Creatine kinase-MB Levels Research Articles

Effect of Different Types of Smoking (Cegarette, hookah and vape) on Neuregulin-1 and Other Biochemical Parameters of Cardiac Health for Al-Mustansiriyah University Students Smoking ( cigarette, hookah and vape) on Heart Health for Mustansiriyah University Students

Tobacco smoking remains a significant contributor to preventable illness and premature mortality worldwide, posing a substantial risk factor for various cardiovascular diseases (CVDs). This study aimed to determine the impact of different smoking methods on cardiac function and oxidative stress parameters, focusing on cigarette smoking, hookah, and vape. A total of 120 male participants were splitted into four groups: healthy controls, cigarette smokers, hookah users, and vape users. Blood samples were collected and analyzed for oxidative stress markers, cardiac function indicators, and neuregulin-1 (NRG-1) levels, a peptide with cardioprotective potential. When compared to controls, the results showed that smokers had significantly higher concentrations of total oxidative stress (TOS) and lower concentrations of total antioxidant capacity (TAC), with hookah having the most noticeable impact. Both the hookah and cigarette groups had noticeably higher levels of neuregulin-1, suggesting possible heart stress. Moreover, smokers showed increased Creatine kinase-MB (CK-MB) levels and lactate dehydrogenase (LDH), which may indicate cardiac injury. The results of correlation analysis showed a strong relationship between LDH and NRG-1, indicating the possibility of using both of them together as markers of smoking-related cardiac risk. The diagnostic usefulness of TOS, TAC, Neuregulin-1, LDH, and CK-MB in differentiating smokers from non-smokers was shown by receiver operating characteristic (ROC) analysis; CK-MB showed the highest sensitivity and specificity. These results highlight how smoking hurts heart health, emphasizing the importance of comprehensive preventive strategies and smoking cessation interventions to mitigate the burden of CVDs associated with tobacco use.

SUZ12-Increased NRF2 Alleviates Cardiac Ischemia/Reperfusion Injury by Regulating Apoptosis, Inflammation, and Ferroptosis.

Nuclear factor erythroid 2-related factor 2 (NRF2) is a redox-sensitive transcriptional factor that enables cells to resist oxidant responses, ferroptosis and inflammation. Here, we set out to probe the effects of NRF2 on cardiomyocyte injury under acute myocardial infarction (AMI) condition and its potential mechanism. Human cardiomyocytes were exposed to hypoxia/reoxygenation (H/R) to induce cell injury. qRT-PCR and western blot assays were used to detect the levels of mRNAs and proteins. Cardiomyocyte injury was determined by detecting the levels of lactate dehydrogenase and creatine Kinase MB(CK-MB). Cell apoptosis was investigated by flow cytometry and related markers. Levels of IL-6, IL-10, and TNF-α were measured by ELISA. Cell ferroptosis was assessed by detecting the production of reactive oxygen species(ROS), malonaldehyde(MDA), reducedglutathione/oxidizedglutathione disulfide (GSH/GSSG)ratio, Fe + content, and related regulators. The interaction between NRF2 and the suppressor of zest 12 (SUZ12) was analyzed by using dual-luciferase reporter and RNA immunoprecipitation assays. AMI rat models were established for in vivo analysis. NRF2 was lowly expressed in AMI patients and H/R-induced cardiomyocytes. Forced expression of NRF2 reduced H/R-induced cardiomyocyte injury, apoptosis, inflammation, and ferroptosis. Moreover, NRF2 overexpression improved cardiac function and injury in vivo. Mechanistically, SUZ12 bound to the promoter of NRF2 and promoted its expression. Further functional analyses showed that SUZ12 overexpression reduced H/R-induced cardiomyocyte injury, apoptosis, inflammation, and ferroptosis, which were reversed by NRF2 silencing. SUZ12-increased NRF2 suppressed H/R-induced cardiomyocyte injury, apoptosis, inflammation, and ferroptosis in vitro and improved cardiac functions in rats with I/R injury, suggesting the potential cardioprotective effect of NRF2 in cardiac injury during AMI.

Alleviation of lipopolysaccharide-induced heart inflammation in poultry treated with carnosic acid via the NF-κB and MAPK pathways.

In intensive poultry farming, environmental stress, pathogen infections, and noise can negatively impact growth or cause sudden death, leading to economic losses. The prevalent use of antibiotics as feed additives to prevent diseases in broilers has raised concerns about antibiotic resistance and highlighted the need for safer and more effective alternatives. Carnosic acid (CA), a bioactive compound derived from rosemary, exhibits notable pharmacological properties, including anti-inflammatory and antioxidant effects. This study investigates CA's efficacy in mitigating lipopolysaccharide (LPS)-induced heart inflammation in broilers. Broilers were pretreated with CA at varying doses (20, 40, and 80mg/kg) for 7 days then exposed to LPS (200mg/kg) for 24h to induce an inflammatory response. LPS treatment increased the levels of the cardiac damage markers creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) and inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), and inducible nitric oxide synthase (iNOS), but these effects were markedly decreased in CA-pretreated poultry. Histopathological analysis indicated that CA mitigated myocardial fiber rupture and inflammatory cell infiltration. Immunohistochemistry showed that CA sustained high expression levels of the protective protein crystallin alpha B (CRYAB), the expression of which was reduced by LPS. Mechanistic studies demonstrated that CA regulates key inflammatory signaling pathways via inhibiting LPS-induced activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) by reducing the phosphorylation of p65 and inhibitor of nuclear factor kappa-B alpha (IκBα). Additionally, CA attenuated mitogen-activated protein kinase (MAPK) pathway activation, as evidenced by decreased phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 in the CA-treated groups compared to the LPS-only groups. These findings suggest that CA exerts a protective effect against LPS-induced cardiac inflammation by enhancing CRYAB expression and modulating the NF-κB and MAPK pathways. Importantly, the findings emphasize CA's potential as a natural feed additive to enhance cardiac health in poultry and present a promising alternative to conventional antibiotics in livestock management. Further research is needed to investigate its broader applications in animal health and other inflammatory conditions.

Sevoflurane attenuates hypoxia/reoxygenation-induced cardiomyocyte injury by regulating miR-4454.

Sevoflurane (Sevo) prevents hypoxia/reoxygenation (H/R)-induced cardiomyocytes injury. The expression of miR-4,454 was increased in individuals experiencing an acute myocardial infarction. The purpose of current investigation was to delved into whether the effects of Sevo on cardiomyocytes are mediated through regulation of miR-4,454 expression. In this study, the expression levels of miR-4,454 and BAG5 were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability was detected by cell counting kit-8 (CCK-8). The levels of creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin I (cTnI) were detected by enzyme-linked immunosorbent assay (ELISA). Reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) were detected using various commercially available kits to assess the level of oxidative stress in the cells. The luciferase reporter gene assay was used to verify the interaction of miR-4,454 with downstream target genes. There was a notable upregulation of miR-4,454 expression in H/R-induced cardiomyocyte models. This was accompanied by a decrease in the viability of myocardial cells induced by H/R and an intensification of the extent of myocardial injury and oxidative stress. However, the detrimental effects were mitigated by the administration of Sevo. miR-4,454 had a target site for binding to BAG5, and its expression was negatively modulated by miR-4,454. An increase in the expression of BAG5 was shown to directly offset the exacerbation of cardiomyocyte damage induced by the overexpression of miR-4,454. Sevo may attenuate H/R-induced cardiomyocyte injury by regulating miR-4454.

Role of del Nido Cardioplegia Solution in Prolonged Aortic Cross-clamp Cardiac Surgery: A Prospective Study.

The myocardial-protective effect of del Nido cardioplegia solution was evaluated in adult patients undergoing prolonged aortic cross-clamping during cardiac surgery. Prospective cohort. Single-center tertiary academic medical center. A total of 462 patients scheduled for cardiac surgery under cardiopulmonary bypass with an expected aortic cross-clamp time >120 minutes between January 2020 and January 2024 were enrolled. Patients with an expected aortic cross-clamp time >120 minutes were randomly assigned to low- and high-risk del Nido and Buckberg groups, with 112 patients in each group. Serum levels of cardiac troponin T and creatine kinase-MB were measured at 1, 24, and 48 hours after operation. The occurrence of atrial fibrillation within 48 hours postoperatively and other intraoperative and postoperative parameters were recorded. No significant differences were observed in preoperative parameters between the groups. The level of cardiac troponin T was significantly higher in the low-risk del Nido group than in the Buckberg group at 24 hours postoperatively (p < 0.05). However, no significant differences were observed in cardiac troponin T or creatine kinase-MB levels at the other time points. The incidence of postoperative atrial fibrillation in the Buckberg group at 48 hours was significantly higher than the del Nido group in both the low- and high-risk groups (p < 0.05). The incidence of postoperative atrial fibrillation at 48 hours was significantly lower in the del Nido group than in the Buckberg group. del Nido cardioplegia solution can be safely used for high-risk patients undergoing prolonged aortic cross-clamping.

Comparison of the effects on coagulation function and safety of bivalirudin and heparin in patients undergoing percutaneous coronary intervention: A randomized trial.

To analyze the effects on coagulation function and safety of bivalirudin and heparin in patients undergoing percutaneous coronary intervention (PCI) and provide clinical evidence for their application. A total of 42 patients with coronary heart disease undergoing PCI treatment from July 2019 to January 2022 at Datong Third People's Hospital in China were divided into 2 groups: the bivalirudin group and the heparin group. The former received perioperative administration of bivalirudin, while the latter received heparin. After 24 hours of treatment, blood indicators, coagulation functions, as well as cardiac, hepatic, and renal markers were evaluated. Additionally, Thrombolysis In Myocardial Infarction (TIMI) flow graded infarct-related vessel blood flow was assessed in both groups. Adverse cardiovascular and cerebrovascular events were monitored for a duration of 12 months. The Activated clotting time (ACT), D-dimer (D-D), and prothrombin time (PT) levels in the bivalirudin group were significantly lower than those in the heparin group (P < .05). Both the bivalirudin and heparin groups showed significant improvement in TIMI flow grade after PCI (P < .05). The levels of Creatine Kinase-MB (CK-MB), N-terminal Pro-B-type Natriuretic Peptide (NT-proBNP) in the bivalirudin group were significantly lower than those in the heparin group (P < .05). There were no serious adverse cardiovascular and cerebrovascular events in either group. Bivalirudin has a slightly superior impact on coagulation function and safety profile in patients undergoing PCI compared to heparin, and the preventive effect of both on postoperative cardiovascular events is similar.

Cocaine-associated Chest Pain: Our Experience with Myocardial Markers and Stress Lexiscans

Abstract Background: Cocaine is a commonly abused recreational drug, leading to frequent emergency room visits. The aim of this study was to check the effect of cocaine on myocardial markers of injury and the stress myocardial imaging patterns. Materials and Methods: All patients with anginal chest pain or equivalents who tested positive for cocaine on urine drug screen with reversible myocardial ischemia on regadenoson stress myocardial perfusion imaging called lexiscans were included and their corresponding myocardial markers of injury and stress imaging were reviewed. Results: Thirty-four patients had tested positive for cocaine in urine, out of the 192 patients with reversible myocardial ischemia on stress testing. The percentage of cocaine-associated myocardial ischemia was up to 17.70% in our study. Creatine kinase-MB levels were above the normal reference value of 5 ng/mL in 72.7% of patients and the combined cardiac troponins by fourth-generation assays were above the detection levels (≥0.02 ng/mL for cardiac troponin I [cTnI] and ≥0.010 ng/mL for cardiac troponin T [cTnT]) in 50% of patients. None of our patients had severe reversible myocardial ischemia on lexicans, but rather minimal-to-mild reversible myocardial ischemia was seen in the majority (76.5%) of patients. cTnI elevation was significantly associated with minimal reversible myocardial ischemia on one-way analysis of variance (P &lt; 0.05). Conclusion: Cocaine was associated with minimal-to-mild reversible myocardial ischemia on stress testing with significant elevation of cTnI.

Impact of a prehospital mobile cloud ECG transmission system on door-to-balloon time, myocardial damage and mid-term all-cause mortality in patients with ST-elevation myocardial infarction

Abstract Background Guidelines recommend to establish a regional reperfusion strategy to maximize the efficiency of care for patients diagnosed with ST-elevation myocardial infarction (STEMI). In Addition, the recently developed mobile cloud-based 12-lead electrocardiogram (ECG) transmission system enables the transmission of prehospital ECGs at a low cost. Medical staff can use electronic devices to access and review ECGs from anywhere. However, the effectiveness of the prehospital mobile cloud ECG system has not yet been clearly established. Objective This single-center study aims to evaluate the impact of the prehospital mobile cloud ECG system on reducing Door-to-Balloon Time (DTBT), myocardial damage, and mid-term all-cause mortality in patients with STEMI. Methods In June 2018, eight prehospital Mobile Cloud ECG Transmission systems were integrated into the regional Emergency Medical Service (EMS) in our region. This study examined and compared Door-to-Catheterization Laboratory Time (DTCT), DTBT, Onset-to-Reperfusion Time (OTRT), peak creatine kinase-MB (CK-MB) levels, and one-year mortality rates of STEMI patients in the five years before and after introducing the prehospital mobile cloud ECG system. From June 2013 to May 2023, our institute received a total of 426 STEMI patients via ambulances from these two EMS departments. After excluding 23 patients with OTRT exceeding 24 hours and 76 patients who were transferred without the system post-introduction, 327 consecutive STEMI patients who underwent emergency percutaneous coronary intervention (PCI) were included in the study. The patients were divided into two groups: 169 patients before the prehospital mobile cloud ECG system introduction and 158 patients after that. Results There were no significant differences in age, gender, past medical history, and Killip Class IV between the two groups, except for the proportion of left main trunk (LMT) lesions, which was significantly higher in the ECG group. Significant reductions were observed in both DTCT and DTBT in the group after introduction, with differences noted as (DTCT: 42 min vs. 26 min; p &amp;lt; 0. 001, and DTBT: 74 min vs. 56 min; p &amp;lt; 0.001, respectively). However, the OTRT did not show a significant difference. Peak creatine kinase-MB (CK-MB) levels did not differ between the two groups, and Kaplan-Meier analysis revealed no significant difference in one-year mortality between them. Multivariate Cox regression analysis, which included variables such as age, peak CK-MB levels, Killip Class IV, LMT lesions, OTRT and the prehospital mobile cloud ECG transmission system usage, revealed that only Killip Class IV was significantly associated with one-year mortality (hazard ratio of 2.82 and a 95% confidence interval of 1.61-4.94; p=0.0003). Conclusion The prehospital mobile cloud ECG transmission system significantly reduced DTBT, but did not lead to a reduction in myocardial damage or an improvement in mid-term prognosis.Effect of the ECG Transmission SystemKaplan-Meier analysis

Bacterial Cellulose Membrane Experimentally Implanted in the Peritoneum of Wistar Rats-Inflammatory Immunoreactivity and Oxidative Stress.

Bacterial cellulose (BC) has been used for various applications; however, studies investigating the immunohistochemical characteristics of the inflammatory and scarring component in BC implanted in the peritoneum in vivo have not yet been fully described. This study aimed to evaluate the systemic and organic safety of BC through oxidative stress, blood, and serum biochemical markers, as well as the late inflammatory response in rats, using histopathology and immunohistochemistry. Forty-three rats (26 males; 17 females) received BC in the peritoneal cavity (implanted group-IG), while twenty-seven rats (12 males; 15 females) served as the control (sham group-SG). Sixty days after surgery, oxidative stress in tissues, blood biochemical markers, and histopathological and immunohistochemical analyses for lymphocytes, macrophages, collagen, and vascular response around the BC were assessed. Only one oxidative stress marker, glutathione peroxidase, was elevated in the liver of IG rats. Creatine kinase MB and lactate dehydrogenase levels were significantly lower in IG animals. Histopathological analysis showed granulomatous inflammation in 93% of IG rats, with 74% of mild intensity. Immunohistochemistry revealed a significant macrophage presence (F4/80), with CD3, CD20, and F4/80 markers indicating differences favoring macrophages. In conclusion, BC implantation in the peritoneum induces a foreign body granulomatous response with prominent macrophage presence (F4/80). Type I and III collagen were observed around the membrane, and vascularization was intense 60 days post-implantation. From a biochemical and oxidative stress perspective, BC seems to be a safe material to be used in the peritoneal cavity.

Machine Learning Diagnostic Model for Early Stage NSTEMI: Using hs-cTnI 1/2h Changes and Multiple Cardiovascular Biomarkers.

This study demonstrates differences in the distribution of multiple cardiovascular biomarkers between non-ST-segment elevation myocardial infarction (NSTEMI) and unstable angina (UA) patients. Diagnostic machine learning predictive models measured at the time of admission and 1/2 h post-admission, achieving competitive diagnostic predictive results. This study aims to explore the diagnostic value of changes in high-sensitivity cardiac troponin I (hs-cTnI) levels in patients with suspected NSTEMI. A total of 267 patients presented with chest pain, requiring confirmation of acute coronary syndrome (ACS) subtypes (NSTEMI vs. UA). Hs-cTnI and other cardiac markers, such as creatine kinase-MB (CK-MB) and Myoglobin (Myo), were analyzed. Machine learning techniques were employed to assess the application of hs-cTnI level changes in the clinical diagnosis of NSTEMI. Levels of CK-MB, Myo, hs-cTnI measured at admission, hs-cTnI measured 1-2 h after admission, and NT-proBNP in NSTEMI patients were significantly higher than those in UA patients (p < 0.001). There was a positive correlation between hs-cTnI and CK-MB, as well as Myo (R = 0.72, R = 0.51, R = 0.60). The optimal diagnostic model, Hybiome_1/2h, demonstrated an F1-Score of 0.74, an AUROC of 0.96, and an AP of 0.89. This study confirms the significant value of hs-cTnI as a sensitive marker of myocardial injury in the diagnosis of NSTEMI. Continuous monitoring of hs-cTnI levels enhances the accuracy of distinguishing NSTEMI from UA. The models indicate that the Hybiome hs-cTnI assays perform comparably well to the Beckman assays in predicting NSTEMI. Moreover, incorporating hs-cTnI measurements taken 1-2 h post-admission significantly enhances the model's effectiveness.

Del Nido versus conventional blood cardioplegia in patients with combined aortic root surgery: A retrospective study.

This study aimed to compare the safety and efficacy of Del Nido cardioplegia (DNC) and conventional blood cardioplegia (CBC) in combined aortic surgery. This retrospective study involved elective patients who underwent combined aortic root surgery between September 2017 and July 2023. Patients were divided into two groups: the DNC and the CBC group. The primary outcome was high-sensitivity cardiac troponin I and creatine kinase-MB levels at the 0, 1, 2, and three postoperative days. The secondary outcomes contained postoperative left ventricular ejection fraction, return to spontaneous rhythm after aortic de-clamping, postoperative myocardial infarction, new-onset atrial fibrillation, postoperative mechanical circulatory support, mechanical ventilation duration, intensive care unit stay, postoperative hospital stay, and the reduction of left ventricle end-diastolic diameter at 3months after surgery. 223 patients were included and divided into the CBC (n = 111) and the DNC group (n = 112). There was no statistical difference in patients' demographics and preoperative parameters between the two groups. No in-hospital mortality. The total cardioplegia volume [35.25 (30.30,43.65) ml/kg versus 21.43 (18.42,25.62) ml/kg, p < 0.001] and infusion times [2 (2,3) times versus 1 (1,2) times, p < 0.001] were less and the incidence of return to spontaneous rhythm after de-clamping was higher in the DNC group [59.5% versus 83%, p < 0.001]. Postoperative high-sensitivity cardiac troponin I and creatine kinase-MB levels were comparable between the two groups. DNC is related to a shorter duration of mechanical ventilation, intensive care unit stay, and hospital stay than CBC. The rate of return to spontaneous rhythm after aortic de-clamping seemed to decrease with the prolongation of aortic cross-clamping (ACC) duration, and there was no difference between the two groups when the time exceeded 120min. The safety and efficacy of using DNC were comparable to CBC in combined aortic surgery. The rate of return to spontaneous rhythm after aortic de-clamping seemed to decrease with the prolongation of ACC time. Further studies may be needed to fully elucidate the advantages of DNC in postoperative recovery and its long-term effects on patient outcomes.

Carbon monoxide-releasing molecule-3 ameliorates traumatic brain injury-induced cardiac dysfunctions via inhibition of pyroptosis and apoptosis.

Traumatic brain injury (TBI) frequently results in cardiac dysfunction and impacts the quality of survivors' life. It has been reported that carbon monoxide-releasing molecule-3 (CORM-3) administration immediately after hemorrhagic shock and resuscitation (HSR) ameliorated the HSR‑induced cardiac dysfunctions. The purpose of this study was to determine whether the application of CORM-3 on TBI exerted therapeutic effects against TBI-induced cardiac dysfunctions. Rats were randomly divided into four groups (n = 12) including Sham, TBI, TBI/CORM-3 and TBI/inactive CORM-3 (iCORM-3) groups. TBI was established by a weight-drop model. The rats in the TBI/CORM-3 group and TBI/iCORM-3 group were intravenously injected with CORM-3 and iCORM-3 (4mg/kg) following TBI, respectively. The time of death in the rats that did not survive within 24h was recorded. 24h post-trauma, the cardiac function, pathological change, serum troponin T and creatine kinase-MB (CK-MB) levels, pyroptosis, apoptosis and expressions of TUNEL staining, Gasdermin D (GSDMD), IL-1β, IL-18, ratio Bax/Bcl-2 were assessed by echocardiography, hematoxylin-eosin staining, chemiluminescence, immunofluorescence, and western blot assays, respectively. TBI-treated rats exhibited dramatically decreased ejection fraction and aggravated myocardial injury, increased mortality rate, elevated levels of serum troponin T and CK-MB, promoted cardiac pyroptosis and apoptosis, and upregulated expressions of cleaved caspase-3, GSDMD N-terminal fragments, IL-1β, IL-18, and ratio of Bax/Bcl-2, whereas CORM-3 partially reversed these changes. CORM-3 ameliorated TBI-induced cardiac injury and dysfunction. This mechanism may be responsible for the inhibition of pyroptosis and apoptosis in cardiomyocyte.

Effect of inflammatory factors on myocardial infarction

BackgroundCohort studies have increasingly shown associations between inflammatory markers and myocardial infarction (MI); however, the specific causal relationships between inflammatory markers and the development of MI remain unclear.Methods and resultsBy utilizing publicly accessible genome-wide association studies, we performed a two-sample Mendelian randomization (MR) analysis to explore the causal associations between inflammatory markers and myocardial infarction (MI). A random-effects inverse-variance weighted method was used to calculate effect estimates. The study included a total of 395,795 European participants for MI analysis and various sample sizes for inflammatory factors, ranging from 3,301 to 563,946 participants.Neutrophil count was found to increase the risk of MI (odds ratio [OR] = 1.08; 95% confidence interval [CI], 1.00–1.17; p = 0.04). C-reactive protein levels correlated positively with MI. No associations were observed with IL-1 beta, IL-6, IL-18, procalcitonin, TNF-α, total white cell count, or neutrophil percentage of white cells. Neutrophil count and C-reactive protein were inversely associated with lactate dehydrogenase: neutrophil cell count (OR 0.95; 95% CI, 0.93–0.98; p < 0.01) and C-reactive protein (OR 0.96; 95% CI, 0.92–1.00; p = 0.02). No associations of MI with myoglobin, troponin I, and creatine kinase-MB levels were found.ConclusionsThis two-sample MR analysis revealed a causal positive association of MI with neutrophil count, C-reactive protein level, and the myocardial injury marker lactate dehydrogenase. These results indicate that monitoring C-reactive protein and neutrophil counts may be useful in management of MI patients.

Impact of Consistent and Inconsistent Creatine Kinase-MB and Troponin Levels on Hospital lethality in Acute Coronary Disorder

Background: Serum CK-MB and cardiac troponin are important diagnostic predictors used to determine the prognosis of patients with acute coronary disorders (ACD). However, the effects of these biomarkers on hospital lethality remain underexplored. Objective: This research aimed to determine the effects of consistent and inconsistent CK-MB and troponin levels on hospital mortality in ACD patients. Methodology: This comparative study was conducted on patients with confirmed ACD admitted to a tertiary care hospital from January 2023 till June 2024. Patients were categorized into two groups based on the consistency of their CK-MB and troponin levels during hospitalization: consistently elevated or normal biomarkers versus those with variable levels. Hospital lethality was defined as mortality occurring during the hospital stay. SPSS version 26 was used for statistical analysis. The study utilized multivariate logistic regression to ascertain independent factors that are associated with hospital death. For continuous variables, t-tests or Mann-Whitney U tests were employed, and for categorical data, chi-square tests. Results: There were 500 patients in the trial; 250 were in the inconsistent group and 250 were in the consistent group. In the inconsistent group, the hospital fatality rate was 18%, while in the consistent group it was 10% (p &lt; 0.05). Variability in biomarker levels was an independent predictor of higher hospital mortality, according to multivariate analysis (OR 2.5, 95% CI 1.5–4.2). Conclusion: Inconsistent CK-MB and troponin levels were associated with higher hospital mortality in ACD patients. Monitoring and stabilizing these biomarkers may be essential for improving patient outcomes and guiding therapeutic interventions in acute care settings.

Troponin I versus Creatinine Kinase-MB as Predictor Markers of the Severity and Outcomes in Acute Theophylline Toxicity

Abstract Theophylline is a type of diethylxanthine that continues to be widely used in many developing countries for the treatment of acute and chronic bronchial asthma, chronic obstructive pulmonary disease (COPD) and apnea of prematurity. Methylxanthine cardiotoxicity is based on diverse, complex mechanisms. PDE inhibition and blocking adenosine receptors cannot explain all the cardiotoxic effects of methylxanthine. In addition, methylxanthines are cardiac stimulants and result in positive inotropy and chronotropy even with therapeutic dosing; myocardial ischemia and myocardial infarction (MI) are associated with acute theophylline poisoning. The current study aimed to investigate troponin I and creatine kinase-MB as predictors of the severity and outcomes in cases of acute theophylline intoxication. No previous studies have proposed early predictors of cardiovascular toxicities among methylxanthine users, early recognition of the severity of theophylline toxicity can be lifesaving and needs aggressive supportive care to improve clinical outcomes in patients. This study was a prospective cohort study conducted on 34 patients admitted to the Poison Control Center at Ain Shams University Hospitals (PCC-ASUH) for a 6-month duration from January 2022 to June 2022 with a history of acute exposure to theophylline toxicity. with history of acute exposure to theophylline toxicity. Patients were subjected to personal and toxicological history taking, vital signs collection, grading of acute theophylline toxicity and measurement of serum theophylline level. Both troponin I and creatine kinase-MB were measured at 6 and 12 hours post admission. Results revealed that, troponin I level at 6 hours post ingestion and 12 hours post ingestion in addition to creatine kinase-MB level at 12 hours post ingestion were significantly higher in cases with severe acute theophylline intoxication and patients who required intensive care unit admission and hemodialysis. It was concluded that, troponin I could predict the severity and the requirement of ICU admission and hemodialysis in patients with acute theophylline toxicity either with early or delayed presentation. On the other hand, CK-MB could be considered for patients with delayed presentation. Depending on time of admission, proper choosing of the biomarker to be investigated will allow for better evaluation of patients with saving extra cost.

Synbiotic supplementation ameliorates anxiety and myocardial ischaemia-reperfusion injury in hyperglycaemic rats by modulating gut microbiota.

Hyperglycaemia, hyperlipidaemia, hypertension and obesity are the main risk factors affecting the development and prognosis of ischaemic heart disease, which is still an important cause of death today. In our study, male Sprague-Dawley rats were fed either a standard diet (SD) or a high fat and high carbohydrate diet (HF-HCD) for 8weeks and streptozotocin (STZ) was injected at the seventh week of the feeding period. In one set of rats, a mixture of a prebiotic and probiotics (synbiotic, SYN) was administered by gavage starting from the beginning of the feeding period. Experimental myocardial ischaemia-reperfusion (30min/60min) was induced at the end of 8weeks. Hyperglycaemia, hypertension and increased serum low-density lipoprotein levels occurred in SD- and HF-HCD-fed and STZ-treated rats followed for 8weeks. Increased density of the Proteobacteria phylum was observed in rats with increased blood glucose levels, indicating intestinal dysbiosis. The severity of cardiac damage was highest in the dysbiotic HF-HCD-fed hyperglycaemic rats, which was evident with increased serum creatine kinase-MB (CK-MB), cardiac troponin I (cTnI), tumour necrosis factor-α, and interleukin-6 levels, along with a decrease in ST-segment resolution index. SYN supplementation to either a normal or a high-fat high-carbohydrate diet improved gut dysbiosis, reduced anxiety, decreased CK-MB and cTnI levels, and alleviated myocardial ischaemia-reperfusion injury in hyperglycaemic rats.

Minocycline alleviates lipopolysaccharide-induced cardiotoxicity by suppressing the NLRP3/Caspase-1 signaling pathway.

Minocycline (Min), as an antibiotic, possesses various beneficial properties such as anti-inflammatory, antioxidant, and anti-apoptotic effects. Despite these known qualities, the precise cardioprotective effect and mechanism of Min in protecting against sepsis-induced cardiotoxicity (SIC) remain unspecified. To address this, our study sought to assess the protective effects of Min on the heart. Lipopolysaccharide (LPS) was utilized to establish a cardiotoxicity model both in vivo and in vitro. Min was pretreated in the models. In the in vivo setting, evaluation of heart tissue histopathological injury was performed using hematoxylin and eosin (H&E) staining and TUNEL. Immunohistochemistry (IHC) was employed to evaluate the expression levels of NLRP3 and Caspase-1 in the heart tissue of mice. During in vitro experiments, the viability of H9c2 cells was gauged utilizing the CCK8 assay kit. Intracellular ROS levels in H9c2 cells were quantified using a ROS assay kit. Both in vitro and in vivo settings were subjected to measurement of oxidative stress indexes, encompassing glutathione (GSH), malondialdehyde (MDA), and superoxide dismutase (SOD) levels. Additionglly, myocardial injury markers like lactate dehydrogenase (LDH) and creatine kinase MB (CK-MB) activity were quantified using appropriate assay kits. Western blotting (WB) analysis was conducted to detect the expression levels of NOD-like receptor protein-3 (NLRP3), caspase-1, IL-18, and IL-1β, alongside apoptosis-related proteins such as Bcl-2 and Bax, and antioxidant proteins including superoxide dismutase-1 (SOD-1) and antioxidant proteins including superoxide dismutase-1 (SOD-2), both in H9c2 cells and mouse heart tissues. In vivo, Min was effective in reducing LPS-induced inflammation in cardiac tissue, preventing cell damage and apoptosis in cardiomyocytes. The levels of LDH and CK-MB were significantly reduced with Min treatment. In vitro studies showed that Min improved the viability of H9C2 cells, reduced apoptosis, and decreased ROS levels in these cells. Further analysis indicated that Min decreased the protein levels of NLRP3, Caspase-1, IL-18, and IL-1β, while increasing the levels of SOD-1 and SOD-2 both in vivo and in vitro. Min alleviates LPS-induced SIC by suppressing the NLRP3/Caspase-1 signalling pathway in vivo and in vitro.

Molecular insight of miRNA-217 role in the pathogenesis of myocardial infarction: Promising diagnostic biomarker and therapeutic target

BackgroundGlobally, myocardial infarction (MI) is one of the main causes of death. This study aims to investigate the role of miR-217 in the pathogenesis through targeting MAPK and PI3K/AKT signaling pathways in experimental model of myocardial infarction and studying the possible cardioprotective role of dihydromyricetin (DHM) through modulation of this pathway. MethodsDihydromyricetin was injected (100 mg/kg; p.o.) in isoprenaline induced myocardial infarction rat model for 14 days. Rats were anaesthetized and blood samples were taken for serum separation, estimation of creatine kinase-MB (CK-MB), and troponin-I levels after 24 h had passed since the last isoprenaline injection. In addition, the hearts were also used for the other biochemical studies and the histological evaluation. ResultsDHM resulted in a significant suppression of the elevated levels miR-217 and MAPK compared to the MI control group and restored the normal level of serum CK-MB. Furthermore, DHM successfully restored the oxidative balance and halted the pro-inflammatory mediators in the cardiac tissue. ConclusionAccordingly, our experiment emphasizes the anti-ischemic property that has been demonstrated through modulation of expression level of miR-217 and consequent deactivation of MAPK and PI3K/AKT signaling pathways, and this was assured by halting downstream pro-inflammatory markers.

Plasma metabolic profiling reveals that crude and processed Polygonatum cyrtonema hua extract ameliorates myocardial ischemia-induced damage by regulating branched-chain amino acid and energy metabolism

Polygonatum cyrtonema Hua and its processed products have demonstrated cardio-protective effects, though the underlying mechanisms remain unclear. In this study, plasma metabolic profiling and pattern recognition were employed to explore the cardio-protective mechanisms of both crude and processed P. cyrtonema in a myocardial ischemia model induced by ligation, using gas chromatography-mass spectrometry. Post-modeling, plasma levels of creatine kinase-MB, lactate dehydrogenase, troponin T, and malondialdehyde were significantly elevated but were notably reduced after treatment. Conversely, plasma levels of glutathione peroxidase and superoxide dismutase, which were significantly decreased post-modeling, were restored following treatment. Hematoxylin-eosin (HE) and Masson staining revealed that both crude and processed P. cyrtonema effectively reduced inflammatory infiltration and fibrosis in cardiac tissue. Metabolic profiling identified 34 differential endogenous metabolites in the treatment groups, with 19 confirmed using standard compounds. The linear correlation coefficients (R2) for these standards ranged from 0.9960 to 0.9996, indicating high accuracy. The method exhibited excellent precision and repeatability, with relative standard deviation (RSD) values below 8.57%. Recovery rates were between 95.02% and 105.15%, and the stability of the standard compounds was confirmed after three freeze–thaw cycles, with RSD values under 4.42%. Both crude and processed P. cyrtonema were found to alleviate myocardial ischemia symptoms by regulating branched-chain amino acid metabolism and energy metabolism. These findings provide a solid foundation for the potential clinical use of this herb and its processed products in treating heart disease.

Clinical Analysis of Myocardial Injury in Highlanders with Pulmonary Hypertension.

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.