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Myocarditis in children is more common in clinical practice, which can cause different degrees of cardiac function damage. We investigated the effects of creatine phosphate in the treatment of myocarditis in children. Children in the control group were treated with sodium fructose diphosphate, and children in the observation group were treated with creatine phosphate on the basis of the control group. After treatment, the myocardial enzyme profile and cardiac function of children in the observation group were better than the control group. The total effective rate of treatment for children in the observation group was higher than that in the control group. In conclusion, creatine phosphate could significantly improve myocardial function, improve myocardial enzyme profile and reduce myocardial damage in children with pediatric myocarditis and had a high safety of use, which was worthy of clinical promotion. [ABSTRACT FROM AUTHOR]

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

American pikas (Ochotona princeps) are small lagomorphs that live in mountainous talus areas of western North America. Studies on the histopathology of American pikas are limited. We summarize here the clinical histories, and gross and histologic findings of 12 American pikas, including 9 captive (wild-caught) and 3 wild animals. Death was often attributed to stress (transport, handling, anesthesia) with few-to-no premonitory clinical signs. Infection was the cause of death in 2 cases: 1 had bacterial pyogranulomatous dermatitis, cellulitis, and lymphadenitis with sepsis; the other case had oomycete-induced necrotizing colitis. Incidental parasitic infections included sarcocystosis, nematodosis (oxyurids), and ectoparasitism. Most animals with adequate nutritional status had periportal hepatic lipidosis; this finding was absent in all animals with adipose atrophy, and it is possible that periportal hepatic lipidosis is non-pathologic in American pikas. Three cases had myocardial necrosis that was considered the cause of death; the cause of necrosis was not determined, but it may have been caused by stress or vitamin E–selenium deficiency. Esophageal hyperkeratosis was noted in animals with a history of anorexia and negative energy balance; accumulation of esophageal keratin can result from lack of mucosal abrasion by ingesta. Several histologic findings that are likely normal in American pikas include splenic extramedullary hematopoiesis, thymic tissue in adults, and Clostridium sp. in the enteric lumen. [ABSTRACT FROM AUTHOR]

The review discusses the pathophysiological mechanisms of SARS-CoV-2, the modes of transmission, and the long-term health consequences of COVID-19, emphasizing the importance of research and successful public health initiatives. COVID-19 taxonomy, pathophysiology, symptomatology, and epidemiological importance are the key objects of this research paper. This review explains how COVID-19 affects different systems of the body, including respiratory, cardiovascular, and reproductive systems of the human body. It describes the modes of entry of the virus into the cell; more precisely, ACE2 and TMPRSS2 in viral entry. In addition, the present study analyzes the situation of COVID-19 in India regarding vaccine development and the transmission rate related to socioeconomic factors. The manifestation of COVID-19 presents a lot of symptoms and post-acute problems, issues which are seriously impacting mental health and physical health as well. The present review summarizes current research into pathogenicity and the mode of virus transmission, together with immunological responses. Coupled with strong vaccination programs, public health initiatives should hold the key to fighting this pandemic. Long-term effects and the development of treatment methods will need further study, as ambiguities on COVID-19 remain. Multidisciplinary collaboration across healthcare sectors in this respect is of paramount importance for the prevention of further spread and protection of public health. [ABSTRACT FROM AUTHOR]

The article focuses on the SPACE trial, which examined the impact of discontinuing renin-angiotensin system inhibitors (RASI) before elective non-cardiac surgery in older patients. It aimed to assess whether stopping RASI prior to surgery would reduce postoperative myocardial injury and other adverse events. It is reported that the results showed that discontinuing RASI did not decrease the incidence of myocardial injury and may have increased the occurrence of hypertensive adverse events.

Objective: To investigate the cardioprotective potential of betulin in isoproterenol (ISO)-induced myocardial injury in rats. Methods: Wistar rats were divided into five groups (n=10): normal, ISO, nebivolol 5 mg/kg, and betulin (20 & 40 mg/kg). Nebivolol and betulin were administered orally for 29 days. ISO (85 mg/kg) was administered subcutaneously on day 27 and day 28 to induce myocardial injury. On day 29, blood was collected for determination of cardiac markers, and hemodynamic parameters were investigated. The levels of oxidative stress markers and the gene expressions of apoptotic markers and inflammatory mediators were evaluated. Moreover, 2,3,5-triphenyltetrazolium chloride staining and histopathological analysis were also performed. Results: Betulin reduced the size of myocardial infarction, decreased elevated levels of cardiac enzymes, and maintained hemodynamic functions. It also inhibited ISO-induced upregulation of Bax, caspase-3, NF-κB, and IL-6, enhanced endogenous antioxidant enzymes, and reduced lipid peroxidation. Additionally, pretreatment with betulin alleviated myocardial ischemic damage, as reflected by reduced myonecrosis, edema, and inflammatory changes. Conclusions: Betulin exhibits strong cardioprotective activity against ISO-induced myocardial injury by anti-inflammatory, antiapoptotic, and antioxidant activities. [ABSTRACT FROM AUTHOR]

The infusion of glucose-insulin-potassium (GIK) has yielded conflicting results in terms of cardioprotective effects. We conducted a meta-analysis to examine the impact of perioperative GIK infusion in early outcome after cardiac surgery. Randomized controlled trials (RCTs) were eligible if they examined the efficacy of GIK infusion in adults undergoing cardiac surgery. The main study endpoint was postoperative myocardial infarction (MI) and secondary outcomes were hemodynamics, any complications and hospital resources utilization. Subgroup analyses explored the impact of the type of surgery, GIK composition and timing of administration. Odds ratio (OR) or mean difference (MD) with 95% confidence interval (CI) were calculated with a random-effects model. Fifty-three studies (n=6129) met the inclusion criteria. Perioperative GIK infusion was effective in reducing MI (k=32 OR 0.66[0.48, 0.89] P=0.0069), acute kidney injury (k=7 OR 0.57[0.4, 0.82] P=0.0023) and hospital length of stay (k=19 MD -0.89[-1.63, -0.16] days P=0.0175). Postoperatively, the GIK-treated group presented higher cardiac index (k=14 MD 0.43[0.29, 0.57] L/min P<0.0001) and lesser hyperglycemia (k=20 MD -30[-47, -13] mg/dL P=0.0005) than in the usual care group. The GIK-associated protection for MI was effective when insulin infusion rate exceeded 2 mUI/kg/min and after coronary artery bypass surgery. Certainty of evidence was low given imprecision of the effect estimate, heterogeneity in outcome definition and risk of bias. Perioperative GIK infusion is associated with improved early outcome and reduced hospital resource utilization after cardiac surgery. Supporting evidence is heterogenous and further research is needed to standardize the optimal timing and composition of GIK solutions. [ABSTRACT FROM AUTHOR]

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Acute myocardial injury (AMI) induced by lipopolysaccharide (LPS) can cause cardiovascular dysfunction and lead to death in poultry. Traditional antibiotic therapy has been found to have many limitations and negative effects. Asiatic acid (AA) is a naturally occurring pentacyclic triterpenoid that is extracted from Centella asiatica and has anti-inflammatory, antioxidant, and anticancer pharmacological properties. Previously, we studied the effect of AA on LPS-induced liver and kidney injury; however, the impact of AA on LPS-induced AMI remained unclear. Sixty 1-day-old broilers were randomly divided into control group, LPS group, LPS + AA 15 mg/kg group, LPS + AA 30 mg/kg group, LPS + AA 60 mg/kg group, and control + AA 60 mg/kg group. The histopathology of cardiac tissues was detected by hematoxylin and eosin (H&E) staining. The mRNA and protein expressions related to mitochondrial dynamics and mitophagy were detected by quantitative real-time PCR, western blot, immunofluorescence, and immunohistochemistry. Disorganized myocardial cells and fractured myocardial fibers were found in the LPS group, and obvious red-blood-cell filling can be seen in the gaps between the myocardial fibers in the low-dose AA group. Nevertheless, the medium and high dose of AA obviously attenuated these changes. Our results showed that AA significantly restored the mRNA and protein expressions related to mitochondrial dynamic through further promoting mitophagy. This study revealed the effect of AA on LPS-induced AMI in broilers. Mechanically, AA regulated mitochondrial dynamic homeostasis and further promoted mitophagy. These novel findings indicate that AA may be a potential drug for LPS-induced AMI in broilers. El ácido asiático como mitigante de las lesiones miocárdicas agudas inducidas por lipopolisacáridos al promover la mitofagia y regular la dinámica mitocondrial en pollos de engorde. La lesión miocárdica aguda (con siglas en inglés IAM) inducida por lipopolisacáridos (LPS) puede causar disfunción cardiovascular y provocar la muerte en las aves comerciales. Se ha descubierto que la terapia tradicional con antibióticos tiene muchas limitaciones y efectos negativos. El ácido asiático (AA) es un triterpenoide pentacíclico natural que se extrae de la planta Centella asiática y que tiene propiedades farmacológicas antiinflamatorias, antioxidantes y anticancerígenas. Anteriormente, se estudió el efecto del ácido asiático sobre la lesión hepática y renal inducida por lipopolisacáridos; sin embargo, el impacto del ácido asiático en las lesiones miocárdicas agudas inducidas por lipopolisacáridos continua sin estar completamente determinada. Sesenta pollos de engorde de un día de edad se dividieron aleatoriamente en los siguientes grupos experimentales: grupo control, grupo que recibió LPS solamente, grupo LPS + ácido asiático 15 mg/kg, grupo LPS + ácido asiático 30 mg/kg, grupo LPS + ácido asiático 60 mg/kg y control + ácido asiático 60 mg./kg grupo. La histopatología de los tejidos cardíacos se detectó mediante tinción con hematoxilina y eosina (H&E). Las expresiones de ARN mensajero y proteínas relacionadas con la dinámica mitocondrial y la mitofagia se detectaron mediante PCR cuantitativa en tiempo real, inmunotransferencia Western, inmunofluorescencia e inmunohistoquímica. Se encontraron células miocárdicas desorganizadas y fibras miocárdicas fracturadas en el grupo que recibió lipopolisacáridos, y se puede observar un evidente acúmulo de glóbulos rojos en los espacios entre las fibras miocárdicas en el grupo de dosis bajas de ácido asiático. Sin embargo, las dosis medias y altas de ácido asiático obviamente atenuaron estos cambios. Nuestros resultados mostraron que el ácido asiático restableció significativamente las expresiones de ARN mensajero y proteínas relacionadas con la dinámica mitocondrial mediante la promoción adicional de la mitofagia. Este estudio reveló el efecto del ácido asiático sobre las lesiones miocárdicas agudas inducidas por lipopolisacáridos en pollos de engorde. Basicamente, el ácido asiático reguló la homeostasis dinámica mitocondrial y promovió aún más la mitofagia. Estos nuevos hallazgos indican que el ácido asiático puede ser un fármaco potencial para mitigar lesiones miocárdicas agudas inducidas por lipopolisacáridos en pollos de engorde. [ABSTRACT FROM AUTHOR]

Objective: To explore the mechanism by which icariin alleviates viral myocarditis. Methods: CVB3-induced cardiomyocytes were used as an in vitro model of viral myocarditis to assess the effects of icariin treatment on cell viability, inflammation, and apoptosis. Moreover, the effects of icariin on ferroptosis and TLR4 signaling were assessed. After AC16 cells were transfected with TLR4 overexpression plasmids, the role of TLR4 in mediating the regulatory effect of icariin in viral myocarditis was investigated. Results: Icariin significantly elevated cell viability and reduced inflammatory factors TNF-α, IL-1β, IL-6, and IL-18. Flow cytometry revealed that icariin decreased apoptosis rate, and the protein expression of Bax and cleaved caspase 3 and 9 in CVB3-induced cardiomyocytes. Additionally, it suppressed ferroptosis including lipid peroxidation and ferrous ion, as well as the TLR4 signaling. However, TLR4 overexpression abrogated the modulatory effects of icariin. Conclusions: Icariin mitigates CVB3-induced myocardial injury by inhibiting TLR4-mediated ferroptosis. Further animal study is needed to verify its efficacy. [ABSTRACT FROM AUTHOR]

Background: The diagnosis and prognosis of cardiovascular disorders are greatly aided by cardiovascular biomarkers. The uses of troponin and B-type natriuretic peptide in situations involving carbon monoxide exposure are examined in this narrative review. These biomarkers are important because they help predict outcomes in cardiovascular disorders, track the effectiveness of therapy, and influence therapeutic choices. Main body: Clinical practice makes considerable use of B-type natriuretic peptide (BNP), which has diuretic and vasodilatory effects, and troponin, a particular marker for myocardial injury. Carbon monoxide (CO) poisoning is a major worldwide health problem because CO, a "silent killer," has significant clinical consequences. Higher risk of cardiac problems, poorer clinical outcomes, and greater severity of carbon monoxide poisoning are all linked to elevated troponin and B-type natriuretic peptide levels. BNP's adaptability in diagnosing cardiac dysfunction and directing decisions for hyperbaric oxygen therapy is complemented by troponin's specificity in identifying CO-induced myocardial damage. When combined, they improve the accuracy of carbon monoxide poisoning diagnoses and offer a thorough understanding of cardiac pathophysiology. Conclusions: To sum up, this review emphasizes the importance of troponin and B-type natriuretic peptide (BNP) as cardiac indicators during carbon monoxide exposure. While BNP predicts long-term cardiac problems, troponin is better at short-term morbidity and death prediction. When highly sensitive troponin I (hsTnI) and B-type natriuretic peptide are combined, the diagnostic accuracy of carbon monoxide poisoning patients is improved. One of the difficulties is evaluating biomarker levels since carbon monoxide poisoning symptoms are not always clear-cut. Accurate diagnosis and treatment depend on the investigation of new biomarkers and the use of standardized diagnostic criteria. The results advance the use of cardiovascular biomarkers in the intricate field of carbon monoxide exposure. [ABSTRACT FROM AUTHOR]

[Display omitted] • S-nanoFe overtly inhibited the survival of bacteria and showed a significant protective effect on septic myocardial injury. • S-nanoFe treatment ameliorated several CLP-related pathological processes and signal pathways, in which AMPK plays a key role in the cardioprotection of S-nanoFe. • The RNA-seq detection further explored the comprehensive mechanisms of S-nanoFe in sepsis. • The surface passivation of nanoFe using sodium sulfide could effectively improve the stability of nanoFe without affecting the efficacy. • Our work provided an alternative strategy of nanoparticle for overcoming sepsis and septic myocardial injury. Myocardial injury is a serious complication in sepsis with high mortality. Zero-valent iron nanoparticles (nanoFe) displayed novel roles in cecal ligation and puncture (CLP)-induced septic mouse model. Nonetheless, its high reactivity makes it difficult for long-term storage. To overcome the obstacle and improve therapeutic efficiency, a surface passivation of nanoFe was designed using sodium sulfide. We prepared iron sulfide nanoclusters and constructed CLP mouse models. Then the effect of sulfide-modified nanoscale zero-valent iron (S-nanoFe) on the survival rate, blood routine parameters, blood biochemical parameters, cardiac function, and pathological indicators of myocardium was observed. RNA-seq was used to further explore the comprehensive protective mechanisms of S-nanoFe. Finally, the stability of S-nanoFe-1d and S-nanoFe-30 d, together with the therapeutic efficacy of sepsis between S-nanoFe and nanoFe was compared. The results revealed that S-nanoFe significantly inhibited the growth of bacteria and exerted a protective role against septic myocardial injury. S-nanoFe treatment activated AMPK signaling and ameliorated several CLP-induced pathological processes including myocardial inflammation, oxidative stress, mitochondrial dysfunction. RNA-seq analysis further clarified the comprehensive myocardial protective mechanisms of S-nanoFe against septic injury. Importantly, S-nanoFe had a good stability and a comparable protective efficacy to nanoFe. The surface vulcanization strategy for nanoFe has a significant protective role against sepsis and septic myocardial injury. This study provides an alternative strategy for overcoming sepsis and septic myocardial injury and opens up possibilities for the development of nanoparticle in infectious diseases. [ABSTRACT FROM AUTHOR]

OBJECTIVE: We aimed to investigate the effects of methoxamine to prevent hypotension in the elderly with intraspinal anesthesia (IA) on myocardial injury and cardiac function. PATIENTS AND METHODS: A retrospective study was conducted by enrolling sixty elderly patients who underwent femoral head replacement (FHR) under IA in our hospital from August 2019 to August 2020. The patients were divided into two groups according to the random number table method. In the control group (CG) (30 patients), 5 mg of ephedrine was administered sedately when patients developed hypotension (20% below basal blood pressure). In the research group (RG) (30 cases), 2 μg/(kg·h) of methoxamine hydrochloride was given as a constant-rate pump before anesthesia, and 1 mg of methoxamine hydrochloride was administered intraoperatively if hypotension occurred. The hemodynamic [systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR)], myocardial injury indexes [cardiac troponin I (cTnI), creatine kinase isoenzyme MB (CK-MB), fatty acid binding protein (FABP), plasma amino-terminal brain natriuretic peptide precursor (NT-proBNP)], cardiac function indexes [systemic vascular resistance (SVR), stroke volume (SV), net percentage ejection time (ET)] were observed before anesthesia (T1), at the end of surgery (T2), and 6 h after surgery (T3) in both groups. The Bruggemann Comfort Score (BCS) and Visual Analog Scale (VAS) scores at T3, 12 h postoperatively (T4) and 24 h postoperatively (T5) in both groups were observed, and the incidence of adverse reactions to intralesional anesthesia in both groups was counted. RESULTS: SBP, DBP and HR at T2 were lower than those at T1 in both groups, and SBP, DBP and HR at T3 were higher than those at T2, and SBP, DBP and HR at T2 and T3 in the RG were higher than those in the CG (p<0.05). In both groups, cTnⅠ, CK-MB and FABP were higher at T2 and T3 than at T1, higher at T3 than at T2, and NT-proBNP was higher at T2 than at T1 and T3, and lower in the RG than in the CG (p<0.05). In both groups, SVR and SV at time point T2 were lower than at time point T1 and ET was higher than at time point T1, SVR and SV at time point T3 were higher than at time point T2 and ET was lower than at time point T2, SVR and SV in the RG were higher than in the CG and ET was lower than in the CG (p<0.05). VAS scores were higher in both groups at T4 and T5 than at T3, and lower in the RG than in the CG (p<0.05). CONCLUSIONS: Methoxamine can effectively reduce the risk of hypotension in geriatric endotracheal anesthesia, which can reduce myocardial injury and stabilize cardiac function in patients. [ABSTRACT FROM AUTHOR]

Background: Cancer patients undergoing major noncardiac surgery are more likely to experience perioperative morbidity and mortality due to myocardial damage. Methods: Comparative study enrolled 80 patients with upper abdominal malignancies subjected to major abdominal surgeries. Of them, seventy-two patients were eligible and randomly assigned into two groups; Epidural catheter group (n = 37), received thoracic epidural infusion of levobupivacaine, and pre-peritoneal catheter group (n = 35), received preperitoneal infusion of levobupivacaine postoperatively. Primary endpoint was pain severity by NRS immediately after recovery, at 2, 4, 6, 12, 24, 36, and 48 hours. Secondary endpoints were: (1) Patient's hemodynamics monitored for postoperative 48 hours. (2) Myocardial injury, confirmed by troponin I & BNP levels preoperatively and on postoperative day 1 and 2 (3) Time of first analgesic demand and total postoperative 48 h morphine consumption. (4) Cardiovascular side effects; hypotension, bradycardia & arrhythmia. (5) Morphine side effects; PONV. Results: NRS scores showed non-significant reduction at most study times between both groups with significant reduction in the ECI group at 6-, 12-, and 24-hour than other group. First analgesic demand was earlier in PCI group than ECI without significant difference, while total 48 h morphine consumption showed a significant reduction in ECI group than PCI group. Hemodynamics were comparable in both groups. Cardiac enzymes, Troponin I and BNP, showed non-significant differences over study time between both groups. Postoperative complications, PONV, were similar in both groups without any significance, but with more cases of hypotension and bradycardia in epidural group. No cases of myocardial injury or heart failure were reported. Conclusions: Preperitoneal analgesia is an effective analgesic method comparable to epidural analgesia limiting the occurrence of major cardiovascular events in cancer patients undergoing major abdominal surgeries and can be utilized when epidural analgesia is not desired or forbidden. [ABSTRACT FROM AUTHOR]

Transient myocardial thickening (TMT) in cats is a poorly characterized clinical entity. Therefore, this study aimed to provide descriptions of additional cats diagnosed with this clinical phenomenon. For this multicenter observational retrospective study, cats diagnosed with TMT were searched in three medical databases. TMT was defined for cats with at least two echocardiograms showing an increased end-diastolic left ventricular wall thickness (LVWTd; i.e. ≥6 mm) at presentation and subsequent echocardiographic normalization (i.e. LVWTd <5.5 mm). Signalment, history, clinical, laboratory, therapeutic, and outcome data were retrieved. Twenty seven cats were included. The median age was 3 years. In 9/27 cats, an antecedent event was documented. At admission, 27/27 cats had evidence of myocardial injury (median value of cardiac troponin I 5.5 ng/mL), 25/27 cats had congestive heart failure, 13/27 cats had hypothermia, 8/27 cats had systemic hypotension, 7/27 cats had bradycardia, and 7/27 cats had electrocardiographic evidence of an arrhythmia. The median LVWTd was 6.4 mm. A potential cause of myocardial injury was identified in 14/27 cats. The median time from diagnosis to a significant reduction in LVWTd was 43 days. TMT can be diagnosed in a wide range of cats, including young subjects. An antecedent predisposing event and/or a possible causative trigger can be identified in some. The reduction in LVWTd that defines this phenomenon usually occurs over a variable time frame. This study represents the largest investigation of TMT in cats and provides additional information on this uncommon clinical entity. [ABSTRACT FROM AUTHOR]

The exact pathogenesis of type 1 diabetes mellitus (DM) is still unclear. Numerous organs, including the heart, will suffer damage and malfunction as a result of long-term hyperglycemia. Currently, insulin therapy alone is still not the best treatment for type 1 DM. In order to properly treat and manage patients with type 1 DM, it is vital to seek a combination that includes both insulin and additional medications. This study aims to explore the therapeutic effect and mechanism of N-acetylcysteine (NAC) combined with insulin on type 1 DM. By giving beagle canines injections of streptozotocin (STZ) and alloxan (ALX) (20 mg/kg each), a model of type 1 DM was created. The results showed that this combination could effectively control blood sugar level, improve heart function, avoid the damage of mitochondria and myocardial cells, and prevent the excessive apoptosis of myocardial cells. Importantly, the combination can activate nuclear factor kappa-B (NF-κB) by promoting linear ubiquitination of receptor-interacting protein kinase 1 (RIPK1) and NF-κB-essential modulator (NEMO) and inhibitor of NF-κB (IκB) phosphorylation. The combination can increase the transcription and linear ubiquitination of Cellular FLICE (FADD-like IL-1β-converting enzyme) -inhibitory protein (c-FLIP), diminish the production of cleaved-caspase-8 p18 and cleaved-caspase-3 to reduce apoptosis. This study confirmed that NAC combined with insulin can promote the linear ubiquitination of RIPK1, NEMO and c-FLIP and regulate the apoptosis pathway mediated by TNF-α to attenuate the myocardial injury caused by type 1 DM. Meanwhile, the research served as a resource when choosing a clinical strategy for DM cardiac complications. [ABSTRACT FROM AUTHOR]

The Lymphocyte-to-C-reactive protein ratio (LCR) combines information on immune and inflammatory status. Lymphocytes reflect immune health, while C-reactive protein (CRP) signals systemic inflammation. Some studies have linked LCR with cardiovascular outcomes, suggesting it could help identify at-risk individuals. However, its clinical utility needs further research validation. To investigate the association between lymphocyte-to-C-reactive protein ratio (LCR) and subclinical myocardial injury (SC-MI) in individuals who are free from cardiovascular disease (CVD) within the general population. The study included individuals in the National Health and Nutrition Examination Survey (NHANES) III. SC-MI was defined as having a Cardiac Infarction Injury Score (CIIS) greater than 10 units on a 12-lead electrocardiogram. Logistic regression models were employed to investigate the association between LCR and SC-MI. In total, 5870 individuals were included in the study, among whom 3266 had a history of SC-MI. Compared with the lowest quartile (Q1) in male, the odds ratios (OR) of SC-MI in Q2, Q3, and Q4 were 0.67 (95%CI: 0.53–0.86), 0.66 (95%CI: 0.51–0.84), and 0.70 (95%CI: 0.55–0.89), respectively. The data shows a trend where the OR of SC-MI are lower in higher quartiles of LCR, compared to the lowest quartile, in the male population (P for trend = 0.006). In other words, the likelihood of SC-MI tends to be lower among males with higher LCR values. However, after adjusting for potential confounding variables, the relationship between LCR and SC-MI displays a pattern of an initial decline, followed by a minor upward shift. LCR is independently and inversely associated with SC-MI risk in the general population free from CVD. Furthermore, the observed association is exclusive to males, indicating a need for further randomized controlled trials to substantiate the efficacy of implementing LCR reduction as a means of CVD prevention in the male population. • LCR is independently and inversely associated with SC-MI risk in the general population free from CVD in US adults. • The relationship between LCR and SC-MI presents a gradual decline initially, followed by a slight increase. • Lymphocyte count may be a useful biomarker in assessing inflammation and predicting CVD risk stratification. [ABSTRACT FROM AUTHOR]

Objective: The objective of this study was to determine the prognostic relevance, clinical characteristics, and 30-day outcomes associated with myocardial injury after noncardiac surgery (MINS) in major general surgery patients. Background: MINS has been independently associated with 30-day mortality after noncardiac surgery. The characteristics and prognostic importance of MINS in major general surgical patients have not been described. Methods: This was an international prospective cohort study of a representative sample of 22,552 noncardiac surgery patients 45 years or older, of whom 4490 underwent major general surgery in 24 centers in 13 countries. All patients had fifth-generation plasma high-sensitivity troponin T (hsTnT) concentrations measured during the first 3 postoperative days. MINS was defined as a hsTnT of 20--65 ng/L and absolute change >5 ng/L or hsTnT ≥65 ng/L secondary to ischemia. The objectives of the present study were to determine (1) whether MINS is prognostically important in major general surgical patients, (2) the clinical characteristics of major general surgical patients with and without MINS, (3) the 30-day outcomes for major general surgical patients with and without MINS, and (4) the proportion of MINS that would have gone undetected without routine postoperative monitoring. Results: The incidence of MINS in the major general surgical patients was 16.3% (95% CI, 15.3--17.4%). Thirty-day all-cause mortality in the major general surgical cohort was 6.8% (95% CI, 5.1%--8.9%) in patients with MINS compared with 1.2% (95% CI, 0.9%--1.6%) in patients without MINS (P< 0.01). MINS was independently associated with 30- day mortality in major general surgical patients (adjusted odds ratio 4.7, 95% CI, 3.0--7.4). The 30-day mortality was higher both among MINS patients with no ischemic features (ie, no ischemic symptoms or electrocardiogram findings) (5.4%, 95% CI, 3.7%--7.7%) and among patients with 1 or more clinical ischemic features (10.6%, 95% CI, 6.7%--15.8%). The proportion of major general surgical patients who had MINS without ischemic symptoms was 89.9% (95% CI, 87.5--92.0). Conclusions: Approximately 1 in 6 patients experienced MINS after major general surgery. MINS was independently associated with a nearly 5-fold increase in 30-day mortality. The vast majority of patients with MINS were asymptomatic and would have gone undetected without routine postoperative troponin measurement. [ABSTRACT FROM AUTHOR]

The incidence, prevalence, and economic burden of heart failure have continued to increase worldwide. It remains unclear whether LCZ696 can ameliorate calcium reuptake in the sarcoplasmic reticulum via the sarcoplasmic endoplasmic reticulum calcium ion-ATPase 2α (SERCA2α)-dependent pathway during cardiac diastole. We investigated whether LCZ696 could ameliorate tachycardia-induced myocardial injury by modulating cardiac SERCA2α levels. A tachycardia-induced myocardial injury model was established by daily intraperitoneal administration of 60 mg/kg isoprenaline (ISO) for 2 weeks. LCZ696 was orally administered for the following 4 weeks. SERCA2α and calcium ion (Ca2+)-related protein expression was assessed by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting. For additional in vitro studies, HL-1 cardiomyocytes were used. A SERCA2α overexpression vector was constructed and transfected into HL-1 cells. The expression of SERCA2α and Ca2+-related proteins were also measured using qRT-PCR and western blotting. Our in vivo results demonstrated that myocardial injury was successfully induced by intraperitoneal administration of ISO. The expression of both SERCA2α - and Ca2+-related proteins was impaired. Oral administration of LCZ696 increased the expression of SERCA2α, alleviated Ca2+-related protein impairment and cardiac Ca2+ dyshomeostasis, and ameliorated myocardial injury. These results were compared with our in vitro findings. Ca2+-related proteins are affected by the overexpression of SERCA2α. LCZ696 improved tachycardia-induced myocardial injury by increasing SERCA2α expression, which reversed the development of heart failure in ISO-induced mice. These results provide new insights into how sustained LCZ696 treatment in heart failure improves cardiac function through intracellular Ca2+-regulatory mechanisms. [ABSTRACT FROM AUTHOR]

Objective: To assess whether the Surgical Apgar Score (SAS) improves re-estimation of perioperative cardiac risk. Background: The SAS is a novel risk index that integrates three relevant and easily measurable intraoperative parameters (blood loss, heart rate, mean arterial pressure) to predict outcomes. The incremental prognostic value of the SAS when used in combination with standard preoperative risk indices is unclear. Methods: We conducted a retrospective cohort study of adults (18 years and older) who underwent elective noncardiac surgery at a quaternary care hospital in Canada (2009–2014). The primary outcome was postoperative acute myocardial injury. The SAS (range 0–10) was calculated based on intraoperative estimated blood loss, lowest mean arterial pressure, and lowest heart rate documented in electronic medical records. Incremental prognostic value of the SAS when combined with the Revised Cardiac Risk Index was assessed based on discrimination (c-statistic), reclassification (integrated discrimination improvement, net reclassification index), and clinical utility (decision curve analysis). Results: The cohort included 16,835 patients, of whom 607 (3.6%) patients had acute postoperative myocardial injury. Addition of the SAS to the Revised Cardiac Risk Index improved risk estimation based on the integrated discrimination improvement [2.0%; 95% confidence interval (CI): 1.5%–2.4%], continuous net reclassification index (54%; 95% CI: 46%–62%), and c-index, which increased from 0.68 (95% CI: 0.65–0.70) to 0.75 (95% CI: 0.73–0.77). On decision curve analysis, addition of the SAS to the Revised Cardiac Risk Index resulted in a higher net benefit at all decision thresholds. Conclusions: When combined with a validated preoperative risk index, the SAS improved the accuracy of cardiac risk assessment for noncardiac surgery. Further research is needed to delineate how intraoperative data can better guide postoperative decision-making. [ABSTRACT FROM AUTHOR]

Despite different prevalence, pathobiology, and prognosis between etiologically distinct myocardial infarction (MI) subtypes, prospective study of risk factor for MI in large NHLBI-sponsored cardiovascular cohorts is limited to acute MI as a singular entity. Therefore, we sought to utilize the Multi-Ethnic Study of Atherosclerosis (MESA), a large prospective primary prevention cardiovascular study, to define the incidence and risk factor profile of individual myocardial injury subtypes. We describe the rationale and design of re-adjudicating 4,080 events that occurred over the first 14 years of follow-up in MESA for the presence and subtype of myocardial injury as defined by the Fourth Universal Definition of MI: MI type 1 to 5, acute non-ischemic myocardial injury, and chronic myocardial injury. The project utilizes a 2-physician adjudication process via examination of medical records, abstracted data collection forms, cardiac biomarker results, and electrocardiograms of all relevant clinical events. Comparison of the magnitude and direction of associations between baseline traditional and novel cardiovascular risk factors with incident and recurrent acute MI subtypes and acute non-ischemic myocardial injury events will be made. This project will result in one of the first large prospective cardiovascular cohort with modern classification of acute MI subtypes, as well as a full accounting of non-ischemic myocardial injury events, with implications for numerous ongoing and future studies in MESA. By creating precise MI phenotypes, and defining their epidemiology, this project will allow for discovery of novel pathobiology-specific risk factors, allow for development of more accurate risk prediction, and suggest more targeted preventive strategies. [ABSTRACT FROM AUTHOR]

The Valve Academic Research Consortium (VARC)-3 definition for myocardial injury after transcatheter aortic valve replacement (TAVR) lacks of clinical validation. This study sought to determine the incidence, predictors, and clinical impact of periprocedural myocardial injury (PPMI) following TAVR as defined by recent VARC-3 criteria. We included 1,394 consecutive patients who underwent TAVR with a new-generation transcatheter heart valve. High-sensitivity troponin levels were assessed at baseline and within 24 hours after the procedure. PPMI was defined according to VARC-3 criteria as an increase ≥70 times in troponin levels (vs ≥15 times according to the VARC-2 definition). Baseline, procedural, and follow-up data were prospectively collected. PPMI was diagnosed in 193 (14.0%) patients. Female sex and peripheral artery disease were independent predictors of PPMI (P < 0.01 for both). PPMI was associated with a higher risk of mortality at 30-day (HR: 2.69, 95% CI: 1.50-4.82; P = 0.001) and 1-year (for all-cause mortality, HR: 1.54; 95% CI: 1.04-2.27; P = 0.032; for cardiovascular mortality, HR: 3.04; 95% CI: 1.68-5.50; P < 0.001) follow-up. PPMI according to VARC-2 criteria had no impact on mortality. About 1 out of 10 patients undergoing TAVR in the contemporary era had PPMI as defined by recent VARC-3 criteria, and baseline factors like female sex and peripheral artery disease determined an increased risk. PPMI had a negative impact on early and late survival. Further studies on the prevention of PPMI post-TAVR and implementing measures to improve outcomes in PPMI patients are warranted. [Display omitted] [ABSTRACT FROM AUTHOR]

Myocardial injury in patients with COVID-19 and suspected cardiac involvement is not well understood. The purpose of this study was to characterize myocardial injury in a multicenter cohort of patients with COVID-19 and suspected cardiac involvement referred for cardiac magnetic resonance (CMR). This retrospective study consisted of 1,047 patients from 18 international sites with polymerase chain reaction–confirmed COVID-19 infection who underwent CMR. Myocardial injury was characterized as acute myocarditis, nonacute/nonischemic, acute ischemic, and nonacute/ischemic patterns on CMR. In this cohort, 20.9% of patients had nonischemic injury patterns (acute myocarditis: 7.9%; nonacute/nonischemic: 13.0%), and 6.7% of patients had ischemic injury patterns (acute ischemic: 1.9%; nonacute/ischemic: 4.8%). In a univariate analysis, variables associated with acute myocarditis patterns included chest discomfort (OR: 2.00; 95% CI: 1.17-3.40, P = 0.01), abnormal electrocardiogram (ECG) (OR: 1.90; 95% CI: 1.12-3.23; P = 0.02), natriuretic peptide elevation (OR: 2.99; 95% CI: 1.60-5.58; P = 0.0006), and troponin elevation (OR: 4.21; 95% CI: 2.41-7.36; P < 0.0001). Variables associated with acute ischemic patterns included chest discomfort (OR: 3.14; 95% CI: 1.04-9.49; P = 0.04), abnormal ECG (OR: 4.06; 95% CI: 1.10-14.92; P = 0.04), known coronary disease (OR: 33.30; 95% CI: 4.04-274.53; P = 0.001), hospitalization (OR: 4.98; 95% CI: 1.55-16.05; P = 0.007), natriuretic peptide elevation (OR: 4.19; 95% CI: 1.30-13.51; P = 0.02), and troponin elevation (OR: 25.27; 95% CI: 5.55-115.03; P < 0.0001). In a multivariate analysis, troponin elevation was strongly associated with acute myocarditis patterns (OR: 4.98; 95% CI: 1.76-14.05; P = 0.003). In this multicenter study of patients with COVID-19 with clinical suspicion for cardiac involvement referred for CMR, nonischemic and ischemic patterns were frequent when cardiac symptoms, ECG abnormalities, and cardiac biomarker elevations were present. [Display omitted] [ABSTRACT FROM AUTHOR]

Perioperative atrial fibrillation (AF) and myocardial injury after noncardiac surgery (MINS) are common complications after noncardiac surgery. Inflammation has been implicated in the pathogenesis of both disorders. The COP-AF trial tests the hypothesis that colchicine reduces the incidence of perioperative AF and MINS in patients undergoing major noncardiac thoracic surgery. The 'COlchicine for the Prevention of Perioperative Atrial Fibrillation' (COP-AF) trial is an international, blinded, randomized trial that compares colchicine to placebo in patients aged at least 55 years and undergoing major noncardiac thoracic surgery with general anesthesia. Exclusion criteria include a history of AF and a contraindication to colchicine (eg, severe renal dysfunction). Oral colchicine at a dose of 0.5 mg or matching placebo is given within 4 hours before surgery. Thereafter, patients receive colchicine 0.5 mg or placebo twice daily for a total of 10 days. The 2 independent co-primary outcomes are clinically important perioperative AF (including atrial flutter) and MINS during 14 days of follow-up. The main safety outcomes are sepsis or infection and non-infectious diarrhea. We aim to enroll 3,200 patients from approximately 40 sites across 11 countries to have at least 80% power for the independent evaluation of the 2 co-primary outcomes. The COP-AF main results are expected in 2023. COP-AF is a large randomized and blinded trial designed to determine whether colchicine reduces the risk of perioperative AF or MINS in patients who have major noncardiac thoracic surgery. [Display omitted] [ABSTRACT FROM AUTHOR]

Myocardial hypoxia is the low oxygen tension in the heart tissue implicated in many diseases, including ischemia, cardiac dysfunction, or after heart procurement for transplantation. Oxygen-generating microparticles have recently emerged as a potential strategy for supplying oxygen to sustain cell survival, growth, and tissue functionality in hypoxia. Here, we prepared oxygen-generating microparticles with poly D,L-lactic-co-glycolic acid, and calcium peroxide (CPO), which yielded a continuous morphology capable of sustained oxygen release for up to 24 h. We demonstrated that CPO microparticles increased primary rat cardiomyocyte metabolic activity while not affecting cell viability during hypoxia. Moreover, hypoxia-inducible factor (HIF)-1α, which is upregulated during hypoxia, can be downregulated by delivering oxygen using CPO microparticles. Single-cell traction force microscopy data demonstrated that the reduced energy generated by hypoxic cells could be restored using CPO microparticles. We engineered cardiac tissues that showed higher contractility in the presence of CPO microparticles compared to hypoxic cells. Finally, we observed reduced myocardial injuries in ex vivo rabbit hearts treated with CPO microparticles. In contrast, an acute early myocardial injury was observed for the hearts treated with control saline solution in hypoxia. In conclusion, CPO microparticles improved cell and tissue contractility and gene expression while reducing hypoxia-induced myocardial injuries in the heart. Oxygen-releasing microparticles can reduce myocardial ischemia, allograft rejection, or irregular heartbeats after heart transplantation. Here we present biodegradable oxygen-releasing microparticles that are capable of sustained oxygen release for more than 24 hrs. We then studied the impact of sustained oxygen release from microparticles on gene expresseion and cardiac cell and tissue function. Previous studies have not measured cardiac tissue or cell mechanics during hypoxia, which is important for understanding proper cardiac function and beating. Using traction force microscopy and an engineered tissue-on-a-chip, we demonstrated that our oxygen-releasing microparticles improve cell and tissue contractility during hypoxia while downregulating the HIF-1α expression level. Finally, using the microparticles, we showed reduced myocardial injuries in rabbit heart tissue, confirming the potential of the particles to be used for organ transplantation or tissue engineering. [Display omitted] [ABSTRACT FROM AUTHOR]

Background: Galectin-3, a biomarker of inflammation and fibrosis, can be associated with renal and myocardial damage and dysfunction in patients with acute heart failure (AHF).Methods and Results: We retrospectively analyzed 790 AHF patients enrolled in the AKINESIS study. During hospitalization, patients with galectin-3 elevation (> 25.9 ng/ml) on admission more frequently had acute kidney injury (assessed by KDIGO criteria), renal tubular damage (peak urine neutrophil gelatinase-associated lipocalin [uNGAL] >150 ng/dl) and myocardial injury (≥ 20% increase in the peak high sensitivity cardiac troponin I [hs-cTnI] value compared to admission). They less frequently had ≥ 30% reduction in B-type natriuretic peptide from admission to last measured value. In multivariable linear regression analysis, galectin-3 was negatively associated with estimated glomerular filtration rate and positively associated with uNGAL and hs-cTnI. Higher galectin-3 was associated with renal replacement therapy, inotrope use and mortality during hospitalization. In univariable Cox regression analysis, higher galectin-3 was associated with increased risk for the composite of death or HF rehospitalization and death alone at one-year. After multivariable adjustment, higher galectin-3 was only associated with death.Conclusions: In patients with AHF, higher galectin-3 values were associated with renal dysfunction, renal tubular damage and myocardial injury, and predicted worse outcomes. [ABSTRACT FROM AUTHOR]

The Amami rabbit (Pentalagus furnessi) is found only on the two islands of Amami-Ōshima and Tokunoshima in southwest Japan. It has a primitive appearance and ecology, is an evolutionarily valuable animal and has been assigned to the International Union for Conservation of Nature Red List of Threatened Species. We describe a case with mild purulent wounds on the distal digital skin of both forelimbs and multiple nodular lesions in various organs, including the heart and kidney. Microscopically, the heart lesions were characterized by disruption of the mitral valve and multifocal myocardial necrosis and abscesses due to infection with gram-positive cocci. Similar bacterial infarctions were also found in other organs, including the kidneys. The bacteria were identified as Staphylococcus aureus by immunohistochemical and molecular biological examinations. This first report of infective endocarditis and systemic infarctions caused by S. aureus in an Amami rabbit indicates the importance of monitoring purulent injuries, even if mild, to prevent secondary infections in this species. [ABSTRACT FROM AUTHOR]

Small ubiquitin-related modifier (SUMOylation) is a dynamic post-translational modification that maintains cardiac function and can protect against a hypertrophic response to cardiac pressure overload. However, the function of SUMOylation after myocardial infarction (MI) and the molecular details of heart cell responses to SUMO1 deficiency have not been determined. In this study, we demonstrated that SUMO1 protein was inconsistently abundant in different cell types and heart regions after MI. However, SUMO1 knockout significantly exacerbated systolic dysfunction and infarct size after myocardial injury. Single-nucleus RNA sequencing revealed the differential role of SUMO1 in regulating heart cells. Among cardiomyocytes, SUMO1 deletion increased the Nppa + Nppb + Ankrd1 + cardiomyocyte subcluster proportion after MI. In addition, the conversion of fibroblasts to myofibroblasts subclusters was inhibited in SUMO1 knockout mice. Importantly, SUMO1 loss promoted proliferation of endothelial cell subsets with the ability to reconstitute neovascularization and expressed angiogenesis-related genes. Computational analysis of ligand/receptor interactions suggested putative pathways that mediate cardiomyocytes to endothelial cell communication in the myocardium. Mice preinjected with cardiomyocyte-specific AAV-SUMO1, but not the endothelial cell-specific form, and exhibited ameliorated cardiac remodeling following MI. Collectively, our results identified the role of SUMO1 in cardiomyocytes, fibroblasts, and endothelial cells after MI. These findings provide new insights into SUMO1 involvement in the pathogenesis of MI and reveal novel therapeutic targets. [Display omitted] • SUMO1 deficiency exacerbated systolic dysfunction and infarct size after myocardial injury. • SnRNA-seq showed cell-specific effects of SUMO1 signaling in infarcted myocardium. [ABSTRACT FROM AUTHOR]

Acute ST-segment elevation myocardial infarction (STEMI) has effects on the myocardium beyond the immediate infarcted territory. However, pathophysiologic changes in the noninfarcted myocardium and their prognostic implications remain unclear. The purpose of this study was to evaluate the long-term prognostic value of acute changes in both infarcted and noninfarcted myocardium post-STEMI. Patients with acute STEMI undergoing primary percutaneous coronary intervention underwent evaluation with blood biomarkers and cardiac magnetic resonance (CMR) at 2 days and 6 months, with long-term follow-up for major adverse cardiac events (MACE). A comprehensive CMR protocol included cine, T2-weighted, T2∗, T1-mapping, and late gadolinium enhancement (LGE) imaging. Areas without LGE were defined as noninfarcted myocardium. MACE was a composite of cardiac death, sustained ventricular arrhythmia, and new-onset heart failure. Twenty-two of 219 patients (10%) experienced an MACE at a median of 4 years (IQR: 2.5-6.0 years); 152 patients returned for the 6-month visit. High T1 (>1250 ms) in the noninfarcted myocardium was associated with lower left ventricular ejection fraction (LVEF) (51% ± 8% vs 55% ± 9%; P = 0.002) and higher NT-pro-BNP levels (290 pg/L [IQR: 103-523 pg/L] vs 170 pg/L [IQR: 61-312 pg/L]; P = 0.008) at 6 months and a 2.5-fold (IQR: 1.03-6.20) increased risk of MACE (2.53 [IQR: 1.03-6.22]), compared with patients with normal T1 in the noninfarcted myocardium (P = 0.042). A lower T1 (<1,300 ms) in the infarcted myocardium was associated with increased MACE (3.11 [IQR: 1.19-8.13]; P = 0.020). Both noninfarct and infarct T1 were independent predictors of MACE (both P = 0.001) and significantly improved risk prediction beyond LVEF, infarct size, and microvascular obstruction (C-statistic: 0.67 ± 0.07 vs 0.76 ± 0.06, net-reclassification index: 40% [IQR: 12%-64%]; P = 0.007). The acute responses post-STEMI in both infarcted and noninfarcted myocardium are independent incremental predictors of long-term MACE. These insights may provide new opportunities for treatment and risk stratification in STEMI. [Display omitted] [ABSTRACT FROM AUTHOR]

Background: Hypothermia is a crucial environmental factor that elevates the risk of cardiovascular disease, but the underlying effect is unclear. Objectives: This study examined the role of cold stress (CS) in cardiac injury and its underlying mechanisms. Methods: In this study, a chronic CS-induced myocardial injury model was used; mice were subjected to chronic CS (4°C) for three hours per day for three weeks. Results: CS could result in myocardial injury by inducing the levels of heat shock proteins 70 (HSP70), enhancing the generation of creatine phosphokinase-isoenzyme (CKMB) and malondialdehyde (MDA), increasing the contents of tumor necrosis factor-α (TNF-α), high mobility group box 1 (HMGB1) interleukin1b (IL-1β), IL-18, IL-6, and triggering the depletion of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Multiple signaling pathways were activated by cold exposure, including pyroptosis-associated NOD-like receptor 3 (NLRP3)-regulated caspase-1-dependent/Gasdermin D (GSDMD), inflammation-related toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)-mediated nuclear factor kappa B (NF-κB), and mitogen-activated protein kinase (MAPK), as well as oxidative stressinvolved thioredoxin-1/thioredoxin-interacting protein (Txnip) signaling pathways, which play a pivotal role in myocardial injury resulting from hypothermia. Conclusions: These findings provide new insights into the increased risk of cardiovascular disease at extremely low temperatures. [ABSTRACT FROM AUTHOR]

High-sensitivity cardiac troponins expedite the evaluation of patients with chest pain in the emergency department. The utility of troponins extends beyond the acute coronary syndromes to accurate the diagnosis of myocardial injury. Troponins are best friends for physicians; however, they are a double-edged sword if not interpreted appropriately. Misdiagnosis is harmful with regard to patient outcomes. The present review focuses on the recent updates in the understanding and interpretation of high-sensitivity troponins in various acute clinical settings. Common mistakes and gray zones in the interpretation of troponins, the concept of myocardial injury versus infarction, newer entities like myocardial infarction (MI) with Nonobstructive Coronary Arteries, recent controversies over the definition of periprocedural MI, complementary role of imaging in the diagnosis of myocardial injury and the role of troponins in the current COVID-19 pandemic are discussed. [ABSTRACT FROM AUTHOR]

Objective: To explore the therapeutic efficacy of L-carvone from Mentha spicata L. leaf extracts against isoproterenol-induced cardiac hypertrophy in rats. Methods: Isoproterenol (5 mg/kg) was injected intraperitoneally into rats for one month to induce cardiac hypertrophy. L-carvone (25 and 100 mg/kg) was administered orally to treat cardiac hypertrophy. The cardioprotective activity of L-carvone was evaluated by electrocardiogram, histopathological analysis as well as determination of biochemical parameters and enzymatic markers. Results: L-carvone from Mentha spicata L. at 25 and 100 mg/kg ameliorated isoproterenol-induced cardiac hypertrophy, as evidenced by reduced QRS interval on electrocardiogram, and decreased heart weight and heart index. In addition, both doses of L-carvone markedly lowered the levels of glucose, total protein, low-density lipoprotein cholesterol, aspartate transaminase, alanine transaminase, lactate dehydrogenase, creatine kinase MB, troponin-Ⅰ, N-terminal pro-B type natriuretic peptide and triglycerides while increasing high-density lipoprotein cholesterol and lipase level (P<0.05). Moreover, L-carvone alleviated contraction band necrosis, and reorganized the myofibrils with normal striations and myocytes as well as normal nuclei in cardiac histoarchitecture of rats with isoproterenol-induced cardiac hypertrophy. Conclusions: L-carvone from Mentha spicata L. leaf extract can restore abnormal cardiac function and may be further explored as a therapeutic agent against the deleterious effects of cardiac hypertrophy after further evaluation. [ABSTRACT FROM AUTHOR]

miR-135 is a highly conserved miRNA in mammals and includes miR-135a and miR-135b. Recent studies have shown that miR-135b is a key regulatory factor in cardio-cerebrovascular diseases. It is involved in regulating the pathological process of myocardial infarction, myocardial ischemia/reperfusion injury, cardiac hypertrophy, atrial fibrillation, diabetic cardiomyopathy, atherosclerosis, pulmonary hypertension, cerebral ischemia/reperfusion injury, Parkinson's disease, and Alzheimer's disease. Obviously, miR-135b is an emerging player in cardio-cerebrovascular diseases and is expected to be an important target for the treatment of cardio-cerebrovascular diseases. However, the crucial role of miR-135b in cardio-cerebrovascular diseases and its underlying mechanism of action has not been reviewed. Therefore, in this review, we aimed to comprehensively summarize the role of miR-135b and the signaling pathway mediated by miR-135b in cardio-cerebrovascular diseases. Drugs targeting miR-135b for the treatment of diseases and related patents, highlighting the importance of this target and its utility as a therapeutic target for cardio-cerebrovascular diseases, have been discussed. [Display omitted] • Targeting miR-135b is an efficient therapeutic approach for cardio-cerebrovascular diseases. • miR-135b exerts consistent protective effect against cerebrovascular diseases. • Abnormal expression of miR-135b may provide early indications for the progression of cardio-cerebrovascular diseases. [ABSTRACT FROM AUTHOR]

With the development of Type 1 diabetes mellitus (T1DM), various complications can be caused. Hyperglycemia affects the microenvironment of cardiomyocytes, changes endoplasmic reticulum homeostasis, triggers unfolding protein response and eventually promotes myocardial apoptosis. However, insulin therapy alone cannot effectively combat the complications caused by T1DM. Forty adult beagles were randomly divided into five groups: control group, diabetes mellitus group, insulin group, insulin combined with NAC group, and NAC group. 24-hour blood glucose, 120-day blood glucose, 120-day body weight, and serum FMN content were observed, furthermore, hematoxylin-eosin staining, Periodic acid Schiff reagent staining, and Sirius red staining of the myocardium were evaluated. The protein expressions of GRP78, ATF6, IRE1, PERK, JNK, CHOP, caspase 3, Bcl2, and Bax were detected. Results of the pathological section of myocardial tissue indicated that insulin combined with NAC therapy could improve myocardial pathological injury and glycogen deposition. Additionally, insulin combined with NAC therapy down-regulates the expression of GRP78, ATF6, IRE1, PERK, JNK, CHOP, caspase3, and Bax. These findings suggest that NAC has a phylactic effect on myocardial injury in beagles with T1DM, and the mechanism may be related to the improvement of endoplasmic reticulum stress-induced apoptosis. • A canine model of T1DM was established by the combination of alloxan and streptozotocin. • NAC combined with insulin therapy maintained glucose stability better than insulin therapy alone. • NAC can reduce myocardial injury by regulating ERs and apoptosis in diabetes myocardium. • NAC can be used as an adjuvant drug for the treatment of T1DM to alleviate the complications of T1DM. [ABSTRACT FROM AUTHOR]

Nimbolide has been demonstrated to possess protective properties against gestational diabetes mellitus and diabetic retinopathy. However, the role and molecular mechanism of nimbolide in diabetic cardiomyopathy (DCM) remain unknown. Diabetes was induced in rats via a single injection of streptozotocin (STZ) and then the diabetic rats were administered nimbolide (5 mg/kg and 20 mg/kg) or dimethyl sulfoxide daily for 12 weeks. H9c2 cardiomyocytes were exposed to high glucose (25 mM glucose) to mimic DCM in vitro. The protective effects of nimbolide against DCM were evaluated in vivo and in vitro. The potential molecular mechanism of nimbolide in DCM was further explored. We found that nimbolide dose-dependently decreased blood glucose and improved body weight of diabetic rats. Additionally, nimbolide dose-dependently improved cardiac function, alleviated myocardial injury/fibrosis, and inhibited endoplasmic reticulum (ER) stress and apoptosis in diabetic rats. Moreover, nimbolide dose-dependently improved mitochondrial function and activated the Akt/mTOR signaling. We consistently demonstrated the cardioprotective effects of nimbolide in an in vitro model of DCM. The involvement of ER stress and mitochondrial pathways were further confirmed by using inhibitors of ER stress and mitochondrial division. By applying a specific Akt inhibitor SC66, the cardioprotective effects of nimbolide were partially blocked. Our study indicated that nimbolide alleviated DCM by activating Akt/mTOR pathway. Nimbolide may be a novel therapeutic agent for DCM treatment. • Nimbolide halted the progression of DCM in animal models. • The cardioprotective effects of nimbolide were demonstrated in vitro. • Nimbolide inhibited the Akt/mTOR signaling in vivo and in vitro. • Akt inhibitor SC66 partially blocked the cardioprotective effects of nimbolide. [ABSTRACT FROM AUTHOR]

Myocardial injury (MI) after acute ischemic stroke (AIS) poses a significant threat to patient prognosis. However, effective intervention strategies are currently lacking. To elucidate the mechanism of MI after AIS and effects of Naoxintong capsule (NXT) therapy. In vivo , after a rat model of middle cerebral artery occlusion (MCAO)-induced MI was established and assessed. NXT was administered prophylactically to evaluate its pharmacodynamic effects and mechanisms. In vitro , a noradrenaline (NA)-induced damage cell model was constructed. Subsequently, the NXT was applied to the cell models to examine its cardioprotective effects and potential mechanisms. The in vivo findings revealed that following MCAO, there was a notable upregulation of TH expression in the rat brain, which subsequently triggered an increase in serum levels of various biomarkers, including AD, NA, AST, cTnT, CK-MB, and NT-proBNP. Histological analysis employing H&E staining and TUNEL assay disclosed significant pathological alterations and an escalation in apoptotic activity within the myocardial tissue. The myocardial tissue exhibited elevated levels of MDA alongside diminished CAT activity. Additionally, a marked increase in the Bax/Bcl-2 ratio, Cytochrome C release, and Caspase-3 activation was observed, all of which are indicative of heightened apoptotic activity. Administration of the NXT intervention successfully attenuated TH expression in the brains of rats subjected to MCAO, consequently leading to a reduction in circulating levels of catecholamines (CAs). NXT also exhibited significant efficacy at ameliorating cardiac oxidative stress and reducing apoptosis. In vitro , stimulation with NA led to an increase in ROS levels and calcium ion concentration in H9c2 cardiomyocytes. However, the administration of NXT has been found to effectively alleviate these adverse effects, thereby protecting H9c2 cardiomyocytes from the deleterious consequences of oxidative stress and calcium dyshomeostasis. Overall, this study has demonstrated that increased CAs synthesis in the brain after AIS in experimental rats led to a surge in circulating CAs, ultimately leading to MI. NXT can alleviate MI due to cerebral ischemia by increasing improving brain catecholamine synthesis, cardiac oxidative stress, and apoptosis. The potential mechanism of NXT intervention on MI after AIS is multifaceted. NXT may ameliorate MI induced by AIS by improving oxidative stress levels, reducing cell apoptosis, and down-regulating the β1-AR-Gs-AC-cAMP-PKA pathway. simultaneously, NXT may regulate MI caused by AIS by reducing CAs synthesis in the brain by suppressing TH expression. Consequently, NXT exhibits a dual effect of simultaneously improving exacerbation of brain CAs synthesis and cardiac oxidative stress and apoptosis resulting from cerebral ischemia, ultimately alleviating AIS-induced MI. [Display omitted] [ABSTRACT FROM AUTHOR]

Introduction: Albeit described since 1763, cardiac contusions is still an under-recognised clinical condition in the acute care setting. This evidence-based review aims to provide an overview of the topic by focusing on etiopathogenesis, classification and clinical presentation of patients with cardiac contusions, as well as on the diagnostic work-up and therapy options available for this subset population in the acute care setting.Methods: A targeted research strategy was performed using PubMed, MEDLINE, Embase and Cochrane Central databases up to June 2022. The literature search was conducted using the following keywords (in Title and/or Abstract): ("cardiac" OR "heart" OR "myocardial") AND ("contusion"). All available high-quality resources written in English and containing information on epidemiology, etiopathogenesis, clinical findings, diagnosis and management of cardiac contusions were included in our research.Results: Biochemical samples of cardiac troponins together with a 12‑lead ECG appear to be sufficient screening tools in hemodynamically stable subjects, while cardiac ultrasound provides a further diagnostic clue for patients with hemodynamic instability or those more likely to have a significant cardiac contusion.Conclusions: The management of patients with suspected cardiac contusion remains a challenge in clinical practice. For this kind of patients a comprehensive diagnostic approach and a prompt emergency response are required, taking into consideration the degree of severity and clinical impairment of associated traumatic injuries. [ABSTRACT FROM AUTHOR]

Ischemic heart disease and the resulting heart failure remain the leading causes of death and disability worldwide. This study aimed to investigate the role of miR-1229-5p in serum extracellular vesicles (EVs) mediated myocardial protection by constructing a hypoxia/reoxygenation model (HR) in H9c2 cells. Cardiomyocytes were cultured and divided into different treatment groups: control group, HR group, serum-EVs group, and serum-EVs + miR-1229-5p inhibitor group. The expression levels of miR-1229-5p were detected using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The changes in cell proliferation and apoptosis were detected by MTT assay and flow cytometry. The myocardial injuryrelated indicators, cardiac troponin I (cTnI), creatinine kinase MB (CK-MB), and lactate dehydrogenase (LDH), were measured by enzyme-linked immunosorbent assay (ELISA). Finally, the luciferase reporter assay was used to verify the miR-1229-5p target. The proliferation of myocardial cells in the HR group was reduced, the number of apoptotic cells was increased, and myocardial injury indicators concentration was decreased. Transfection of miR-1229-5p inhibitor under serum-EVs treatment reduced the protective effect of serum-EVs on myocardial cell injury, decreased cell proliferation, increased the number of apoptotic cells, and increased myocardial injury indicator concentration. Additionally, FOXO4 may be the target of miR-1229-5p. Our data suggest that serum-EVs alleviate HR-induced cardiomyocyte injury by regulating miR-1229-5p/FOXO4. [ABSTRACT FROM AUTHOR]

Pre-excitation syndrome can either mimic or mask myocardial infarction, making the diagnosis of acute myocardial infarction difficult. Herein, we report the case of a male patient with Wolf-Parkinson-White (WPW) syndrome who presented to our emergency department with severe chest pain. Non-ST-elevation myocardial infarction was suspected because of cardiac enzyme elevation and abnormal ST-T changes identified through electrocardiography. The patient underwent percutaneous coronary intervention; a left anterior descending artery stenotic lesion was dilated, and drug-eluting stents were implanted. One month later, he underwent successful radiofrequency catheter ablation for his accessory pathway and tachycardia. We present the series of electrocardiographic ST-T abnormalities to raise awareness of the value of diagnosing myocardial injury early in patients with WPW syndrome. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The severe acute respiratory syndrome coronavirus 2 (SARSCoV-2), also known as COVID-19, a viral outbreak that started in December 2019, eventually lead to a worldwide pandemic. COVID-19 usually presents with flu-like symptoms, such as headaches, dry cough, fever, fatigue, myalgia, shortness of breath, diarrhea and loss of smell or taste. However, it can also have major effects on the cardiovascular system. Based on the available relevant literature, we aimed to elaborate the possible mechanisms influencing cardiovascular damage, myocardial injury and thromboembolic disease process in particular. MATERIALS AND METHODS: After considering our inclusion and exclusion criteria, the systematic review included 8 studies in total. RESULTS: In general, underlying cardiovascular diseases were associated with poorer clinical outcomes. This may be due to immunological dysregulation. The disease outcomes were also positively correlated with the severity of the disease, especially with myocardial injury. Thus, cardiac biomarkers, such as Troponin T, CK-MB and myoglobin could be utilized in prediction algorithms for deciphering the clinical outcome in COVID-19 patients. CONCLUSIONS: Venous thromboembolisms were commonly encountered complications despite the administration of thromboprophylaxis, and they mostly presented as pulmonary embolisms, warranting the need for relevant investigations in hemodynamically unstable patients. However, more studies need to be conducted to better understand the mechanisms at play and the ensuing complications, to better treat COVID-19 patients. [ABSTRACT FROM AUTHOR]

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Exposure to fine particulate matter (PM 2.5) and polycyclic aromatic hydrocarbons (PAHs) is known to be associated with the polarization of pro-inflammatory macrophages and the development of various cardiovascular diseases. The pro-inflammatory polarization of resident cardiac macrophages (cMacs) enhances the cleavage of membrane-bound myeloid-epithelial-reproductive receptor tyrosine kinase (MerTK) and promotes the formation of soluble MerTK (solMER). This process influences the involvement of cMacs in cardiac repair, thus leading to an imbalance in cardiac homeostasis, myocardial injury, and reduced cardiac function. However, the relative impacts of PM 2.5 and PAHs on human cMacs have yet to be elucidated. In this study, we aimed to investigate the effects of PM 2.5 and PAH exposure on solMER in terms of myocardial injury and left ventricular (LV) systolic function in healthy children. A total of 258 children (aged three to six years) were recruited from Guiyu (an area exposed to e-waste) and Haojiang (a reference area). Mean daily PM 2.5 concentration data were collected to calculate the individual chronic daily intake (CDI) of PM 2.5. We determined concentrations of solMER and creatine kinase MB (CKMB) in plasma, and hydroxylated PAHs (OH-PAHs) in urine. LV systolic function was evaluated by stroke volume (SV). Higher CDI values and OH-PAH concentrations were detected in the exposed group. Plasma solMER and CKMB were higher in the exposed group and were associated with a reduced SV. Elevated CDI and 1-hydroxynaphthalene (1-OHNa) were associated with a higher solMER. Furthermore, increased solMER concentrations were associated with a lower SV and higher CKMB. CDI and 1-OHNa were positively associated with CKMB and mediated by solMER. In conclusion, exposure to PM 2.5 and PAHs may lead to the pro-inflammatory polarization of cMacs and increase the risk of myocardial injury and systolic function impairment in children. Furthermore, the pro-inflammatory polarization of cMacs may mediate cardiotoxicity caused by PM 2.5 and PAHs. [Display omitted] • PM 2.5 and PAH exposure was higher in e-waste-exposed children. • Elevated soluble form of MerTK (solMER) in exposed children was observed. • PM 2.5 and PAH exposure was related to reduced left ventricular systolic function. • PM 2.5 and PAH exposure was related to myocardial injury and mediated by solMER. [ABSTRACT FROM AUTHOR]

Background: Magnolol is a component of the bark of Magnolia officinalis, which is a traditional herbal remedy used in China. In this study, we investigated whether magnolol can reduce myocardial injury induced by renal ischemia and reperfusion (I/R). Methods: Renal I/R was elicited by a 60-minute occlusion of the bilateral renal arteries and a 24-hour reperfusion in Sprague-Dawley rats. Magnolol was administered intravenously 10 minutes before renal I/R to evaluate its effects on myocardial injury induced by renal I/R. Results: Renal I/R significantly increased the serum levels of creatine phosphokinase (CPK), lactate dehydrogenase (LDH), and cardiac troponin I and caused myocardial damage. The terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive nuclei and caspase-3 activation was significantly increased in the myocardium, indicating increase of apoptosis. Echocardiography revealed left ventricular dysfunction, as evidenced by reduction of left ventricular ejection fraction and left ventricular fractional shortening. Furthermore, serum levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 were significantly elevated, while the IL-10 level was suppressed. However, intravenously, pretreatment with magnolol at doses of 0.003 and 0.006 mg/kg 10 minutes before renal I/R significantly prevented the increases of CPK, LDH, and cardiac troponin I levels, as well as the histological damage and the apoptosis in the myocardium. Echocardiography showed significant improvement of left ventricular function. Furthermore, the increases in TNF-α, IL-1β, and IL-6 and the decrease in IL-10 were significantly limited, while Bcl-2 was increased and Bax was decreased in the myocardium. Phosphorylation of Akt and extracellular signal-regulated kinases 1 and 2 was increased, while phosphorylation of p38 and c-Jun N-terminal kinase was reduced. Conclusion: Magnolol reduces myocardial injury induced by renal I/R. The underlying mechanisms for this effect might be related to modulation of the production of pro- and anti-inflammatory cytokines and the limiting of apoptosis. [ABSTRACT FROM AUTHOR]

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COVID-19 is associated with myocardial injury caused by ischemia, inflammation, or myocarditis. Cardiovascular magnetic resonance (CMR) is the noninvasive reference standard for cardiac function, structure, and tissue composition. CMR is a potentially valuable diagnostic tool in patients with COVID-19 presenting with myocardial injury and evidence of cardiac dysfunction. Although COVID-19–related myocarditis is likely infrequent, COVID-19–related cardiovascular histopathology findings have been reported in up to 48% of patients, raising the concern for long-term myocardial injury. Studies to date report CMR abnormalities in 26% to 60% of hospitalized patients who have recovered from COVID-19, including functional impairment, myocardial tissue abnormalities, late gadolinium enhancement, or pericardial abnormalities. In athletes post–COVID-19, CMR has detected myocarditis-like abnormalities. In children, multisystem inflammatory syndrome may occur 2 to 6 weeks after infection; associated myocarditis and coronary artery aneurysms are evaluable by CMR. At this time, our understanding of COVID-19–related cardiovascular involvement is incomplete, and multiple studies are planned to evaluate patients with COVID-19 using CMR. In this review, we summarize existing studies of CMR for patients with COVID-19 and present ongoing research. We also provide recommendations for clinical use of CMR for patients with acute symptoms or who are recovering from COVID-19. [Display omitted] • Given the high rate of acute cardiovascular abnormalities in COVID-19 reported in clinical and pathologic series, concern exists for long-term myocardial injury in convalescent patients. • We review existing studies of CMR in COVID-19 and discuss the use of CMR for the acute and convalescent patients, including athletes. • Existing evidence is limited by small cohort sizes; absence of longitudinal follow-up; and, in some cases, lack of appropriate controls. • Evaluation of emerging evidence from ongoing and planned international studies will be essential for more robust evidence-based clinical decision making. [ABSTRACT FROM AUTHOR]

Background: Clinical congestion is associated with adverse outcomes in patients with heart failure. The pathophysiological mediators of this association remain uncertain.Methods and Results: We prospectively enrolled a cohort of patients with heart failure and reduced left ventricular ejection fraction and performed a detailed clinical examination followed on the same day by an invasive right heart catheterization and blood sampling for biomarkers. High-sensitivity troponin T and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were measured. A clinical congestion score was calculated based on jugular venous pressure (cm H20 <10 = 0, 10-14 = 1, >14 = 2 points), bendopnea (0 vs 1), a third heart sound (0 vs 1), or peripheral edema (0-2). Congestion was categorized into tiers as absent (0 points), mild (1 point), or moderate to severe (≥ 2 points). We tested for associations of high-sensitivity troponin T, NT-proBNP, and elevated ventricular filling pressures with clinical congestion in both univariate and multivariable analyses. Of 153 participants, 65 (42%) had absent, 35 mild (23%), and 53 (35%) had moderate to severe clinical congestion. Congestion tier was associated with higher NT-proBNP and hs-troponin levels, and the right atrial pressure and pulmonary capillary wedge pressure (P < .001 for each). Increased congestion tier was also associated with the coexistent presence of elevated troponin T (≥52 ng/L), NT-proBNP (≥1000 pg/mL), and pulmonary capillary wedge pressure (≥22 mm Hg). Specifically, 78% of those with absent clinical congestion had 0 to 1 of these findings, whereas 75% of those with moderate-severe congestion had 2 or all 3 of these abnormalities (P < .001). An elevated hs-troponin was associated with mild or greater clinical congestion (odds ratio 3, 95% confidence interval 1.2-7.5, P = .02) in multivariable analysis adjusting for potential confounders including the right atrial pressure, pulmonary capillary wedge pressure, and NT-proBNP levels.Conclusions: Clinical congestion is a phenotype in which there is a high coexistent presence of elevated ventricular filling pressures, elevated natriuretic peptide levels, and subclinical myocardial injury. An elevated troponin was associated with clinical congestion in multivariable models that adjusted for ventricular filling pressures and natriuretic peptide levels. These data strengthen the evidence base for an association of elevated troponin with clinical congestion, suggesting that subclinical myocardial injury may be an important contributor to the pathophysiology of the congested state. [ABSTRACT FROM AUTHOR]

Other than respiratory disease, patients with coronavirus disease 2019 (COVID-19) commonly have cardiovascular manifestations, which are recognized as significant risk factors for increased mortality. COVID-19 patients may present with a wide spectrum of clinical presentations ranging from asymptomatic heart disease detected incidentally by cardiac investigations (troponin, BNP, and imaging) to cardiogenic shock and sudden cardiac death. In this broad clinical course, advanced imaging plays an important role in the diagnosis of different patterns of myocardial injury, risk stratification of COVID-19 patients, and in detecting potential cardiac side effects of the current treatments and vaccines against the severe acute respiratory syndrome. [ABSTRACT FROM AUTHOR]

Severe acute respiratory syndrome coronavirus-2 can affect the cardiovascular system yielding a wide range of complications, including acute myocardial injury. The myocardium can be damaged by direct viral invasion or indirect mechanisms, sustained by systemic inflammation, immune-mediated response, and dysregulation of the renin-angiotensin system. Myocardial injury affects about one-quarter of patients with COVID-19, can manifest even in the absence of previous cardiovascular disease, and is associated to higher mortality rates and long-term sequelae. This review describes the pathophysiological mechanisms of myocardial injury and infarction and discusses the main clinical outcomes and diagnostic challenges associated with myocardial damage during COVID-19. [ABSTRACT FROM AUTHOR]