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BACKGROUND: It has been shown that long non-coding RNA (lncRNA) plays an important role in the development and progression of cardiac diseases, and whether it is involved in daisy leaf gentianone antagonizing adriamycin-induced cardiac injury in mice has not been reported. OBJECTIVE: To screen differentially expressed lncRNAs in myocardial tissue of mice with adriamycin-induced myocardial injury antagonized with daisy leaf gentianone and conduct a bioinformatics analysis. METHODS: Forty-eight C57 mice were randomly divided into normal group, model group, daisy leaf gentianone group and positive drug group, with 12 mice in each group. The mice in the model group, daisy leaf gentianone group and positive drug group were injected with adriamycin intraperitoneally once every other day for 8 times in total. The daisy leaf gentianone group and positive drug group were given daisy leaf gentianone suspension and captopril solution by gavage based on adriamycin injection once a day for 21 continuous days. After medication, mice in each group underwent electrocardiogram examination and the myocardial tissue was taken for pathomorphological observation. At the same time, high-throughput sequencing analysis of mouse myocardial tissue was carried out, differentially expressed lncRNAs were screened, and target genes were predicted for differentially expressed lncRNAs. Gene ontology enrichment and Kyoto Encyclopedia of Genes and Genomes signaling pathway analyses of target genes were performed. RESULTS AND CONCLUSION: The ST segment of the electrocardiogram of mice in the model group was significantly elevated. Compared with the model group, the degree of ST-segment elevation on the electrocardiogram was reduced in the daisy leaf gentianone group. Results from hematoxylin-eosin, Masson, and Sirius red staining indicated that in the model group, the myocardial cytoplasm was unevenly colored with varying shades of color, the integrity and continuity of myocardial fibers were poor, and a large number of collagen fibers were deposited. After treatment with gentianone daisy leaves, the abnormalities in myocardial tissue of mice were improved. The results of high-throughput sequencing analysis showed that compared with the model group, a total of 270 lncRNAs were identified in the myocardial tissue of mice in the daisy leaf gentianone group, including 165 up-regulated and 105 down-regulated lncRNAs. Combining the experimental results with related literature, three lncRNAs (NONMMUT149833.1, NONMMUT003237.2, and ENSMUST00000219015) and four related mRNAs (Alas2, Igf2, Acta1, and Cilp) were finally identified. The results of target gene prediction, gene ontology enrichment and Kyoto Encyclopedia of Genes and Genomes signaling pathway analyses showed that differentially expressed lncRNAs in myocardial tissue of mice with myocardial injury could regulate the expression of their target protein-coding genes through cis- and/or trans-regulation, and participate in regulating molecular functions and biological processes. To conclude, daisy leaf gentianone significantly improves cardiac function and partial lncRNA expression in mice with adriamycin-induced myocardial injury. [ABSTRACT FROM AUTHOR]

AbstractBackgroundMethodsResultsConclusionHigh-sensitivity cardiac troponins (Hs-cTns) are reliable indicators of myocardial injury, but their relationship with cardiovascular outcomes remains less understood. This study explored the association between adverse cardiac events and Hs-cTnT levels exceeding 14ng/L in patients with stable CAD.Thirteen pertinent studies were identified using specific keywords from a pool of 208 articles retrieved from PubMed, Scopus, and Google Scholar, spanning 2013 to 2023. The primary outcomes included all-cause mortality (ACM), myocardial infarction (MI), cardiovascular death (CVD), rehospitalization due to decompensated heart failure (RDHF), need for revascularization, and stroke. Comprehensive meta-analysis (CMA) was employed to analyze the data for odds ratios (OR) and 95% confidence intervals (CI). Heterogeneity was assessed using I2 statistics, and both qualitative assessment (Newcastle-Ottawa Scale) and quantitative analysis (Egger's and Beggs test, funnel plots) were conducted.The analysis included 29,115 participants (74.72% male) with a mean age of 68.34 years. It revealed a significantly elevated risk of ACM among stable CAD patients with Hs-cTnT levels > 14ng/L compared to those with levels <14ng/L (11.2% vs. 3.3%; OR 5.46; 95% CI: [1.53, 19.54]; p = 0.009). Similarly, higher risks were observed for MI (10.9% vs 3.6%; OR 3.12;, 95% CI: [0.98, 9.95], p = 0.053, CVD (8.1% vs. 2.1%; OR 3.37; 95% CI: [1.74, 6.50]; p < 0.0001), and RDHF (6.62% vs. 0.92%; OR 9.46; 95% CI: [4.65, 19.24]; p < 0.0001). Notably, major adverse cardiovascular events (MACE) exhibited a stronger association with Hs-cTnT levels (18.2% vs 7.81%; OR of 1.89; 95% CI: [0.80, 4.43]; I2 = 97%; p = 0.14) compared to Hs-cTnI levels (20.1% vs 21.1%; OR 1.30; 95% CI: [1.03, 1.64]; I2 = <0.0001%; p = 0.03).Elevated levels of Hs-cTnT (>14ng/L) are significantly associated with increased risks of RDHF and ACM in patients with stable CAD. Further large-scale prospective studies are warranted to refine risk assessment strategies and mitigate cardiovascular mortality in this population. [ABSTRACT FROM AUTHOR]

Aims Methods and results Conclusion Abnormalities in specific echocardiographic parameters and cardiac biomarkers have been reported among individuals with diabetes. However, a comprehensive characterization of diabetic cardiomyopathy (DbCM), a subclinical stage of myocardial abnormalities that precede the development of clinical heart failure (HF), is lacking. In this study, we developed and validated a machine learning‐based clustering approach to identify the high‐risk DbCM phenotype based on echocardiographic and cardiac biomarker parameters.Among individuals with diabetes from the Atherosclerosis Risk in Communities (ARIC) cohort who were free of cardiovascular disease and other potential aetiologies of cardiomyopathy (training, n = 1199), unsupervised hierarchical clustering was performed using echocardiographic parameters and cardiac biomarkers of neurohormonal stress and chronic myocardial injury (total 25 variables). The high‐risk DbCM phenotype was identified based on the incidence of HF on follow‐up. A deep neural network (DeepNN) classifier was developed to predict DbCM in the ARIC training cohort and validated in an external community‐based cohort (Cardiovascular Health Study [CHS]; n = 802) and an electronic health record (EHR) cohort (n = 5071). Clustering identified three phenogroups in the derivation cohort. Phenogroup‐3 (n = 324, 27% of the cohort) had significantly higher 5‐year HF incidence than other phenogroups (12.1% vs. 4.6% [phenogroup 2] vs. 3.1% [phenogroup 1]) and was identified as the high‐risk DbCM phenotype. The key echocardiographic predictors of high‐risk DbCM phenotype were higher NT‐proBNP levels, increased left ventricular mass and left atrial size, and worse diastolic function. In the CHS and University of Texas (UT) Southwestern EHR validation cohorts, the DeepNN classifier identified 16% and 29% of participants with DbCM, respectively. Participants with (vs. without) high‐risk DbCM phenotype in the external validation cohorts had a significantly higher incidence of HF (hazard ratio [95% confidence interval] 1.61 [1.18–2.19] in CHS and 1.34 [1.08–1.65] in the UT Southwestern EHR cohort).Machine learning‐based techniques may identify 16% to 29% of individuals with diabetes as having a high‐risk DbCM phenotype who may benefit from more aggressive implementation of HF preventive strategies. [ABSTRACT FROM AUTHOR]

The aim of the study was to analyze the Canadian Cardiovascular Society (CCS) guidelines for routine postoperative troponin testing after elective total hip arthroplasty (THA) to reduce the mortality rate resulting from myocardial injury. The purpose of this study was to assess the prognostic relevance of implementing these guidelines to minimize cardiac events in patients undergoing elective THA. Patients who underwent THA surgery in 2020 were included in the study. The inclusion criteria were elective THA patients aged ≥45 years, while emergency, revision, and simultaneous bilateral THA surgeries were excluded. The patients were categorized into 4 groups based on the CCS guidelines. The study included 669 patients who had an average age of 67 years. There were 43 patients (6.4%), who experienced a rise in troponin levels ≥30 ng/L and developed myocardial injury after noncardiac surgery. Among these patients, 8 developed cardiac complications, and one experienced a serious cardiac event that resulted in death. Notably, there was a significant increase in the length of hospital stay for patients who received the postoperative screening protocol. The implementation of the CCS guidelines for routine postoperative troponin testing in elective THA surgery did not significantly decrease the rate of cardiac events or mortality. [ABSTRACT FROM AUTHOR]

Introduction: Ventricular arrhythmia is commonly provoked by acute cardiac ischemia through sympathetic exaggeration and is often resistant to anti-arrhythmic therapies. Thoracic epidural anesthesia has been reported to terminate fatal ventricular arrhythmia; however, its underlying mechanism is unknown. Methods: Rats were randomly divided into four groups: sham, sham plus bupivacaine, ischemia/reperfusion (IR), and IR plus bupivacaine groups. Bupivacaine (1 mg/mL, 0.05 mL/100 g body weight) was injected intrathecally into the L5–L6 intervertebral space prior to establishing a myocardial IR rat model. Thereafter, cardiac arrhythmia, cardiac function, myocardial injury, and electrical activities of the heart and spinal cord were evaluated. Results: Intrathecal bupivacaine inhibited spinal neural activity, improved heart rate variability, reduced ventricular arrhythmia score, and ameliorated cardiac dysfunction in IR rats. Furthermore, intrathecal bupivacaine attenuated cardiac injury and myocardial apoptosis and regulated cardiomyocyte autophagy and connexin-43 distribution during myocardial IR. Conclusion: Our results indicate that intrathecal bupivacaine blunts spinal neural activity to prevent cardiac arrhythmia and dysfunction induced by IR and that this anti-arrhythmic activity may be associated with regulation of autonomic balance, myocardial apoptosis and autophagy, and cardiac gap junction function. [ABSTRACT FROM AUTHOR]

Perioperative myocardial injury (PMI) is a common syndrome in high-risk surgical populations, with an estimated incidence of 19.6%. Reliable detection of PMI is only possible with active surveillance strategies, such as serial cardiac troponin (cTn) measurements. PMI can have different causes and carries different prognoses, so it is important to distinguish the etiology for proper management. The European Society of Cardiology offers a pragmatic approach for clinicians, and personalized, etiology-driven management is recommended. Prevention and early identification of PMI are crucial, and preoperative cTn surveillance can provide additional predictive value. Treatment should be tailored according to the specific cause of PMI. [Extracted from the article]

Limited data are available regarding myocardial injury and its risk factors in percutaneous coronary interventions (PCI) of severe calcified lesions using orbital atherectomy (OA). Patients who underwent OA at our institution were retrospectively enrolled into the present registry. High-sensitive Troponin I (hsTroponin I), EKG and echocardiography were used to assess myocardial injury after the procedure. A total of 27 patients between who underwent OA between January 2022 and June 2023 were included. Myocardial injury (elevation of hsTroponin I above the 99th percentile upper reference limit) occurred in all patients. Median hsTroponin I on the first day after the procedure was 1093 (557–4037) ng/l with a minimum of 86 ng/l and a maximum of 25,756 ng/l. Myocardial infarction occurred in two patients (7 %), who had severe coronary dissection after OA. Lesions were longer (47 [38–52] mm vs. 20 [14–47] mm; p = 0.009) in patients with hsTroponin I levels above the median compared to those with levels below. Furthermore, a moderate correlation between hsTroponin I and lesion length was detected (r = 0.54; p = 0.004). In the present study myocardial injury occurred in all patients after OA without loss of viable myocardium in the majority of patients. Lesions length was found to be a significant factor associated with markedly increased hsTroponin I after the OA procedure. • Myocardial injury defined as elevation of hsTroponin I above the upper reference limit occurred in all patients after OA. • However, the incidence of myocardial infarction in this complex coronary anatomy population was rather low (7%). • Lesion length was identified as risk factor for myocardial injury. [ABSTRACT FROM AUTHOR]

Background: Pulmonary hypertension (PH) is a prevalent adverse cardiovascular event at high-altitude environments. Prolonged exposure to high altitudes may result in myocardial injury, which is associated with poor clinical outcomes. This study aims to investigate the clinical characteristics of myocardial injury in patients with PH at high altitude. Methods: Consecutive patients admitted to a general tertiary hospital at the altitude of 3,650 m were selected into this retrospective study. Clinical and biochemical data were collected, as well as based on cardiac troponin I (cTnI) and echocardiography, patients were divided into myocardial injury group and non-myocardial injury group. Results: A total of 231 patients were enrolled, among whom 29 (12.6%) had myocardial injury. We found that body mass index, left ventricular end-diastolic dimension, and serum level of creatine kinase-MB (CK-MB) in myocardial injury group were significantly higher than non-myocardial injury group. Spearman correlation analysis revealed that cTnI has a significant positive correlation with CK-MB and lactic dehydrogenase instead of aspartate aminotransferase. A receiver operating characteristic curve was drawn to demonstrate that CK-MB could significantly predict the occurrence of myocardial injury with an area under the curve of 0.749, and a level of 3.035 (sensitivity = 59.3%, specificity = 90.5%) was optimal cutoff value. Conclusion: The incidence of myocardial injury in highlanders with PH is significant. CK-MB, as a convenient and efficient marker, has been found to be closely associated with cTnI and plays a predictive role in the occurrence of myocardial injury with PH in individuals exposed to high altitude. [ABSTRACT FROM AUTHOR]

Myocardial injury and cardiovascular dysfunction are the most common complications of sepsis, and effective therapeutic candidate is still lacking. This study aims to investigate the protective effect of oxycodone in myocardial injury of lipopolysaccharide‐induced sepsis and its related signalling pathways. Wild‐type and nuclear factor erythroid 2‐related factor 2 (Nrf2)‐knockout mice, as well as H9c2 cardiomyocytes cultures treated with lipopolysaccharide (LPS) were used as models of septic myocardial injury. H9c2 cardiomyocytes culture showed that oxycodone protected cells from pyroptosis induced by LPS. Mice model confirmed that oxycodone pretreatment significantly attenuated myocardial pathological damage and improved cardiac function demonstrated by increased ejection fraction (EF) and fractional shortening (FS), as well as decreased cardiac troponin I (cTnI) and creatine kinase isoenzymes MB (CK‐MB). Oxycodone also reduced the levels of inflammatory factors and oxidative stress damage induced by LPS, which involves pyroptosis‐related proteins including: Nod‐like receptor protein 3 (NLRP3), Caspase 1, Apoptosis‐associated speck‐like protein contain a CARD (ASC), and Gasdermin D (GSDMD). These changes were mediated by Nrf2 and heme oxygenase‐1 (HO‐1) because Nrf2‐knockout mice or Nrf2 knockdown in H9c2 cells significantly reversed the beneficial effect of oxycodone on oxidative stress, inflammatory responses and NLRP3‐mediated pyroptosis. Our findings yielded that oxycodone therapy reduces LPS‐induced myocardial injury by suppressing NLRP3‐mediated pyroptosis via the Nrf2/HO‐1 signalling pathway in vivo and in vitro. [ABSTRACT FROM AUTHOR]

Schematic illustration of CeCH for sepsis-induced myocardial injury. (A) Preparation of CeCH with self-assembled by HSA. (B) The mechanism of CeCH to show protective effect for sepsis-induced cardiac injury by inhibiting ferroptosis and inflammation. [Display omitted] • CeCH was successfully developed by a green self-assembled method with human serum albumin to increase the water solubility and poor bioavailability of curcumin. • CeCH performed SOD-like and CAT-like activities to eliminate ROS generation and inhibit ferroptosis in H9C2 cells. • CeCH reduced the secretion of inflammatory factors by M1 macrophages to suppress the inflammation. • CeCH protected the heart against sepsis-induced cardiac injury and reversed cardiac dysfunction in vivo. • A promising strategy with Cur and nanozyme for septic cardiomyopathy by inhibiting ferroptosis and inflammation in clinical application. Sepsis-induced cardiac injury is the leading cause of death in patients. Recent studies have reported that reactive oxygen species (ROS)-mediated ferroptosis and macrophage-induced inflammation are the two main key roles in the process of cardiac injury. The combination of ferroptosis and inflammation inhibition is a feasible strategy in the treatment of sepsis-induced cardiac injury. In the present study, ceria nanozyme coordination with curcumin (CeCH) was designed by a self-assembled method with human serum albumin (HSA) to inhibit ferroptosis and inflammation of sepsis-induced cardiac injury. The formed CeCH obtained the superoxide dismutase (SOD)-like and catalase (CAT)-like activities from ceria nanozyme to scavenge ROS, which showed a protective effect on cardiomyocytes in vitro. Furthermore, it also showed ferroptosis inhibition to reverse cell death from RSL3-induced cardiomyocytes, denoted from curcumin. Due to the combination therapy of ceria nanozyme and curcumin, the formed CeCH NPs could also promote M2 macrophage polarization to reduce inflammation in vitro. In the lipopolysaccharide (LPS)-induced sepsis model, the CeCH NPs could effectively inhibit ferroptosis, reverse inflammation, and reduce the release of pro-inflammatory factors, which markedly alleviated the myocardial injury and recover the cardiac function. Overall, the simple self-assembled strategy with ceria nanozyme and curcumin showed a promising clinical application for sepsis-induced cardiac injury by inhibiting ferroptosis and inflammation. [ABSTRACT FROM AUTHOR]

Background: The study aimed to explore clinical indicators that can predict the prognosis of children with acute fulminant myocarditis (AFM) through a retrospective analysis. Methods: A retrospective analysis was conducted on the clinical indices of 79 children diagnosed with AFM and hospitalized from March 2013 to March 2023. Relevant demographic and clinical data, including symptoms at admission, laboratory results, and outcomes were extracted to identify factors associated with in-hospital mortality. Results: A total of 79 children with AFM were analyzed. The survival group (n = 61) had a longer median hospital stay and higher medical expenses compared to the death group (n = 18). Significant differences in the levels of left ventricular ejection fraction (LVEF)(P < 0.001), myoglobin (MYO)(P < 0.001), aspartate aminotransferase (AST)(P < 0.001), lactate dehydrogenase (LDH)(P = 0.004), B-type natriuretic peptide (BNP)(P = 0.005), arterial potential hydrogen (PH)(P < 0.001), bicarbonate (HCO3-)(P = 0.003), serum lactate (Lac)(P = 0.001), peripheral oxygen saturation (SpO2)(P = 0.008), and white blood cell count (WBC)(P = 0.007) were observed between the two groups. Additionally, there were significant differences in the incidences of multi-organ failure (P = 0.003) and respiratory failure (P = 0.001) between the two groups. Conclusions: Severe myocardial injury (AST > 194.00 U/L, LDH > 637.50 U/L, MYO > 265.75 µg/L, BNP > 1738.50 ng/L), acidosis (PH < 7.29, HCO3− <18.45 mmol/L, Lac > 12.30 mmol/L), hypoxia (SpO2 < 97.50%), inflammatory response (WBC > 9.69*109/L), left ventricular systolic dysfunction (LVEF < 28.25%), multi-organ failure, and respiratory failure are significantly associated with higher mortality rates. These factors can accurately identify AFM children at an increased risk of death. [ABSTRACT FROM AUTHOR]

The major contribution of myocardial damage to global mortalities raises debate regarding the exploration of new therapeutic strategies for its treatment. Therefore, our study investigated the counteracting effect of tiron against isoprenaline (ISO)-mediated cardiac infarction in mice. Tiron was administered tomice for 7 days prior to two consecutive injections of ISOon days 8 and 9 of the treatment protocol. Tiron significantly reduced the levels of CK-MB, LDH, and AST in serum samples of ISO-challenged mice. A considerable increase in the cardiac antioxidant response was observed in tiron-treated mice, as indicated by depletion of MDA and enhancement of antioxidant activities. Furthermore, tiron induced amarked decrease in NLRP3, ASC, and caspase-1 levels accompanied by weak immune reactions of IL-1β, NF-kB, TLR4, and iNOS in the infarct cardiac tissues. Histopathological screening validated these variations observed in the cardiac specimens. Thus, tiron clearly mitigated the oxidative and inflammatory stress by repressing the NLRP3 inflammasome and the TLR4/NF-kB/iNOS signaling cascade. [ABSTRACT FROM AUTHOR]

Objective: The study aimed to examine the role of the C-reactive protein to albumin ratio (CAR) as an inflammatory biomarker in relation to subclinical myocardial injury (SC-MI), addressing the limited knowledge of their association. Methods: The study included 5,949 individuals without cardiovascular disease (CVD) from the National Health and Nutrition Examination Survey. SC-MI was identified through a Cardiac Infarction Injury Score (CIIS) of ≥ 10 units based on a 12-lead electrocardiogram. The study used multivariate logistic regression models, adjusted for potential confounders, to evaluate the relationship between CAR and SC-MI. Subgroup analyses were conducted to substantiate the results, and the non-linear correlation was assessed via restricted cubic spline (RCS) regression. Results: The RCS curve showed a significant positive correlation between CAR and SC-MI (P for nonlinear = 0.2496). When adjusted for all confounders, individuals in the highest tertile of CAR exhibited a higher likelihood of SC-MI compared to those in the lowest tertile, with an odds ratio (OR) of 1.21 (95% CI: 1.06–1.39, P for trend = 0.029). A 10-unit increment in CAR was linked to a 3.6% heightened risk of SC-MI [OR = 1.036 (95% CI: 1.006, 1.066)], with this association being more prominent among male adults, non-smokers, married individuals, those without diabetes mellitus, and those with no history of cancer. Conclusion: The findings of this study suggest a positive correlation between CAR and SC-MI among the US adult population, indicating the potential of CAR in enhancing SC-MI prevention strategies in the general population. [ABSTRACT FROM AUTHOR]

Given the global high prevalence of MASLD and its poor CVD prognosis, it is essential to perform risk stratification for MASLD patients. The specific impact of High Sensitivity Troponins (hs-cTn) on mortality in MASLD patients remains unexplored. The NHANES databases from 1999 to 2004, which include data on high-sensitivity cardiac troponin (hs-cTn) levels and comorbidities, were linked with the most recent mortality dataset. Myocardial injury was determined using the 99th upper reference limits (URL) for hs-cTn. Our study included 3460 MASLD patients. The mean follow-up duration was 192 months, during which 1074 (23%) MASLD participants died from all-cause mortality, and 363 (7.3%) died from CVD mortality. Our findings indicate that MASLD patients with elevated levels of hs-cTnT (> 99th URL) exhibit increased risks of all-cause mortality [adjusted hazard ratio (aHR) = 1.93] and CVD mortality (aHR = 2.4). Similar results were observed for hs-cTnI, where the aHRs for all-cause mortality and CVD mortality were 2.03 and 2.97, respectively. Furthermore, we identified a nonlinear dose-response relationship between hs-cTn levels and the risk of mortality (P for nonlinearity < 0.001). Our findings suggest that hs-cTn can predict mortality risk in MASLD, aiding clinicians in risk-stratifying this population. Therefore, we recommend considering hs-cTn detection in individuals with MASLD to effectively assess their future mortality risk. [ABSTRACT FROM AUTHOR]

Background: Buyang Huanwu Decoction (BYHWD) is a traditional Chinese medicine to treat the syndrome of qi deficiency and blood stasis. Platelets play an important role in regulating thrombus and inflammation after ischemic injury, studies have shown that BYHWD regulate myocardial fibrosis and exert anti-inflammatory effects through IL-17 and TLR4 pathways, but the mechanism of platelet activation by BYHWD in stable coronary heart disease is still unknown. In the present study, model of left anterior descending coronary artery ligation was applied to investigate the mechanisms of BYHWD on modulating platelets hyperreactivity and heart function after fibrosis of ischemic myocardial infarction (MI). Methods: Myocardial infarction model was constructed by ligation of the left anterior descending coronary artery. The rats were randomly divided into five groups: sham, model, MI with aspirin (positive), MI with a low dosage of BYHWD (BYHWD-ld) and MI with a high dosage of BYHWD (BYHWD-hd) for 28 days. Results: Coronary artery ligation prominently induced left ventricle dysfunction, increased cardiomyocyte fibrosis, which was accompanied by platelets with hyperreactivity, and high levels of inflammatory factors. BYHWD obviously reversed cardiac dysfunction and fibrosis, increased the thickness of the left ventricular wall, and inhibited aggregation ratio and CD62p expression. BYHWD restored the mitochondrial respiration of platelets after MI, concomitant with an increased telomere expression and decreased inflammation. According to the result of transcriptome sequencing, we found that 106 differentially expressed genes compared model with BYHWD treatment. Enrichment analysis screened out the Ras-related protein Rap-1 (Rap1) signaling pathway and platelet activation biological function. Quantitative real-time PCR and Western blotting were applied to found that BYHWD reduced the expression of Rap1/PI3K-Akt/Src-CDC42 genes and attenuated the overactivity of PI3 kinase/Rap1/integrin α(IIb)β(3) pathway. Conclusion: BYHWD reduced inflammation and platelet activation via the PI3 kinase/Rap1/integrin α(IIb)β(3) pathway and improved heart function after MI. [ABSTRACT FROM AUTHOR]

Ischemia-reperfusion (I/R) injury, a multifaceted pathological process, occurs when the prolongation of reperfusion duration triggers ferroptosis-mediated myocardial damage. Isoliquiritigenin (ISL), a single flavonoid from licorice, exhibits a wide range of pharmacological impacts, but its function in ferroptosis caused by myocardial I/R injury remains unclear. This study delved into the protective effect of ISL on myocardial I/R injury-induced ferroptosis and its mechanism. Neonatal mouse cardiomyocytes (NMCM) underwent hypoxia/reoxygenation (H/R) to simulate the pathological process of myocardial I/R. ISL significantly attenuated H/R-triggered production of reactive oxygen species in NMCM, reduced the expression of malondialdehyde and the activity of lactate dehydrogenase, enhanced superoxide dismutase and catalase activity, and increased the expression of nuclear factor E2-related factor 2 (Nrf2) and its downstream heme oxygenase 1 (HO-1), thereby mitigating oxidative stress damage. CCK8 experiment revealed that the ferroptosis inhibitor Ferrostatin-1 significantly improved myocardial cell viability after 24 h of reoxygenation, and ISL treatment showed a similar effect. ISL reduced intracellular free iron accumulation, up-regulated glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) expression, and inhibited lipid peroxidation accumulation, thereby alleviating ferroptosis. The Nrf2-specific inhibitor ML385 counteracted ISL's defensive role against H/R-triggered oxidative stress damage and ferroptosis. In vivo experiments further confirmed that by regulating the translocation of Nrf2 into the nucleus, ISL treatment increased the levels of HO-1, GPX4, and SLC7A11, inhibited the expression of ACSL4, Drp1 to exert the antioxidant role, alleviated mitochondrial damage, and ferroptosis, ultimately reducing myocardial infarction area and injury induced by I/R. ML385 nearly abolished ISL's protective impact on the I/R model by inhibiting Nrf2 function. In summary, ISL is capable of mitigating oxidative stress, mitochondrial damage, and cardiomyocyte ferroptosis caused by I/R, thereby reducing myocardial injury. A key mechanism includes triggering the Nrf2/HO-1/SLC7A11/GPX4 pathway to prevent oxidative stress damage and cardiomyocyte ferroptosis caused by I/R. [Display omitted] • Isoliquiritigenin mitigates myocardial oxidative stress, and mitochondrial damage induced by I/R. • Cardiomyocyte ferroptosis has an essential role in mediating myocardial I/R injury. • Isoliquiritigenin activates the Nrf2/HO-1/SLC7A11/GPX4 pathway to reduce cardiomyocyte ferroptosis to protect hearts against myocardial I/R injury. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusions Dyslipidaemia, inflammation and elevated Lp(a) levels are associated with the progression of atherosclerosis. This study investigates whether patients with a first‐time presentation of chest pain and on‐target LDL‐C levels and intermediate FRS/ESC‐Score risks, display a high inflammatory burden linked to myocardial injury and whether inflammation at admission affects the re‐event rate up to 6 years follow‐up.Blind assessments of novel inflammatory markers such as Glycoprotein A and B via nuclear magnetic resonance (NMR), cytokines, hsCRP, Neutrophil‐to‐Lymphocyte ratio (NLR) and Lipoprotein(a) levels were examined. Out of 198 chest pain patients screened, 97 met the inclusion criteria at admission.cTnI(+) patients (>61 ng/L) with elevated Lipoprotein(a), showed significantly increased levels of Glycoprotein A and B, hsCRP, IL‐6, a high NLR and a reduced left ventricular ejection fraction (%) compared to cTnI(−) individuals. Those patients, with a higher inflammatory burden at hospital admission (hsCRP, IL‐6, Glycoprotein A and B, and Lipoprotein(a)) had a higher re‐event rate at follow‐up.Inflammation and Lipoprotein(a) levels were particularly prominent in patients presenting with reduced left ventricular ejection fraction. Notably, Glycoproteins A/B emerge as novel markers of inflammation in these patients. Our study highlights the significantly higher impact of inflammatory burden in patients with chest pain and high level of myocardial damage than in those with lower myocardial affectation, even when they all had lipid levels well controlled. Inflammation at the time of admission influenced the re‐event rate over a follow‐up period of up to 6 years. [ABSTRACT FROM AUTHOR]

Background: The protective effects of metformin (Met) against doxorubicin (Dox)-induced cardiotoxicity via potential hypotheses of mechanisms of action with unknown reliability and credibility. Objectives: This study aimed to investigate the protective effects of Met against Dox-induced cardiotoxicity and the underlying mechanisms of action, as well as examine their reliability and credibility. Methods: A comprehensive search was conducted within the PubMed, Embase, Web of Science, Science Direct, Scopus, and CNKI databases from inception to 31 December 2023. Animal experiments evaluating the efficacy of Met against Dox-induced cardiotoxicity were included in this study. The primary efficacy outcomes were markers of myocardial injury. Effect size was measured using the standardized mean difference for continuous variables. Data were pooled using a random-effects model in the Stata 18 statistical software package. Results: Twenty-one studies involving 203-208 animals treated with Dox and 271-276 animals treated with Dox and Met were included in this analysis. Quality assessment revealed high-quality scores. Pooled results favored Met treatment based on the serum lactate dehydrogenase (LDH), creatine kinase-myocardial band (CK-MB), cardiac troponin I (cTnI), and aspartate aminotransferase levels. Sensitivity analysis using the leave-one-out method demonstrated stable results. Funnel plots, Egger's test, and Begg's test confirmed potential publication bias. The oxidative stress hypothesis has been investigated extensively based on abundant evidence. Conclusion: Met is effective and safe for protecting against Dox-induced cardiotoxicity, thus making it an appropriate drug for clinical investigation. The oxidative stress hypothesis of mechanism of action is well established with highest reliability and credibility. [ABSTRACT FROM AUTHOR]

Background: Acute coronary syndrome (ACS) is a type of coronary heart disease (CHD), which is responsible for one-third of total deaths in people older than 35 years. Even though cardiac troponin is the gold standard for myocardial necrosis it is blind for ischemia without necrosis. Studies demonstrate that Ischaemia Modified Albumin (IMA) is more sensitive in diagnosing ischemic chest pain compared to cardiac troponin T and electrocardiogram, and its combination with these tests significantly increases the sensitivity for diagnosing unstable angina, non-ST-elevation myocardial infarction (NSTEMI), or ST-elevation myocardial infarction (STEMI), with high positive and negative predictive values, making it a valuable tool for ruling out ACS in patients with inconclusive diagnoses in the emergency department. Methods: This prospective cohort study, conducted at the Teaching Hospital, Peradeniya, Sri Lanka, from 2015 to 2019, investigated ischemia-modified albumin (IMA) levels in 330 acute coronary syndrome (ACS) patients. Excluding those with various chronic conditions and those on specific medications, serum IMA was analyzed using a colorimetric assay based on cobalt (II) binding to human serum albumin affected by myocardial ischemia. Serum IMA levels were measured, and statistical analyses, including non-parametric tests and correlation analyses, were conducted to evaluate the association between IMA levels and various demographic and clinical factors. Results: IMA concentrations were found to be non-normally distributed, with an average concentration of 0.252 ± 0.123 AU. No overall significant gender-based difference in IMA levels was observed, though within the younger age group (< 59 years), males exhibited higher IMA concentrations than females. Significant gender differences were observed in the younger age group, with males showing higher IMA levels than females (p = 0.033). No significant differences in IMA levels were found across different ethnicities (p = 0.217) or BMI categories (p = 0.056). A significant increase in IMA levels was noted in ACS patients compared to control subjects (p < 0.001). Correlation analysis revealed significant associations between IMA levels and total cholesterol (r = 0.262, p = 0.009) and low-density lipoprotein (LDL) levels (r = 0.280, p = 0.006). Notably, a significant gender difference in IMA levels was found in obese patients, suggesting physiological differences in response to obesity. The study also revealed higher IMA concentrations in NSTEMI and STEMI patients compared to those with unstable angina. Conclusion: The study confirms elevated IMA levels in ACS patients, supporting its diagnostic potential. It reveals demographic influences, such as higher IMA levels in younger males and significant gender-specific differences in obese patients. Personalized approaches considering demographics and lipid management are essential for ACS risk reduction and IMA's role in management. [ABSTRACT FROM AUTHOR]

Introduction: Isoproterenol (ISO) is regarded as an adrenergic non-selective β agonist. It regulates myocardial contractility and may cause damage to cardiac tissues. Alchemilla vulgaris (AV) is an herbal plant that has garnered considerable attention due to its anti-inflammatory and antioxidant bioactive components. The present investigation assessed the cardioprotective potential of AV towards ISOinduced myocardial damage. Methods: Four groups of mice were utilized: control that received saline, an ISO group (85 mg/kg, S.C.), ISO + AV100, and ISO + AV200 groups (mice received 100 or 200 mg/kg AV orally along with ISO). Results and discussion: ISO induced notable cardiac damage demonstrated by clear histopathological disruption and alterations in biochemical parameters. Intriguingly, AV treatment mitigates ISO provoked oxidative stress elucidated by a substantial enhancement in superoxide dismutase (SOD) and catalase (CAT) activities and reduced glutathione (GSH) content, as well as a considerable reduction in malondialdehyde (MDA) concentrations. In addition, notable downregulation of inflammatory biomarkers (IL-1β, TNF-α, and RAGE) and the NF-κB/p65 pathway was observed in ISO-exposed animals following AV treatment. Furthermore, the pro-apoptotic marker Bax was downregulated together with autophagy markers Beclin1 and LC3 with in ISO-exposed animals when treated with AV. Pre-treatment with AV significantly alleviated ISO-induced cardiac damage in a dose related manner, possibly due to their antioxidant and antiinflammatory properties. Interestingly, when AV was given at higher doses, a remarkable restoration of ISO-induced cardiac injury was revealed. [ABSTRACT FROM AUTHOR]

Objective: The main pathological change of myocarditis is an inflammatory injury of cardiomyocytes. Long noncoding RNAs (lncRNAs) are closely related to inflammation, and our previous study showed that differential expression of lncRNAs is associated with myocarditis. This study aimed to investigate the impact of lncRNAs on the onset of myocarditis. Methods: RNA expression was measured by quantitative reverse-transcription polymerase chain reaction (RT-qPCR). Lipopolysaccharide (LPS) was used to induce inflammation in human cardiomyocytes (HCMs). The expression of inflammatory cytokines and myocardial injury markers was detected by enzyme-linked immunosorbent assay (ELISA) and RT-qPCR. Cell viability and apoptosis were measured by the cell counting kit-8 assay and flow cytometry. The binding force between lncRNA NONHSAT122636.2 and microRNA miRNA-2110 was detected using the dual-luciferase assay. Results: NONHSAT122636.2 was dynamically expressed in patients with myocarditis and negatively correlated with inflammation severity. The overexpression of NONHSAT122636.2 improved inflammatory injury in LPS-stimulated HCMs. The study observed that there was a weak binding force between NONHSAT122636.2 and miR-2110. Conclusion: NONHSAT122636.2 attenuates myocardial inflammation and apoptosis in myocarditis. Additionally, its expression decreases in the peripheral blood of children suffering from myocarditis and in patients who are diagnosed for the first time showing higher diagnostic sensitivity and specificity. This decrease is negatively correlated with the degree of inflammation. Overall, the study suggests that NONHSAT122636.2 can be exploited as a potential diagnostic biomarker for pediatric myocarditis. [ABSTRACT FROM AUTHOR]

Tissue vascularization plays a critical role in the regeneration and repair of damaged tissues. However, in certain instances of tissue injury, the pace and effectiveness of vascularization can be limited. Innovative strategies leveraging magnetic fields and magnetic nanoparticles (MNPs) are devised to enhance the efficacy of tissue vascularization. This review explores the potential of magnetic field‐assisted strategies in augmenting tissue vascularization and repair. Direct application of static or dynamic magnetic fields, alone or in combination with MNPs, offers a means to modulate cellular behaviors and gene expression, thereby promoting angiogenesis and tissue regeneration. Techniques such as cell labeling, gene delivery using MNPs, and magnetic targeting have shown promise in efficiently repairing various ischemic tissue injuries by enhancing tissue vascularization. These strategies have broad applications in bone and skin tissue regeneration, limb ischemia treatment, myocardial injury treatment, and diabetic wound therapy. By summarizing recent advancements in magnetically controlled strategies, this review aims to shed light on their future prospects in tissue regeneration and clinical treatment. [ABSTRACT FROM AUTHOR]

Background: Subclinical myocardial injury (SCMI) is associated with an increased risk of poor cardiovascular disease (CVD) outcomes. Understanding the underlying risk factors for SCMI is crucial for the prevention and management of CVD. We hypothesized that atherogenic dyslipidemia, a combination of high triglycerides (TG) and low high-density lipoprotein cholesterol (HDL-C), is associated with an increased risk of SCMI. Methods: This analysis from the third National Health and Nutrition Examination Survey (NHANES-III) included 7093 participants (age 59.3 ± 13.4 years, 52.8% women, and 49.4% White) free of CVD. Atherogenic dyslipidemia was defined as TG ≥ 150 mg/dL and HDL-C < 40 mg/dL in men or <50 mg/dL in women. A validated electrocardiographic-based cardiac infarction injury score (CIIS) ≥ 10 was considered positive for SCMI. Multivariable logistic regression analysis was used to examine the association of different combinations of TG and HDL-C groups, including atherogenic dyslipidemia with SCMI. Results: About 22.5% (n = 1594) of participants had atherogenic dyslipidemia, and 26.3% (n = 1862) had SCMI. Compared to participants with normal TG and normal HDL-C, those with atherogenic dyslipidemia had a higher prevalence of SCMI (31.2% vs. 23.9%, p-value < 0.001). In a multivariable logistic regression model, atherogenic dyslipidemia was associated with the highest odds of SCMI followed by high TG/normal HDL-C, then low HDL-C/normal TG [OR (95% CI): 131 (1.14, 1.52), 1.13 (0.97, 1.33), and 1.01 (0.86, 1.20), respectively). Conclusions: Atherogenic dyslipidemia is associated with a higher risk of SCMI, which highlights the role of nontraditional risk factors in the development of subclinical CVD. [ABSTRACT FROM AUTHOR]

Cardiovascular magnetic resonance (CMR) imaging is widely regarded as the gold-standard technique for myocardial tissue characterization, allowing for the detection of structural abnormalities such as myocardial fatty replacement, myocardial edema, myocardial necrosis, and/or fibrosis. Historically, the identification of abnormal myocardial regions relied on variations in tissue signal intensity, often necessitating the use of exogenous contrast agents. However, over the past two decades, innovative parametric mapping techniques have emerged, enabling the direct quantitative assessment of tissue magnetic resonance (MR) properties on a voxel-by-voxel basis. These mapping techniques offer significant advantages by providing comprehensive and precise information that can be translated into color-coded maps, facilitating the identification of subtle or diffuse myocardial abnormalities. As unlikely conventional methods, these techniques do not require a substantial amount of structurally altered tissue to be visually identifiable as an area of abnormal signal intensity, eliminating the reliance on contrast agents. Moreover, these parametric mapping techniques, such as T1, T2, and T2* mapping, have transitioned from being primarily research tools to becoming valuable assets in the clinical diagnosis and risk stratification of various cardiac disorders. In this review, we aim to elucidate the underlying physical principles of CMR parametric mapping, explore its current clinical applications, address potential pitfalls, and outline future directions for research and development in this field. [ABSTRACT FROM AUTHOR]

Background: This study aimed to determine the roles of interleukin (IL)-17, TAO kinase 1 (TAOK1), and NOD-like receptor protein 3 (NLRP3) in cardiomyocyte pyroptosis and proliferation. Methods: The IL-17-treated H9C2 cells were used as in vitro heart failure (HF) models. These cells were subjected to TAOK1 overexpression or knockdown and treated with BMS-986299 (NLRP3 inflammasome agonist), MCC950 (NLRP3 inflammasome inhibitor), or verteporfin (Yes-associated protein [YAP] inhibitor). Thereafter, their pyroptosis, proliferative capacity, and gene and protein expression levels were detected. Doxorubicin-induced HF rats were used as in vivo models and subjected to TAOK1 overexpression. Thereafter, their myocardial pathology, NLRP3 inflammasome-mediated pyroptosis, and YAP/TEAD pathway function were evaluated. Results: IL-17 treatment increased the pyroptosis and decreased the proliferative capacity of H9C2 cells. Additionally, IL-17 treatment inducedto the activation of the NLRP3 inflammasomes and inhibition of the YAP/TEAD pathway in the H9C2 cells. Moreover, the IL-17-mediated effects on the H9C2 cells were alleviated by TAOK1 overexpression and augmented by TAOK1 knockdown. Furthermore, treatment with BMS-986299 or verteporfin affected the pyroptosis, proliferative capacity, and NLRP3 inflammasome activation of the H9C2 cells independently of TAOK1 expression. In the doxorubicin-induced HF rat model, TAOK1 overexpression mitigated myocardial injury, suppressed NLRP3 inflammasome pathway activation, and restored the YAP/TEAD pathway activity. Conclusion: TAOK1 played a crucial role in regulating IL-17-mediated increase in the pyroptosis and decrease in the proliferation of cardiomyocytes by regulating the activities of the NLRP3 inflammasomes and the YAP/TEAD pathway. [ABSTRACT FROM AUTHOR]

Background: Perinatal asphyxia remains a significant cause of morbidity and mortality among neonates, often leading to hypoxic-ischemic encephalopathy (HIE) and myocardial injury. Understanding the predictors and markers of these conditions is crucial for improving clinical management and outcomes. Methods: A prospective cohort study enrolled 50 asphyxiated neonates at Tirunelveli Medical College Hospital, assessing demographic factors, clinical parameters, and Troponin I levels. Data were analyzed using Chi-square test to determine associations and significance. Results: Demographic factors including gravida (χ²(2) = 0.499, p = 0.499), gestational age (χ² = 0.961, p = 0.961), mode of delivery (χ² = 0.507, p = 0.507), sex (χ² = 0.982, p = 0.982), and birth weight (χ² = 0.499, p = 0.499) showed no significant association with HIE severity. However, seizures (p = 0.001), ventilator requirement (p = 0.006), and shock (p = 0.001) were strongly associated with elevated Troponin I levels, indicative of myocardial injury. Conclusion: Clinical parameters such as seizures, ventilator requirement, and shock are critical indicators of myocardial injury in asphyxiated neonates. Early recognition and management of these factors may improve outcomes and guide therapeutic interventions in neonatal intensive care settings. [ABSTRACT FROM AUTHOR]

The incidence and mortality of ST-elevated myocardial infarction are increasing year by year, causing a huge economic burden to patients' families due to its severe clinical symptoms, high mortality, and poor prognosis. Percutaneous coronary intervention is the best treatment strategy for reducing myocardial infarction area, prolonging survival, and improving prognosis. To further improve the clinical effect of percutaneous coronary intervention in the treatment of ST-elevated myocardial infarction, this study explored the application value of nicorandil in the procedure. Oral nicorandil tablets were found to improve the cardiac function and myocardial microcirculation of patients with ST-elevated myocardial infarction, enhance their nutritional status, and reduce the risk of malnutrition. In the 6-month prognostic follow-up, nicorandil tablets provided more effective prognostic myocardial protection for patients. Therefore, we recommend the use of nicorandil tablets for adjuvant therapy during primary percutaneous coronary intervention in the future. [ABSTRACT FROM AUTHOR]

Aim: Sepsis‐induced myocardial injury (SIMI) may be associated with insufficient mitophagy in cardiomyocytes, but the exact mechanism involved remains unknown. Sirtuin 3 (Sirt3) is mainly found in the mitochondrial matrix and is involved in repairing mitochondrial function through means such as the activation of autophagy. Previously, we demonstrated that the annexin‐A1 small peptide (ANXA1sp) can promote Sirt3 expression in mitochondria. In this study, we hypothesized that the activation of Sirt3 by ANXA1sp induces mitophagy, thereby providing a protective effect against SIMI in mice. Methods: A mouse model of SIMI was established via cecal ligation and puncture. Intraperitoneal injections of ANXA1sp, 3TYP, and 3MA were administered prior to modeling. After successful modeling, IL‐6, TNF‐α, CK‐MB, and CTn‐I levels were measured; cardiac function was assessed using echocardiography; myocardial mitochondrial membrane potential, ROS, and ATP production were determined; myocardial mitochondrial ultrastructure was observed using transmission electron microscopy; and the expression levels of Sirt3 and autophagy‐related proteins were detected using western blotting. Results: ANXA1sp significantly reduced serum IL‐6, TNF‐α, CK‐MB, and CTn‐I levels; decreased myocardial ROS production; increased mitochondrial membrane potential and ATP synthesis; and improved myocardial mitochondrial ultrastructure in septic mice. Furthermore, ANXA1sp promoted Sirt3 expression and activated the AMPK‐mTOR pathway to induce myocardial mitophagy. These protective effects of ANXA1sp were reversed upon treatment with the Sirt3 blocker, 3‐TYP. Conclusion: ANXA1sp can reverse SIMI, and the underlying mechanism may be related to the activation of the AMPK‐mTOR pathway following upregulation of Sirt3 by ANXA1sp, which, in turn, induces autophagy. [ABSTRACT FROM AUTHOR]

• NPY levels were significantly higher in patients with worse myocardial function. • High NPY concentrations were significantly associated with infarct severity. • NPY can be used as novel clinical risk marker post STEMI. Acute myocardial infarction is associated with the release of the co-transmitter neuropeptide-Y (NPY). NPY acts as a potent vasoconstrictor and is associated with microvascular dysfunction after ST-elevation myocardial infarction (STEMI). This study comprehensively evaluated the association of plasma NPY with myocardial function and infarct severity, visualized by cardiac magnetic resonance (CMR) imaging, in STEMI patients revascularized by primary percutaneous coronary intervention (PCI). In this observational study, we included 260 STEMI patients enrolled in the prospective MARINA-STEMI (NCT04113356) study. Plasma NPY concentrations were measured by an immunoassay 24h after PCI from peripheral venous blood samples. Left ventricular ejection fraction (LVEF), global longitudinal strain (GLS), infarct size (IS) and microvascular obstruction (MVO) were determined using CMR imaging. Median plasma concentrations of NPY were 70 [interquartile range (IQR):35-115] pg/ml. NPY levels above median were significantly associated with lower LVEF (48%vs.52%, p=0.004), decreased GLS (-8.8%vs.-12.6%, p<0.001) and larger IS (17%vs.13%, p=0.041) in the acute phase after infarction as well as after 4 months (LVEF:50%vs.52%, p=0.030, GLS:-10.5vs.-12.9,p<0.001,IS:13%vs.10%,p=0.011). In addition, NPY levels were significantly related to presence of MVO (58%vs.52%, p=0.041). Moreover, in multivariable linear regression analysis, NPY remained significantly associated with all investigated CMR parameters (LVEF:p<0.001,GLS:p<0.001,IS:p=0.003,MVO:p=0.042) independent of other established clinical variables including high-sensitivity cardiac troponin T, pre-interventional TIMI flow 0 and left anterior descending artery as culprit lesion location. High plasma levels of NPY, measured 24h after STEMI, were independently associated with lower LVEF, decreased GLS, larger IS as well as presence of MVO, indicating plasma NPY as a novel clinical risk marker post STEMI. [ABSTRACT FROM AUTHOR]

Ischemic heart disease, manifesting as myocardial infarction (MI), remains the leading cause of death in the western world. Both ischemia and reperfusion (I/R) cause myocardial injury and result in cardiac inflammatory responses. This sterile inflammation in the myocardium consists of multiple phases, involving cell death, tissue remodeling, healing, and scar formation, modulated by various cytokines, including the macrophage migration inhibitory factor (MIF). Meanwhile, different immune cells participate in these phases, with myeloid cells acting as first responders. They migrate to the injured myocardium and regulate the initial phase of inflammation. The MIF modulates the acute inflammatory response by affecting the metabolic profile and activity of myeloid cells. This review summarizes the role of the MIF in regulating myeloid cell subsets in MI and I/R injury and discusses emerging evidence of metabolism-directed cellular inflammatory responses. Based on the multifaceted role of the MIF affecting myeloid cells in MI or I/R, the MIF can be a therapeutic target to achieve metabolic balance under pathology and alleviate inflammation in the heart. [ABSTRACT FROM AUTHOR]

Intraoperative hypotension (IOH) is a common issue associated with acute kidney injury, myocardial injury, stroke, and death. IOH may be avoided with the incorporation of newer advanced hemodynamic monitoring technologies. This case study examines the use of advanced hemodynamic monitoring with an early warning system for the intraoperative hemodynamic management of a patient presenting for pancreaticoduodenectomy. Incorporating the hypotension prediction index and other hemodynamic parameters to anticipate impending hypotension and treat potential causative factors is an emerging technological advancement. Understanding and embracing the potential for new advanced hemodynamic technology to reduce intraoperative hypotension's severity, duration, and occurrence is key to reducing negative patient outcomes. [ABSTRACT FROM AUTHOR]

To detect the acute myocardial injury in fulminant myocarditis (FM) survivors after extracorporeal membrane oxygenation (ECMO) and to demonstrate its significant differences from non-FM patients by cardiac magnetic resonance (CMR). This retrospective study enrolled 59 patients with acute myocarditis (AM), including 35 non-FM patients, 24 FM patients, and 54 controls. The peak value of cardiac troponin T (cTnT) was recorded. Tissue parameters, including native T1, extracellular volume (ECV), late gadolinium-enhancement (LGE)%, and T2 by CMR were assessed. The mean age was 35 ± 14 years, and 45.8% of the population were males in the AM group. Patients had higher levels of peak cTnT, peak NT-proBNP and peak C-reactive protein in the FM group (all p<0.05). Comparing with non-FM, the values of T1-based imaging parameters were significantly higher in the FM group (all p<0.05). In contrast, no difference was observed among the two groups in terms of T2 value (p=0.707). The septal area was more frequently involved in FM survivors after ECMO treatment, both in T1 and T2-based images. In addition, the cubic relationship was the relative best fit of LGE% against logcTnT and indicated that cTnT value exceeding 300ng/L exhibited a rapid upward trend of LGE%. Comparing to non-FM, higher myocardial necrosis and fibrosis but similar edema determined by T1 and T2 based imaging was found in FM survivors after ECMO treatment. Furthermore, the inter-ventricular septal area was more frequently involved by acute myocardial injury in FM survivors after ECMO treatment. In addition, LGE% showed an overall increasing trend with cTnT values elevating with rapidly increasing with cTnT exceeding 300 ng/L. • To detect the acute cardiac injury defined by CMR in FM survivors after ECMO. • Higher myocardial necrosis and fibrosis but similar edema was found in FM survivors. • The septal area was more frequently involved by acute myocardial injury in FM group. • LGE% showed an overall increasing trend with cTnT values elevating. [ABSTRACT FROM AUTHOR]