UNASSIGNED: Ischemic preconditioning-induced serum exosomes (IPC-exo) protected rat heart against myocardial ischemia/reperfusion injury. However, whether IPC-exo regulate replacement fibrosis after myocardial infarction (MI) and the underlying mechanisms remain unclear. MicroRNAs (miRs) are important cargos of exosomes and play an essential role in cardioprotection. We aim to investigate whether IPC-exo regulate post-MI replacement fibrosis by transferring cardioprotective miRs and its action mechanism.
UNASSIGNED: Exosomes obtained from serum of adult rats in control (Con-exo) and IPC groups were identified and analyzed, subsequently intracardially injected into MI rats following ligation. Their miRs profiles were identified using high-throughput miR sequencing to identify target miRs for bioinformatics analysis. Luciferase reporter assays confirmed target genes of selected miRs. IPC-exo transfected with selected miRs antagomir or NC were intracardially administered to MI rats post-ligation. Cardiac function and degree of replacement fibrosis were detected 4 weeks post-MI.
UNASSIGNED: IPC-exo exerted cardioprotective effects against excessive replacement fibrosis. MiR sequencing and RT-qPCR identified miR-133a-3p as most significantly different between IPC-exo and Con-exo. MiR-133a-3p directly targeted latent transforming growth factor beta binding protein 1 (LTBP1) and protein phosphatase 2, catalytic subunit, alpha isozyme (PPP2CA). KEGG analysis showed that transforming growth factor-β (TGF-β) was one of the most enriched signaling pathways with miR-133a-3p. Comparing to injection of IPC-exo transfected with miR-133a-3p antagomir NC, injecting IPC-exo transfected with miR-133a-3p antagomir abolished protective effects of IPC-exo on declining excessive replacement fibrosis and cardiac function enhancement, while increasing the messenger RNA and protein expression of LTBP1, PPP2CA, and TGF-β1in MI rats.
UNASSIGNED: IPC-exo inhibit excessive replacement fibrosis and improve cardiac function post-MI by transferring miR-133a-3p, the mechanism is associated with directly targeting LTBP1 and PPP2CA, and indirectly regulating TGF-β pathway in rats. Our finding provides potential therapeutic effect of IPC-induced exosomal miR-133a-3p for cardiac repair.

UNASSIGNED: Abnormal electrocardiogram (ECG) findings can be seen in traumatic brain injury (TBI) patients. ECG may be an inexpensive tool to identify patients at high risk for developing cardiac dysfunction after TBI. This study aimed to examine abnormal ECG findings after isolated TBI and their association with true cardiac dysfunction based on echocardiogram.
UNASSIGNED: This prospective observational study examined the data from adult patients with isolated and non-operated TBI between 2020 and 2021. Patients aged <18 years and >65 years with and presence of extracranial injuries including orthopedic, chest, cardiac, abdominal, and pelvis, pre-existing cardiac disease, patients who have undergone cardiothoracic surgery, with inotrope drugs, acute hemorrhage, and brain death were excluded from the study.
UNASSIGNED: We examined data from 100 patients with isolated TBI who underwent ECG and echocardiographic evaluation. ECG changes among 53% of mild cases showed a heart rate of 60-100/min, and 2% of cases showed more than 100/min. Prolonged pulse rate (PR) interval was observed in 8%, 11%, and 16% of mild, moderate, and severe cases, while no changes in PR interval were observed in 65% of cases. A prolonged QRS pattern was observed in 5%, 7%, and 15% of mild, moderate, and severe cases. A normal QRS complex was observed in 71% of cases. Prolonged QTc was observed in 3%, 10%, and 15% of cases in mild, moderate, and severe cases, respectively.
UNASSIGNED: Repolarization abnormalities, but not ischemic-like ECG changes, are associated with cardiac dysfunction after isolated TBI. 12-lead ECG may be an inexpensive screening tool to evaluate isolated TBI patients for cardiac dysfunction.

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BACKGROUND: Stimulator of interferons genes (STING) is crucial for innate immune response. It has been demonstrated that cGAS-STING pathway was the driver of aging-related inflammation. However, whether STING is involved in cardiac dysfunction during the physiological aging process remains unclear.
METHODS: Gene expression profiles were obtained from the Gene Expression Omnibus database, followed by weighted gene co-expression network analysis, gene ontology analysis and protein network interaction analysis to identify key pathway and genes associated with aging. The effects of STING on cardiac function, glucose homeostasis, inflammation, and autophagy in physiological aging were investigated with STING knockout mice.
RESULTS: Bioinformatics analysis revealed STING emerged as a hub gene of interest. Subsequent experiments demonstrated the activation of STING pathway in the heart of aged mice. Knockout of STING alleviated the inflammation in aged mice. However, Knockout of STING impaired glucose tolerance, inhibited autophagy, enhanced oxidative stress and aggravated cardiac dysfunction in aged mice.
CONCLUSIONS: Although reducing inflammation, long-term STING inhibition by genetic ablation exacerbated cardiac dysfunction in aged mice. Given the multifaceted nature of aging and the diverse cellular functions of STING beyond immune regulation, the negative effects of targeting STING as a strategy to mitigate aging phenotype should be fully considered.

UNASSIGNED: The prognosis of Duchenne muscular dystrophy (DMD) is poor once it develops to the stage of cardiac impairment. Recent studies have demonstrated that electrocardiogram (ECG), which consists of general ECG and vectorcardiogram (VCG), retains an extremely powerful role in the assessment of patients with reduced left ventricular (LV) systolic dysfunction. However, data regarding VCG recordings in DMD and its prognostic value for reduced left ventricular ejection fraction (LVEF) of DMD have never been reported. This study aims to describe the characteristics of VCG in children with DMD and to explore the predictive value of VCG for reduced LVEF in children with DMD.
UNASSIGNED: A total of 306 patients with a known diagnosis of DMD confirmed by the genetic test were retrospectively enrolled at our hospital between August 2018 and August 2022. This resulted in a total study group of 486 VCG recordings. Among them, 75 DMD patients who underwent cardiac magnetic resonance (CMR) later after one year follow-up were prospectively enrolled. The trend of VCG parameters of DMD patients across the different age span were compared with age-matched normal children. Concordance statistic analysis was further performed to assess the validity of VCG parameters in predicting the occurrence of reduced LVEF in patients with DMD.
UNASSIGNED: DMD patients have a significantly higher heart rate, R waves in V1, QRS loop percentage in the right anterior quadrant in the horizontal plane (horizontal quadrant II) and QRS loop percentage in the anterior superior quadrant in the sagittal plane (sagittal quadrant IV) than normal children. Concordance statistic (C-statistic) showed an area under the curve of quadrant IV in the sagittal plane of baseline was 0.704. The receiver operating characteristic (ROC) curve shows that quadrant IV in the sagittal plane of 7.57% was the optimal cutoff with a sensitivity of 53.3% and a specificity of 88.3% for predicting reduced LVEF in DMD patients.
UNASSIGNED: Our study firstly showed that QRS loop percentage in the right anterior quadrant in the horizontal plane (horizontal quadrant II) and QRS loop percentage in the anterior superior quadrant in the sagittal plane (sagittal quadrant IV) could be abnormal in DMD boys as early as before 5 years old. Evaluation of the myocardium by VCG in the early age to predict possible cardiac systolic dysfunction may have important implications for the ongoing management of DMD boys.

Heart failure is a prevalent and life-threatening syndrome characterized by structural and/or functional abnormalities of the heart. As a global burden with high rates of morbidity and mortality, there is growing recognition of the beneficial effects of exercise on physical fitness and cardiovascular health. A substantial body of evidence supports the notion that exercise can play a protective role in the development and progression of heart failure and improve cardiac function through various mechanisms, such as attenuating cardiac fibrosis, reducing inflammation, and regulating mitochondrial metabolism. Further investigation into the role and underlying mechanisms of exercise in heart failure may uncover novel therapeutic targets for the prevention and treatment of heart failure.

Tyrosine kinase inhibitors (TKIs) offer targeted therapy for cancers but can cause severe cardiotoxicities. Determining their dose‑dependent impact on cardiac function is required to optimize therapy and minimize adverse effects. The dose‑dependent cardiotoxic effects of two TKIs, imatinib and ponatinib, were assessed in vitro using H9c2 cardiomyoblasts and in vivo using zebrafish embryos. In vitro, H9c2 cardiomyocyte viability, apoptosis, size, and surface area were evaluated to assess the impact on cellular health. In vivo, zebrafish embryos were analyzed for heart rate, blood flow velocity, and morphological malformations to determine functional and structural changes. Additionally, reverse transcription‑quantitative PCR (RT‑qPCR) was employed to measure the gene expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), established markers of cardiac injury. This comprehensive approach, utilizing both in vitro and in vivo models alongside functional and molecular analyses, provides a robust assessment of the potential cardiotoxic effects. TKI exposure decreased viability and surface area in H9c2 cells in a dose‑dependent manner. Similarly, zebrafish embryos exposed to TKIs exhibited dose‑dependent heart malformation. Both TKIs upregulated ANP and BNP expression, indicating heart injury. The present study demonstrated dose‑dependent cardiotoxic effects of imatinib and ponatinib in H9c2 cells and zebrafish models. These findings emphasize the importance of tailoring TKI dosage to minimize cardiac risks while maintaining therapeutic efficacy. Future research should explore the underlying mechanisms and potential mitigation strategies of TKI‑induced cardiotoxicities.

OBJECTIVE: Cardiac dysfunction is a key factor in the pathogenesis of hepatorenal syndrome, for which terlipressin is the recommended first-line treatment. This study investigates whether long-term terlipressin can ameliorate the subclinical cardiac dysfunction observed in decompensated cirrhosis.
METHODS: Twenty-two patients with decompensated cirrhosis and ascites enrolled in a prospective study of home continuous terlipressin infusion were included. Cardiac function was assessed using dobutamine stress echocardiogram before and after 12 weeks of terlipressin. The primary outcome was the impact of terlipressin on cardiac reserve; the change in cardiac output (CO) in response to stress.
RESULTS: Median age was 61 years (IQR 56-64), median MELD score was 15 (IQR 12.3-17.0) and 72.7% were male. The increase in CO in response to low-dose dobutamine was significantly higher following terlipressin (↑4.0L/min [↑57.8%]) as compared to baseline (↑1.8L/min [21.3%], p=0.0001). The proportion of patients with impaired cardiac reserve (defined by ΔCO <25% after low-dose dobutamine) reduced from 81.8% at baseline to 40.9% after terlipressin, (p=0.02), driven primarily by improvement in inotropic function. Resting cardiac output (CO) decreased significantly after terlipressin from 8.9±2.2L/min to 7.2±1.8 L/min (p<0.001, normal range 5-6L/min), due to a decrease in stroke volume from 108 to 86mL/beat (p=0.006).
CONCLUSIONS: Long-term continuous terlipressin infusion resulted in a significant increase in cardiac reserve and attenuation of the hyperdynamic state usually observed in decompensated cirrhosis. These data provide important mechanistic insight into the pathogenesis and reversibility of cardiac dysfunction in cirrhosis. Future studies are required to evaluate whether long-term terlipressin can prevent hepatic decompensating events such as hepatorenal syndrome in high-risk individuals. ANZCTR NUMBER: (http://www.anzctr.org.au/): ACTRN12619000891123.

In modern oncology, despite the efficacy of chemotherapy, there is a risk of cardiotoxicity resulting in heart failure. This necessitates early diagnosis to prevent complications and improve prognosis. The study is aimed at analysing the abilities of speckle-tracking echocardiography as a modern tool in detecting cardiotoxicity in the early stages. This non-invasive method allows evaluating myocardial strain and its contractility. During a thorough analysis and extensive review of the scientific literature, it was found that the speckle-tracking echocardiography technique demonstrates an exceptionally high sensitivity to detecting early signs of cardiotoxicity, significantly outpacing conventional echocardiography methods in this aspect. This advantage makes it an invaluable tool in the early detection of potentially dangerous changes in the myocardium, which is especially important for patients at risk of developing cardiotoxic reactions as a result of chemotherapy. Speckle-tracking echocardiography has a unique ability to identify even the slightest local abnormalities in the structure and function of the myocardium, significantly before any clinical symptoms become apparent, thereby allowing doctors to take preventive measures at the earliest stages. This outstanding diagnostic ability is supported by an extensive body of scientific research and publications that unequivocally confirm the effectiveness of speckle-tracking echocardiography as an advanced tool for the early diagnosis of cardiotoxic changes. Thus, the timely application of this technique can significantly reduce the risks to the cardiac health of patients and contribute to more effective treatment of oncological diseases. Speckle-tracking echocardiography serves as an important tool in the early detection of cardiotoxicity in patients undergoing chemotherapy, allowing clinicians to timely adapt treatment protocols and prevent the development of serious cardiovascular complications, thereby improving the prognosis and quality of life of cancer patients.

UNASSIGNED: Non-ST-segment elevation myocardial infarction (NSTEMI) is a common form of coronary artery disease, and its prognosis is influenced by multiple factors. This study aimed to analyze the predictive role of the combined application of cardiac troponin and cardiac function indices in NSTEMI patients\' prognosis.
UNASSIGNED: NSTEMI patients were screened and included in the study. Cardiac troponin elevation ratio (cardiac troponin I (cTnI)/upper limit of normal (ULN)) was measured upon admission, and cardiac function was assessed. General clinical data, laboratory parameters, Grace score, New York Heart Association (NYHA) functional class, complications, and mortality data were collected. The correlation between mortality in NSTEMI patients and clinical parameters was analyzed, and a nomogram prediction model for NSTEMI patient mortality was established.
UNASSIGNED: A total of 252 NSTEMI patients were included. Female gender, elevated high-sensitivity C-reactive protein (H-CRP), left ventricular ejection fraction (LVEF) < 50%, NYHA class III and IV, and cTnI/ULN elevation by 36.25-fold were significantly independently associated with mortality outcomes. Multifactorial logistic analysis indicated that these indices remained associated with mortality. A nomogram model predicting NSTEMI patient mortality was constructed using these indices, with an area under the curve (AUC) of 0.911, sensitivity of 97.5%, and specificity of 72.8%. This predictive model outperformed the Grace score (AUC = 0.840).
UNASSIGNED: In NSTEMI patients, a 36.25-fold increase in cTnI/ULN, coupled with NYHA class III and IV, independently predicted prognosis. We developed a nomogram model integrating cTnI/ULN and cardiac function indices, aiding clinicians in assessing risk and implementing early interventions for improved outcomes.