Could extracellular vesicles derived from mesenchymal stem cells be a potential therapy for acute pancreatitis-induced cardiac injury?

Acute pancreatitis(AP)often leads to a high incidence of cardiac injury,posing significant challenges in the treatment of severe AP and contributing to increased mortality rates.Mesenchymal stem cells(MSCs)release bioactive molecules that participate in various inflammatory diseases.Similarly,extracellular vesicles(EVs)secreted by MSCs have garnered extensive attention due to their comparable anti-inflammatory effects to MSCs and their potential to avoid risks associated with cell transplantation.Recently,the therapeutic potential of MSCs-EVs in various inflammatory diseases,including sepsis and AP,has gained increasing recognition.Although preclinical research on the utilization of MSCs-EVs in AP-induced cardiac injury is limited,several studies have demonstrated the positive effects of MSCs-EVs in regulating inflammation and immunity in sepsis-induced cardiac injury and cardiovascular diseases.Furthermore,clinical studies have been conducted on the therapeutic application of MSCs-EVs for some other diseases,wherein the contents of these EVs could be deliberately modified through prior modulation of MSCs.Consequently,we hypothesize that MSCs-EVs hold promise as a potential therapy for AP-induced cardiac injury.This paper aims to discuss this topic.However,additional research is essential to comprehensively elucidate the underlying mechanisms of MSCs-EVs in treating AP-induced cardiac injury,as well as to ascertain their safety and efficacy.

Relation between Cardiac Injury and Elevated Levels of Inflammatory Biomarkers in Patients with Severe COVID-19

Background:Since early December 2019,coronavirus disease 2019(COVID-19)has emerged as a global pandemic and public health crisis.This study aims to explore the relationship between cardiac injury and infl ammatory biomarkers in patients with severe COVID-19.Methods:We collected data on 91 patients with a confi rmed diagnosis of severe COVID-19 from February 8 to March 31,2020.Demographic characteristics,clinical data,and in-hospital outcomes were compared.The relationship between cardiac injury and infl ammatory biomarkers was analyzed.Logistic regression was used to explore the independent risk factors for cardiac injury.Results:The mean age of all patients was 61 years±14 years.About half of the patients were male.Hypertension and coronary heart disease were more common in the cardiac injury group.The levels of infl ammatory biomarkers in patients who experienced cardiac injury were generally higher than the levels of those without cardiac injury,including interleukin-6,interleukin-2 receptor(IL-2R),procalcitonin,and high-sensitivity C-reactive protein.There were positive correlations between the levels of high-sensitivity troponin I and N-terminal prohormone of brain natriuretic peptide and the levels of infl ammatory biomarkers.Logistic regression shows that IL-2R(odds ratio 1.001,95%confi dence interval 1.000–1.002,P=0.045)and comorbidities(odds ratio 4.909,95%confi dence interval 1.231–19.579,P=0.024)are independent risk factors for cardiac injury in patients with severe COVID-19.Conclusion:High levels of infl ammatory biomarkers are associated with higher risk of cardiac injury in patients with severe COVID-19.IL-2R and comorbidities are predictors of cardiac injury.

Unstable cardiac injury complicated with septic shock—a challenge

Background:Road traffic accident accounts for 70%to 80%of the blunt cardiac injury.The true incidence varies in the literature due to non-uniform criteria for diagnosis.Case Presentation:Here,we describe the case of a young male presenting after blunt chest injury and hemodynamic instability.Initially,the patient had frequent episodes of arrhythmias and hypotension due to cardiac injury per se.However,he was stabilized by day 2.Subsequently,patient developed cellulitis followed by septic shock and succumbed to cellulitis on day 5 of injury.Conclusion:Sepsis is difficult to be diagnosed and treated in the presence of cardiac injury.Myocardial depression has been found in sepsis,which contributes as an added comorbidity in an already compromised heart function.Sepsis also interferes with the diagnosis and follow-up of progress of blunt cardiac injury.

Acupuncture Therapy Related Cardiac Injury

Cardiac injury is the most serious adverse event in acupuncture therapy. The causes include needling chest points near the heart, the cardiac enlargement and pericardial effusion that will enlarge the projected area on the body surface and make the proper depth of needling shorter, and the incorrect needling method of the points. Therefore, acupuncture practitioners must be familiar with the points of the heart projected area on the chest and the correct needling methods in order to reduce the risk of acupuncture therapy related cardiac injury.

Epileptic Seizure‑induced Cardiac Injury as a Cause of Sudden Unexpected Death in Epilepsy:Evidence from Pathological Analyses

Sudden unexpected death in epilepsy(SUDEP)is the most frequent cause of death in people with epilepsy.The detailed mechanisms of SUDEP have not been elucidated.Moreover,it is still difficult for clinicians to predict and prevent the occurrence of sudden death in patients with epilepsy.Seizure‑related cardiac complications were considered to play a significant role in the physiological changes that lead to SUDEP.This report described a case of sudden death of an 11‑year‑old boy with epilepsy.Detailed autopsy and pathological analyses were performed to determine the cause of death.Seizure‑induced myocardial fibrosis was observed and deemed to be the cause of SUDEP.This study clearly showed the importance of improving the protection of cardiac function in the reductions of sudden deaths among patients with epilepsy.In addition,further studies in the pathophysiology of patients with epilepsy may help in improving our understanding of the mechanisms of SUDEP and adding new insight into the development of seizure‑induced cardiovascular and respiratory changes that may contribute to sudden death in epileptics.

Traumatic cardiac injury： Experience from a level-1 trauma centre

Purpose： Traumatic cardiac injury （TCI） is a challenge for trauma surgeons as it provides a short thera- peutic window and the management is often dictated by the underlying mechanism and hemodynamic status, The current study is to evaluate the factors influencing the outcome of TCI. Methods： Prospectively maintained database of TCI cases admitted at a Level-I trauma center from July 2008 to June 2013 was retrospectively analyzed. Hospital records were reviewed and statistical analysis was performed using the SPSS version 15. Results： Out of 21 cases of TCI, 6 （28.6%） had isolated and 15 （71.4%） had associated injuries. Ratio be- tween blunt and penetrating injuries was 2：1 with male preponderance. Mean ISS was 31.95. Thirteen patients （62%） presented with features suggestive of shock. Cardiac tamponade was present in 12 （57%） cases and pericardiocentesis was done in only 6 cases of them. Overall 19 patients underwent surgery, Perioperatively 8 （38,1%） patients developed cardiac arrest and 7 developed cardiac arrhythmia. Overall survival rate was 71.4%. Mortality was related to cardiac arrest （p = 0.014）, arrhythmia （p = 0.014）, and hemorrhagic shock （p = 0.04）. The diagnostic accuracy of focused assessment by sonography in trauma （FAST） was 95.24%. Conclusion： High index of clinical suspicion based on the mechanism of injury, meticulous examination by FAST and early intervention could improve the overall outcome.

Changes of cTnI in myocardial ischemic and reperfusion injury during correction of cardiac defects in children

Objective The purpose of this study is to investgate changes of cTnI in myocardial ischemic and reperfusion injury during correction of cardiac defects in children. Methods From June, 1999 to May,2000,45 children (30 male, 15 female) undergoing correction of cardiac defects were divided into three groups randomly: group Ⅰ no myocardial ischemia,group Ⅱ myocardial ischemia less than 60 minutes, group Ⅲmyocardial ischemia 】 60 minutes. There were no significant differences in the three groups in age, sex ratio, C/T ratio, or left ventricular function. Blood samples for analysis were collected before skin incision and at time intervals up to 6 days postoperatively. Analysis of creatine kinase MB.LDH and cardiac-specific troponin I was used for the detection of myocardial damage. Meantime, the ECG was checked for myocardial infarction. After the reperfusion, myocardial tissue was obtained from the free wall of right ventricle myocardial structure studies. Results The level of cTnI was increased

SiO_(2) Induces Iron Overload and Ferroptosis in Cardiomyocytes in a Silicosis Mouse Model

Objective The aim of this study was to explore the role and mechanism of ferroptosis in SiO_(2)-induced cardiac injury using a mouse model.Methods Male C57BL/6 mice were intratracheally instilled with SiO_(2) to create a silicosis model.Ferrostatin-1(Fer-1)and deferoxamine(DFO)were used to suppress ferroptosis.Serum biomarkers,oxidative stress markers,histopathology,iron content,and the expression of ferroptosis-related proteins were assessed.Results SiO_(2) altered serum cardiac injury biomarkers,oxidative stress,iron accumulation,and ferroptosis markers in myocardial tissue.Fer-1 and DFO reduced lipid peroxidation and iron overload,and alleviated SiO_(2)-induced mitochondrial damage and myocardial injury.SiO_(2) inhibited Nuclear factor erythroid 2-related factor 2(Nrf2)and its downstream antioxidant genes,while Fer-1 more potently reactivated Nrf2 compared to DFO.Conclusion Iron overload-induced ferroptosis contributes to SiO_(2)-induced cardiac injury.Targeting ferroptosis by reducing iron accumulation or inhibiting lipid peroxidation protects against SiO_(2) cardiotoxicity,potentially via modulation of the Nrf2 pathway.

Upregulated IRF9 promotes cell apoptosis of hyperlipidemia acute pancreatitis with heart injury by regulating SIRT1

Hyperlipidemia acute pancreatitis(HLAP)is a significant cause of AP,characterized by recurrent attacks,more complications and high incidence and mortality.HLAP is often accompanied by single or multiple organ damage.Negative regulation of interferon-regulatory factor 9(IRF9)on sirtuin-1(SIRT1)contributes to a range of diseases.However,the function of IRF9 and SIRT1,and the relationship of the two in HLAP with heart injury remain to be illustrated so far.Animal models of HLAP were set up by feeding with high-fat chow and subsequently injecting 20%L-arginine intraperitoneally.The degree of pancreas and heart tissue injury was evaluated.Heart cell apoptosis was assayed by the TUNEL technique.IRF9,SIRT1,p53 and acetylated p53(Ac-p53)expression levels were measured by qRT-PCR and western blot.The correlation between SIRT1 and IRF9 expression levels was analyzed.Results showed that the damage degree in rat pancreas and heart tissues of AP and HLAP group was more distinctly and heart cell apoptosis was elevated.Pancreas,heart injury and cell apoptosis of the HLAP group were more remarkable than that of the AP group.Apparent increases of IRF9 and Ac-p53/p53 expression and a marked drop of SIRT1 expression were observed in the AP and HLAP group rather than NC and HLNC group.IRF9 and Ac-p53/p53 expression levels of the HLAP group were markedly raised compared with the AP group.SIRT1 expression of the HLAP group was obviously lower than that of the AP group.There was an inverse correlation between the decrease of SIRT1 and the increase of IRF9 in AP and HLAP groups.Based on the above findings,we drew a conclusion that in pancreatitis with heart injury,upregulated IRF9 inhibited SIRT1 expression,elevated the acetylation of p53,and increased myocardial cell apoptosis.Hyperlipidemia further exacerbated pancreas and heart injury and accelerated myocardial cell apoptosis.These results would furnish an experimental and theoretical basis to diagnose and therapy diseases.

Dengue hemorrhagic fever and cardiac involvement

Dengue viral infection(DVI)is one of the world’s most significant viral infections spreading.Most of the patients have been asymptomatic,with relatively benign clinical manifestations and outcomes.However,a small number of patients have progressed to severe dengue diseases,including hemorrhage,multi-organ impairment,and increased vascular leakage causing hypovolemic shock,which can cause cardiovascular collapse and death.Numerous lines of evidence have demonstrated that DVI could also cause cardiac dysfunction,arrhythmias,and severe myocarditis.The treatment for dengue hemorrhagic fever(DHF)patients remains symptomatic and supportive,with close monitoring of hemodynamic status.The contributory role of cardiac dysfunction in DHF patients has potentially critical implications on the management.This review will address the current knowledge of cardiac involvement in DHF patients and the management strategy to reduce the fatality outcome.

Research progress on ferroptosis in septic cardiac function injury

Sepsis is a common cause of death for critically ill patients in clinical practice,which can cause death of patients.Septic cardiac function injury refers to cardiac dysfunction caused by sepsis,which is directly related to the high mortality rate of sepsis.In recent years,it has found that ferroptosis is a new form of programmed cell death,which may be a potential mechanism for septic cardiac function injury.Therefore,we summarize the relevant evidence for ferroptosis in septic cardiac function injury,providing new ideas and directions for further research and treatment of septic cardiac functioninjury.

Effect of Xuebijing injection on myocardium during cardiopulmonary bypass:A prospective,randomized,double blind trial

BACKGROUND Cardiopulmonary bypass(CPB)is an essential procedure for maintaining the blood supply to vital organs in patients undergoing cardiac surgery.However,perioperative cardiac injury related to CPB remains a severe complication in these patients.Cardiac protection is important for patients undergoing CPB.AIM To evaluate the potential cardioprotective efficacy of the Chinese medicine preparation Xuebijing injection(XBJ)in patients undergoing CPB.METHODS Sixty patients undergoing cardiac surgery with CPB were randomly allocated to the XBJ and control groups(saline).XBJ was administered intravenously three times:12 h prior to surgery,at the beginning of the surgery,and 12 h after the second injection.Cardiac function was evaluated by echocardiography 48 h after surgery.Circulating inflammation-and oxidative-stress-related markers were measured.Clinical outcomes related to intensive care unit(ICU)stay were recorded.RESULTS Compared to control treatment,XBJ was associated with improved PaO2/FiO2 and cardiac systolic function,but reduced troponin I and creatine kinase fraction after surgery(all P<0.05).The circulating concentrations of tumor necrosis factor-α,interleukin(IL)-1βand IL-8 in the XBJ group were significantly lower than those in the control group(all P<0.05),whereas the circulating concentration of IL-10 was significantly higher in the XBJ group(P<0.05).In addition,the lengths of ICU stay and hospitalization after surgery tended to be shorter in the XBJ group than in the control group,although the differences were not significant.CONCLUSION Perioperative administration of XBJ was associated with attenuated cardiac injury during CPB,likely via anti-inflammatory and antioxidative mechanisms.

Phloretin-induced suppression of oxidative and nitrosative stress attenuates doxorubicin-induced cardiotoxicity in rats

Objective:To compare the cardioprotective efficacy of equimolar doses(50 mM/kg,p.o.)of phloretin and genistein against doxorubicin-induced cardiotoxicity in rats.Methods:Cardiotoxicity was induced in rats by intraperitoneal injection of 6 mg/kg doxorubicin on alternative days till the cumulative dose reached 30 mg/kg.This study included four treatment groups of rats(n=6):the control group(0.5%carboxymethyl cellulose solution-treated),the doxorubicin-treated group(0.5%carboxymethyl cellulose solution along with doxorubicin),the genistein-treated group(50 mM/kg/day;p.o.along with doxorubicin)and phloretin-treated group(50 mM/kg/day;p.o.along with doxorubicin).On the 10th day of dosing,rats were anesthetized for recording ECG,mean arterial pressure,and left ventricular function.Oxidative stress,nitric oxide levels,and inflammatory cytokines were estimated in the cardiac tissue.Cardiac function parameters(creatine kinase MB,lactate dehydrogenase,aspartate aminotransferase,and alanine transaminase)were estimated in the serum samples.Results:Phloretin treatment inhibited doxorubicin-induced oxidative stress and also reduced nitric oxide levels in cardiac tissues of rats.Phloretin administration attenuated doxorubicin-induced alterations in hemodynamic parameters(heart rate,mean arterial blood pressure,and left ventricular function)and suppressed the expression of pro-inflammatory cytokines.The cardiac injury markers like creatine kinase MB,lactate dehydrogenase,aspartate aminotransferase,and alanine transaminase were reduced by both genistein and phloretin.All these effects of phloretin were more prominent than genistein.Conclusions:Phloretin offers cardioprotection that is comparable to genistein,a clinically validated cardioprotectant against doxorubicin-induced cardiotoxicity.Further studies are needed to confirm and establish the therapeutic utility of phloretin as a chemopreventive adjuvant to doxorubicin chemotherapy.

Renewal of embryonic and neonatal-derived cardiac-resident macrophages in response to environmental cues abrogated their potential to promote cardiomyocyte proliferation via Jagged-1-Notch1

Cardiac-resident macrophages(CRMs)play important roles in homeostasis,cardiac function,and remodeling.Although CRMs play critical roles in cardiac regeneration of neonatal mice,their roles are yet to be fully elucidated.Therefore,this study aimed to investigate the dynamic changes of CRMs during cardiac ontogeny and analyze the phenotypic and functional properties of CRMs in the promotion of cardiac regeneration.During mouse cardiac ontogeny,four CRM subsets exist successively:CX3CR1+CCR2-Ly6C-MHCII-(MP1),CX3CR1lowCCR2lowLy6C-MHCII-(MP2),CX3CR1-CCR2+Ly6C+MHCII-(MP3),and CX3CR1+CCR2-Ly6C-MHCII+(MP4).MP1 cluster has different derivations(yolk sac,fetal liver,and bone marrow)and multiple functions population.Embryonic and neonatal-derived-MP1 directly promoted cardiomyocyte proliferation through Jagged-1-Notch1 axis and significantly ameliorated cardiac injury following myocardial infarction.MP2/3 subsets could survive throughout adulthood.MP4,the main population in adult mouse hearts,contributed to inflammation.During ontogeny,MP1 can convert into MP4 triggered by changes in the cellular redox state.These findings delineate the evolutionary dynamics of CRMs under physiological conditions and found direct evidence that embryonic and neonatal-derived CRMs regulate cardiomyocyte proliferation.Our findings also shed light on cardiac repair following injury.

Changes and significance of serum troponin in trauma patients: A retrospective study in a level I trauma center

BACKGROUND: Elevated troponin I(TnI) is common among trauma patients. TnI is an indicator of myocardial injury, but clinical diagnosis of blunt cardiac injury cannot be based solely on an increase in TnI. Therefore, this study aims to explore the changes and clinical significance of serum TnI in trauma patients. METHODS: The clinical data of consecutive trauma patients admitted to our trauma center between July 1, 2017 and July 31, 2020 were retrospectively analyzed. According to TnI levels within 24 hours of admission, patients were divided into the elevated and normal TnI groups. According to the TnI levels after 7 days of admission, a graph depicting a change in trend was drawn and then analyzed whether TnI was related to in-hospital mortality. RESULTS: A total of 166 patients(69 and 97 cases with elevated and normal TnI, respectively) were included in this study. The average hospital stay, intensive care time, mechanical ventilation time, and in-hospital mortality were higher in the elevated TnI group than in the normal TnI group(P<0.05). The TnI level of trauma patients gradually increased after admission and peaked at 48 hours(7.804±1.537 ng/mL). Subsequently, it decreased, and then recovered to normal within 7 days. However, 13 patients did not recover. Logistic regression analysis revealed that abnormal TnI at 7 days was independently related to in-hospital mortality. CONCLUSIONS: Trauma patients with elevated TnI levels may have a worse prognosis. Monitoring the changes in serum TnI is important, which can reflect the prognosis better than the TnI measured immediately after admission.

The early risk stratification of the patients with acute chest pain

Objective： This investigation was designed to stratify patients with acute chest pain based on their symptoms, electrocardiogram （ECG）, cardiac injury markers and the number of accompanying traditional risk factors（smoking, obesity, hyperlipemia, hypertension, diabetes）, and to assess the effect of the above factors to obtain a risk stratification for patients with chest pain. Methods： We identified 139 patients with acute chest pain, including 45 myocardiac infarction patients, 65 unstable angina patients and 29 chest pain patients without identified acute coronary syndrome（ACS） admitted to our Coronary Heart Center during December 2004 to February 2005. All patients accepted coronary angiography. All data was collected using questionnaires. Based on reported symptom, electrocardiogram （ECG）, cardiac injury markers and the number of the accompanying traditional risk factors, we stratified all patients into four groups： Group 1, patients with acute chest pain, ECG changes and abnormal cardiac injury biomarkers. Group 2, patients with acute chest pain and ECG changes（without abnormal cardiac injury biomarkers）. Group 3, patients with acute chest pain, normal ECG, normal cardiac injury biomarkers and 〉2 traditional risk factors. Group 4, patients with acute chest pain, normal ECG and normal cardiac injury biomarkers, but only ≤ 2 traditional risk factors. From this data we examined the difference of ACS incidence in the four groups. Results：After stratification the ACS incidence of the grouped patients in turn was 100%, 84%, 69.6% and 53.3%. The combination of early phase ECG and cardiac injury markers identified 70.9% patients with ACS（the specificity being 90.7%）. The mortality of group 3 was higher compared with group 4（69.6% vs 53.3%）, however the P value was more than 0.05 and didn＇ t show significant statistical difference. The correlation analysis found the number of the traditional risk factors had a significant positive correlation （r= 0.202, P = 0.044） with the number of stenosis being more than 50% of the artery diameter. Multiple linear regression showed the hypertension had a significant correlation with the number of the diseased regions（P= 0.014）. Conclusions：The risk stratification based on the symptom, ECG, cardiac injury markers and accompanying traditional risk factors is both important and available in practice. It is unsuitable for patients with a normal ECG and cardiac injury markers to differentiate ACS from non-cardiac chest pain relying only on the number of the accompanying traditional risk factors. However we found the number of the risk factors can indicate the disease severity.

INCREASED VULNERABILITY OF HYPERTROPHIED MYOCARDIUM TO ISCHEMIA AND REPERFUSION INJURY RELATION TO CARDIAC RENIN-ANGIOTENSIN SYSTEM

Hearts of pressure-overload hypertrophy show an increased activation of intracardiac renin-angiotensin system which may contribute to ischemia and reperfusion injury. The purpose of this study is to evaluate whether the hypertrophied myocardium is more vulnerable to ischemia and reperfusion injury and to find out its relation to the cardiac renin-angiotensin system. Hypertrophied rat hearts induced by abdominal aortic banding for 6 weeks were subjected to 2 hours of hypothermic ischemic arrest followed by 30 minutes of reperfusion, and their cardiac function recovery was compared with that of sham-operated normal control hearts. The cardiac renin activity and angiotensin II content before ischemia and after reperfusion were determined. It was found that both the pre-ischemic renin activity and angiotensin II level were higher in hypertrophied myocardium than those in the control: ischemia and reperfusion injury increased both renin activity and angiotensin II content in the two groups, but the renin activity and angiotensin II level were further elevated after reperfusion in the hypertrophied hearts than those in the control hearts. Meanwhile, the cardiac function recovery after 30 minutes reperfusion in the hypertrophied hearts was poorer than that in the control. Correlation analysis revealed that there was a negative correlation between the cardiac output recovery and the myocardial angiotensin II content (r=-0.841), P<0.001), It is concluded that ischemia and reperfusion injury can activate cardiac renin-angiotensin system in isolated rat heart, which may be responsible for the increased susceptibility of the hypertrophied myocardium to ischemia and reperfusion injury.

Urine neutrophil gelatinase-associated lipocalin at SICU admission predicts for cardiac surgery-associated acute kidney injury

Background Acute Kidney Injury （AKI） is a common and serious complication of cardiovascular surgery. There is a need to find biomarkers that are involved in the etiology of cardiac surgery-associated acute kidney injury （CSA-AKI） and have an earlier response to acute kidney injury. The association between urine neutrophil gelatinase-associated lipocalin （NGAL） concentrations and AKI progression is not well established. Methods The prospective-cohort study included 1631 consecutive adult patients undergoing cardiac surgery at Fuwai Hospital between September 2012 and November 2013. AKI defined by Acute Kidney Injury Network （AKIN） criteria with a postoperative increase in plasma creatinine 〉/50% baseline or/〉0.3 mg/dL. Urine NGAL was measured us- ing latex particle-enhanced turbidimetric immunoassay. Associations between Urine NGAL levels and AKI were determined by estimating areas under receiver operating characteristic curves （AUC）. Results A total of 438 （26.9%） patients developed CSA-AKI. And the patients were divided into four groups： 1193 non-AKI patients, 368（22.6%） patients with AKIN stage I AKI, 49（3.0%） with AKIN stage 2 AKI and 21（1.3%） with AKIN stage 3 AKI. urine NGAL concentrations at surgical intensive care unit （SICU） admission were significantly related to AKI severity. The AUCs for urine NGAL were for AKIN stage 1 （0.54±0.02）, AKIN stage 2 （0.67±0.04）, and AKIN stage 3 （0.76±0.06）, respectively. Conclusions Urinary NGAL is associated with CSA-AKI and its progression, indicating their potential use as prognostic markers. Urine NGAL level measured at SICU admission predicts the development of severe AKI after cardiac surgery.

RELEASE OF SERUM TROPONIN I AND ITS RELATIONSHIP TO MULTIFACTORS FOLLOWING OPEN HEART SURGERY IN CHILDREN

Objective To be released specifically after myocardial damage. The goal of this study was to measure serum cardiac troponin I levels after open heart surgery in children, and to evaluate relevance between TnTi and perioperative multi-factors. Methods Fifty-seven consecutive pediatric patients undergoing elective correction of congenital heart diseases were divided into group A （ TOF, n =31 ） and group B （ VSD, n =26）. Blood sampies were drawn preoperatively, 5min（ T0 ） , 6h（ T6 ） , 12h（ T12 ） , 24h（ T24 ） , 48h（ T48 ） , 72h（ T72 ） after removal of aortic cross clamping. Myocardial protection consisted of moderate systemic hypothermia （ 30℃- 32℃ ）, cold crystalloid cardioplegia and topical cooling. Demographic information, cardiac defect, repair procedure, duration of bypass （ CPBT） , cross-clamping time （ CCT） , clinical score for cardiac function, electrocardiographic changes and outcomes were recorded. Results Compared with the baseline value, serum concentration of troponin I peaked at T0 （ P 〈 0. 01 ）, and fell to normal level at T72 （ P 〉 0. 05 ）. Peak CTnI was 118 and 55 times higher than the baseline value, respectively in group A and group B. There was a positive correlation between peak CTnI and CPBT, CCT （ r = 0. 51 ; P 〈 0. 01 ）, myocardial operative injury after ventriculotomy and muscle resection （ r = 0. 35, P 〈0. 01 ）. Also the peak CTnl value was correlated to the clinical score for cardiac function （r = -0. 52; P 〈0. 01）. 2.3μg/L was a cutoff value which was highly predictive for postoperative recovery and inotropic support. Conclusion Postoperative serum troponin I is a highly specific and sensitive marker for myocardial ischemia and injury; therefore, its measurement may contribute to the assessment of recovery and outcome after open heart surgery.

Optimization of different intensities of exercise preconditioning in protecting exhausted exercise induced heart injury in rats

This study was to optimize the exercise preconditioning(EP)intensity in protecting from exhaustive exercise-induced cardiac injury(EECI).A total of 98 male Sprague-Dawley rats were divided into 7 groups(n=14):the control group(C),the exhaustive exercise group(EE)and the EP+EE groups,which include the V10(53.0%VO_(2max)),V15(58.4%VO_(2max)),V20(67.0%VO_(2max)),V26(74.0%VO_(2max))and V30(80.0%VO_(2max))groups.Except the C group,the other groups were subjected to treadmill running.The serum contents of N terminal pro B type natriuretic peptide(NT-proBNP)and cardiac troponin I(cTn-I)were detected by the enzyme-linked immunosorbent assay method,ECG was recorded,heart function was detected by pressure volume catheter and the activities of mitochondrial electron transfer pathway(ET pathway)complexesⅠ,ⅡandⅣwere measured by high-resolution respiration instrument.Compared to the EE group,the EP groups have shown decrease of NT-proBNP and cTn-I,improvement of mitochondrial respiratory function and car-diac function.Compared to other EP groups,the V26 group has shown significant decrease of myocardial enzymes and improvement of mitochondrial function.The correlation analysis showed the EP effect was proportional to EP intensity in the range of 53.0%VO_(2max)-74.0%VO_(2max).High intensity and long duration of exhaustive exercise caused cardiac injury and EP could decrease serum level of NT-proBNP and cTn-I,improve electrical derangement and the left ventricular function,and raise the activities of ET pathway complexesⅠ,ⅡandⅣ.The protection of EP on EECI was improved as the EP intensity was increased from 53.0%VO_(2max)to 74.0%VO_(2max)and when EP intensity was 74.0%VO_(2max),the effect was the most obvious among all the setting EP groups.