Creatine Kinase-myocardial Band Research Articles

Punicalagin attenuates isoproterenol-induced myocardial infarction through nuclear factor erythroid 2-related factor 2/silent information regulator transcript-1-mediated inhibition of inflammation and cardiac stress markers in experimental animal models.

Myocardial infarction (MI) is a significant global health issue and the leading cause of death. Myocardial infarction (MI) is characterized by events such as damage to heart cells and stress generated by inflammation. Punicalagin (PCN), a naturally occurring bioactive compound found in pomegranates, exhibits a diverse array of pharmacological effects against many disorders. This study aimed to assess the preventive impact of PCN, with its potential anti-inflammatory and antioxidant properties, on myocardial injury caused by isoproterenol (ISO) in rats and elucidate the possible underlying mechanisms. Experimental rats were randomly categorized into four groups: control group (fed a regular diet for 15 days), PCN group (orally administered PCN at 50 mg/kg body weight (b.w.) for 15 days), ISO group (subcutaneously administered ISO (85 mg/kg b.w.) on days 14 and 15 to induce MI), and PCN+ISO group (orally preadministered PCN (50 mg/kg b.w.) for 15 days and administered ISO (85 mg/kg b.w.) on days 14 and 15). The rat cardiac tissue was then investigated for cardiac marker, oxidative stress marker, and inflammatory marker expression levels. PCN prevented ISO-induced myocardial injury, suppressing the levels of creatine kinase-myocardial band, C-reactive protein, homocysteine, cardiac troponin T, and cardiac troponin I in the rats. Moreover, PCN treatment reversed (P<0.01) the ISO-induced increase in blood pressure, attenuated lipid peroxidation markers, and depleted both enzymatic and nonenzymatic markers in the rats. Additionally, PCN inhibited (P<0.01) ISO-induced overexpression of oxidative stress markers (p-38, p-c-Jun N-terminal kinase, and p-extracellular signal-regulated kinase 1), inflammatory markers (nuclear factor-kappa B, tumor necrosis factor-alpha, and interleukin-6), and matrix metalloproteinases and decreased the levels (P<0.01) of apoptosis proteins in the rats. Nuclear factor erythroid 2-related factor 2/silent information regulator transcript-1 (Nrf2/Sirt1) is a major cellular defense protein that regulates and scavenges oxidative toxic substances through apoptosis. Therefore, overexpression of Nrf2/Sirt1 to inhibit inflammation and oxidative stress is considered a novel target for preventing MI. PCN also significantly enhanced the expression of Nrf2/Sirt1 in ISO-induced rats. Histopathological analyses of cardiac tissue revealed that PCN treatment exhibited a protective effect on the heart tissue, mitigating damage. These findings show that by activating the Nrf2/Sirt1 pathway, PCN regulates oxidative stress, inflammation, and apoptosis, hence providing protection against ISO-induced myocardial ischemia.

Protective effect of thymoquinone nanoemulsion in reducing the cardiotoxic effect of 5-fluorouracil in rats.

5-Fluorouracil (5-FU), which is one of the most widely used chemotherapy drugs, has various side effects on the heart. Thymoquinone (TMQ), the main bioactive component of Nigella sativa, has antioxidant and protective effects against toxicity. In this study, we investigated the protective effect of thymoquinone against cardiotoxicity caused by 5-FU in vitro and in vivo models. H9C2 cells were exposed to 5-FU and TMQ, and cell viability was evaluated in their presence. Also, 25 male Wistar rats were divided into five control groups, 5-FU, 2.5, and 5 mg TMQ in nanoemulsion form (NTMQ) + 5-FU and 5 mg NTMQ. Cardiotoxicity was assessed through electrocardiography, cardiac enzymes, oxidative stress markers, and histopathology. 5-FU induced cytotoxicity in H9c2 cells, which improved dose-dependently with NTMQ cotreatment. 5-FU caused body weight loss, ECG changes (increased ST segment, prolonged QRS, and QTc), increased cardiac enzymes (aspartate aminotransferase [AST], creatine kinase-myocardial band [CK-MB], and lactate dehydrogenase [LDH]), oxidative stress (increased malondialdehyde, myeloperoxidase, nitric acid; decreased glutathione peroxidase enzyme activity), and histological damage such as necrosis, hyperemia, and tissue hyalinization in rats. NTMQ ameliorated these 5-FU-induced effects. Higher NTMQ dose showed greater protective effects. Thus, the results of our study indicate that NTMQ protects against 5-FU cardiotoxicity likely through antioxidant mechanisms. TMQ warrants further research as an adjuvant to alleviate 5-FU chemotherapy side effects.

Nicotinamide ribose ameliorates myocardial ischemia/reperfusion injury by regulating autophagy and regulating oxidative stress.

Nicotinamide riboside (NR) has been reported to play a protective role in myocardial ischemia-reperfusion (I/R) injury when used in association with other drugs; however, the individual effect of NR is unknown. In the present study Evan's blue/triphenyl tetrazolium chloride staining, hematoxylin and eosin staining, echocardiography, western blotting, reverse transcription-quantitative PCR, and the detection of myocardial injury-associated markers and oxidative stress metabolites were used to explore the ability of NR to alleviate cardiac I/R injury and the relevant mechanisms of action. In a mouse model of I/R injury, dietary supplementation with NR reduced the area of myocardial ischemic infarction, alleviated pathological myocardial changes, decreased inflammatory cell infiltration and attenuated the levels of mitochondrial reactive oxygen species (ROS) and creatine kinase myocardial band (CK-MB). In addition, echocardiography suggested that NR alleviated the functional damage of the myocardium caused by I/R injury. In H9c2 cells, NR pretreatment reduced the levels of lactate dehydrogenase, CK-MB, malondialdehyde, superoxide dismutase and ROS, and reduced cell mortality after the induction of hypoxia/reoxygenation (H/R) injury. In addition, the results indicated NR activated sirt 1 via the upregulation of nicotinamide adenine dinucleotide (NAD+) and protected the cells against autophagy. The sirt 1 inhibitor EX527 significantly attenuated the ability of NR to inhibit autophagy, but had no significant effect on the ROS content of the H9c2 cells. In summary, the present study suggests that NR protects against autophagy by increasing the NAD+ content in the body via the sirt 1 pathway, although the sirt 1 pathway does not affect oxidative stress.

Risk Factors of Convulsions in Children With Rotavirus Gastroenteritis and Construction of a Nomogram Prediction Model.

This study aims to investigate and analyze the risk factors of convulsions in children with rotavirus gastroenteritis and to construct a nomogram prediction model. A retrospective analysis was performed on 940 cases of pediatric patients with rotavirus gastroenteritis treated in our hospital from December 2017 to December 2022. Based on whether convulsions occurred during hospitalization, patients were divided into the convulsion group (n = 135) and the convulsion-free group (n = 805). Clinical information of patients in both groups was collected, logistic regression analysis was carried out to analyze the convulsion risk factors pertaining to children with rotavirus gastroenteritis, and a nomogram prediction model was constructed. The univariate analysis revealed that fever, frequency of diarrhea, white blood cell count, blood calcium level, blood glucose level, CO 2 CP, creatine kinase myocardial band (CK-MB), and blood pH value were all factors that display statistically significant differences at the level of P = 0.05. Then, logistic regression analysis was carried out, taking the occurrence of such convulsions as the dependent variable and the aforementioned factors as independent variables. The results show that fever, frequency of diarrhea, blood calcium, CO 2 CP, and CK-MB were the independent risk factors ( P < 0.05), whereas the area under the receiver operating characteristic curve (area under the curve) of the constructed nomogram prediction model based on these factors was 0.842 (95% confidence interval, 0.821-0.914). Frequency of diarrhea, blood calcium, CO 2 CP, and CK-MB are independent risk factors for the occurrence of convulsions in children with rotavirus gastroenteritis. The nomogram prediction model constructed based on these risk factors provides guidance and value in effectively preventing and controlling convulsions in children with rotavirus gastroenteritis.

Mutation of PTEN: Loss and Likelihood of Being a Non-responder to Trastuzumab in a Sample of Iraqi Her2+ Breast Cancer Patients.

PTEN controls upstream PI3K relatives, such as AKT. PTEN gene mutations have been documented to affect outcomes in main or distant malignancies, including breast cancer (BC). PTEN gene deletions are common in a variety of humancancers. A key factor in the response to this kind of therapy is genetic diversity. The purpose of this research is to determine whether a PTEN loss mutation influences a patient's propensity to not respond to trastuzumab (TRS) in cases of Her2+ BC. Diwaniya Teaching Hospital's oncology ward provided 60 patients with Her2+ BC who had been on TRS for at least 12 months for this study. Patients were split in half using the RECIST criteria for evaluating responses to therapy in solid tumors: responders and non-responders. A PTEN polyclonal primary antibody was used for the detection of PTEN in breast tissue in the current study. This research employs a rating system based on eight specimens (26.67%) among non-responsive women who demonstrated PTEN loss compared with one specimen (3.33%) among responsive women. Statistically, PTEN loss varied significantly between the responsive and non-responsive groups. Loss of PTEN was also not linked to shifts in creatine kinase-myocardial band (CK-MB), troponin T (TnT), or any other biomarker, or troponin I (Tn1) at baseline or after 12 months of TRS therapy. These results give us important information about how PTEN deletion mutations might work as a predictor for TRS response in women with Her2+ BC.

Efficacy and Safety of Multidose del Nido Cardioplegia for Optimal Myocardial Protection in Isolated Coronary Artery Bypass Grafting Surgery: A Comparative Retrospective Cohort Study

Background: The perioperative outcomes of del Nido cardioplegia (DNC) as a single-dose solution have been investigated in cardiac surgical procedures. However, the optimal redosing interval for multiple doses of DNC remains an area of ongoing debate. The purpose of this study is to evaluate the safety and efficacy of multidose DNC administered according to our protocol in comparison to intermittent cold blood cardioplegia (BC) in isolated coronary artery bypass grafting (CABG) patients. Methods: A retrospective analysis was conducted on 79 consecutive isolated CABG patients between January 2022 and March 2023. The Patients were divided into two groups: the DNC group (n = 35), and the BC group (n = 44). Perioperative clinical characteristics, cardiac enzyme levels, and postoperative complications were compared between the groups. DNC was applied in a 1:4 (crystalloid:blood) ratio, with an initial dose of 20 mL/kg. Maintenance doses of 10 mL/kg were given every 45 to 50 minutes. A half dose was given if the aortic cross-clamp was expected to last less than 60 minutes. Warm blood was applied before releasing the aortic cross-clamp. Results: Both groups demonstrated comparable mean aortic cross-clamp and cardiopulmonary bypass times. At 24 hours postoperatively, troponin T levels were significantly lower in the DNC group (p ˂ 0.001), while creatine kinase-myocardial band (CK-MB) levels were higher (p ˂ 0.001). The DNC group required lower defibrillation rates than the BC group (p = 0.008). Multivariate logistic regression analysis revealed that the requirement for defibrillation (odds ratio (OR) = 10.9, 95% confidence interval (CI): 2.9–41.8, p &lt; 0.001), cross-clamp time (OR = 1.04, 95% CI: 1.02–1.1, p = 0.002) and body mass index (BMI) (OR = 0.8, 95% CI: 0.7–0.9, p = 0.030) were independent risk factors for low cardiac output syndrome. DNC and left ventricle ejection fraction &gt;40% were associated with a return to sinus rhythm (OR = 3.6, 95% CI: 1.3–10.1, p = 0.013 and OR = 3.1, 95% CI: 1.1–8.7, p = 0.035, respectively). No significant differences were found in terms of postoperative adverse events, and in-hospital mortality. Conclusion: Multidose DNC in CABG patients provides equivalent clinical outcomes and myocardial protection compared to BC. In addition, the findings suggest that the redosing interval strategy employed in the DNC protocol is acceptable.

Complexity of coronary artery disease and the release of cardiac biomarkers after CABG.

In patients with complex coronary artery disease (CAD) undergoing cardiac surgery, myocardial protection might be impaired due to microvascular obstruction, resulting in myocardial injury and subsequent biomarker release. Therefore, this study investigated the correlation between the complexity of CAD, reflected by the SYNTAX Score, and the release of cardiac biomarkers after CABG. In a consecutive series of 919 patients undergoing isolated CABG SYNTAX scores I and II were calculated to assess the complexity of CAD. Levels of high sensitivity cardiac troponin T (hs-cTnT) and creatine kinase-myocardial band (CK-MB) were routinely measured once before and serially after surgery. Patients were divided into tertiles according to their SYNTAX Scores I and II. Spearman correlations and regression models were performed to measure the degree of association between the release of hs-cTnT and CK-MB and the SYNTAX Scores. Patients with a higher SYNTAX Score I had more comorbidities reflected in a higher EuroSCORE II. Preoperatively, higher levels of cardiac biomarkers were found in patients with higher SYNTAX Score II. No correlation was observed between hs-cTnT, CK-MB and SYNTAX Score I or II. Regression models did not show any association between cardiac biomarkers and the complexity of CAD. The complexity of CAD is not associated with the release of cardiac biomarkers after CABG. Factors influencing postoperative biomarker release need to be elucidated in future trials to include postoperative biomarker release into risk stratification models predicting outcome after cardiac surgery.

Clinical characteristics, diagnosis and management of nivolumab-induced myocarditis.

Nivolumab can cause fatal myocarditis. We aimed to analyze the clinical characteristics of nivolumab-induced myocarditis and provide evidence for clinical diagnosis, treatment, and prevention. Studies involving nivolumab-induced myocarditis were identified in electronic databases from 2000 to 2023 for retrospective analysis. A total of 66 patients were included, with a median age of 68 years. The median onset time of myocarditis is 11.5 days. The main organs affected in persons presented with myocarditis are heart (100.0%) and skeletal muscle (22.7%). The main clinical manifestations are dyspnea (49.2%), fatigue (47.6%), and myalgias (25.4%). The levels of troponin, troponin T, troponin I, creatine kinase, creatine kinase myocardial band, creatine phosphokinase, C-reactive protein, brain natriuretic peptide, and N-terminal brain natriuretic peptide precursor were significantly increased. Histopathology often shows lymphocyte infiltration, myocardial necrosis, and fibrosis. Myocardial immunological parameters usually present positive. Cardiac imaging often suggests complete heart block, intraventricular conduction delay, arrhythmia, myocardial infarction, edema, left ventricular ejection fractions reduction, ventricular dysfunction, and other symptoms of myocarditis. Forty-two (63.6%) patients achieved remission within a median time of 8 days after discontinuation of nivolumab and treatment with systemic corticosteroids, immunoglobulins, plasmapheresis, and immunosuppressant. Thirty-five patients eventually died attributed to myocarditis (68.6%), cancer (20.0%), respiratory failure (5.7%), and other reasons (5.7%). Nivolumab-induced myocarditis should be comprehensively diagnosed based on clinical symptoms, histopathological manifestations, immunological parameters, and cardiac function imaging examinations. Nivolumab should be discontinued immediately, plasmapheresis and systemic corticosteroids combined with immunoglobulins or immunosuppressants may be an effective treatment.

Anterior-wall and non-anterior-wall STEMIs do not differ in long-term mortality: results from the augsburg myocardial infarction registry.

Different ST-segment elevation myocardial infarction (STEMI) localizations go along with dissimilarities in the size of the affected myocardium, the causing coronary vessel occlusion, and the right ventricular participation. Therefore, this study aims to clarify if there is any difference in long-term survival between anterior- and non-anterior-wall STEMI. This study included 2,195 incident STEMI cases that occurred between 2009 and 2017, recorded by the population-based Augsburg Myocardial Infarction Registry, Germany. The study population comprised 1.570 men and 625 women aged 25-84 years at acute myocardial infarction. The patients were observed from the day of their first acute event with an average follow-up period of 4.3 years, (standard deviation: 3.0). Survival analyses and multivariable Cox regression analyses were performed to examine the association between infarction localizations and long-term all-cause mortality. Of the 2,195 patients, 1,118 had an anterior (AWS)- and 1,077 a non-anterior-wall-STEMI (NAWS). No significant associations of the STEMI localization with long-term mortality were found. When comparing AWS with NAWS, a hazard ratio of 0.91 [95% confidence interval: 0.75-1.10] could be calculated after multivariable adjustment. In contrast to NAWS, AWS was associated with a greater <28 day mortality, less current or former smoking and higher creatine kinase-myocardial band levels (CK-MB) and went along with a higher frequency of impaired left ventricular ejection fraction (<30%). Despite pathophysiological differences between AWS and NAWS, and identified differences in multiple clinical characteristics, no significant differences in long-term mortality between both groups were observed.

Glycyrrhizic acid alleviated MI/R-induced injuries by inhibiting Hippo/YAP signaling pathways

BackgroundPrevious research has demonstrated that glycyrrhizic acid (GA) exhibits antioxidant, anti-inflammatory, and antiapoptotic characteristics. Using myocardial ischemia/reperfusion injury as a case study, this study aims to clarify the functional significance of GA and to elucidate the mechanisms involved. Materials and methodsIn this study, an MI/R injury model was established both in vivo and in vitro to investigate the impact of GA on MI/R injury. The viability of H9c2 cells was evaluated using the Cell Counting Kit-8. Myocardial damage was assessed through the measurement of creatine kinase myocardial band (CK-MB) levels and lactate dehydrogenase (LDH), HE staining, and MASSON staining. Inflammatory cytokine levels (IL-6, IL-1β, IL-10, and TNF-α) were measured to determine the presence of inflammation. Cellular oxidative stress was evaluated by measuring ROS and MMP levels, while cardiac function was assessed using cardiac color Doppler ultrasound. Immunofluorescence staining to determine the nuclear translocation of YAP, TUNEL to determine apoptosis, and western blotting to determine gene expression. ResultsGA treatment effectively alleviated myocardial injury induced by MI/R, as evidenced by reduced levels of inflammatory cytokines (IL-1β, IL-6, IL-10, and TNF-α) and cardiac biomarkers (CK-MB, LDH) in MI/R rats. Moreover, There was a significant increase in cell viability in vitro after GA treatment and inhibited reactive oxygen species (ROS) during oxidative stress, while also increasing mitochondrial membrane potential (MMP) in vitro. The Western blot findings indicate that GA treatment effectively suppressed apoptosis in both in vivo and in vitro settings. Additionally, GA demonstrated inhibitory effects on the activation of the Hippo/YAP signaling pathway triggered by MI/R and facilitated YAP nuclear translocation both in vitro and in vivo. It has been found, however, in vitro, that silencing the YAP gene negates GA's protective effect against hypoxia/reoxygenation-induced myocardial injury. ConclusionThis study suggests that GA regulates YAP nuclear translocation by inhibiting the Hippo/YAP signaling pathway, which protects ists against MI/R injury. This finding may present a novel therapeutic approach for the treatment of MI/R.

Antihyperlipidemic and cardiopreventive properties of Arabic gum in nicotinamide/streptozotocin-induced diabetic rats

Background/Aim Diabetes mellitus (DM) and its complications have a negative impact on human health and the economy worldwide. Diabetic patients are at a high risk of dying from cardiovascular diseases. Arabic gum (AG) is a natural product that exhibits potent anti-inflammatory, antioxidant and hypoglycemic properties. The purpose of this study was to scrutinize the antihyperlipidemic and cardiopreventive efficacy and to assess the antioxidant and anti-inflammatory roles of AG in nicotinamide (NA)/streptozotocin (STZ)-induced DM in rats. Material and methods Three groups of 18 adult (6 each) male Wistar rats each were used for the experiment. The first group was the normal control group, which received 0.9% NaCl daily by oral gavage for 8 weeks. The rats in the second group were injected with 60 mg/kg b.w. STZ in citrate buffer (pH 4.5) intraperitoneally (IP), after being given intraperitoneally 120 mg/kg b.w. NA. They also received 0.9% NaCl daily by oral gavage for 8 weeks. The third group was treated with 20 mg AG/kg b.w./day suspended in 0.9% NaCl by oral gavage for 8 weeks after inducing DM in the same way as the second group. Results Hyperglycemia and hyperlipidemia were observed in DM rats. They also had significantly higher levels (P&lt;0.05) of serum creatine kinase (CK), creatine kinase myocardial band (CK-MB), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH), which indicate heart dysfunction. The diabetic heart suffered from oxidative stress, as shown by significant increases (P&lt;0.05) of malondialdehyde (MDA) and decreased glutathione (GSH), glutathione peroxidase (GPx), and superoxide dismutase values (SOD). AG treatment improved blood glucose and serum lipid levels, as well as heart function biomarkers in serum. AG also reduced oxidative stress and enhanced antioxidant defenses in the diabetic heart. Immune-inflammatory markers, such as nuclear factor-kappa B and tumor necrosis factor-α and apoptotic protein p53 expressions were elevated in diabetic rats (P&lt;0.05) markedly, but the treatment with AG exhibited normal levels for them. Conclusion In conclusion, this study demonstrated that AG has a preventive role against heart injury in NA/STZ-induced DM in rats. AG improved the metabolic, oxidative, and inflammatory status as well as apoptosis and their cardiac function in diabetic rats. Moreover, AG improved the histological picture of cardiac myocytes and therefore, it may be a potential natural remedy for diabetic cardiomyopathy.

Reliability of Metformin's protective effects against doxorubicin-induced cardiotoxicity: a meta-analysis of animal studies.

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

A retrospective cohort study of myocarditis prevalence and diagnosis in Al‐Baha region, Saudi Arabia

Background: Carditis describes heart inflammation with a variety of symptoms ranging from mild chest pain to cardiac shock or even sudden death. Myocarditis will result in heart failure (HF) in around 12%–17% of adults, with a death rate of approximately 8.4/100,000. The causatives of myocarditis include viral, bacterial, fungal, and protozoan infections. Aims: This retrospective cohort study aimed to statistically analyze the prevalence and diagnosis of myocarditis and other cardiovascular diseases (CVDs) among admitted patients to Al-Baha Hospitals in Saudi Arabia. Setting and Design: The study involved 384 patients diagnosed with CVDs at Al-Baha Hospital between January 2017 and December 2022. Statistical Analysis and Results: Overall, patients’ ages ranged from 25 to 94 years, averaging 59 ± 14. The majority of patients with different CVDs were aged between 41 and 70 years (69% myocardial infarction (MI), 48% HF, and 56% heart block). Most of the patients were male (80%), and 90% of the participants were Saudis. The incidence of CVDs showed a gradual increase between 2017 and 2019 and a dramatic increase in 2020 and 2022 compared to other years. The analysis included the most common laboratory markers aimed for the diagnosis. The result of the study showed an increase in lactate dehydrogenase (91%), creatine kinase (CK) (95%), CK-myocardial band (93%), aspartate aminotransferase (94%), and white blood cells (89%) of the patients who were diagnosed with MI compared to the other CVDs. Conclusions: It is important to note that while electrocardiogram, complete blood count, and cardiac profile form the core of the diagnostic protocol, additional diagnostic measures may be considered depending on the specific circumstances.

Melatonin reduces myocardial cell damage in myocardial ischemia/reperfusion rats by inhibiting NLRP3 activation.

Melatonin (Mel) is an endogenous hormone with many pharmacological effects, such as sedation, hypnosis, antidepressant, blood pressure regulation, anti-inflammatory and anti-tumor. It is mainly synthesized by pineal gland in vivo. Mel can regulate the function of cardiovascular system and effectively reduce myocardial cell injury, thus playing a role in myocardial protection, but its specific mechanism is unclear. Ischemia-reperfusion injury (IRI) often leads to poor prognosis and complications in patients with cardiovascular diseases, and inflammatory reaction mediated by nod-like receptor thermoprotein domain-related protein 3(NLRP3) is an important reason for the further aggravation of subsequent injury after IRI. Rats were intervened with Mel or NLRP3 inhibitor MCC950 for 10 days, and then the IRI rat model was established. After that, rats were anesthetized and killed, and myocardial tissues were collected for experiments. The experimental results showed that Mel reduced the myocardial infarction area, decreased aspartate aminotransferase (AST), creatine kinase myocardial band (CK-MB), lactate dehydrogenase (LDH) and malondialdehyde (MDA), and significantly inhibited the expression of reactive oxygen species (ROS), NLRP3, caspase-1 and apoptosis-associated speck-like protein containing a CARD (ASC), but its effect on superoxide dismutase (SOD) was opposite. Therefore, Melmay improve autophagy and inflammation during myocardial ischemia/reperfusion and may decrease myocardial cell damage by inhibitingNLRP3.

Pinostrobin attenuated cadmium instigated cardiotoxicity in albino rats: A biochemical, inflammatory, apoptotic and histopathological examination

Cadmium (Cd) is a noxious and non-biodegradable heavy metal which instigates various organ toxicities such as cardiac injuries. Pinostrobin (PSB) is a potent dietary bioflavonoid, which shows various pharmacological potentials. The current research was designed to evaluate the ameliorative effects of PSB against Cd elicited cardiac dysfunction in rats. Twenty-four albino rats were apportioned into four equal groups viz. control, Cd (5 mg/kg), Cd (5 mg/kg) + PSB (40 mg/kg) and PSB (40 mg/kg) only treated group. It was observed that Cd intoxication reduced catalase (CAT), glutathione reductase (GSR), superoxide dismutase (SOD), glutathione peroxidase (GPx), activities and glutathione S-transferase (GST) contents while escalating the levels of reactive oxygen species (ROS), hydrogen peroxide (H2O2) and malondialdehyde (MDA). Furthermore, Cd exposure escalated the levels of cardiac injury markers such as creatine phosphokinase (CPK), creatine kinase-myocardial band (CK-MB), troponin I and lactate dehydrogenase (LDH). Besides, the levels of inflammatory cytokines nuclear factor- κB (NF-κB), interleukin 1beta (IL-1ß), tumor necrosis factor- α (TNF-α), interleukin-6 (IL-6) levels and cyclooxygenase-2 (COX-2) activity were upregulated in Cd intoxicated group. Similarly, Caspase-3, Bax and Caspase-9 levels were augmented, and Bcl-2 levels were reduced after Cd administration. In addition, the histopathological examination revealed a notable cardiac tissue impairment in the Cd exposed group. Nonetheless, PSB treatment significantly (p < 0.05) recovered the abovementioned Cd-induced impairments. Therefore, the current study revealed that PSB might be a promising ameliorative agent to ameliorate Cd instigated cardiac damages.

Postoperative cardiac biomarker release is not associated with myocardial mass in computer tomography scans.

Myocardial hypertrophy results in increased levels of cardiac biomarkers in healthy individuals and in patients suffering from acute myocardial infarction. The influence of cardiac mass on postoperative cardiac biomarkers release remains unclear. This study investigated the correlation between myocardial mass and the release of high-sensitivity cardiac Troponin T (hs-cTnT) and creatine kinase-myocardial band (CK-MB) after isolated aortic valve replacement (AVR) or bypass surgery. Myocardial mass of a consecutive retrospective series of patients was measured automatically using preoperative computer tomography scans (636 patients, AVR = 251; bypass surgery = 385). Levels of cardiac biomarkers were measured before and serially after surgery. Spearman and Pearson correlation and a multivariate regression model was performed to measure the degree of association between myocardial mass and the release of hs-cTnT and CK-MB. Patients were divided into 3 tertiles according to their myocardial mass index. Higher biomarker levels were measured preoperatively in the upper tertile of patients undergoing AVR (P = 0.004) or bypass surgery (P < 0.001). Patients with different heart sizes showed no differences in postoperative biomarker release neither after AVR nor bypass surgery. No statistical significant correlation was observed between myocardial mass index and postoperative release of hs-cTnT or CK-MB in any subgroup (ρ maximum 0.106). Postoperative biomarker release is not correlated with myocardial mass. Patient factors leading to increased postoperative biomarker levels need to be elucidated in future studies.

Taohong Siwu decoction reduces acute myocardial ischemia–reperfusion injury by promoting autophagy to inhibit pyroptosis

Ethnopharmacological relevanceTaohong Siwu decoction (TSD) is a classic traditional Chinese medicine (TCM) prescription used to promote the blood circulation and alleviate blood stasis. TSD consists of Paeonia lactiflora Pall., Conioselinum anthriscoides (H. Boissieu) Pimenov & Kljuykov, Rehmannia glutinosa (Gaertn.) DC., Prunus persica (L.) Batsch, Angelica sinensis (Oliv.) Diels, and Carthamus creticus L. in the ratio of 3:2:4:3:3:2. Studies on the effects of TSD on myocardial ischemia–reperfusion injury (MIRI) from the perspective of autophagy and pyroptosis have not been reported. Aim of the studyInvestigate the effect of TSD on MIRI and explore the underlying mechanisms. Materials and methodsWe searched the main components and corresponding potential targets of TSD on The Pharmacology of Traditional Chinese Medicine Systems database for target prediction. We identified targets for MIRI on Online Mendelian Inheritance in Man and GeneCards databases. The intersection of the compound target and disease target was obtained and a protein–protein interaction network constructed. We undertook enrichment analyses using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes databases. The results of network pharmacology were verified by in vivo experiments in mice. ResultsIn mice, TSD significantly reduced the volume of the myocardial infarct, significantly reduced serum levels of cardiac troponin-nI (CTnI), creatine kinase-myocardial band (CK-MB), malonaldehyde (MDA), interleukin (IL)-6, increased the activity of superoxide dismutase (SOD) and IL-10 level, reduced the level of pyroptosis in myocardial tissue, increased the number of autophagosomes, and significantly reduced the fluorescence intensity of apoptosis-associated speck-like protein (ASC), Nod-like receptor protein 3 (NLRP3), and caspase-1. TSD administration increased the protein expression of microtubule-associated protein light chain 3 (LC3), but reduced the protein expression of p62, NLRP3, ASC, caspase-1, cleaved caspase-1, pro-caspase-1, gasdermin D (GSDMD), GSDMD-N-terminal, IL-18, and IL-1β. Administration of 3-Methyladenin could reverse the effect of TSD in inhibiting inflammation and the release of proinflammatory factors. ConclusionTSD treatment alleviated MIRI by promoting autophagy to suppress activation of the NLRP3 inflammasome and reducing the release of proinflammatory factors.

Melatonin mitigates oxidative damage induced by anthracycline: a systematic-review and meta-analysis of murine models

BackgroundOxidative stress induced by the excessive production of reactive oxygen species is one of the primary mechanisms implicated in anthracycline (ANT)-induced cardiotoxicity. There is a strong clinical need for a molecule capable of effectively preventing and reducing the oxidative damage caused by ANT. In vitro and in vivo studies conducted in mice have shown that melatonin stimulates the expression of antioxidative agents and reduces lipid peroxidation induced by ANT.MethodsWe investigated this issue through a meta-analysis of murine model studies. The outcome of the meta-analysis was to compare oxidative damage, estimated by products of lipid peroxidation (MDA = Malondialdehyde) and markers of oxidative stress (SOD = Superoxide Dismutase, GSH = Glutathione), along with a marker of cardiac damage (CK-MB = creatine kinase–myocardial band), assessed by measurements in heart and/or blood samples in mice undergoing ANT chemotherapy and assuming melatonin vs. controls. The PubMed, OVID-MEDLINE and Cochrane library databases were analysed to search English-language review papers published from the inception up to August 1st, 2023. Studies were identified by using Me-SH terms and crossing the following terms: “melatonin”, “oxidative stress”, “lipid peroxidation”, “anthracycline”, “cardiotoxicity”.ResultsThe metanalysis included 153 mice administered melatonin before, during or immediately after ANT and 153 controls from 13 studies. Compared with controls, the levels of all oxidative stress markers were significantly better in the pooled melatonin group, with standardized mean differences (SMD) for MDA, GSH and SOD being −8.03 ± 1.2 (CI: −10.43/−5.64, p &amp;lt; 0.001), 7.95 ± 1.8 (CI: 4.41/11.5, p &amp;lt; 0.001) and 3.94 ± 1.6 (CI: 0.77/7.12, p = 0.015) respectively. Similarly, compared with controls, CK-MB levels reflecting myocardial damage were significantly lower in the pooled melatonin group, with an SMD of −4.90 ± 0.5 (CI: −5.82/−3.98, p &amp;lt; 0.001).ConclusionMelatonin mitigates the oxidative damage induced by ANT in mouse model. High-quality human clinical studies are needed to further evaluate the use of melatonin as a preventative/treatment strategy for ANT-induced cardiotoxicity.

Cardiorenal protective effects of extracts of bitter leaf (Vernonia amygdalina) in animal model of metabolic syndrome

Every year, metabolic syndrome and cardiorenal diseases cause many deaths worldwide. African bitter leaf (Vernonia amygdalina) is known for its numerous therapeutic effects. Potentially, it can lower plasma lipid and glucose levels, which, in turn, may improve the condition of patients with the abovementioned diseases. This research featured the antihyperlipidemic and antihyperglycemic effects of methanol extract of V. amygdalina in an animal model of metabolic syndrome.&#x0D; Twenty albino rats were divided into four groups. Groups A to C were orally administered with ghee (3 mL/kg) + high-cholesterol diet (500 mg/kg) + high-sugar diet (10 mL/kg) to induce metabolic syndrome. Group A served as negative control and received no treatment with bitter leaf methanol extract. Groups B and C received 200 and 400 mg/kg of V. amygdalina methanol extract, respectively. Group D received no administration. The cardiorenal injuries and alterations in blood lipids and sugar levels wereassessed via various biochemical analyses.&#x0D; The combination of ghee + high-cholesterol diet + high-sugar diet triggered a significant elevation of creatine kinase myocardial band, lactate dehydrogenase, aspartate aminotransferase, triglycerides, total cholesterol, low density lipoprotein-cholesterol, glucose, urea, creatinine, and potassium levels. The histopathological results agreed with the biochemical findings. However, the treatment with 200 and 400 mg/kg of V. amygdalina methanol extract was able to inhibit the adverse alterations causing a dosedependent significant antihyperlipidemic and antihyperglycemic effect (p &lt; 0.05).&#x0D; Bitter leaf (V. amygdalina) demonstrated cardiorenal protective effects and may be used to manage metabolic syndrome.

Biomarker associated trends in mortality in myocardial infarction as an example of clinical data warehouse analyses - new opportunities of data-driven cardiovascular research

Abstract Background Healthcare data collected during clinical routine bears an immense potential for various clinical research questions. With the rapid use and development of structured electronic health records, this abundant source of data can be utilized to efficiently comprise large datasets based on actual, unselected patients. In this study, we examined 4,205 patients who presented with myocardial infarction (MI) since the implementation of a new hospital information system at a tertiary hospital. We sought to evaluate mortality trends using routinely collected biomarkers. Methods 4,205 patients admitted with MI at a high-volume tertiary hospital between September 2016 and September 2022, were retrospectively analyzed. Statistical analyses comprised data from a data warehouse sourced from the hospital information system including ICD and OPS codes, biometric data, and biomarker values. Results Of the 4,205 patients with MI, 28% (1,176) were female, the mean age was 67 years. 28% (1,171) were diagnosed with ST-segment elevation myocardial infarction (STEMI). 15% of all MI patients (645) showed coronary single-vessel disease, whereas 65% of patients (2.746) suffered from multi-vessel disease. Percutaneous coronary intervention was performed in 47% (1,961) of all included NSTEMI and STEMI patients. Concomitant arterial hypertension was present in 51% of STEMI patients compared to 65% of the NSTEMI population. Regarding STEMI, diabetes mellitus (DM) was prevalent in 22% of cases, whereas 31% in NSTEMI were diagnosed with DM. We observed a significant linear association between in-hospital mortality and peak biomarker levels of high-sensitive Troponin I (hsTnI), serum lactate, and creatine kinase myocardial band (CKMB) (figure 1). MI patients with a peak lactate measurement of &amp;gt; 17.01 mmol/l had a mortality rate of &amp;gt; 80%. Two-thirds of patients (66%) with CKMB values of &amp;gt; 1474.50 U/I died during the index hospitalization. Conclusion In our study, we observed significant linear associations between biomarker levels and in-hospital mortality in patients with myocardial infarction. Furthermore, we demonstrated that hospital information systems can efficiently be used to generate large, comprehensive datasets not only to characterize real-world patient populations but also to evaluate data of prognostic relevance. With careful evaluation of data quality and within the frameworks of patient privacy, future research in this field holds promising potential.