Serum BNP Research Articles

Studying Hemodynamics during Weaning from Mechanical Ventilation among Critically ill Pediatric Patients

Abstract Background Among the multiple causes of weaning failure from mechanical ventilation, cardiovascular dysfunction is increasingly recognized as a quite frequent cause that can be treated successfully. Knowledge of the changes in the cardiopulmonary pathophysiology occurring during mechanical ventilation and its withdrawal is a prerequisite for early recognition of weaning failure of cardiovascular origin and optimal patient management. Aim of the Work Identification of hemodynamic and biomarkers changes during weaning process from mechanical ventilation and how these changes predict weaning success Methodology This cross sectional study was conducted on 50 children who were admitted to Pediatric Intensive Care Units and were mechanically ventilated and ready to be weaned according to weaning criteria. assessment of hemodynamic changes during weaning was done by tracing and comparing vital data, echocardiography parameters and levels of serum BNP and troponin in all patients during pressure support ventilation and at the end of spontaneous breathing trial (SBT) for identification of changes during weaning and risk factors for weaning failure. Results There was statistically significant increase in heart rate, cardiac index and E/A ratio at the end of SBTin all studied patients with lower cardiac index in patients who failed weaning, significant increase in TAPSE at the end of SBT with lower TAPSE in patients who failed weaning. Levels of BNP1 during pressure support were significantly higher in patients who failed weaning however levels of troponin didn’t show significant changes. Conclusion Transthoracic echocardiography can accurately detect changes in central hemodynamics induced by the SBT. It helps the attending physician to identify patients at high risk of weaning failure, when documenting a lower cardiac index, low TAPSE values.

Sex-related differences in clinical outcomes of patients with atrial fibrillation and heart failure with preserved ejection fraction

Abstract Background Heart failure with preserved ejection fraction (HFpEF) and atrial fibrillation (AF) are both highly prevalent diseases that commonly coexist, sharing clinical features and pathomechanisms. While prevalence of AF is higher in men compared to women with HFpEF, outcomes appear to be worse in women. However, there are no studies systematically examining gender-specific differences. Purpose Aiming for deeper insights into the effects of gender on clinical outcomes of patients with AF and HFpEF. Methods AF patients with HFpEF were included. HFpEF was diagnosed according to the current ESC guideline. Outcomes of men and women were compared. The primary endpoint was the time to heart failure hospitalization. Secondary endpoints were maintenance of sinus rhythm, as well as clinical and functional parameters. Factors related to a primary endpoint event were assessed. Results A total of 161 patients were included in our study (69 male patients, 92 female patients). Assessment of patient characteristics at baseline showed that male patients suffered more often from coronary artery disease (male: 45/69 patients (65%); female: 45/92 patients (49%); p=0.039), and OSAS (male: 14/69 patients (20%); female: 5/92 patients (5%); p=0.004). After a follow-up of 3 years, occurrence of the primary endpoint event was less frequent in women than in men (Hazard Ratio (HR): 0.61; 95% Confidence Interval (CI): 0.38-0.97; p=0.36; Figure A). By logistic regression analysis, we identified female sex (HR 0.48; 95%CI: 0.23-0.97; p=0.041), AF ablation (HR: 0.26; 0.13-0.53; p<0.001), and decrease in Left Ventricular Mass Index (LVMI) (HR:0.66; 95%CI: 0.44-0.98; p=0.041) as preventive factors with regard to heart failure hospitalization. Subgroup analysis for AF ablation versus medical therapy showed that patients who underwent ablation had lower hospitalization events (AF (HR: 0.49; 95% CI: 0.25-0.98; p=0.45). Additionally, left ventricular reverse remodeling, as assessed by the decrease of LVMI had a "dose-dependent" protective effect on heart failure hospitalizations (p=0.024, Figure B). Evaluation of functional HFpEF parameters revealed that only in women LVMI (baseline: 111 [99; 133] g/m2; follow-up: 105 [93; 127] g/m2; p=0.006), E/E’ ratio (baseline: 13.0 [10.2; 15.3]; follow-up: 11.5 [8.6; 14.7]; p=0.046), and NT-pro BNP serum levels (baseline: 1367 [352; 3605]; follow up: 987 [438; 2579]; p=0.039) improved. Discussion Our study suggests that women with AF and HFpEF have better outcomes as compared to men regarding heart failure hospitalization. LVMI and AF ablation are ssociated with fewer heart failure hospitalizations. Assessment of LVMI and further markers of HFpEF (E/E’ ratio and NT-pro BNP) only improved in women, suggesting that the gender-difference in heart failure hospitalization might be mediated by left ventricular induced remodeling following AF ablation. Further studies are necessary to verify this hypothesis generating results.Kaplan-Meier Analysis

Effect and mechanism of gomisin D on the isoproterenol induced myocardial injury in H9C2 cells and mice

We established myocardial injury models in vivo and in vitro to investigate the cardioprotective effect of gomisin D obtained from Schisandra chinensis. Gomisin D significantly inhibited isoproterenol-induced apoptosis and hypertrophy in H9C2 cells. Gomisin D decreased serum BNP, ANP, CK-MB, cTn-T levels and histopathological alterations, and inhibited myocardial hypertrophy in mice. In mechanisms research, gomisin D reversed ISO-induced accumulation of intracellular ROS and Ca2+. Gomisin D further improved mitochondrial energy metabolism disorders by regulating the TCA cycle. These results demonstrated that gomisin D had a significant effect on isoproterenol-induced myocardial injury by inhibiting oxidative stress, calcium overload and improving mitochondrial energy metabolism.

Network and Experimental Pharmacology on Mechanism of Yixintai Regulates the TMAO/PKC/NF-κB Signaling Pathway in Treating Heart Failure.

This study aims to explore the mechanism of action of Yixintai in treating chronic ischemic heart failure by combining bioinformatics and experimental validation. Five potential drugs for treating heart failure were obtained from Yixintai (YXT) through early mass spectrometry detection. The targets of YXT for treating heart failure were obtained by a search of online databases. Gene ontology (GO) functional enrichment analysis and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analyses were conducted on the common targets using the DAVID database. A rat heart failure model was established by ligating the anterior descending branch of the left coronary artery. A small animal color Doppler ultrasound imaging system detected cardiac function indicators. Hematoxylin-eosin (HE), Masson's, and electron microscopy were used to observe the pathological morphology of the myocardium in rats with heart failure. The network pharmacology analysis results were validated by ELISA, qPCR, and Western blotting. A total of 107 effective targets were obtained by combining compound targets and eliminating duplicate values. PPI analysis showed that inflammation-related proteins (TNF and IL1B) were key targets for treating heart failure, and KEGG enrichment suggested that NF-κB signaling pathway was a key pathway for YXT treatment of heart failure. Animal model validation results indicated the following: YXT can significantly reduce the content of intestinal microbiota metabolites such as trimethylamine oxide (TMAO) and improve heart failure by improving the EF and FS values of heart ultrasound in rats and reducing the levels of serum NT-proBNP, ANP, and BNP to improve heart failure. Together, YXT can inhibit cardiac muscle hypertrophy and fibrosis in rats and improve myocardial ultrastructure and serum IL-1β, IL-6, and TNF-α levels. These effects are achieved by inhibiting the expressions of NF-κB and PKC. YXT regulates the TMAO/PKC/NF-κB signaling pathway in heart failure.

Ultrasound-targeted microbubble destruction rapidly improves left ventricular function in rats with ischemic cardiac dysfunction

BackgroundPrevious studies have demonstrated the efficacy of ultrasound-targeted microbubble destruction (UTMD) in the treatment of ischemic heart failure (HF). The purpose of this study was to explore the mechanism by which UTMD improves ischemic HF. MethodsAn ischemic heart failure model was established using Sprague-Dawley rats. Rats were randomly divided into 7 groups: sham group, HF group, HF + MB group, HF + ultrasound (US) group, HF + UTMD group, HF + UTMD+LY294002 group, and HF + LY294002 group. Serum BNP level and echocardiographic parameters were measured to evaluate cardiac function. PI3K/Akt/eNOS signaling pathway protein levels were detected by immunohistochemistry (IHC) and western blotting. The concentrations of nitrous oxide (NO) and ATP were detected by ELISA, and hematoxylin and eosin (HE) staining was used to evaluate myocardial tissue. ResultsUTMD rapidly improved ejection fraction (EF) (HF: 37.16 ± 1.21% vs. HF + UTMD: 46.31 ± 3.00%, P < 0.01) and fractional shortening (FS) (HF: 18.53 ± 0.58% vs. HF + UTMD: 24.05 ± 1.84%, P < 0.01) in rats with ischemic HF. UTMD activated the PI3K/AKT/eNOS signaling pathway (HF vs. HF + UTMD, P < 0.01) and promoted the release of NO and ATP (HF vs. HF + UTMD, both, P < 0.05). Inhibition of the PI3K/AKT/eNOS signaling pathway by LY294002 worsened EF (HF: 37.16 ± 1.21% vs. HF + LY294002: 32.73 ± 3.05%, P < 0.05), and the release of NO and ATP by UTMD (HF + UTMD vs. HF + UTMD+LY294002, P < 0.05). ConclusionsUTMD can rapidly improve cardiac function in ischemic HF by activating the PI3K/Akt/eNOS signaling pathway and promoting the release of NO and ATP.

The association of plasma connective tissue growth factor levels with left ventricular diastolic dysfunction in patients with overt hyperthyroidism.

Left ventricular (LV) diastolic dysfunction is an independent predictor of future cardiovascular events. Early detection of patients with LV diastolic dysfunction can improve clinical outcomes through active management. However, the assessment of diastolic function is very complicated, and there are currently lack of effective biomarkers to assess the risk of LV diastolic dysfunction. Connective tissue growth factor (CTGF) plays a significant role in cardiac remodeling and dysfunction. We aimed to investigate the associations between plasma CTGF level and the risk of LV diastolic dysfunction in this study and judge its effectiveness in diagnosing LV diastolic dysfunction. A total of 169 patients with overt hyperthyroidism were included. LV diastolic function was evaluated and the subjects were divided into normal LV diastolic function group and LV diastolic dysfunction group. Routine clinical medical data, biochemical data, thyroid related parameters and echocardiographic parameters were recorded for analysis. Compared with normal LV diastolic function group, the LV diastolic dysfunction group had higher age and BMI, as well as lower heart rate, lower serum albumin, lower eGFR, higher serum TgAb and BNP level, and the incidences of hypertension were also higher (all P <0.05). Circulating plasma CTGF levels in the LV diastolic dysfunction group were significantly higher (normal LV diastolic function group: 7.026 [5.567-8.895], LV diastolic dysfunction group: 8.290 [7.054-9.225] ng/ml, median [(Interquartile range)], P = 0.004); Compared with the lowest quartile group, the crude odds ratios (OR) of LV diastolic dysfunction in the second, third, and fourth quartile group were 3.207, 5.032 and 4.554, respectively (all P<0.05). After adjustment for the potentially confounding variables, the adjusted OR values of the third and fourth quartile group had no obvious change. The results of ROC showed that the plasma CTGF had the largest area under the ROC curve, and the value was 0.659 (P = 0.005). The level of circulating plasma CTGF in the LV diastolic dysfunction group was significantly increased. Plasma CTGF level is an independent risk factor for LV diastolic dysfunction. Compared with serum BNP level, the plasma CTGF level may have auxiliary diagnostic value for LV diastolic dysfunction in hyperthyroid patients.

The Clinical Effects of Pharmacotherapy Combined with Blood Flow Restriction and Isometric Exercise Training in Rehabilitating Patients with Heart Failure with Reduced Ejection Fraction.

Heart failure with reduced ejection fraction (HFrEF) is associated with reduced cardiac function and impaired quality of life. Blood flow restriction (BFR) training is emerging as a potential adjunctive therapy. This study aimed at evaluating the efficacy of combination of BFR and isometric exercises on cardiac function, functional status, and quality of life in HFrEF patients. Totally 44 patients with HFrEF were equally divided into a control group and a combined treatment group. Both groups received standard pharmacotherapy and upper limb exercise, with the combined group also undergoing BFR and isometric exercise training. We assessed demographic and clinical characteristics, New York Heart Association (NYHA) functional classification, cardiac function parameters, serum Brain Natriuretic Peptide levels, physical capacity via the 6-minute walking test, and quality of life using the Heart Failure Questionnaire (Minnesota Living with Heart Failure Questionnaire). Post-treatment, the combined group significantly improved in NYHA classification (p = 0.012), with more patients shifting to a better class. Cardiac function improved in both groups, with the combined group showing a greater increase in mean left ventricular ejection fractions (p < 0.001), and reductions in left ventricular end-diastolic and end-systolic diameters (p < 0.05). The addition of BFR training to standard pharmacotherapy with upper limb exercise in HFrEF patients led to significant enhancements in cardiac function, functional status, and quality of life. These findings support the integration of BFR training into conventional HFrEF treatment regimens to maximize patient recovery outcomes.

Coenzyme Q10 mitigates macrophage mediated inflammation in heart following myocardial infarction via the NLRP3/IL1β pathway

BackgroundThe protective effect of Coenzyme Q10 (CoQ10) on the cardiovascular system has been reported, however, whether it can promote early recovery of cardiac function and alleviate cardiac remodeling after myocardial infarction (MI) remains to be elucidated. Whether CoQ10 may regulate the macrophage-mediated pro-inflammatory response after MI and its potential mechanism are worth further exploration.MethodsTo determine the baseline plasma levels of CoQ10 by LC-MS/MS, healthy controls and MI patients (n = 11 each) with age- and gender-matched were randomly enrolled. Additional MI patients were consecutively enrolled and randomized into the blank control (n = 59) or CoQ10 group (n = 61). Follow-ups were performed at 1- and 3-month to assess cardiac function after percutaneous coronary intervention (PCI). In the animal study, mice were orally administered CoQ10/vehicle daily and were subjected to left anterior descending coronary artery (LAD) ligation or sham operation. Echocardiography and serum BNP measured by ELISA were analyzed to evaluate cardiac function. Masson staining and WGA staining were performed to analyze the myocardial fibrosis and cardiomyocyte hypertrophy, respectively. Immunofluorescence staining was performed to assess the infiltration of IL1β/ROS-positive macrophages into the ischemic myocardium. Flow cytometry was employed to analyze the recruitment of myeloid immune cells to the ischemic myocardium post-MI. The expression of inflammatory indicators was assessed through RNA-seq, qPCR, and western blotting (WB).ResultsCompared to controls, MI patients showed a plasma deficiency of CoQ10 (0.76 ± 0.31 vs. 0.46 ± 0.10 µg/ml). CoQ10 supplementation significantly promoted the recovery of cardiac function in MI patients at 1 and 3 months after PCI. In mice study, compared to vehicle-treated MI mice, CoQ10-treated MI mice showed a favorable trend in survival rate (42.85% vs. 61.90%), as well as significantly alleviated cardiac dysfunction, myocardial fibrosis, and cardiac hypertrophy. Notably, CoQ10 administration significantly suppressed the recruitment of pro-inflammatory CCR2+ macrophages into infarct myocardium and their mediated inflammatory response, partially by attenuating the activation of the NLR family pyrin domain containing 3 (NLRP3)/Interleukin-1 beta (IL1β) signaling pathway.ConclusionsThese findings suggest that CoQ10 can significantly promote early recovery of cardiac function after MI. CoQ10 may function by inhibiting the recruitment of CCR2+ macrophages and suppressing the activation of the NLRP3/IL1β pathway in macrophages.Trial registrationDate of registration 09/04/2021 (number: ChiCTR2100045256).

Charlson and Elixhauser Comorbidity Indices for Prediction of Mortality and Hospital Readmission in Patients With Acute Pulmonary Embolism.

Several risk stratification systems aid clinicians in classifying pulmonary embolism (PE) severity and prognosis. We compared 2 clinical PE scoring systems, the PESI and sPESI scores, with 2 comorbidity indices, the Charlson Comorbidity Index (CCI) and the val Walraven Elixhauser Comorbidity Index (ECI), to determine the utility of each in predicting mortality and hospital readmission. Information was collected from 436 patients presenting with PE via retrospective chart review. The PESI, sPESI, CCI, and ECI scores were calculated for each patient. Multivariate analysis was used to determine each system's ability to predict in-hospital mortality, 90-day mortality, overall mortality, and all-cause hospital readmission. The impact of various demographic and clinical characteristics of each patient on these outcomes was also assessed. The PESI score was found to be an independent predictor of in-hospital mortality and 90-day mortality. The PESI score and the CCI were able to independently predict overall mortality. None of the 4 risk scores independently predicted hospital readmission. Other factors including hypoalbuminemia, serum BNP, coagulopathy, anemia, and diabetes were associated with increased mortality and readmission at various endpoints. The PESI score was the best tool for predicting mortality at any endpoint. The CCI may have utility in predicting long-term outcomes. Further work is needed to better determine the roles of the CCI and ECI in predicting patient outcomes in PE. The potential prognostic implications of low serum albumin and anemia at the time of PE also warrant further investigation.

Platelet Analysis in the Thrombus Plus Serum BNP for Detecting Clot-Related Atrial Fibrillation. Results From the ITACAT Multicentric Registry

Platelet Analysis in the Thrombus Plus Serum BNP for Detecting Clot-Related Atrial Fibrillation. Results From the ITACAT Multicentric Registry

Treatment of ischemic heart failure through ultrasound-targeted microbubble destruction and it's mechanism

Abstract Background The cavitation effect mediated by ultrasonic-targeted microbubble destruction (UTMD) can regulate the microenvironment and circulation of ischemic myocardium. The UTMD cavitation effect can rapidly enhance blood perfusion and improve cardiac function in patients with ischemic heart failure. However, the internal mechanism of this treatment has yet to be reported. Objective The objective of this study was to explore the underlying mechanism of UTMD-mediated cavitation effect to rapidly improve cardiac function in rats with ischemic heart failure. Methods In the first part of the study, the ischemic heart failure model was induced by ligation of the left anterior descending branch coronary in Sprague-Dawley rats, the rats were randomly divided into 7 groups: sham group, HF group, HF+MB(microbubble) group, HF+US(ultrasound) group, HF+UTMD group, HF+UTMD+LY294002(PI3K inhibitor) group, and HF+LY294002 group. Serum BNP level and echocardiographic parameters were measured to evaluate cardiac function. Thereafter, SD rats were treated with UTMD by specific ultrasonic parameters and microbubble concentration, cardiac function should be reassessed after treatment. Finally, the myocardial tissues were extracted for Western Blot and immunohistochemical analysis to detect the protein expression of the PI3K/Akt/eNOS signaling pathway, and the contents of serum nitric oxide(NO) and myocardial ATP were detected by Elisa. Results The application of UTMD resulted in significant improvements in ejection fraction (EF) and fractional shortening (FS) in rats with ischemic heart failure, as compared to the HF group (EF: 37.16 ± 1.21% vs. HF+UTMD: 46.31 ± 3.00%, P=0.0057; FS: 18.53 ± 0.58% vs. HF+UTMD: 24.05 ± 1.84%, P=0.0089). Additionally, UTMD treatment led to the activation of the PI3K/Akt/eNOS signaling pathway (HF vs. HF+UTMD, P &amp;lt; 0.01), and promoted the production of NO and ATP (HF vs. HF+UTMD, both, P&amp;lt; 0.05). However, when a PI3K inhibitor was used, the cardiac protective effects of UTMD treatment were largely eliminated. EF and FS deteriorated significantly (EF: HF+UTMD+LY294002: 42.84±2.88% vs. HF+LY294002: 32.73±3.05%, P&amp;lt;0.0001; FS: HF+UTMD+LY294002: 21.94±1.69% vs. HF+LY294002: 16.36±1.76%, P&amp;lt;0.0001), and the production of NO and ATP decreased significantly (HF+UTMD+LY294002 vs. HF+LY294002, both, P&amp;lt; 0.05). Conclusion The UTMD-mediated cavitation effect can rapidly improve the cardiac function of ischemic heart failure rats by activating PI3K/Akt/eNOS signaling pathway and promoting the release of NO and ATP.

Abstract 17284: Prognostic Impact of Silent Cerebral Microbleeds in Patients Undergoing Transcatheter Aortic Valve Replacement

Introduction: Cerebral microbleeds (CMBs) are known to be associated with age, various cardiovascular risk factors, cognitive impairment, the use of antithrombotic drugs, and future neurological or cardiovascular events. Transcatheter aortic valve implantation (TAVR) has emerged as a rapidly evolving treatment for patients with severe aortic stenosis (AS). However, data on CMBs in those patients are scarce. Hypothesis: We hypothesized that the presence of CMBs in patients with severe aortic stenosis (AS) undergoing TAVR may be associated with some clinical factors or have prognostic implications. Methods: A retrospective analysis was conducted on data from 137 consecutive patients (mean age: 84 ± 5 years, 55 male) with severe AS who underwent T2*-weighted brain magnetic resonance imaging (MRI) prior to TAVR. The brain MRI was assessed by researchers blinded to the patients' clinical information. Additionally, conventional echocardiography was performed to evaluate left ventricular function and valvular abnormalities. Results: CMBs were identified in 42 out of 137 patients (31%). No significant differences were observed between patients with and without CMBs in age, gender, serum BNP levels, or antiplatelet/anticoagulant therapy. However, there were significant differences in left ventricular ejection fraction (LVEF) and left ventricular end-systolic volume (LVESV) between the two groups (LVEF: 58 ± 14% vs. 64 ± 10%, p = 0.01; LVESV: 38 ± 25 ml vs. 28 ± 16 ml, p &lt; 0.01, respectively). Over a median follow-up period of 618 days, patients with CMBs had a higher incidence of major adverse cardiac events (defined as death or heart failure re-hospitalization) compared to those without CMBs (24.0% vs. 13.0%, log-rank test, p = 0.04). (Figure). Conclusions: Our study reveals a high prevalence of CMBs in patients with severe AS. The presence of CMBs is associated with lower LVEF, increased LVESV, and poor prognosis following TAVR.

Abstract 16532: Mosaic Loss of Y Chromosome in Leukocytes Predicts Death in Patients With Chronic Heart Failure Across the Whole Spectrum of Ejection Fraction

Aims: Mosaic loss of Y chromosome (LOY) in men increases with age and correlates with clonal expansion of myeloid cells. Experimental modeling demonstrated that LOY in hematopoietic cells leads to diffuse cardiac fibrosis and subsequent development of heart failure in mice. Cardiac fibrosis is an important pathogenic feature in heart failure irrespective of etiology. Therefore, we investigated the prognostic significance of LOY in men with chronic heart failure. Methods and Results: In a total of 705 male patients with chronic heart failure with reduced and preserved ejection fraction, LOY was determined by digital PCR of peripheral blood cells by assessing the 6bp sequence difference between the AMELX and AMELY genes. ROC analysis relating the extent of LOY to mortality revealed a LOY of 17% as the optimal cut-off value to predict death during follow-up. LOY &gt;17% was observed in 18.6% of all patients, increased with age and was associated with increased mortality after three years (13,7% in patients without LOY compared to 29.0% in patients with LOY, p&lt;0.001, Figure 1). LOY remained an independent predictor of death in multivariate analysis including, age, LVEF and nt-pro BNP serum levels (HR 1,67; 95% CI 1.08-2.57; p=0.017). Importantly, LOY was associated with increased mortality in patients with heart failure with reduced ejection fraction defined as LVEF &lt; 50% (p&lt;0.001) as well as in patients with preserved LVEF ≥ 50% (p=0.01). Conclusion: Among patients with heart failure, LOY in blood cells is associated with increased risk of death across the complete range of ejection fraction. Further studies are warranted to discern if LOY associates with cardiac fibrosis in men with heart failure and triggers increased profibrotic signaling. The results of this study may inform trials evaluating precision-targeted anti-fibrotic therapies in patients with chronic heart failure.

Activation of AHR by ITE improves cardiac remodelling and function in rats after myocardial infarction.

Left ventricular remodelling subsequent to myocardial infarction (MI) constitutes a pivotal underlying cause of heart failure. Intervention with the nontoxic endogenous aryl hydrocarbon receptor (AHR) agonist 2-(1'H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) in the acute phase of MI has been shown to ameliorate cardiac function, but its role in the chronic phase remains obscured. This study explores the beneficial role of ITE in delaying the progression of heart failure in the chronic phase of MI. MI rats established by ligating the left anterior descending coronary artery were treated with the indicated concentration of the AHR agonist ITE or vehicle alone. Echocardiography was performed to determine cardiac structure and function; myocardial morphology and fibrosis were observed by haematoxylin and eosin and Masson's trichrome staining; serum biochemical indices, BNP, and inflammatory cytokine levels were detected by enzyme-linked immunosorbent assay; F4/80+ iNOS+ M1 macrophages and F4/80+ CD206+ M2 macrophages were detected by immunofluorescence; the terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling assay was used to detect the apoptosis of cardiomyocytes; ultrastructural changes in myocardial tissue were observed by transmission electron microscopy; and Cyp1a1, Akt, P-Akt, p70S6K, P-p70S6K, Bcl-2, Bax, caspase-3, and cleaved caspase-3 protein levels were determined via Western blotting. We found that therapy with the AHR agonist ITE rescued cardiac remodelling and dysfunction in rats with MI and attenuated myocardial fibrosis, inflammation, and mitochondrial damage. Further studies confirmed that ITE dose-dependently improved myocardial cell apoptosis after MI, as demonstrated by reduced levels of the apoptosis-related proteins cleaved caspase-3 and Bax but increased expression levels of Bcl-2. These effects were attributed to ITE-induced activation of AHR receptors, leading to the down-regulation of Akt and p70S6K phosphorylation. The AHR agonist ITE alleviates cardiomyocyte apoptosis through the Akt/p70S6K signalling pathway, thereby rescuing left ventricular adverse remodelling and cardiac dysfunction after MI.

Investigating the Effects and Mechanism of Rhodiola Rosea Injection on Cardiac Function in Rats with Chronic Heart Failure.

To study the effect of Rhodiola Rosea injection on cardiac function and the reninangiotensin- aldosterone system (RASS) in rats with chronic heart failure. Rhodiola Rosea injection, a traditional Chinese medication for relieving blood stasis and improving blood circulation, is an excellent therapeutic for treating coronary heart disease-angina pectoris. Rhodiola Rosea injection's major component, salidroside, protects the cardiovascular system. But there isn't much first-hand evidence about how injectable Rhodiola Rosea affects heart failure. In this study, a rat model of heart failure was established, and the effect of Rhodiola rosea injection on myocardial cell morphology, cardiac function, and ventricular remodelling in rats with heart failure was investigated. 66 SD male rats were selected; 10 were randomly selected as a blank control group, and 56 were treated intraperitoneally with doxorubicin (4 g/g). After 6 weeks, all animals had LVEF 60%. Established a heart failure model. Each group had 14 rats: model control, low-dose, mediumdose, and high-dose Rhodiola Rosea injection. The 2 mL/kg of Rhodiola Rosea injection was injected into the tail vein once a day for 2 weeks. Both the blank and control groups received normal daily saline. After 2 weeks, the echocardiographic index, RASS-related index, and serum BNP level were assessed in all rats, and myocardial tissue morphology was observed. MiRNA423-5p, miRNA499-5p, and miRNA210-3p were extracted from peripheral blood. Rhodiola rosea injection on its expression was compared to healthy control rats. 6 mL/kg Rhodiola Rosea injection lowered LVEDV and LVESV while increasing LVEF and LVFS. Injections of 6 mL/kg Rhodiola Rosea reduce plasma levels of miR-210-3p, miR-423- 5p, miRNA-499, and BNP in heart failure model rats. The 6 mL/kg Rhodiola Rosea injection can restore the RASS indexes of heart failure rats to the level of the normal group. The present study offers preliminary evidence supporting the use of Rhodiola Rosea injection in the treatment of heart failure and offers a solid foundation for clinical off-label medication use.

Anti-heart failure mechanism of saponin extract of black ginseng based on metabolomics

ObjectiveThis study aimed to explore the mechanism of total saponin of black ginseng (TSBG) in treating heart failure (HF) in DOX-induced HF model rats. MethodsRats with HF induced by the intraperitoneal injection of DOX were treated with TSBG (low dose, 30 mg/kg/day; medium dose, 60 mg/kg/day; high dose, 120 mg/kg/day) and shakubar trivalsartan (80 mg/kg/day, positive control) for four weeks. Serum BNP and ANP levels were tested by ELISA, and pathological tissue sections were examined. Serum metabolites were measured using nontargeted metabolomic techniques. The expression of Akt/mTOR autophagy-associated proteins in heart tissue was detected using Western blot, including Beclin1, p62, LCII and LC3I. ResultsCompared with the model group, rats in the TSBG-H group had a significantly lower heart index (p < 0.05), significantly lower serum levels of BNP (p < 0.01) and ANP (p < 0.01) and significantly fewer cardiac histopathological changes. Metabolomic results showed that TSBG significantly back-regulated 12 metabolites (p < 0.05), including cholesterol, histamine, sphinganine, putrescine, arachidonic acid, 3-sulfinoalanine, hypotaurine, gluconic acid and lysoPC (18:0:0). These metabolite changes were involved in taurine and hypotaurine metabolism, arachidonic acid metabolism, sphingolipid metabolism, etc. The protein expression level of p-Akt/Akt and p-mTOR/mTOR was significantly up-regulated (p < 0.001), whereas that of Beclin1, p62 (p < 0.001) and LCII/LC3I was down-regulated (p < 0.05). ConclusionTSBG has an excellent therapeutic effect on DOX-induced HF in rats, probably by regulating the Akt/mTOR autophagy signalling pathway, resulting in the improvement of taurine and hypotaurine metabolism, arachidonic acid metabolism and sphingolipid metabolism, which may provide a reference for elucidating the potential mechanism of action of TSBG against HF.

Retracted: Early Diagnosis and Prediction of Death Risk in Patients with Sepsis by Combined Detection of Serum PCT, BNP, Lactic Acid, and Apache II Score.

[This retracts the article DOI: 10.1155/2022/8522842.].

Significance of electrocardiogram abnormalities in children presenting to the emergency department with acute COVID-19 infection

ObjectivesAcute COVID-19 infection may be associated with electrocardiogram (EKG) abnormalities in pediatric patients. We have anecdotally observed EKG abnormalities in patients without MIS-C or significant cardiac disease requiring intervention or further follow-up. Our aim was to determine the incidence of abnormal EKG findings and correlate with evidence of significant cardiac pathology in pediatric patients who present to the emergency department during an acute COVID-19 infection. MethodsWe conducted a retrospective chart review of 209 pediatric patients diagnosed in the emergency department with acute COVID-19 infection and had an EKG during the same encounter; patients with MIS-C were excluded. Primary objectives included determination of the incidence of EKG abnormalities in patients presenting to the emergency department (ED) with acute COVID-19 infection who did not require hospitalization. Secondary objectives included correlation of these findings with other concomitant testing of possible cardiac pathology (echocardiograms, biomarkers), and clinical outcomes. ResultsEKG abnormalities were identified in 84 (40%) patients. Echo was performed in 28 (13.4%) patients; only 1 was abnormal, and considered an incidental finding. The most common EKG abnormality involved nonspecific ST-T wave patterns, suggestive of but not diagnostic for underlying pericardial or myocardial disease. Serum troponin and BNP values were normal in all patients tested, either with a normal or abnormal EKG. A normal EKG had a 100% sensitivity and negative predictive value in predicting a normal echocardiogram. No patients were hospitalized and there was normalization of EKG abnormalities during short-term follow up. ConclusionsDespite a high incidence of abnormal EKG repolarization patterns in pediatric patients presenting with acute (non-MIS-C) COVID-19 infections, these patients generally do not have abnormal cardiac biomarkers or echocardiograms, and the risk for adverse cardiac events is low.

P173 THERAPEUTIC MANAGEMENT OF FLUOROPYRIMIDINE CARDIOTOXICITY: AN ANECDOTAL CASE

Abstract Background Fluoropirimidine represents one of the staple treatment of metastatic colorectal cancer; chemoterapy–based cardiotoxicity is unfortunately habitual in clinical practice. Raltitrexed could represent a valid alterantive to 5–FU in patients with cardiovascular comorbidities or in which 5–FU Has not been tolerated. Case Report Our patient is a 73 years–old woman, who underwent left colon surgical resection due to subocclusion; a whola body staging was not performed. After surgery, patient underwent CT scan,i n which multiple liver, lung and peritoneal metastases were identified. Biomolecular profiling assessment was perfomed (RAS, BRAF Wild type, DPYD*6 heterozigosis mutation). On January 2020, patient began FOLFIRI + PANITUMUMAB scheme as first line treatment (total cycles perfomed: 15). On January 2021, PD was detected though restaging imaging, and patient was subsequently treated with FOLFOX + BEvacizumab as second line. After 5 cycles, patient developed dyspnoea and palpitation; EKG was performed depicting Atrial fibrillation with heart rate: 73bpm, preserved biventricular systolic function and increased BNP and NT–pro–BNP serum concentration. According to patient’s high thromboembolic risk, oral anticoagulation (NOAC) was administered and multidisciplinary discussion was scheduled. NAO were preferred to Vitamin K antagonists due to drug–drug interactions; the treatment–of–choice was Apixaban 2.5 mg bis in die. Given the fact that aforementioned condition could have been attributed to 5–FU cardiologic toxicity, Raltitrexed was administered in lieu thereof 5–FU once synusal rythm was restored (TOMOX scheme). Bevacizumab administration was restored after a longer waiting (ca 2 months); the patient uderwent systematic and serial cardiologic assessment through clinical and EKG consults. Conclusion Our case report depicts the undelayable necessity of a Multidisciplinar collaboration in which oncologists and cardiologists could propose personalized treatment strategies which ensure correct antitumoral activities without significant and life–threatening toxicities.

Serum B-type natriuretic peptide levels (BNP) can be used as a predictor of complications in patients undergoing non-cardiac surgery: a prospective observational study

ObjectivesWorldwide, an estimated 10 million adults annually experience significant myocardial injury after non-cardiac surgery. Our aim is to assess whether preoperative and postoperative serum B-type natriuretic peptides levels (BNP) could...