric oxygen and ulinastatin treatment, whereas the N and M groups were gavaged with an equivalent volume of saline. The rats' myocardial function was assessed through cardiac echocardiography, brain tissue pathology was examined using hematoxylin and eosin (HE) staining and Nissl staining, cardiomyocyte apoptosis was evaluated by TUNEL assay, and ChAT and acetylcholine (Ach) content in rat brain tissues were determined through histochemical methods. Serum levels of MDA and superoxide dismutase (SOD) were measured using the thiobarbituric acid reactive substances (TBARS) assay. Statistical analysis was performed by SPSS 22.0. Results Compared with Group N, the left ventricular end systolic dimension (LVSD) and left ventricular end diastolic dimension (LVDD) in Group M were both enlarged, with increased interventricular septum (IVS) thickness, aggravated left ventricular strain (LVS), increased number of apoptotic cardiomyocytes, and elevated Ach and MDA levels (P<0.05). Additionally, the left ventricular ejection fraction (LVEF) decreased, while ChAT and SOD levels also decreased (P<0.05). When compared to Group M, both Groups H and U exhibited reduced LVSD and LVDD, thinner IVS, decreased LVS, and fewer apoptotic cardiomyocytes. Furthermore, Ach and MDA levels were lower (P<0.05), while LVEF, ChAT, and SOD levels were higher (P<0.05). No statistically significant difference was observed between Groups U and H (P>0.05), while Group O showed more pronounced changes compared to Group U (P<0.05). Rats in Group N exhibited normal brain tissue pathological morphology, while those in Group M suffered severe damage to brain tissue structure. Compared to Group M, significant improvements in symptoms were observed in Groups H, U, and O. Conclusions Hyperbaric oxygen combined with ulinastatin has a significant effect on acute organophosphorus pesticide poisoning rats, which can significantly increase ChAT content, decrease MDA content, and effectively improve myocardial function. [ABSTRACT FROM AUTHOR]

Acute myocardial infarction has the characteristics of rapid progression, dangerous condition, unstable hemodynamics, and is prone to thrombosis, resulting in a high clinical mortality rate. Intra-aortic balloon counterpulsation (IABP) has the function of increasing intra-aortic diastolic pressure, reducing left ventricular afterload, and enhancing coronary artery blood supply. It is a common auxiliary and transitional treatment method for coronary intervention, which can significantly improve the safety and clinical efficacy of coronary intervention. Therefore, it is widely used in high-risk and complex coronary heart disease, mainly acute myocardial infarction. This article reviews the research progress on the application effect and thrombosis management of IABP in acute myocardial infarction in recent years. [ABSTRACT FROM AUTHOR]

Objective To investigate the changes in the myocardial fibrosis indexes of myocardial infarction mice with transient receptor potential channel C1(TRPC1） knockout. Methods Twenty wild type mice and 20 TRPC1-/- mice were divided into four groups: the wild control group, wild experimental group, TRPC1-/-control group, and TRPC1-/- experimental group, with 10 mice in each. In the wild experimental group and TRPC1-/- experimental group, the left anterior descending coronary artery was lapped and sutured to establish the myocardial infarction models. In the the wild control group and TRPC1-/- control group, mice were only threaded without ligature. Twenty-four hours later, the mice were sacrificed to obtain the hearts. Normal tissues from the left ventricle were taken from the mice in the two control groups, and infarcted tissues from the anterior wall of the left ventricle were taken from the mice in the two experimental groups. RT-PCR was used to detect the expression of TRPC1 mRNA, and Western blotting was used to detect the TRPC1 protein and Collagen Ⅰ(Col-Ⅰ） and α-smooth muscle actin(α-SMA). ResultsThe mRNA expression of TRPC1 in the wild experimental group was higher than that in the TRPC1-/- experimental group, and that in the wild control group was higher than that in the TRPC1-/- control group（ both P<0. 05). The expression of TRPC1 protein in the wild experimental group was higher than that in the wild control group and the TRPC1-/- experimental group, and the expression of TRPC1 protein in the TRPC1-/-experimental group was higher than that in the TRPC1-/- control group(all P<0. 05). Col-Ⅰ and α -SMA protein expression levels in the wild experimental group were higher than those in the wild control group and TRPC1-/- experimental group, and Col-Ⅰ and α-SMA protein expression levels in the wild control group were higher than those in the TRPC1-/- control group； the expression levels of Col-Ⅰ and α-SMA in the TRPC1-/- experimental group were higher than those in the TRPC1-/- control group（all P<0. 05). Conclusion Knocking down TRPC1 gene expression can down-regulate the expression of myocardial fibrosis indexes of myocardial infarction mice. [ABSTRACT FROM AUTHOR]

Objective: To investigate the relationship between serum γ-glutamyl transferase (GGT), cystatin C (CysC), apolipoprotein B/apolipoprotein A1 (ApoB/ApoA1) ratio and the prognosis of patients with acute ST elevation myocardial infarction (ASTEMI) complicated with type 2 diabetes mellitus (T2DM). Methods: The clinical data of 175 patients with ASTEMI complicated with T2DM who underwent percutaneous coronary intervention (PCI) in Guangdong Provincial Hospital of Traditional Chinese Medicine were retrospectively collected, patients were divided into poor prognosis group (63 cases) and good prognosis group (112 cases) according to the prognosis at 1 month after PCI, Serum GGT and CysC levels were detected and ApoB/ApoA1 ratio was calculated. The factors affecting the poor prognosis of ASTEMI patients complicated with T2DM after PCI were analyzed by multivariate Logistic regression, the predictive value of serum GGT, CysC and ApoB/ApoA1 ratio for the poor prognosis of ASTEMI patients complicated with T2DM after PCI were analyzed by receiver operating characteristic curve(ROC). Results: 1 month after follow-up, the incidence of poor prognosis after PCI in 175 ASTEMI patients complicated with T2 DM was 36.00 %(63/175). Compared with good prognosis group, the serum GGT, CysC and ApoB/ApoA1 ratio in poor prognosis group increased(P<0.05). Killip grade≥II and elevated serum GGT, CysC, ApoB ApoA1 ratio were independent risk factors for poor prognosis in ASTEMI patients complicated with T2 DM after PCI(P<0.05). The area under the curve (AUC) of serum GGT, CysC and ApoB/ApoA1 ratio combined to predict the poor prognosis of ASTEMI patients complicated with T2DM after PCI was 0.924, which was greater than the 0.776, 0.778 and 0.785 predicted by serum GGT, CysC and ApoB/ApoA1 ratio alone. Conclusion: Elevated serum GGT, CysC and ApoB/ApoA1 ratio are relate to the poor prognosis of ASTEMI patients complicated with T2DM after PCI, and the combined detection of serum GGT, CysC and ApoB/ApoA1 ratio has a high predictive value for the poor prognosis of ASTEMI patients complicated with T2DM after PCI. [ABSTRACT FROM AUTHOR]

Objective To investigate the relationship between the expression of serum angiopoietin-like protein 8 (ANGPTL8) and Kruppel-like factor 2 (KLF2) and the degree of coronary artery disease and the occurrence of major adverse cardiac events (MACE) in patients with acute myocardial infarction (AMI). Methods A total of 106 patients with AMI who were hospitalized in our hospital from January 2021 to June 2023 were selected as the research objects. According to the degree of coronary artery disease, the patients were grouped into mild group (52 cases) and severe group (54 cases). According to the occurrence of MACE, the patients were grouped into MACE group (18 cases) and non-MACE group (88 cases). General patient data were collected. Serum ANGPTL8 and KLF2 levels were detected by enzyme-linked immunosorbent assay (ELISA). Spearman correlation analysis was applied to analyze the correlation between serum ANGPTL8 and KLF2 levels and Gensini score in AMI patients. Multivariate logistic regression was applied to analyze the influencing factors of coronary artery disease degree in patients with AMI. Receiver operating characteristic (ROC) curves were drawn to analyze the value of serum ANGPTL8 and KLF2 levels in predicting the occurrence of MACE in AMI patients. Results The proportions of patients with history of hypertension and hyperlipidemia, systolic blood pressure, diastolic blood pressure, levels of triacylglycerol (TG), N-terminal pro-B-type natriuretic peptide (NT-proBNP), cardiac troponin I (cTnI), Gensini score, and level of serum ANGPTL8 in the severe group were higher than those in the mild group (P < 0.05). The level of high- density lipoprotein cholesterol (HDL-C) and serum KLF2 in the severe group were lower than those in the mild group (P < 0.05). The number of lesions in the mild group and the severe group was statistically obvious (P < 0.05). Serum ANGPTL8 level in AMI patients was positively correlated with Gensini score (r = 0.638, P < 0.05), and serum KLF2 level was negatively correlated with Gensini score (r = -0.612, P < 0.05). History of hypertension, hyperlipidemia, cTnI and ANGPTL8 were risk factors for the progression of severe coronary artery disease in patients with AMI (P < 0.05), while HDL-C and KLF2 were protective factors (P < 0.05). The serum level of ANGPTL8 in AMI patients in the MACE group was higher than that in the non-MACE group (P < 0.05), and the serum KLF2 level in the MACE group was lower than that in the non-MACE group (P < 0.05). The area under the curve of serum ANG- PTL8 and KLF2 levels and their combination in predicting the occurrence of MACE in AMI patients was 0.740 (95%CI: 0.646 ~ 0.820), 0.799 (95%CI: 0.710 ~ 0.870), and 0.806 (95%CI: 0.717 ~ 0.876), respectively. Conclusion The expressions of serum ANGPTL8 and KLF2 are closely related to the degree of coronary artery disease in patients with AMI, and have certain predictive value for the occurrence of MACE. [ABSTRACT FROM AUTHOR]

Objective To investigate the role of H9c2-derived exosomes in regulating angiogenesis in rat cardiomyocytes under hypoxia. Methods The hypoxia model of H9c2 cells was prepared by mixed gas method (the hypoxia model group), and the normal cultured cells were used as the control group. The exosomes secreted by the two groups of cells were extracted respectively. The concentration and particle size of exosomes were detected by nanoparticle tracking analysis. The morphology and size of exosomes were detected by transmission electron microscopy. Western blot assay was used to verify the exosome marker proteins. The hypoxia model of human umbilical vein endothelial cells (HUVEC) was established. HUVECs were incubated with H9c2 exosomes and divided into the normoxia group, the hypoxia group, the hypoxia + normal H9c2 exosomes (EXO-C) group and the hypoxia + hypoxia H9c2 exosomes (EXO-M) group. The proliferation, migration and tube formation of HUVECs were detected by CCK-8 method, cell scratch test and Matrigel in vitro three-dimensional forming test. Results The results of exosome identification showed that the particle concentration of H9c2 exosome samples was 1×107 -1×1012 particles/mL and the particle size was 40-160 nm in the normoxia group and the hypoxia group. The morphological characteristics were spherical or saucer-like structure, uniform in size and complete in shape. Exosome marker proteins TSG101, CD63 and CD9 were expressed, and there was no expression of negative protein Calnexin. Compared with the normoxic group, the proliferation ability, migration area and migration rate of HUVEC were significantly decreased in the hypoxic group, and the length of tube, the number of branches and the number of nodes were decreased (P＜ 0.01). Compared with the hypoxia group, the proliferation ability of HUVEC cells was decreased, the migration area was decreased, the migration rate was decreased and the length and number of branches involved in tube formation were further decreased in the EXO-M group (P＜0.05). Compared with the EXO-C group, the proliferation ability of the EXO-M group decreased, the cell migration area decreased and the migration rate decreased (P＜0.01). Conclusion Exosomes derived from hypoxic H9c2 can inhibit the proliferation, migration and tube formation of HUVEC. [ABSTRACT FROM AUTHOR]

Myocardial infarction is the most common cause of heart failure, and myocardial remodeling can occur after infarction, thus contributing to the progression of heart failure. The occurrence of post-infarction ventricular remodeling is closely related to m6 A methylation. m6 A methylation is a reversible and highly dynamic process. This process is mainly mediated by m6 A methylation positive and negative regulatory enzymes and is involved in the occurrence of post-infarction myocardial remodeling through mechanisms such as cellular autophagy. This article mainly reviews relevant literature in recent years. Firstly, a brief introduction is given to m6 A methylation, followed by an introduction to the role of m6 A methylase in regulating myocardial remodeling. Finally, a summary analysis is conducted on the mechanism of m6 A methylation in regulating myocardial remodeling from the perspectives of autophagy, inflammation, cell apoptosis, calcium ion homeostasis, extracellular matrix remodeling, and ferroptosis. The feasibility of using m6 A methylation serological detection as a diagnostic tool for myocardial remodeling after myocardial infarction is discussed, in order to provide reference for related research. [ABSTRACT FROM AUTHOR]

Objective: To study Effects of levosimendan on myocardial perfusion and electrocardiogram indexes in patients with acute myocardial infarction after Percutaneous coronary intervention (PCI). Methods: 113 patients with acute myocardial infarction who received PCI treatment in our hospital from January 2020 to December 2022 were selected and divided into experimental group (n=57) and control group (n=56) by random number table method. The control group was treated with clopidogrel after PCI, and the experimental group was treated with levosimendan. The clinical efficacy, myocardial perfusion grade, ST segment retreat within 2 h, Tp-e/QT, CI, LVEF, LVESD, LVEDD and the incidence of complications were compared between the two groups. Results: The total effective rate of the experimental group was 89.13%, higher than that of the control group 71.11%(P<0.05). After treatment, the myocardial perfusion grade level of both groups was increased, and the increase of experimental group was more obvious(P<0.05). The ST segment in test group was better than that in control group within 2 h(P<0.05). After treatment, the Tp-e/QT level in both groups was decreased, and the decrease in test group was more obvious (P<0.05). After treatment, CI and LVEF levels were increased in both groups, more significantly in experimental group(P<0.05); LVESD and LVEDD levels were decreased in both groups, more significantly in experimental group (P<0.05); During treatment, the main adverse reactions were nausea, fever, recurrent angina pectoris and arrhythmia, and the incidence rate was compared between the two groups (P>0.05). Conclusion: Levosimendan has a good effect in PCI treatment of patients with acute myocardial infarction, which can effectively improve the level of myocardial perfusion and electrocardiogram. [ABSTRACT FROM AUTHOR]

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Objective To investigate the effect of indoxyl sulfate (IS) on myocardial remodeling in a mouse model of myocardial infarction (MI). Methods A total of 50 adult male C57BL/6J mice were randomly divided into sham-operation group (Sham group) with 10 mice, sham operation+indoxyl sulfate group (Sham+IS group) with 10 mice, myocardial infarction group (MI group) with 15 mice, and myocardial infarction+indoxyl sulfate group (MI+IS group) with 15 mice. Left anterior descending coronary artery ligation was performed to establish a mouse model of MI, and at 24 hours after surgery, the mice in the Sham+IS group and the MI+IS group were given intraperitoneal injection of IS (100 mg/kg), while those in the Sham group and the MI group were given intraperitoneal injection of an equal volume of PBS, once a day for 28 consecutive days. The survival status of the mice in each group was recorded during this period of time. On day 30 of the experiment, echocardiography was performed to evaluate the cardiac function of mice in each group. Ultra-performance liquid chromatography was used to measure the serum concentration of IS. Masson staining was used to assess the degree of myocardial fibrosis in the infarct zone. RT-qPCR was used to measure the mRNA expression levels of α-sma and Collagen Ⅰ in myocardial tissue. Western blot was used to measure the protein expression levels of the TGF-β signaling pathway marker proteins TGF-β, p-Smad2, and p-Smad3 in myocardial tissue. Results On day 30 of the experiment, the MI+IS group had a significant reduction in the survival rate of mice compared with the MI group (χ2=5.02,P0.05). Compared with the MI group, the MI+IS group had significant increases in LVIDd and LVIDs (t=3.96,4.31,P

Myocardial infarction without obstructive coronary artery (MINOCA) refers to myocardial infarction (MI) that occurs when the lumen area of coronary artery stenosis is ≤50%, accounting for 1% to 14% of the total MI. The etio-logy of MINOCA is complex and diverse, and accurate diagnosis and identification of the potential causes of MINOCA are crucial for guiding subsequent clinical management. Based on the unique advantages of myocardial tissue imaging, non-invasive cardiac magnetic resonance (CMR) examination has been widely recognized for its value in the management of MINOCA patients. CMR can be used to exclude diseases similar to MI, such as myocarditis and stress-induced cardio-myopathy, and identify the potential causes of MINOCA. It is a necessary diagnostic tool in the diagnostic process, helping to reduce overdiagnosis, misdiagnosis, and missed diagnosis of true MINOCA. Currently, it has been recommended by the American Heart Association (AHA) and the European Society of Cardiology (ESC) as an essential examination method in the MINOCA management process. In addition, compared with patients with coronary artery occlusion, MINOCA patients have a better short-term prognosis, but the risk of poor prognosis increases in long-term follow-up. It is necessary to pay more attention to the prognosis and risk stratification of MINOCA patients and management process. The traditional MI prognosis evaluation system is not entirely applicable to MINOCA patients, and CMR can provide valuable information for the prognosis evaluation of MINOCA patients. Currently, there are no standardized norms or guidelines for the application of CMR in the management of MINOCA patients in China. This article aims to review the application norms and prognostic value of CMR technology in clinical management of MINOCA, providing reference for clinical practice and enhancing understanding and management of this special MI lesion.

Objective To investigate the efficacy of indobuprofen combined with nicodil for the treatment of acute coronary syndromes (ACS) and the effects of percutaneous coronary intervention on patients Effects of myocardial injury markers, platelet function and inflammatory factors after intervention (PCI). Method A total of 150 patients with ACS admitted to the hospital from January 2021 to December 2022 were divided into groups according to different treatment methods. The control group (n = 75) was given nicodil combined with antiplatelet therapy, and the study group (n = 75) was given indobufen combined with nicodil combined with antiplatelet therapy. Both groups were treated for 2 weeks. The clinical efficacy of the two groups was compared, the changes of myocardial injury markers, platelet function and inflammatory factors before and after treatment were monitored, and the total incidence of adverse reactions was recorded. Results The total effective rate of the group treated with nicodil combined with indobufen was 98.67% higher than that of the control group treated with nicodil alone, 90.67% (χ2 = 4.754, P < 0.05). The levels of myocardial injury markers such as cTnI and CK-MB in the study group after treatment were lower than those in the control group (t = 15.492, 3.250, P < 0.05). The levels of platelet function indexes such as CD62p, CD63, GP'b/IIIa in the study group after treatment were lower than those in the control group (t = 2.034, 3.257, 2.221, P < 0.05). The levels of CRP, TNF- α, IL-6 and other inflammatory factors in the study group were lower than those in the control group after treatment (t = 21.862, 3.378, 2.131, P < 0.05). The total incidence of adverse reactions after treatment was 4.00% in the study group and 2.67% in the control group (P > 0.05). Conclusion The efficacy of indobufien combined with nicodil in the treatment of ACS is better than that of nicodil alone, and it can improve myocardial injury and platelet function after PCI, inhibit the release of inflammatory factors, and the incidence of adverse reactions is lower. [ABSTRACT FROM AUTHOR]

Objective To investigate changes in serum complement C1 tumor necrosis factor-related protein family 12 (CTRP12) level before and after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI) and the relationship of CTRP12 level with in-stent restenosis (ISR). Methods A total of 104 patients who had been diagnosed with AMI and had undergone PCI at Danyang People's Hospital in Jiangsu Province from January 2021 to June 2023 were selected. The incidence of ISR within 12 months after PCI was counted, and they were divided into an ISR group and a non-ISR group according to the results of reviewed coronary angiography. Serum CTRP12 levels were compared between the two groups before PCI and on one day before discharge. Logistic regression was used to analyze the influencing factors of ISR in AMI patients after PCI. Receiver operating characteristic (ROC) curve was used to analyze the predictive value of CTRP12 for ISR in AMI patients after PCI. Results The incidence of ISR in 104 AMI patients at 12 months after PCI was 14.4% (15/104). As compared with the non-ISR group, the ISR group had significant increases in preoperative TIMI flow of ≤ 1, white blood cell count, neutrophil count, TC, and LDL-C, and a significant decline in serum CTRP12 level on one day before discharge (P < 0.05). In the non-ISR group, serum CTRP12 level was significantly higher on one day before discharge than its baseline (P < 0.05). In the ISR group, serum CTRP12 level on one day before discharge was lower than its baseline, but the difference was not statistically significant (P > 0.05). Logistic regression analysis showed that a lower CTRP12 level on one day before discharge was an independent risk factor for ISR in AMI patients after PCI (P < 0.05). ROC curve analysis showed that the optimal cut-off point of serum CTRP12 on one day before discharge for predicting ISR in AMI patients after PCI was 3.89 ng/mL (sensitivity 93.3% and specificity 73.0%), and the area under the ROC curve (AUC) was 0.849. Conclusions Serum CTRP12 level inone day before discharge has certain predictive value for ISR in AMI patients after PCI. CTRP12 may be a therapeutic target for ISR in AMI patients after PCI. [ABSTRACT FROM AUTHOR]

AIM: This study employs Brainbow 2. 1 mice to trace myocardial cell lineage and investigates the optimal dose of tamoxifen for labeling proliferating myocardial cells. METHODS: Four-week-old Brainbowfl/+; Myh6-Mer-CreMer+ mice were administered tamoxifen at three different doses (3, 9 and 27 mg/kg) via intraperitoneal injection to induce Cre recombinase expression and label myocardial cells with specific colors. Four weeks later, the samples were stained, and the number of myocardial cells labeled with varying doses of tamoxifen was quantified under confocal micro -scope. This quantification included the proportion of individually labeled cells, adjacent clusters of two cells, and clusters of three or more cells. An appropriate dose (9 mg/kg) of tamoxifen for labeling Brainbow mice was selected to compare myocardial cell proliferation between sham and myocardial infarction (MI) model groups. RESULTS: (1) After 9 mg/kg tamoxifen injection, the proportion of individually labeled cells was 99. 13%±0. 03%, that of adjacent 2-cell clusters was 0. 82%±0. 09%, and that of ^3-cell clusters was 0. 05%±0. 01%. The 3 mg/kg group had fewer total labeled cells, while the 27 mg/kg group showed significant clonal expansion and enrichment. ( 2) After labeling myocardial cells with 9 mg/kg tamoxifen, the MI mice showed increased proportions of 2-cell and ^3-cell clusters compared with sham group (P<0.01), indicating an increase in myocardial cell proliferation after MI. CONCLUSION: The proportion of adjacent myocardial cell clusters labeled with 9 mg/kg tamoxifen more closely approximates the physiological myocardial cell proliferation rate, indicating 9 mg/kg as the most suitable tamoxifen dose for tracing myocardial cell proliferation. [ABSTRACT FROM AUTHOR]

Aim Previous studies have indicated that H2 S can attenuate myocardial fibrosis. However, it is unclear whether mitochondria-targeted H2 S can attenuate myocardial fibrosis after myocardial infarction and whether its mechanism is associated with the regulation of mitochondrial fusion and fission. To investigate this relationship, this study was conducted. Methods Isoproterenol (ISO, 50 mg / (kg·d)) was injected intraperitoneally to induce myocardial infarction in SD rats. Electrocardiograms were performed on each group of rats, and the rats were treated with AP39 (36 μg / (kg·d), intraperitoneal) for 4 weeks. Masson's staining was used to assess the extent of myocardial fibrosis. Western blot was used to measure the expression of relevant proteins. In vitro experiments were performed to induce hypoxic injury in H9c2 cardiomyocytes with CoCl 2(800 μmol / L), H9c2 cells were treated with AP39 (100 nmol / L), and the endogenous hydrogen sulfide synthase cystathionine-γ-lyase ( CSE) was inhibited using DL-propargylglycine ( PAG, 2 mmol / L), and fluorescence probe was used to measure the level of reactive oxygen species(ROS) in myocardial cells. Results Myocardial fibrosis was evident in infarcted rat hearts, with a significant accumulation of collagen fibers. Additionally, the expression of CSE and mitofusin 2 (MFN2) proteins was downregulated, while dynamin-related protein 1 (DRP1) protein expression was increased. Intervention with AP39 significantly improved the above changes, and the addition of CSE inhibitor PAG reversed the effects of AP39. In in vitro experiments, when H9c2 myocardial cells were subjected to hypoxic injury induced by CoCl 2, intracellular ROS levels increased, MFN2 expression was downregulated, and DRP1 expression was upregulated. AP39 upregulated MFN2 protein expression, inhibited DRP1 protein expression, and reduced ROS levels in myocardial cells. The addition of PAG reversed these changes. Conclusion The mitochondria-targeted H2 S donor, AP39, can improve myocardial fibrosis in rats with myocardial infarction and promote mitochondrial fusion and inhibit excessive mitochondrial division. [ABSTRACT FROM AUTHOR]

Objective: This study observed the effect of Wendan Ningxin Granules (WDNX) on the BDNF/TrkB/PI3K/Akt signaling pathway in rats with myocardial infarction and depression, and explored its possible mechanism of action. Methods: A rat model of myocardial infarction combined with depression was prepared by subcutaneous multi-point injection of isoproterenol (ISO) and chronic unpredictable mild stress (CUMS). After 28 days of intervention with WDNX, changes in cardiac function were detected by transthoracic echocardiography; Evaluate the depression status of rats based on sugar preference and open field experiments; Using hematoxylin eosin (HE) and Nissl staining to observe pathological changes in myocardial and brain tissue, as well as neuronal damage; Finally, the expression levels of the BDNF/TrkB/PI3K/Akt pathway were detected using immunohistochemistry and Western blotting techniques. Results: In vivo experiments have confirmed that compared with the blank group, the left ventricular ejection fraction (LVEF) and left ventricular short axis shortening rate (LVFS) of the model group rats were significantly reduced (P<0.01). A large amount of fiber edema and cytoplasmic looseness were observed in the myocardial tissue, and myocardial fiber dissolution was observed at the tissue edge, accompanied by a small amount of lymphocyte infiltration; There is obvious diffuse damage to brain tissue, interstitial swelling, aggregation of inflammatory cells, and irregular morphology; Nissl staining observation showed that the number of neurons in the model group significantly decreased, with irregular morphology, loose and disordered arrangement, increased intercellular spaces, and also led to the consolidation of Nissl body morphology, resulting in pathological changes; The preference for sugar water, activity time in the central region, and number of central crossings in the model rats were significantly reduced (P<0.01); Compared with the model group, the WDNX group showed a significant increase in LVEF and LVFS (P<0.01), with improvements in myocardial fiber edema, cytoplasmic looseness, inflammatory infiltration, cell cavity degeneration, and fiber dissolution. The morphology of neurons in the brain tissue was more regular, arranged neatly and tightly, and the number of neurons was relatively increased. It was also possible to restore the morphology of Nissl bodies; The preference for sugar water, activity time in the central region, and number of central crossings in the WDNX group of rats significantly increased (P<0.05). Immunohistochemical staining results; Compared with the blank group, the BDNF protein expression in the myocardial and brain tissues (hippocampus, cortex, and hypothalamus) of the model group rats was significantly reduced (P<0.01), while the expression of TrkB, PI3K, and Akt proteins in the myocardium was significantly reduced (P<0.01); Compared with the model group, the expression of BDNF protein in the myocardium and brain tissues (hippocampus, cortex, and hypothalamus) of the WDNX group was significantly increased (P<0.05), while the expression of TrkB, PI3K, and Akt proteins in the myocardium were significantly increased (P<0.01); Western blotting test results: Compared with the blank group, the expression of BDNF, TrkB, PI3K, and Akt proteins in the myocardium of the model group rats was significantly reduced (P<0.01); Compared with the model group, the expression of BDNF, TrkB, PI3K, and Akt proteins in the myocardium of the WDNX group was significantly increased (P<0.05). Conclusion: WDNX can effectively improve myocardial injury and depressive behavior in rats with myocardial infarction and depression, which may be related to the activation of the BDNF/ TrkB/PI3K/Akt pathway. [ABSTRACT FROM AUTHOR]

Objective To investigate the relationship between serum C-reactive protein (CRP).procalcitonin (PCT), calcineurin (CaN) and ventricular remodeling in patients with acute myocardial infarction (AMI) and its impact on prognosis. Methods A total of 126 patients with AMI admitted to Puyang County People's Hospital from January 2020 to August 2022 were divided into ventricular remodeling group (54 cases) and non-ventricular remodeling group (72 cases). According to the prognosis at 12 months after treatment, they were divided into poor prognosis group (25 cases) and good prognosis group (101 cases). In addition, 63 healthy subjects were selected as the normal control group. The levels of serum CRP, PCT and CaN at admission were compared among the three groups. The relationship between serum CRP,PCT, CaN and ventricular remodeling [left ventricular end-systolic volume (LVESV), end-systolic dispersion (DISPES), left ventricular end-diastolic volume (LVEDV), end-diastolic dispersion (DISPED), left ventricular ejection fraction (LVEF),etc. was analyzed. The levels of serum CRP, PCT and CaN in patients with different prognosis were compared. The predictive value of serum CRP, PCT and CaN on prognosis and its impact on prognosis were analyzed. Results The levels of serum CRP, PCT, CaN, LVEDV, LVESV, DISPES and DISPED in the ventricular remodeling group were significantly higher than those in the non-ventricular remodeling group and the normal control group, and the LVEF in the ventricular remodeling group was significantly lower than that in the non-ventricular remodeling group and the normal control group. The levels of serum CRP, PCT and CaN in the poor prognosis group were significantly higher than those in the good prognosis group. Serum CRP,PCT and CaN were negatively correlated with LVEF, and positively correlated with LVEDV.LVESV, DISPES and DISPED, with statistically significant differences (P<0.05). The area under the receiver operating characteristic curve of serum CRP, PCT and CaN combined to predict the poor prognosis of AMI patients was 0.912, which was better than that of each serum index alone, and the difference was statistically significant (P<0.05). The risk of poor prognosis in AMI patients with high levels of serum CRP, PCT and CaN was 2.522,3. 024 and 3.958 times higher than that in patients with low levels. Conclusion The high expression of serum CRP, PCT and CaN is not only related to ventricular remodeling in AMI patients, but also affects their prognosis. Combined detection can be used as an important auxiliary index to predict poor prognosis. [ABSTRACT FROM AUTHOR]

BACKGROUND: Conductive biomaterials are considered potential candidates for transmitting electrical signals for myocardial repair. Combining cell-based or cellfree strategies with conductive biomaterials to replenish cardiomyocytes and/or restore electrical signaling pathways is a promising approach for cardiac repair. OBJECTIVE: To evaluate the effect of polypyrrole-chitosan conductive composite hydrogel on cardiac function in rats with myocardial ischemia-reperfusion injury. METHODS: The polypyrrole-chitosan conductive composite hydrogel was prepared by chemical oxidative polymerization. The micromorphology, biocompatibility and conductivity of the hydrogels were characterized. Thirty adult SD rats were selected to establish a myocardial ischemia-reperfusion injury model by clamping the left anterior descending branch of the heart and then releasing it. After 21 days of modeling, the rats were divided into three groups by the random number table method: Normal saline was injected into the left ventricular infarction area and infarction margin area in the blank group. Chitosan hydrogel was injected into the left ventricular infarction area and infarction margin area in the ordinary hydrogel group. The polypyrrole-chitosan conductive composite hydrogel was injected into the left ventricular infarction area and infarction margin area, with 10 rats in each group. The corresponding time points after modeling were set, and cardiac mechanical function (echocardiogram, pressure-volume analysis), cardiac electrophysiology (electrocardiogram, programmed electrical stimulation, optical mapping technology, microelectrode array technology, eight-lead electrocardiogram, and electrical resistivity of the scar area) and cardiac histology were detected. RESULTS AND CONCLUSION: (1) There were a lot of pores on the surface of the conductive composite hydrogel, and the conductivity was (3.19±0.03)× 10-3 mS/cm, which had good biocompatibility co-cultured with smooth muscle cells. (2) After 105 days of modeling, echocardiogram and pressure-volume analysis showed that compared with the blank group and the ordinary hydrogel group, the conductive composite hydrogel could significantly improve the contractile function of the heart of rats with myocardial ischemia-reperfusion injury. The results of electrocardiogram, programmed electrical stimulation, optical mapping technology, microelectrode array technology, eight-lead electrocardiogram, and electrical resistivity of the scar area examination at 105 days after modeling displayed that, compared with the blank group and the ordinary hydrogel group, the conductive composite hydrogel could significantly improve the electrical conduction function of the heart of rats with myocardial ischemia-reperfusion injury and reduce the occurrence of arrhythmia. Masson staining of heart tissue at 105 days after modeling exhibited that there were different degrees of fibrosis in the myocardial infarction area of the three groups. Compared with the normal saline group and the ordinary hydrogel group, the conductive hydrogel group had more normal myocardial tissue and less fibrosis in the myocardial infarction area. (3) The results verify that polypyrrole-chitosan conductive composite hydrogel may promote the repair of infarcted heart after ischemia-reperfusion injury by increasing the electrical conduction velocity of infarct scar area tissue, increasing scar thickness, enhancing synchronous cardiac contraction, and reducing damaged tissue. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of remimazolam on myocardial injury in rats with acute myocardial infarction (AMI) by regulating exchange proteins directly activated by cAMP (EPAC1)/RAS-related protein 1 (RAP1) signaling pathway. Methods Rats were divided into the sham operation group, the model group, the remazolam group and the remazolam+8-CPT (EPAC1 agonist) group according to random number table method, with 20 rats in each group. Except for the sham operation group, AMI rat model was constructed by ligation of left anterior descending branch in the other groups. Ultrasonic apparatus for small animals was applied to detect cardiac function indicators. HE staining was applied to detect the pathological condition of myocardial tissue. Chemical colorimetry was applied to detect levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in myocardial tissue of rats. JC-1 staining method was applied to detect the mitochondrial membrane potential of rat cardiomyocytes. TUNEL staining was used to detect the TUNEL positive rate of myocardial cells. Western blot assay was applied to detect expression levels of EPAC1, RAP1 and Caspase-3 proteins in myocardial tissue. Results Compared with the sham operation group, the myocardial tissue structure of rats in the model group was severely damaged and infiltrated with a large number of inflammatory cells. Cardiac function indicators left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), myocardial tissue MDA level, myocardial cell TUNEL positive rate, and myocardial tissue EPAC1, RAP1 and Caspase-3 protein expression levels were obviously increased, and the left ventricular ejection fraction (LVEF), left ventricular fraction shortening (LVFS), myocardial tissue SOD level, cardiomyocytes mitochondrial membrane potential were obviously decreased (P＜0.05). Compared with the model group, the myocardial tissue structure of rats in the ramazolam group was obviously restored, and inflammatory cell infiltration was reduced. The cardiac function indicators LVEDD, LVESD, myocardial tissue MDA level, myocardial cell TUNEL positive rate, and myocardial tissue EPAC1, RAP1 and Caspase-3 protein expression levels were obviously decreased, and LVEF, LVFS, myocardial tissue SOD level, cardiomyocytes mitochondrial membrane potential were obviously increased (P＜0.05). Agonists of EPAC1 attenuated the mitigating effect of remazolam on myocardial injury in AMI rats. Conclusion Remimazolam may inhibit the EPAC1/RAP1 signaling pathway, inhibit myocardial cell apoptosis and alleviate myocardial injury in AMI rats. [ABSTRACT FROM AUTHOR]

Copyright of Traditional Chinese Drug Research & Clinical Pharmacology is the property of Traditional Chinese Drug Research & Clinical Pharmacology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the influence of sulforaphane （SFN） on ventricular remodeling in myocardial infarction （MI） rat model by regulating extracellular regulated protein kinase （ERK）/nuclear respiratory factor 1 （NRF1） signaling pathway. Methods: Among 48 SD male rats, 12 were randomly selected as Sham group. The remaining rats were treated with ligation of left anterior descending coronary artery to establish myocardial infarction model. After modeling, 36 rats were randomly divided into MI model group, SFN treatment group （10 mg/kg）, SFN+SCH772984 （ERK inhibitor） group （10 mg/kg+15 mg/kg）, with 12 rats in each group. Animal ultrasound was performed to detect cardiac structure and function. Histological analysis was performed to evaluate myocardial fibrosis and cell apoptosis. ELISA was used to measure pro-inflammatory factor levels in serum, and Western blot assay was used to observe the expression of ERK/NRF1 pathway related proteins in myocardium of rats in each group. Results: Compared with rats in Sham group, rats in MI model group showed a loss of myocardial compliance and disarray of ventricular myocardial fibers, along with increased myocardial fibrosis and myocardial cell apoptosis. Moreover, rats in MI model group also exhibited overactive inflammatory response and inhibition of the ERK/NRF1 signaling pathway in cardiac tissues（ P <0.05）. Notably, SFN treatment significantly not only improved cardiac function, but also ameliorated myocardial fibrosis and cell apoptosis （P <0.05）. SFN treatment inhibited inflammatory cytokine expression and activated the ERK/NRF1 pathway as well （P <0.05）. However, SCH772984 significantly abrogated the protective effect of SFN against myocardial fibrosis and apoptosis in MI rats. Conclusion: SFN may protect against ventricular remodeling in MI rat by activating ERK/NRF1 pathway. [ABSTRACT FROM AUTHOR]

Aim To reveal the mechanism of cross-species ischemic heart failure from the perspective of spatial and gene co-expression networks. Methods GSE210374 and GSE57338 high-throughput sequencing datas were retrieved from the national center for biotechnology information gene expression database (NCBI-GEO), and R language software packages was used to analyze and screen differentially expressed genes (DEG) in different myocardial regions of myocardial infarction rats, as well as DEG of myocardial samples from patients with ischemic heart failure and healthy controls, and the regional expression of common genes was analyzed. Weighted gene co-expression network analysis (WGCNA) was used to screen the genes related to myocardial infarction and to carry out enrichment analysis, protein-protein interaction network (PPI) was constructed to screen core genes (HG). Results A total of 4 835 differentially expressed genes were screened out in myocardial infarction rats and normal controls, and 51 differentially expressed genes were screened out in ischemic heart failure patients and normal control samples, which revealed representative gene sets in the left ventricular myocardial infarction area (I area), border area (BZ area), and remote area (R area) after myocardial infarction. Spatial expression analysis revealed that there were 20 co-expressed genes in each myocardial region, 16 of which were expressed in all three regions, the number of genes specifically expressed in I, BZ and R regions were 2, 0 and 2, respectively. Enrichment analysis showed that the functions of co-expressed genes were different in different region. The I and BZ regions were related to collagen fiber assembly, stress-induced cardiomyocyte hypertrophy, down-regulation of c-Jun amino terminal kinase (JNK signal) and cell proliferation, and complement signaling pathways; The I and R regions were enriched in the binding of Wnt and collagen; As a non-ischemic distal R region, the co-expressed genes were significantly enriched in the extracellular matrix for functions such as compressive resistance, cytolysis and inhibition of T cell proliferation. Furthermore, it was worth noting that the products of co-expressed genes in the three regions were mostly located in the extracellular space and extracellular matrix, suggesting that there may be active cellular secretion and interaction regulation. Further PPI analysis suggested that asporin (ASPN), osteoglycin (OGN) and collagentype ⅩⅣ alpha chain (COL14A1) gene might be the core genes of the mechanism mentioned above. Conclusions The common mechanism of ischemic heart failure in rats and human involves multiple signaling pathways such as complement and coagulation cascade signaling and Wnt; which may be closely related to cell apoptosis mediated by extracellular matrix and exosomes; ASPN, OGN, and COL14A1 may be the core genes. This work is expected to provide spatial and pathway reference for the selection of intervention targets and pathway in the transformation research related to ischemic heart failure. [ABSTRACT FROM AUTHOR]

Objective：To explore the evaluation of myocardial microcirculation characteristics and predictive value for left ventricular remodeling in patients with myocardial infarction using three ⁃ dimensional speckle tracking imaging. Methods：A total of 165 patients with myocardial infarction admitted to Chest Hospital affiliated to Zhengzhou University from August 2020 to August 2023 were selected for the study. According to the increase rate of left ventricular end⁃diastolic volume index（ΔLVEDVI），the patients were divided into left ventricular remodeling group（ΔLVEDVI>20%，74 cases）and non⁃left ventricular remodeling group（ΔLVEDVI≤20%， 91 cases）. The predictive value of myocardial microcirculation characteristics for left ventricular remodeling in patients with myocardial infarction was evaluated using receiver operating characteristic（ROC）curve. The influencing factors of left ventricular remodeling in patients with myocardial infarction were screened by stepwise regression analysis. A risk prediction model for left ventricular remodeling in patients with myocardial infarction was established and validated. Results：Coronary intervention time，myocardial infarction area，C⁃reactive protein（CRP），matrix metalloproteinase⁃（9 MMP⁃9），vascular endothelial growth factor⁃A（VEGF⁃A），index of microcirculatory resistance（IMR），fractional flow reserve（FFR），and coronary flow reserve（CFR）were all independent risk factors affecting left ventricular remodeling in patients with myocardial infarction（P < 0.05）. The calibration curve results showed that the multivariate logistic regression model had good accuracy. Conclusion：Myocardial microcirculation characteristics in patients with myocardial infarction have certain predictive value for left ventricular remodeling [ABSTRACT FROM AUTHOR]

Copyright of Journal of Clinical Nursing in Practice is the property of Journal of Clinical Nursing in Practice (Editorial Board, Shanghai Jiao Tong University Press) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the effect of overwork on the hemopoietic function of spleen in mice. Methods A total of 18 C57BL/6J mice were randomly divided into 3 groups, i.e., control group (C), 15-day-overworked group (W1) and 30-day-overworked group (W2). The mice from Groups W1 and W2 were forced to keep standing in water for 8 h and restrained for 3 h for consecutive 15 and 30 d, respectively, while those of Group C had no special treatment. The general condition, food intake and body weight of the mice were observed and measured. After modelling, the mice were euthanatized, and the spleen and heart were isolated to calculate spleen index and observe spleen pathological changes after HE staining, and then blood routine test was performed. The mRNA expression levels of CXCL12 and SCF in the spleen and that of connexin 45 (Cx45) in the heart were detected by RT-qPCR, and the protein levels of CXCL12 and SCF in spleen were detected by ELISA. The cardiac protein level of Cx45 was quantified with immunohistochemical assay. Results ① General condition showed that Groups W1 and W2 showed coarse hairs, increased at first and then decreased in activities, poor mental state, and larger food intake when compared with Group C. The body weight of Group C was increased with the feeding time, but that of Groups W1 and W2 had no such change. The spleen index was decreased significantly in Group W2 (P < 0.05). ② The results of blood routine test showed that WBC and RBC counts and HGB level were significantly increased in Group W2(P < 0.05), and PLT count in Groups W1 and W2 was significantly increased compared with Group C (P < 0.05). ③ Spleen HE staining displayed that the boundary between red pulp and white pulp was not clear, and the region of red pulp was enlarged in Group W2 when compared with Group C. ④ RT-qPCR showed that the mRNA level of Cx45 was significantly higher in heart tissue of Group W2 than that of Group C (P < 0.05), and that of SCF in spleen tissue of Group W2 was also higher than that in Groups C and W1 (P < 0.05). ⑤ Immunohistochemical assay indicated that the protein expression of Cx45 in myocardium of Groups W1 and W2 was significantly higher than that in Group C (P < 0.05). ⑥ ELISA revealed that the content of SCF in the spleen of Group W2 was notably higher than that of Groups C and W1 (P < 0.05), but there was no statistical difference between Groups W1 and C. Conclusion Overwork destroys the tight connection between cardiac myocytes, enhances the hemopoietic function of spleen, increases WBC count, and then forms a hypercoagulable state, which may be one of the precipitating factors for cardiovascular diseases related to overwork.

BACKGROUND: Exercise is an effective strategy to prevent and treat various cardiovascular diseases and protect the heart from ischemia-reperfusion injury. Its mechanism of action needs to be studied in depth. OBJECTIVE: To observe the effect of aerobic exercise preconditioning on myocardial ischemia-reperfusion injury and to explore the effect of endothelial nitric oxide synthase (eNOS) activation (including coupling and phosphorylation). METHODS: Eighty adult Wistar rats were randomly divided into sedentary (n=40) and exercise (n=40) groups. The rats in the exercise group were subjected to aerobic exercise for 8 weeks while those in the sedentary group were quietly fed and caged. After 8 weeks of intervention, three experiments were performed. (1) Experiment 1: After the last training, cardiac function, cardiac nitric oxide metabolite content and cardiac eNOS, phosphorylated eNOS-S1177, eNOS dimer and eNOS monomer protein expression levels were detected. (2) Experiment 2: Rats were divided into sedentary control group, exercise control group, sedentary+eNOS inhibitor group, exercise+eNOS inhibitor group, all of which were subjected to an in vitro myocardial ischemia-reperfusion injury experiment. eNOS inhibitor was continuously infused into the sedentary+eNOS inhibitor group and exercise+eNOS inhibitor group 10 minutes before reperfusion, and cardiac function and myocardial infarction area were detected 3 hours after reperfusion. (3) Experiment 3: Rats were divided into sedentary control group, exercise control group, sedentary+eNOS coupler group and exercise+eNOS coupler group, all of which were subjected to an in vitro myocardial ischemiareperfusion injury experiment. The rats in the sedentary+eNOS coupler group and exercise+eNOS coupler group were treated with eNOS coupler. Myocardial infarct area, cardiac nitric oxide metabolite content, cardiac protein expression of eNOS, phosphorylated eNOS-S1177, eNOS dimer, eNOS monomer and 3-nitrotyrosine were detected 3 hours after reperfusion. The phosphorylated eNOS-S1177/eNOS ratio reflected the phosphorylated/dephosphorylated level of eNOS and eNOS dimer/monomer ratio reflected eNOS coupling/uncoupling level. RESULTS AND CONCLUSION: Experiment 1: Compared with the sedentary group, the exercise group had increased cardiac output and left ventricular ejection fraction (P < 0.05), increased nitrite and S-nitrosothiol contents (P < 0.05), upregulated phosphorylated eNOS-S1177, eNOS protein expression and phosphorylated eNOS-S1177/eNOS ratio (P < 0.05), eNOS dimer protein expression and eNOS dimer/monomer ratios were elevated (P < 0.05). Experiment 2: Compared with the sedentary control group, left ventricular development pressure increased (P < 0.05) and myocardial infarct area decreased (P < 0.05) in the exercise control group. Compared with the exercise control group, left ventricular development pressure decreased (P < 0.05) and myocardial infarct area increased (P < 0.05) in the exercise+eNOS inhibitor group. Experiment 3: Compared with the sedentary control group, the exercise control group had increased left ventricular developmental pressure (P < 0.05), decreased myocardial infarct area (P < 0.05), decreased phosphorylated eNOS-S1177/eNOS ratio (P < 0.05), decreased eNOS dimer/monomer ratio (P < 0.05), increased S-nitrosothiol content (P < 0.05), and decreased 3-nitrotyrosine protein expression (P < 0.05). Compared with the exercise control group, the exercise+eNOS coupler group had decreased left ventricular developmental pressure (P < 0.05), increased myocardial infarct area (P < 0.05), increased phosphorylated eNOS-S1177/eNOS ratio (P < 0.05), increased eNOS dimer/monomer ratio (P < 0.05), and elevated 3-nitro tyrosine protein expression (P < 0.05). To conclude, aerobic exercise preconditioning could induce cardioprotection, which is related to uncoupling and dephosphorylation of eNOS during cardiac ischemia-reperfusion, thereby inhibiting the excessive production of nitric oxide and reducing nitro-oxidative stress. [ABSTRACT FROM AUTHOR]

BACKGROUND: Although traditional therapies, including drugs and surgery, cannot repair the damaged myocardial tissue, the mortality rate of myocardial infarction remains high. Stem cells provide the possibility to solve this problem due to their self-renewal and multi-directional differentiation potential. OBJECTIVE: To analyze the research progress of stem cell therapy for myocardial infarction in recent ten years by bibliometric analysis. METHODS: The related articles on stem cells and myocardial infarction published in SCI-E and SSCI from January 1, 2012 to December 1, 2022 in the Web of Science database were searched. EXCEL, CiteSpace and VOSviewer software were used to make statistical and visualization analyses of the data such as the number of publications, authors, institutions, journals, countries and keywords. RESULTS AND CONCLUSION: A total of 3 210 core articles were published, and the total number increased year by year. hausenloy,derek j. is the author with the largest number of publications, China is the country with the largest number of publications, and the Fourth Military Medical University is the institution with the largest number of publications. The research hotspots in this field are changing from cell experiments and animal experiments to clinical trials. In the past ten years, research in this field has been highly popular and still has great development prospects. It is necessary to promote international and interagency exchange and learning, and further explore the role of stem cells in the treatment of myocardial infarction. [ABSTRACT FROM AUTHOR]

BACKGROUND: Myocardial infarction is one of the most serious cardiovascular diseases at present, and the existing clinical treatment options such as thrombolytic therapy, percutaneous coronary intervention and coronary artery bypass grafting cannot fully restore the myocardial damage caused by ischemia. Stem cell-derived exosomes for the treatment of myocardial infarction have been a hot research topic in recent years, but the low yield of natural-derived exosomes, the difficulty and time consuming nature of obtaining them, and the poor homing effect have limited their clinical application. In this context, the construction of artificial exosomes as an alternative to natural exosomes has become an effective strategy to solve the above problems. OBJECTIVE: To expound the research status of artificial exosomes in the treatment of myocardial infarction, and classify them into two design modes: semiartificial and full-artificial, and discuss the research progress and problems of the two modes, finally, make the evaluation and prospect of its clinical application in the future. METHODS: PubMed and CNKI were searched for relevant articles with “artificial exosomes, myocardial infarction, engineering” in Chinese, and “artificial exosome, hybrid exosome, myocardial infarction, nanoparticle, drug delivery system” in English. The focus of the search was from January 2017 to December 2022, and some of the classic forward literature was included. A preliminary selection was conducted through reading titles and abstracts. Repetitive studies, low-quality journals and irrelevant articles were excluded. Finally, 73 articles were included for review. RESULTS AND CONCLUSION: (1) By semi-artificially modifying exosomes, whether it is the modification of targeting peptides, hybridization of biofilms or the assistance of magnetic substances, traditional exosome therapies with insufficient targeting and low retention rate and easy to be cleared by the reticuloendothelial system have improved the efficiency of traditional exosome therapy for myocardial infarction. However, these strategies have problems such as unclear modification efficiency, medical ethics, and biotoxicity. (2) Fully artificial bionic exosomes have a higher degree of design freedom compared to exosome modification, which can solve the problems of high extraction and storage difficulties of exosomes of natural origin and limitations of large-scale production; however, this artificial exosome strategy still lacks reliable preclinical data support and biosafety testing, and has not yet formed a standardized process required for large-scale production; therefore, before applying to the clinic, the artificial exosome solution as an alternative to natural exosomes still needs continuous in-depth research by researchers. [ABSTRACT FROM AUTHOR]

Ischemic heart disease is one of the main causes of death worldwide. In this study, the plasma samples of 47 patients with angina, 51 patients with myocardial infarction, and 80 patients with heart failure were collected. Ultra-performance liquid chromatography-high resolution mass spectrometry (UPLC-HRMS) and chemometrics were used to analyze the plasma metabolic disorder in disease progression for patients with ischemic heart disease. Chromatographic separation was performed on an ACE3 C18 column (150 mm×3.0 mm×3 μm), and MS analysis was carried out by electrospray ionization (ESI) source at positive and negative modes combined with full scanning. In total, 97 endogenous metabolites were identified and quantitative analyzed. Principal component analysis and partial least square-discriminant analysis were applied in combination with variable importance projection (VIP) and t-test to screen differentially characteristic metabolites. Metabolite concentration was analyzed using SPSS and the metabolites with significant differences (P<0.05) were found between different processes of diseases. Discriminant analysis using partial least squares-discriminant analysis (PLS-DA) was conducted on various disease processes. Classification models were established for angina, myocardial infarction, and heart failure patients. The variables with VIP>1 were selected using Variable Importance in Projection screening. Finally, disease-specific metabolites were identified using VIP>1 and t-test P<0.05. Accordingly, 28 and 32 characteristic metabolites were selected to distinguish between patients with angina and myocardial infarction, and with myocardial infarction and heart failure, respectively. The metabolic pathway analysis revealed disorders in both amino acid metabolism and the tricarboxylic acid cycle during the progression from angina to myocardial infarction, and from myocardial infarction to heart failure. In the progression from myocardial infarction to heart failure, there is a significant disturbance in lipid metabolism, including glycerophospholipid metabolism and fatty acid biosynthesis. Based on the results of 1 receiver operating character (ROC) analysis, several indicators including glycocholic acid, fumaric acid, palmitic acid, troponin, high-density lipoprotein, alanine aminotransferase, and aspartate aminotransferase, were found to have diagnostic significance for distinguishing between angina and myocardial infarction, with respective area under curve (AUC) values of 0.737 6, 0.831 9, 0.827 7, 0.938 7, 0.646 0, 0.704 5 and 0.758 9. When these indicators were combined, the AUC was increased to 1.000 0. Similarly, citrulline, citric acid, stearic acid, glycerophospholine, and NT-proBNP were found to have diagnostic significance for distinguishing between myocardial infarction and heart failure, with respective AUC values of 0.619 4, 0.748 7, 0.878 4, 0.636 0 and 0.812 1. When these indicators were combined, the AUC was increased to 0.957 0. At present, there have been some advances in understanding the metabolic characteristics of patients with angina or heart failure based on metabolomics, but there is limited research on the metabolic characteristics of patients with ischemic heart disease. The findings of this study can provide important metabolic targets for precise diagnosis of ischemic heart disease and drug and nutritional interventions during disease development. [ABSTRACT FROM AUTHOR]

AIM: To examine the effects of borneol on inflammation and myocardial remodeling after myocardial infarction (MI) in mice, and to investigate the underlying mechanisms. METHODS: Eight-week-old wild-type (WT) C57BL/6 mice and transient receptor potential cation channel subfamily M member 8 (TRPM8) gene knockout ( TRPM8-/-) mice were randomly divided into sham and MI groups, and were subsequently treated with normal saline (control group) or borneol (borneol group) via gavage. Survival curves were plotted for WT and TRPM8mice with MI treated with or without borneol. After 28 d, cardiac function of the mice was assessed through echocardiography, and haemodynamic indexes were evaluated using a multi-channel physiological instrument. Infarct size, myocardial hypertrophy and interstitial fibrosis were assessed via pathological staining. In addition, inflammatory response in the peri-infarct region was detected. RESULTS: The TRPM8 expression was up-regulated in the peri-infarct region of the mice with MI (P<0. 05), and borneol had no effect on TRPM8 expression (P>0. 05). Borneol increased the survival rate, reduced the infarct size, inhibited cardiac remodeling and improved cardiac function in WT mice with MI (P<0. 05 or P<0. 01). However, it did not affect the survival rate, infarct size, myocardial hypertrophy, myocardial fibrosis or cardiac function in TRPM8mice (P>0. 05). Furthermore, borneol reduced inflammatory cell infiltration and the expression of inflammatory cytokines, tumor necrosis factor-α (TNF-α ), interleukin-1β (IL-1β), IL-6 and monocyte chemotactic protein-1 (MCP-1), in WT mice (P<0. 05 or P<0. 01) but not in TRPM8-/- mice (P>0. 05). CONCLUSION: Borneol attenuates inflammation, inhibits cardiac remodeling and improves cardiac function in mice with MI via TRPM8. [ABSTRACT FROM AUTHOR]

Objective To observe and compare in-hospital and 1-year survival and prognosis of patients with 4b acute myocardial infarction (AMI) caused by early and late stent thrombosis (ST). Methods A total of 302 patients with 4b acute myocardial infarction caused by ST were enrolled in this study from January 2015 to February 2018. ST patients were confirmed by coronary angiography. These patients were divided into two groups: the early ST group (n=26) and the late ST group (n=276) according to the time of ST occurrence. Endpoint events during hospitalization and one year of follow up were compared between the two groups of patients. The primary endpoint events included cardiac death and recurrent AMI. The secondary endpoint events included target lesion revascularization (TLR), re-stent thrombosis, heart failure and stroke. The incidence of no endpoint events was compared between two groups of patients by Kaplan and Meier survival analysis. Cox regression analysis was used to analyze risk factors for endpoint events in patients with type 4b AMI. Results There was no significant difference in the incidence of the primary endpoint events during hospitalization between the two groups (7.7% vs. 3.3%，P=0.243). The incidence of heart failure was higher in the early ST group than that of the late ST group (11.5% vs.1.4%, P=0.016). There was no significant difference in the incidence rates of other secondary endpoint events between the two groups (P＞0.05). After a mean follow-up of 1 year, the incidence rates of primary endpoint events and the secondary eendpoint events were higher in the early ST group (20.0% vs. 5.9%，P＜0.05 and 36.0% vs. 11.5%，P＜0.01）than that of the late ST group. Kaplan and Meier survival analysis showed that the 1-year cumulative incidences of non-primary (P= 0.022) and non-secondary events (P＜0.001) were lower in the early ST group than those of the late ST group. Cox regression analysis showed that hypertension and history of coronary artery bypass grafting were independent risk factors for primary endpoint events in patients with 4b AMI, and intraoperative implantation of intraaortic balloon pump (IABP) and shortening the time from stent thrombosis to balloon dilation (ST to B) were independent protective factor. Conclusion Early ST patients have similar in-hospital outcomes and poor long-term prognosis compared with late ST induced 4b type AMI patients. Intraoperative implantation of IABP and shortening of ST to B time may improve the prognosis of 4b type AMI patients. [ABSTRACT FROM AUTHOR]

Copyright of Journal of China Medical University is the property of Journal of China Medical University Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To explore the characteristics of myocardial injury in patients with acute myocardial infarction (AMI) complicated by pleural effusion and its effect on long-term prognosis. Methods It was a prospective single-center study. Patients with AMI who were admitted to hospital within 15 days from symptom onset and performed echocardiography and cardiac magnetic resonance imaging (CMR) during hospitalization were consecutively enrolled and assigned to the withpleural effusion group and the without-pleural effusion group according to the echocardiography result. Baseline data, cardiac magnetic resonance myocardial injury index and echocardiography characteristics were compared between the two groups. The occurrence of major adverse cardiovascular and cerebrovascular events (MACCE) was recorded through outpatient follow-up and telephone follow-up, including all-cause death, re-infarction, revascularization, rehospitalization for congestive heart failure and stroke. Cox regression analysis was performed to analyze influencing factors of all-cause death. Results Among 211 patients, 31 (14.7%) patients had pleural effusion and 180 (85.3%) had no pleural effusion. Compared with the group without pleural effusion, the left ventricular end-diastolic diameter was larger, and left ventricular ejection fraction assessed by echocardiography was lower in the group with pleural effusion (P＜0.05). There were no significant differences in infarct size, left ventricular end-diastolic volume, left ventricular end-systolic volume, left ventricular ejection fraction and the presence of microvascular obstruction and intramyocardial hemorrhage between the two groups in CMR (all P＞0.05). At a median follow-up of 31 months, MACCE occurred in 43 (20.4%) patients, and there was no significant difference between the two groups (χ2 =3.160，P=0.075). Six cases (2.8%) had all-cause death. The incidence of all-cause death was higher in the group with pleural effusion than that in the group without pleural effusion (9.7% vs. 1.7%, P < 0.05). There was no significant difference in the incidence of other adverse events between the two groups (P＞ 0.05). Multivariate Cox regression analysis showed that advanced age and presence of pleural effusion were independent risk factors of all-cause death during follow-up. Conclusion Patients with AMI combined with pleural effusion have more severe myocardial injury and higher all-cause mortality. [ABSTRACT FROM AUTHOR]

Objective To investigate the efficacy and safety of sacubitril valsartan in the treatment of heart failure (HF) of midrange ejection fraction（HFmrEF）in patients after acute myocardial infarction (AMI). Methods A total of 102 patients with HFmrEF after AMI were divided into the control group and the experimental group, with 51 cases in each group. The control group was given conventional treatment for AMI and anti-HF treatment, and the angiotensin-converting enzyme inhibitor (ACEI)/ angiotensin Ⅱ receptor blocker (ARB) was used without contraindications. The experimental group was replaced by ACEI/ARB with sacubitril valsartan on the basis of the control group. After 6 months of treatment, the total effective rates of the two groups after treatment were analyzed, and the cardiac function, N-terminal pro-brain natriuretic peptide (NT-proBNP) and serum inflammatory factor C-reactive protein (CRP) were compared before and after treatment. The occurrence of adverse reactions after treatment was recorded. Kaplan-Meier method was used to analyze the cumulative cardiovascular mortality, HF rehospitalization rate and end-event-free survival after 6 months of treatment in two groups. Results After treatment, there was no significant difference in the occurrence of adverse reactions between the two groups (P＞0.05). The total effective rate was higher in the experimental group than that of the control group (P＜0.05). Compared with before treatment, left ventricular ejection fraction (LVEF), stroke volume (SV), mitral diastolic blood flow velocity E peak and A peak ratio (E/A) and 6 min walking distance (6MWD) were increased in the two groups, and left ventricular enddiastolic diameter (LVEDD) and left atrial diameter (LAD) were decreased in the two groups after treatment (all P＜0.05). After treatment, LVEF, SV, E/A and 6MWD were higher in the experimental group than those in the control group (P＜0.05). LVEDD and LAD were lower than those in the control group (all P＜0.05). Compared with results before treatment, NT proBNP and CRP were decreased after treatment in the experiment group than those in the control group (P＜0.05). There was no significant difference in the cumulative cardiovascular mortality between the experiment group and the control group (3.9% vs. 5.9%，P=0.524). The cumulative HF rehospitalization rate was lower in the experimental group than that of the control group (9.8% vs. 23.5%，P=0.042). The cumulative end-point-free survival rate was higher in the experiment group than that of the control group (86.3% vs. 70.6%, P=0.037). Conclusion Sacubitril valsartan is safer and more effective than ACEI/ARB in the treatment of AMI patients with HFmrEF, and it is worthy of clinical promotion. [ABSTRACT FROM AUTHOR]

BACKGROUND: Our previous experimental results have shown that hyaluronic acid hydrogel can act as a vehicle for bone marrow mesenchymal stem cell delivery to improve the cardiac function of rats with myocardial infarction. OBJECTIVE: To explore the molecular mechanism of bone marrow mesenchymal stem cells and hyaluronic acid hydrogel in promoting damaged heart repair. METHODS: Bone marrow mesenchymal stem cells from male Sprague-Dawley rats were isolated and cultured, and then hyaluronic acid-encapsulated bone marrow mesenchymal stem cells were cultured in vitro in a three-dimensional manner. A model of myocardial infarction was made by ligating the left anterior descending artery of female Sprague-Dawley rats. After 1 week, the model rats were screened by ultrasonic testing and then eligible ones were randomly divided into four groups: PBS group (n=12), hyaluronic acid group (n=12), bone marrow mesenchymal stem cell group (n=15), and hyaluronic acid-encapsulated bone marrow mesenchymal stem cell group (n=15). At 1 week after ligation, the model rats underwent the secondary thoracotomy followed by corresponding injections into the infarcted region and its marginal zone. The expression levels of matrix metalloproteinase-2, vascular endothelial growth factor, thymosin β4 and c-Kit were examined at post-injection day 1, week 1 and week 2 by western blot assay. At post-injection week 2, immunofluorescence staining was used to detect the differentiation of transplanted cells. RESULTS AND CONCLUSION: (1) The expression levels of matrix metalloproteinase-2 and vascular endothelial growth factor protein in the infarct zone in the bone marrow mesenchymal stem cell group were significantly up-regulated at week 1 compared with the other three groups (P < 0.05). At week 2, the hyaluronic acid group had a lower expression of matrix metalloproteinase-2 and vascular endothelial growth factor protein than the other three groups (P < 0.05). However, the expression of matrix metalloproteinase-2 and vascular endothelial growth factor protein in the hyaluronic acid+bone marrow mesenchymal stem cell group was not significantly different compared with the bone marrow mesenchymal stem cell group. This was primarily attributable to a prolonged paracrine effect via the controlled release of the hyaluronic acid hydrogel. This prolonged paracrine effect offsets the inhibitory effect induced by hyaluronic acid hydrogel at 2 weeks. (2) Compared with the PBS group, thymosin β4 and c-Kit expression levels in the hyaluronic acid group, bone marrow mesenchymal stem cell group and bone marrow mesenchymal stem cell+hyaluronic acid group were significantly increased (P < 0.05). (3) No differentiation of transplanted cells into cardiomyocytes or blood vessels was detected 2 weeks after transplantation. (4) It is indicated that transplanted bone marrow mesenchymal stem cells promote myocardial repair through the paracrine effect, and hyaluronic acid hydrogel prolongs the paracrine effect of transplanted bone marrow mesenchymal stem cells. [ABSTRACT FROM AUTHOR]

Currently, revascularization is an effective rescue strategy for patients with acute myocardial infarction. However, myocardial ischemia/reperfusion （I/R） injury induced by revascularization has become a significant risk factor affecting the long-term prognosis of patients with ischemic cardiomyopathy after revascularization, without precise treatment. Extracellular vehicles derived from mesenchymal stem cells are characterized by easy access, editability, and easy absorption of cells, and their application in treating myocardial I/R injury is considered valuable to study. This review focuses on the advances in research on mesenchymal stem cell-derived extracellular vehicles and their function of regulating myocardial I/R injury after natural drug intervention, hopefully offering ideas for the research of prevention and treatment of myocardial I/R injury. [ABSTRACT FROM AUTHOR]

Exosomes are the means of intercellular communication, and long non-coding RNAs (lncRNA), as the cargo of exosomes, are involved in regulating various physiological and pathological processes of cardiovascular system due to their rich functions. This article reviews the relevant research on extracellular lncRNA in the field of acute myocardial infarction, summarizes the regulatory role of extracellular lncRNA, analyzes the current research status of extracellular lncRNA as a biomarker and treatment strategy for myocardial infarction, and selects potential biomarkers through sequencing information in public databases. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Inorganic Analytical Chemistry / Zhongguo Wuji Fenxi Huaxue is the property of Beijing Research Institute of Mining & Metallurgy Technology Group and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background The mortality of acute myocardial infarction complicated with cardiogenic shock (AMI-CS) is very high, timely and effective circulatory support is essential to save the lives of patients. It is important to explore the clinical efficacy, complications and prognosis of combined auxiliary sequence of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) and intra-aortic balloon pumps (IABP) in patients with AMI-CS. Objective To observe the effect of the auxiliary sequence of VA-ECMO and IABP on the therapeutic effect and prognosis of patients with AMI-CS in the combination of VA-ECMO and IABP, explore the causes and significance of changes in relevant indicators, compare the incidence of complications, analyze the factors affecting prognosis, so as to find a relatively safe and effective mechanical circulatory support (MCS) method for patients with AMI-CS. Methods AMI-CS patients who received VA-ECMO combined with IABP in the Department of Intensive Care Medicine of the Second Affiliated Hospital of Zhengzhou University and Fuwai Central China Cardiovascular Hospital from 2021 to 2022 were retrospectively included as the study objects, and all patients were treated with the combined auxiliary mode of VA-ECMO and IABP, and divided into the group A (IABP followed by VA-ECMO, n=42) and group B (VA-ECMO followed by IABP or VA-ECMO combined with IABP at the same time, n=40). Baseline data, clinical indicators, treatment status, related complications and prognosis before, 24 h and 72 h after combination therapy were collected by the electronic medical record system. Results The results of two-factor repeated measures ANOVA showed that there were interactions of time and intergroup on mean arterial pressure (MAP), heart index (CI), arterial blood lactate (Lac), and troponin I (cTnI) (P0.05). The main effects of time on MAP, CI, GFR, Lac, cTnI and BNP were significant (P0.05). MAP, CI and GFR at 24 h and 72 h after treatment were higher than those before treatment, while Lac, cTnI and BNP were lower than those before treatment, the differences were statistically significant (P

Objective To investigate risk factors for short-term major adverse cardiovascular events (MACE) following percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI) with type 2 diabetes mellitus (T2DM). Methods We retrospectively analyzed the clinical data of 147 patients with AMI with T2DM who underwent PCI in Kaifeng people’s Hospital from August 2016 to January 2020 as well as their information on MACE within 3 months after PCI. The patients were divided into MACE group and normal group according to whether MACE occurred or not within 3 months after operation. The two groups were compared in terms of blood glucose variability [standard deviation of blood glucose (SDBG), mean amplitude of glycemic excursions (MAGE), absolute mean of daily differences (MODD), and postprandial glucose excursions (PPGE)] within 72 h after operation as well as total cholesterol (TC), high-sensitivity C-reactive protein (hs-CRP), and left ventricular ejection fraction (LVEF) after operation. The risk factors for the occurrence of MACE were analyzed. Results The incidence of MACE within 3 months after PCI was 23.81%. The MACE group showed significantly higher levels of SDBG, MAGE, MODD, and PPGE within 72 h after operation and a significantly higher hs-CRP level after operation (t=10.206-24.388,P

Background Important predictive value of platelet-lymphocyte ratio (PLR) for adverse outcomes of cardiovascular disease has been proved in previous studies, however, the predictive value of PLR for short-term prognosis in elderly patients with acute myocardial infarction (AMI) remains to be explored. Objective To determine the predictive ability of PLR for mortality risk during hospitalization in elderly patients with AMI. Methods The medical history data of 1 423 elderly patients with AMI treated in the Department of Cardiology of the Second Hospital of Dalian Medical University from December 2015 to December 2021 was retrospectively collected, mainly including gender, age, BMI, blood pressure classification, glycated hemoglobin, platelet count, neutrophil count, lymphocyte count, estimated glomerular filtration rate, lipid related indices, the combination of heart failure and diabetes, the use of statins and antiplatelet agents during hospitalization, with the final outcome defined as all-cause death during hospitalization. The included patients were divided into the non-death group (n=1 315) and death group (n=108) according to the occurrence of death. ROC curve was used to determine the predictive ability of PLR for in-hospital mortality risk in elderly patients with AMI, and the clinical application value of PLR and its combined indicators by decision curve analysis (DCA) . Results There were significant differences in age, BMI, PLR, white blood cell count, neutrophil count, lymphocyte count, red blood cell count, hemoglobin, fasting blood glucose level, AST, TG, CTNI, eGFR grade, proportion of heart failure, proportion of antiplatelet drugs, and proportion of lipid-lowering drugs between the death group and the non-death group (P

BACKGROUND: Histone modification is a reversible post-translational modification that acts as a marker of transcriptional activation or inhibition and controls cell metabolism, damage, and repair. Deacetylation, as one of the histone posttranslational modifications, plays an important role in the occurrence and development of cardiovascular diseases. OBJECTIVE: To mainly review the mechanisms of histone deacetylation in atherosclerosis, myocardial hypertrophy, heart failure, myocardial infarction, and hypertension, in order to further understand the pathological processes related to the occurrence and development of cardiovascular diseases, providing theoretical reference for the diagnosis, treatment and prognosis of cardiovascular diseases. METHODS: Related articles published from 1979 to 2022 were retrieved from PubMed, Web of Science and CNKI database. The keywords were “histone, histone modification, histone acetylation, histone deacetylation, histone transacetylase, histone deacetylase, cardiovascular, atherosclerosis, cardiac hypertrophy, heart failure, myocardial infarction, hypertension” in English and Chinese. Ultimately, we included 64 articles for review. RESULTS AND CONCLUSION: Histone acetylation modifications occur mainly at the more conserved N-terminal lysine residues of core histones and are regulated synergistically by histone acetyltransferases and histone deacetylases, which have emerged as an important form of epigenetic regulation. Histone deacetylation modifications regulate the occurrence and development of cardiovascular diseases and the following conclusions can be drawn: (1) At the protein level, histone deacetylation modifications increase the diversity and complexity of mechanisms between cellular pathways, mainly by changing the localization, activity or function of proteins, which then affect a variety of important cellular life activities, thus playing an important role in the diagnosis, treatment and prognosis of cardiovascular diseases. (2) Histone acetyltransferase and histone deacetylase molecules are closely related to cardiovascular diseases such as atherosclerosis, myocardial hypertrophy, myocardial infarction and hypertension, and their corresponding inhibitors can be used as targeted drugs for these diseases. (3) Research on histone acetylation and deacetylation modifications in cardiovascular diseases is still at the basic research stage and the specific mechanisms of histone deacetylation modifications in some diseases are still being investigated. As research progresses, new breakthroughs in histone acetylation modifications are expected in the treatment of cardiovascular disease and in clinical translation. [ABSTRACT FROM AUTHOR]

Aim To investigate the clinical predictive value of free thyroid hormone (FT4) / free triiodothyronine (FT3) ratio for the risk of all-cause death in hospital in acute myocardial infarction (AMI) patients. Methods The clinical data of AMI patients who underwent coronary angiography or percutaneous coronary intervention (PCI) in the Department of Cardiology of the Second Affiliated Hospital of Dalian Medical University from January 2016 to December 2022 were collected retrospectively, a total of 63 patients with complete medical history and died during hospitalization were selected, 180 AMI patients who did not die during hospitalization in the same period were selected as the control group. Results Age, ST elevation myocardial infarction (STEMI), renal insufficiency, atrial fibrillation, heart rate, Killip III/ IV, multi-vessel disease, cardiac troponin I and brain natriuretic peptide (BNP) in the in-hospital death group were higher than those in the survival group, while ejection fraction (EF) was lower than that in the survival group, the difference was statistically significant (P<0. 05). FT4 and FT4/ FT3 ratio in the in-hospital death group was higher than those in the survival group, and the FT3 was lower than that in the survival group, the difference was statistically significant (P < 0. 05). Multivariate Logistic regression analysis showed that the FT4/ FT3 ratio was associated with the risk of all-cause death in hospital in AMI patients (OR=1. 844, 95% CI: 1. 193 ~2. 850, P<0. 05). In addition, age, heart rate, Killip III/IV grade, STEMI, renal insufficiency and low EF were also positively correlated with the risk of all-cause death in hospital in AMI patients (OR=1. 084, 1. 031, 2. 847, 2. 508, 4. 085, 4. 407, P<0. 05). The results of the ROC curve analysis showed that the FT4/ FT3 ratio (AUC=0. 774, 95%CI: 0. 708 ~0. 839, P<0. 001) predicted the risk of all-death in hospital better than FT4 (AUC=0. 640, 95%CI: 0. 561 ~0. 719, P =0. 001) or FT3 (AUC=0. 719, 95%CI: 0. 647 ~ 0. 790, P<0. 001) alone. The difference in area under the ROC curve was statistically significant (P = 0. 001 and P = 0. 042). Conclusions FT4/ FT3 ratio is related to the risk of all-cause death in hospital in AMI patients, which can predict the risk of all-cause death in hospital in AMI patients. Compared with FT3 or FT4 alone, FT4/ FT3 ratio has better clinical predictive value for all-cause death in hospital in AMI patients. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Clinical Nursing in Practice is the property of Journal of Clinical Nursing in Practice (Editorial Board, Shanghai Jiao Tong University Press) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective Fourier transform infrared spectroscopy (FTIR) was used to analyze myocardial infarction tissues at different stages of pathological change to achieve the forensic pathology diagnosis of acute and old myocardial infarction. MethodsFTIR spectra data of early ischemic myocardium, necrotic myocardium, and myocardial fibrous tissue in the left ventricular anterior wall of the sudden death group of atherosclerotic heart disease and the myocardium of the normal control group were collected using hematoxylin-eosin (HE) and immunohistochemistry (IHC) staining as a reference, and the data were analyzed using multivariate statistical analysis. Results The mean normalized spectra of control myocardium, early ischemic myocardium and necrotic myocardium were relatively similar, but the mean second derivative spectra were significantly different. The peak intensity of secondary structure of proteins in early ischemic myocardium was significantly higher than in other types of myocardium, and the peak intensity of the α-helix in necrotic myocardium was the lowest. The peaks of amide and amide in the mean normalized spectra of myocardial fibrous tissue significantly shifted towards higher wave numbers, the peak intensities of amide and amide were higher than those of other types of myocardium, and the peak intensities at 1 338, 1 284, 1 238 and 1 204 cm-1 in the mean second derivative spectra were significantly enhanced. Principal component analysis (PCA) and partial least square-discriminant analysis (PLS-DA) showed that FTIR could distinguish different types of myocardium. ConclusionFTIR technique has the potential to diagnose acute and old myocardial infarction, and provides a new basis for the analysis of the causes of sudden cardiac death. [ABSTRACT FROM AUTHOR]

Objective To investigate the biological role of methyltransferase-like 14 （METTL14）-mediated m6A modification in myocardial infarction （MI）. Methods A total of 40 mice were randomly divided into 4 groups: Sham+AAV9-NC group （n = 10）, Sham+AAV9-METTL14 group （n = 10）, MI+AAV9-NC group （n = 10） and MI+AAV9-METTL14 group （n = 10）. Mice in each group were injected with AAV9-METTL14 or AAV9-NC through the tail vein one week before MI induction. Cardiac function was measured non-invasively by transthoracic echocardiography, and microvascular injury were measured by immunofluorescence. CMECs were isolated from mouse myocardial tissue, and the cells were treated with oxygen-glucose deprivation （OGD）. Results METTL14 was downregulated in MI mouse heart tissue as well as in OGD-treated CMECs. Compared with the Sham+AAV9-NC group, the expression of VE-cadherin was significantly down-regulated （P < 0.05）, ROS levels increased significantly （P < 0.05） in the MI+AAV9-NC group. MI+AAV9-METTL14 suppressed these changes and enhanced cardiac function in mice. Compared with the NC group, a significant increase in mitochondrial ROS levels was observed in the OGD group （P < 0.05）. Knockdown of METTL14 in CMECs exacerbated ROS levels （P < 0.05）, and the addition of USP48 overexpression plasmid reversed these changes （P < 0.05）. Conclusion METTL14 was lowly expressed in MI and mediates mitochondrial dysfunction in CMECs by increasing the m6A modification level of USP48 in CMECs to reduce its stability. [ABSTRACT FROM AUTHOR]