The expression of oxidative stress genes related to myocardial ischemia reperfusion injury in patients with ST-elevation myocardial infarction

BACKGROUND:We aimed to investigate the gene expression of myocardial ischemia/reperfusion injury(MIRI)in patients with acute ST-elevation myocardial infarction(STEMI)using stress and toxicity pathway gene chip technology and try to determine the underlying mechanism.METHODS:The mononuclear cells were separated by ficoll centrifugation,and plasma total antioxidant capacity(T-AOC)was determined by the ferric reducing ability of plasma(FRAP)assay.The expression of toxic oxidative stress genes was determined and verified by oligo gene chip and quantitative real-time polymerase chain reaction(qRT-PCR).Additionally,gene ontology(GO)enrichment analysis was performed on DAVID website to analyze the potential mechanism further.RESULTS:The total numbers of white blood cells(WBC)and neutrophils(N)in the peripheral blood of STEMI patients(the AMI group)were significantly higher than those in the control group(WBC:11.67±4.85×10^(9)/L vs.6.41±0.72×10^(9)/L,P<0.05;N:9.27±4.75×10^(9)/L vs.3.89±0.81×10^(9)/L,P<0.05),and WBCs were significantly associated with creatine kinase-myocardial band(CK-MB)on the first day(Y=8.945+0.018X,P<0.05).In addition,the T-AOC was significantly lower in the AMI group comparing to the control group(12.80±1.79 U/mL vs.20.48±2.55 U/mL,P<0.05).According to the gene analysis,eight up-regulated differentially expressed genes(DEGs)included GADD45A,PRDX2,HSPD1,DNAJB1,DNAJB2,RAD50,TNFSF6,and TRADD.Four down-regulated DEGs contained CCNG1,CAT,CYP1A1,and ATM.TNFSF6 and CYP1A1 were detected by polymerase chain reaction(PCR)to verify the expression at different time points,and the results showed that TNFSF6 was up-regulated and CYP1A1 was down-regulated as the total expression.GO and kyoto encyclopedia of genes and genomes(KEGG)enrichment analysis suggested that the oxidative stress genes mediate MIRI via various ways such as unfolded protein response(UPR)and apoptosis.CONCLUSIONS:WBCs,especially neutrophils,were the critical cells that mediating reperfusion injury.MIRI was regulated by various genes,including oxidative metabolic stress,heat shock,DNA damage and repair,and apoptosis-related genes.The underlying pathway may be associated with UPR and apoptosis,which may be the novel therapeutic target.

Effect of reperfusion strategy on QT dispersion in patients with acute myocardial infarction:Impact on in-hospital arrhythmia

BACKGROUND Myocardial ischemia and ST-elevation myocardial infarction(STEMI)increase QT dispersion(QTD)and corrected QT dispersion(QTcD),and are also associated with ventricular arrhythmia.AIM To evaluate the effects of reperfusion strategy[primary percutaneous coronary intervention(PPCI)or fibrinolytic therapy]on QTD and QTcD in STEMI patients and assess the impact of the chosen strategy on the occurrence of in-hospital arrhythmia.METHODS This prospective,observational,multicenter study included 240 patients admitted with STEMI who were treated with either PPCI(group I)or fibrinolytic therapy(group II).QTD and QTcD were measured on admission and 24 hr after reperfusion,and patients were observed to detect in-hospital arrhythmia.RESULTS There were significant reductions in QTD and QTcD from admission to 24 hr in both group I and group II patients.QTD and QTcD were found to be shorter in group I patients at 24 hr than those in group II(53±19 msec vs 60±18 msec,P=0.005 and 60±21 msec vs 69+22 msec,P=0.003,respectively).The occurrence of in-hospital arrhythmia was significantly more frequent in group II than in group I(25 patients,20.8%vs 8 patients,6.7%,P=0.001).Furthermore,QTD and QTcD were higher in patients with in-hospital arrhythmia than those without(P=0.001 and P=0.02,respectively).CONCLUSION In STEMI patients,PPCI and fibrinolytic therapy effectively reduced QTD and QTcD,with a higher observed reduction using PPCI.PPCI was associated with a lower incidence of in-hospital arrhythmia than fibrinolytic therapy.In addition,QTD and QTcD were shorter in patients not experiencing in-hospital arrhythmia than those with arrhythmia.

Long-Term Prognosis of Different Reperfusion Strategies for ST-Segment Elevation Myocardial Infarction in Chinese County-Level Hospitals:Insight from China Acute Myocardial Infarction Registry

Objective To evaluate the long-term prognosis of patients with ST-segment elevation myocardial infarction(STEMI)treated with different reperfusion strategies in Chinese county-level hospitals Methods A total of 2,514 patients with STEMI from 32 hospitals participated in the China Acute Myocardial Infarction registry between January 2013 and September 2014.The success of fibrinolysis was assessed according to indirect measures of vascular recanalization.The primary outcome was 2-year mortality.Results Reperfusion therapy was used in 1,080 patients(42.9%):fibrinolysis(n=664,61.5%)and primary percutaneous coronary intervention(PCI)(n=416,38.5%).The most common reason for missing reperfusion therapy was a prehospital delay>12 h(43%).Fibrinolysis[14.5%,hazard ratio(HR):0.59,95%confidence interval(CI)0.44–0.80]and primary PCI(6.8%,HR=0.32,95%CI:0.22–0.48)were associated with lower 2-year mortality than those with no reperfusion(28.5%).Among fibrinolysistreated patients,510(76.8%)achieved successful clinical reperfusion;only 17.0%of those with failed fibrinolysis underwent rescue PCI.There was no difference in 2-year mortality between successful fibrinolysis and primary PCI(8.8%vs.6.8%,HR=1.53,95%CI:0.85–2.73).Failed fibrinolysis predicted a similar mortality(33.1%)to no reperfusion(33.1%vs.28.5%,HR=1.30,95%CI:0.93–1.81).Conclusion In Chinese county-level hospitals,only approximately 2/5 of patients with STEMI underwent reperfusion therapy,largely due to prehospital delay.Approximately 30%of patients with failed fibrinolysis and no reperfusion therapy did not survive at 2 years.Quality improvement initiatives are warranted,especially in public health education and fast referral for mechanical revascularization in cases of failed fibrinolysis.

EFFECT OF REPERFUSION THERAPY ON SOLUBLE CELL ADHESION MOLECULES IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION

Objective To observe the changes of serum soluble intercellular adhesion moiecuie type-1(ICAM-1) and E-selectin in patients with acute myocardial inlarction (AMI) receiving reperfusiontherapy. Methods Peripheral venous blood samples were taken from 21 patients with AMI before and4,8,12,24,48,72h after thrombolytic treatment or direct percutaneous transluminal coronary angioplasty (PTCA).Blood samples from 16 control subjects were drawn for one time. Serum concentration of ICAM-1 and E-selectinwas determined by double antibodies sandwich enzyme-linked immunosorbent assay. Results Serum levels ofICAM-1 and E-selectin were higher in patients with AMI than those in controls. Sixteen patients with AMIand successful roperfusion therapy had signifcantly reduction in serum concentration of ICAM-1 and E-selectinat 24 and 48h, but had a peak at 4h. The remaining live patients who failed in mperfusion theropy didn’t show anysignificant changes in these values. Conclusion The serum concentration of ICAM-1 and E-selectin waselevated significantly in patients with AMI Successful reperfusion therapy can reduce the increased serumconcentration.

Delay Times and Clinical Outcomes in Acute Myocardial Infarction: Comparison of Periods before and during the COVID-19 Pandemic—Myocardial Infarction and the Pandemic

Introduction: At the beginning of the COVID-19 pandemic, a drop in the number of patients treated for cardiac emergencies raised concern about cardiovascular mortality in that period. An increase in care delay for patients with ST-segment elevation myocardial infarction (STEMI) may have affected clinical outcomes. Objectives: To analyze delay times and clinical outcomes of patients with STEMI undergoing primary percutaneous coronary intervention (PPCI), before and during the COVID-19 pandemic. Methods: Retrospective observational study that included patients with STEMI undergoing PPCI from December 2018 to July 2021. The COVID-19 pandemic cases were divided into two groups: pandemic I—from March to August 2020;and pandemic II—from September 2020 to July 2021. Patients were compared according to the period of hospitalization. Primary outcomes were delay times in assistance and clinical outcomes (acute kidney injury [AKI], post-procedural vascular complications and in-hospital mortality). Results: 108 patients were included, 39 (36.1%) in the pre-pandemic period, 13 (12.1%) in pandemic I and 56 (51.8%) in pandemic II. Time from onset of symptoms to arrival at the service and door-to-balloon time did not differ significantly among groups. Vascular complications were more frequent during the pandemic (I and II) than in the pre-pandemic period (2.5% pre-pandemic vs 15.4% pandemic vs 12.5% pandemic II;p = 0.03). AKI incidence was similar in all three periods. There was a non-significant increase in in-hospital mortality during the COVID-19 pandemic. Conclusion: In patients with STEMI, there was an increase in vascular complications and a trend toward increased mortality during the COVID-19 pandemic. Delay times to admission and reperfusion did not differ significantly between before and during the pandemic.

Autonomic function and ventricular tachyarrhythmias during acute myocardial infarction

Most cases of sudden cardiac death are attributed to sustained ventricular tachyarrhythmias(VTs), triggered by acute coronary occlusion. Autonomic dysfunction, an important arrhythmogenic mechanism in this setting, is being actively investigated, aiming at the advent of preventive strategies. Recent experimental studies have shown vagal withdrawal after anterior myocardial infarction, coinciding with high incidence of VTs, followed by more gradual sympathetic activation coinciding with a second arrhythmia peak. This article summarizes recent knowledge on this intriguing topic, generating hypotheses that can be investigated in future experimental and clinical studies.

Bifunctional staining for ex vivo determination of area at risk in rabbits with reperfused myocardial infarction

AIM: To develop a method for studying myocardial area at risk(AAR) in ischemic heart disease in correlation with cardiac magnetic resonance imaging(c MRI). METHODS: Nine rabbits were anesthetized, intubated and subjected to occlusion and reperfusion of the left circumflex coronary artery(LCx) to induce myocardial infarction(MI). ECG-triggered c MRI with delayed en-hancement was performed at 3.0 T. After euthanasia, the heart was excised with the LCx re-ligated. Bifunctional staining was performed by perfusing the aorta with a homemade red-iodized-oil(RIO) dye. The heart was then agar-embedded for ex vivo magnetic resonance imaging and sliced into 3 mm-sections. The AAR was defined by RIO-staining and digital radiography(DR). The perfusion density rate(PDR) was derived from DR for the AAR and normal myocardium. The MI was measured by in vivo delayed enhancement(i DE) and ex vivo delayed enhancement(e DE) c MRI. The AAR and MI were compared to validate the bifunctional straining for cardiac imaging research. Linear regression with Bland-Altman agreement, one way-ANOVA with Bonferroni's multiple comparison, and paired t tests were applied for statistics.RESULTS: All rabbits tolerated well the surgical procedure and subsequent c MRI sessions. The openchest occlusion and close-chest reperfusion of the LCx, double suture method and bifunctional staining were successfully applied in all animals. The percentage MI volumes globally(n = 6) and by slice(n = 25) were 36.59% ± 13.68% and 32.88% ± 12.38% on i DE, and 35.41% ± 12.25% and 32.40% ± 12.34% on e DE. There were no significant differences for MI determination with excellent linear regression correspondence(r global = 0.89; r slice = 0.9) between i DE and e DE. The percentage AAR volumes globally(n = 6) and by slice(n = 25) were 44.82% ± 15.18% and 40.04% ± 13.64% with RIO-staining, and 44.74% ± 15.98% and 40.48% ± 13.26% by DR showing high correlation in linear regression analysis(r global = 0.99; r slice = 1.0). The mean differences of the two AAR measurements on BlandAltman were almost zero, indicating RIO-staining and DR were essentially equivalent or inter-replaceable. The AAR was significantly larger than MI both globally and slice-by-slice(P < 0.01). After correction with the background and the blank heart without bifunctional staining(n = 3), the PDR for the AAR and normal myocardium was 32% ± 15% and 35.5% ± 35%, respectively,which is significantly different(P < 0.001), suggesting that blood perfusion to the AAR probably by collateral circulation was only less than 10% of that in the normal myocardium.CONCLUSION: The myocardial area at risk in ischemic heart disease could be accurately determined postmortem by this novel bifunctional staining, which may substantially contribute to translational cardiac imaging research.

Calpain system and its involvement in myocardial ischemia and reperfusion injury

Calpains are ubiquitous non-lysosomal Ca2+-dependent cysteine proteases also present in myocardial cytosol and mitochondria.Numerous experimental studies reveal an essential role of the calpain system in myocardial injury during ischemia,reperfusion and postischemic structural remodelling.The increasing Ca2+-content and Ca2+-overload in myocardial cytosol and mitochondria during ischemia and reperfusion causes an activation of calpains.Upon activation they are able to injure the contractile apparatus and impair the energy production by cleaving structural and functional proteins of myocytes and mitochondria.Besides their causal involvement in acute myocardial dysfunction they are also involved in structural remodelling after myocardial infarction by the generation and release of proapoptotic factors from mitochondria.Calpain inhibition can prevent or attenuate myocardial injury during ischemia,reperfusion,and in later stages of myocardial infarction.

Cardioprotection and pharmacological therapies in acute myocardial infarction: Challenges in the current era

In patients with an acute ST-segment elevation myocardial infarction, timely myocardial reperfusion using primary percutaneous coronary intervention is the most effective therapy for limiting myocardial infarct size, preserving left-ventricular systolic function and reducing the onset of heart failure. Within minutes after the restoration of blood flow, however, reperfusion itself results in additional damage, also known as myocardial ischemia-reperfusion injury. An improved understanding of the pathophysiological mechanisms underlying reperfusion injury has resulted in the identification ofseveral promising pharmacological(cyclosporin-A, exenatide, glucose-insulin-potassium, atrial natriuretic peptide, adenosine, abciximab, erythropoietin, metoprolol and melatonin) therapeutic strategies for reducing the severity of myocardial reperfusion injury. Many of these agents have shown promise in initial proofof-principle clinical studies. In this article, we review the pathophysiology underlying myocardial reperfusion injury and highlight the potential pharmacological interventions which could be used in the future to prevent reperfusion injury and improve clinical outcomes in patients with coronary heart disease.

Effects of intracoronary injection of nicorandil and tirofiban on myocardial perfusion and short-term prognosis in elderly patients with acute ST-segment elevation myocardial infarction after emergency PCI

BACKGROUND:This study investigated the effects of the intracoronary injection of nicorandil and tirofiban on myocardial perfusion and short-term prognosis in elderly patients with acute ST-segment elevation myocardial infarction(STEMI)after emergency percutaneous coronary intervention(PCI).METHODS:Seventy-eight STEMI patients with age>65 years who underwent emergency PCI were consecutively enrolled.These patients received conventional PCI and were randomly divided into a control group and a treatment group(n=39 per group).The control group received an intracoronary injection of tirofiban followed by a maintenance infusion for 36 hours after surgery.The treatment group received intracoronary injection of tirofiban and nicorandil,and then intravenous infusion of tirofiban and nicorandil 36 hours after surgery.The following parameters were measured:TIMI grade,corrected TIMI frame count(c TFC),TIMI myocardial perfusion grade(TMPG),STsegment resolution(STR)rate 2 hours post-operatively,resolution of ST-segment elevation(STR)at 2 hours postoperatively,peak level of serum CK-MB,left ventricular end diastolic diameter(LVEDD)and left ventricular ejection fraction(LVEF)at 7–10 days postoperatively,and major adverse cardiac events(MACEs)in-hospital and within 30 days post-operatively.RESULTS:Compared with the control group,more patients in the treatment group had TIMI 3 and TMPG 3,and STR after PCI was significantly higher.The treatment group also had significantly lower c TFC,lower infarction relative artery(IRA),lower peak CK-MB,and no reflow ratio after PCI.The treatment group had significantly higher LVEDD and LVEF but lower incidence of MACEs than the control group.CONCLUSION:The intracoronary injection of nicorandil combined with tirofiban can effectively improve myocardial reperfusion in elderly STEMI patients after emergency PCI and improve shortterm prognoses.

GYY4137 protects against myocardial ischemia and reperfusion injury by attenuating oxidative stress and apoptosis in rats

Hydrogen sulfide （H2S） is a gasotransmitter that regulates cardiovascular functions. The present study aimed to determine the protective effect of slow-releasing H2S donor GYY4137 on myocardial ischemia and reperfusion （I/R） injury and to investigate the possible signaling mechanisms involved. Male Sprague-Dawley rats were treated with GYY4137 at 12.5 mg/（kg.day）, 25 mg/（kg.day） or 50 mg/（kg.day） intraperitoneally for 7 days. Then, rats were subjected to 30 minutes of left anterior descending coronary artery occlusion followed by reperfusion for 24 hours. We found that GYY4137 increased the cardiac ejection fraction and fractional shortening, reduced the ischemia area, alleviated histological injury and decreased plasma creatine kinase after myocardial I/R. Both H2S concentration in plasma and cystathionine-γ-lyase （CSE） activity in the myocardium were enhanced in the GYY4137 treated groups. GYY4137 also decreased malondialdehyde and myeloperoxidase levels in serum, attenuated superoxide anion level and suppressed phosphorylation of mitogen activated protein kinases in the myocardium after I/R. Meanwhile, GYY4137 increased the expression of Bcl-2 but decreased the expression of Bax, caspase-3 activity and apoptosis in the myocardium. The data suggest that GYY4137 protects against myocardial ischemia and reperfusion injury by attenuating oxidative stress and apoptosis.

ST-segment elevation: Distinguishing ST elevation myocardial infarction from ST elevation secondary to nonischemic etiologies

The benefits of early perfusion in ST elevation myocardial infarctions(STEMI) are established; howeverearly perfusion of non-ST elevation myocardial infarctions has not been shown to be beneficial. In additionST elevation(STE) caused by conditions other thanacute ischemia is common. Non-ischemic STE may beconfused as STEMI, but can also mask STEMI on electrocardiogram(ECG). As a result, activating the primarypercutaneous coronary intervention(pPCI) protocooften depends on determining which ST elevation patterns reflect transmural infarction due to acute coronary artery thrombosis. Coordination of interpreting theECG in its clinical context and appropriately activatingthe pPCI protocol has proved a difficult task in borderline cases. But its importance cannot be ignored, asreflected in the 2013 American College of CardiologyFoundation/American Heart Association guidelines concerning the treatment of ST elevation myocardial infarction. Multiples strategies have been tested and studiedand are currently being further perfected. No mattethe strategy, at the heart of delivering the best care lies rapid and accurate interpretation of the ECG. Here, we present the different patterns of non-ischemic STE and methods of distinguishing between them. In writing this paper, we hope for quicker and better stratification of patients with STE on ECG, which will lead to be bet-ter outcomes.

Thrombus aspiration in acute myocardial infarction:Rationale and indication

Reperfusion of myocardial tissue is the main goal of primary percutaneous coronary intervention(PPCI) with stent implantation in the treatment of acute ST-segment elevation myocardial infarction(STEMI). Although PPCI has contributed to a dramatic reduction in cardiovascular mortality over three decades, normal myocardial perfusion is not restored in approximately one-third of these patients. Several mechanisms may contribute to myocardial reperfusion failure, in particular distal embolization of the thrombus and plaque fragments. In fact, this is a possible complication during PPCI, resulting in microvascular obstruction and no-reflow phenomenon. The presence of a visible thrombus at the time of PPCI in patients with STEMI is associated with poor procedural and clinical outcomes. Aspiration thrombectomy during PPCI has been proposed to prevent embolization in order to improve these outcomes. In fact, the most recent guidelines suggest the routine use of manual aspiration thrombectomy during PPCI(class Ⅱa) to reduce the risk of distal embolization. Even though numerous international studies have been reported, there are conflicting results on the clinical impact of aspiration thrombectomy during PPCI. In particular, data on long-term clinical outcomes are still inconsistent. In this review, we have carefully analyzed literature data on thrombectomy during PPCI, taking into account the most recent studies and meta-analyses.

Effect of rosiglitazone on rabbit model of myocardial ischemia-reperfusion injury

To explore mechanism and protective effect of rosiglitazone on myocardial ischemia reperfusion(I/R) injury.Methods:A total of 48 male Japanese white big-ear rabbits were randomly divided into control group(A),I/R group(B),low dose of rosiglitazone group(C),high dose of rosiglitazone group(D).Plasma concentration of and also reduced the concentration of plasma serum creatine kinase(CK),CK-MB.high-sensitivity C-reactive protein(hsCRP).ultrasuperoxide dismutase(SOD),malondialdehyde(MD.A).lactic acid glutathione skin peroxidase (C-SH-PX).nitric oxide(NO)and endothelin(ET) were measured 1 h later after I/R.Twenty-four hours after I/R the hearts were harvested for pathological and ultrastructural analysis.Area of myocardial infarction were tested.Results:Plasma concentration of CK,Ck-MB.hsCRP,NO. MDA and ET were decreased in C,D group compared with group B.Plasma concentration of T-SOD and GSH-Px were increased significantly in C.D group compared with group B.Compared with group B.pathological and ullraslructural changes in C and D group were slightly.There was significant difference in myocardial infarction area between group C.D and group B(P【0.05). Myocardial infarction area and arrhythmia rate were lower in group C,D compare with group B. Rosiglitazone may protect myocardium from I/R injury by enhancing T-SOD and GSH-Px concentration,inhibit inflammatory reaction,and improve endothelial function.

Predictors and in-hospital prognosis of recurrent acute myocardial infarction

Objective To investigate the contributing factors and in-hospital prognosis of patients with or without recurrent acute myocardial infarction （AMI）. Methods A total of 1686 consecutive AMI patients admitted to Peking University People＇s Hospital from January 2010 to December 2015 were recruited. Their clinical characteristics were retrospectively compared between patients with or without a recurrent AMI. Then multivariable logistic regression was used to estimate the predictors of recurrent myocardial infarction. Results Recurrent AMI patients were older （69.3 ± 11.5 vs. 64.7 ± 12.8 years, P 〈 0.001） and had a higher prevalence of diabetes mellitus （DM） （52.2% vs. 35.0%, P 〈 0.001） compared with incident AMI patients, they also had worse heart function at admission, more severe coronary disease and lower reperfusion therapy. Age （OR = 1.03, 95% CI： 1.02-1.05; P 〈 0.001）, DM （OR = 1.86, 95% CI： 1.37-2.52; P 〈 0.001） and reperfusion therapy （OR = 0.74; 95% CI： 0.52-0.89; P 〈 0.001） were independent risk factors for recurrent AMI Recurrent AMI patients had a higher in-hospital death rate （12.1% vs. 7.8%, P = 0.039） than incident AMI patients. Conclusions Recurrent AMI patients presented with more severe coronary artery conditions. Age, DM and reperfusion therapy were independent risk factors for recurrent AMI, and recurrent AM1 was related with a high risk of in-hospital death.

Effect and mechanism of salvianolic acid B on the myocardial ischemiareperfusion injury in rats

Objective:To investigate the effect of salvianolic acid B on rats with myocardial ischemiareperfusion injury.Methods:SD rats were randomly divided into five groups(n=10 in each group):A sham operation group,B ischemic reperfusion group model group,C low dose salvianolic acid B group,D median dose salvianolic acid B group,E high dose salvianolic acid B group.One hour after establishment of the myocardial ischemia-reperfusion model,the concentration and the apoptotic index of the plasma level of myocardial enzymes(CTnⅠ,CKMB),SOD,MDA,NO,ET were,measured.Heart tissues were obtained and micro-structural changes were observed.Results:Compared the model group,the plasma CTnⅠ,CK-MB,MDA and ET contents were significantly increased,NO,T-SOD contents were decreased in the treatment group(group C,D,and E)(P<0.05);compared with group E,the plasma CTnⅠ,CKMB,MDA and ET levels were increased,the NO,T-SOD levels were decreased in groups C and D(P<0.05).Infarct size was significantly reduced,and the myocardial ultrastructural changes were improved significantly in treatment group.Conclusions:Salvianolic acid B has a significant protective effect on myocardial ischemia-reperfusion injury.It can alleviate oxidative stress,reduce calcium overload,improve endothelial function and so on.

Typical rise and fall of troponin in(peri-procedural) myocardial infarction:A systematic review

AIM: To identify the typical shape of the rise and fall curve of troponin(Tn) following the different types of myocardial infarction(MI). METHODS: We conducted a systematic search in PubM ed and Embase including all studies which focused on the kinetics of Tn in MI type 1, type 4 and type 5. Tn levels were standardized using the 99 th percentile, a pooled mean with 95%CI was calculated from the weighted means for each time point until 72 h. RESULTS: A total of 34 of the 2528 studies identified in the systematic search were included. The maximum peak level of the Tn was seen after 6 h after successful reperfusion of an acute MI, after 12 h for type 1 MI and after 72 h for type 5 MI. In type 1 MI there were additional smaller peaks at 1 h and at 24 h. After successful reperfusion of an acute MI there was a second peak at 24 h. There was not enough data available to analyze the Tn release after MI associated with percutaneous coronary intervention(type 4).CONCLUSION: The typical rise and fall of Tn is different for type 1 MI, successful reperfusion of an acute MI and type 5 MI, with different timing of the peak levels and different slopes of the fall phase.

Myocardial ischemia-reperfusion injury:Possible role of melatonin

Our knowledge and understanding of the pathophysiology of coronary atherosclerosis has increased enormously over the last 20 years.Reperfusion through thrombolysis or percutaneous coronary angioplasty is the standard treatment for preventing acute myocardial infarction.Early reperfusion is an absolute prerequisite for survival of the ischemic myocardium,but reperfusion itself may lead to accelerated and additional myocardial injury beyond that generated by ischemia alone.These outcomes,in a range of reperfusion-associated pathologies,are collectively termed "reperfusion injuries".Reactive oxygen species are known to be produced in large quantities in the first few minutes of the post-ischemia reperfusion process.Similarly,scientific evidence from the last 15 years has suggested that melatonin has beneficial effects on the cardiovascular system.The presence of vascular melatoninergic receptor binding sites has been demonstrated;these receptors are functionally linked to vasoconstrictor or vasodilatory effects of melatonin.It has been shown that patients with coronary heart disease have a low melatonin production rate,especially those with higher risk of cardiac infarction and/or sudden death.Melatonin attenuates molecular and cellular damage resulting from cardiac ischemia-reperfusion in which destructive free radicals are involved.

Acute Myocardial Infarction in a 26-Year-Old Man with Normal ST-Segment

Acute myocardial infarction (AMI) is rare in young adults. The management of these patients is considered as a clinical challenge. We report the case of a 26-year-old man who was presented to the Emergency Room of Affiliated Hospital of Guilin Medical University with an acute onset of chest pain. Initially electrocardiogram (ECG) with no evidence of ST-segment abnormalities but QT prolongation a signal of sudden cardiac death, 20 minutes later, it revealed ST-segment elevation myocardial infarction (STEMI). Coronary angiography (CAG) demonstrated left main coronary artery occlusion. AMI was diagnosed based on clinical symptom, elevated cardiac biomarkers, electrocardiographic dynamic monitoring and CAG. The awareness of chest pain as possible underlying AMI symptom—especially in young patients presenting with QT prolongation—is crucial for clinical treatment, as a missed diagnosis can worsen the patient’s further prognosis. In addition, reperfusion arrhythmia is a challenge to short-term outcomes of young patients with AMI, so it is necessary to make preoperative risk stratification.

Comparison between primary angioplasty and thrombolytic therapy on erectile dysfunction after acute ST elevation myocardial infarction

Acute ST elevation myocardial infarction has high mortality and morbidity rates. The majority of patients with this condition face erectile dysfunction in addition to other health problems. In this study, we aimed to investigate the effects of two different reperfusion strategies, primary angioplasty and thrombolytic therapy, on the prevalence of erectile dysfunction after acute myocardial infarction. Of the 71 patients matching the selection criteria, 45 were treated with primary coronary angioplasty with stenting, and 26 were treated with thrombolytic agents. Erectile function was evaluated using the International Index of Erectile Function in the hospital to characterize each patient＇s sexual function before the acute myocardial infarction and 6 months after the event. The time required to restore blood flow to the artery affected by the infarct was found to be associated with the occurrence of erectile dysfunction after acute myocardial infarction. The increase in the prevalence of erectile dysfunction after acute myocardial infarction was 44.4% in the angioplasty group and 76.9% in the thrombolytic therapy group （P= 0.008）. In conclusion, this study has shown that reducing the time of reperfusion decreases the erectile dysfunction prevalence, and primary angioplasty is superior to thrombolytic therapy for decreasing the prevalence of erectile dysfunction after acute myocardial infarction.