AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsHealth Care
Myocardial Reperfusion InjuryReperfusion InjuryMyocardial InfarctionMyocardial ReperfusionIschemic Preconditioning, MyocardialMyocardial IschemiaMyocardiumIschemiaCardiotonic AgentsReperfusionHydroxy AcidsDecanoic AcidsIschemic PreconditioningCreatine KinaseBrain IschemiaIschemic PostconditioningHemodynamicsDisease Models, AnimalCoronary CirculationRats, Sprague-DawleyImino PyranosesTime FactorsDogsRats, WistarHeartVectorcardiographyVentricular Function, LeftRabbitsMyocytes, CardiacPeroxidaseMitochondria, HeartNecrosisAnesthetics, InhalationRandom AllocationIsofluraneCerebral InfarctionElectrocardiographyL-Lactate DehydrogenaseMyocardial ContractionHeart RateCoronary VesselsMice, Inbred C57BLVentricular RemodelingNicorandilBlood PressureApoptosisStreptokinase1-DeoxynojirimycinInfarction, Middle Cerebral ArteryHeart VentriclesSwineKATP ChannelsHeart Function TestsVentricular FibrillationDiazoxidePotassium ChannelsMice, KnockoutEnzyme InhibitorsThrombolytic TherapyOxidative StressNitric OxideCreatine Kinase, MB FormArrhythmias, CardiacTechnetium Tc 99m PyrophosphateNitric Oxide Synthase Type IIGlyburideTechnetiumNitric Oxide Synthase Type IIIIschemic Attack, TransientReactive Oxygen SpeciesSuperoxide DismutaseNeuroprotective AgentsWarm IschemiaMitochondrial Membrane Transport ProteinsSignal TransductionBrain InfarctionProto-Oncogene Proteins c-aktMethyl EthersPerfusionNeutrophilsDose-Response Relationship, DrugCoronary DiseaseProtective AgentsMalondialdehydeNitric Oxide SynthaseAdenosine TriphosphateAnalysis of VarianceEchocardiographyNeutrophil InfiltrationTetrazolium SaltsCold IschemiaVentricular PressureModels, AnimalDiphosphatesCells, CulturedIsoenzymesLigationMyocardial StunningPhosphorylationConstriction
InfarctionSTEMIPercutaneous coronary intNecrosisMyocardiumPerfusionAcute ischemia-reperfusion injuryEarly reperfusionIschemicThrombolysisThrombolytic therapyArteryHypoxiaInjuryOxidative stressFibrinolyticSegment elevationFinal infarctVentricularMortalityPatientsInfarctions occurReflowVivoSymptomsCardioprotectionTherapeuticHeartDecreaseLeft ventricleAtherosclerosisOccursPhenomenonTROPONINOutcomeSubsequentTissue
Infarction78
STEMI8
  • Large infarct size and coronary microvascular injury, as the consequence of ischaemia-reperfusion injury and distal embolization of atherothrombotic debris, account for suboptimal long-term prognosis of STEMI patients. (ox.ac.uk)
  • Primary PCI is defined as the performance of percutaneous coronary intervention (PCI) (either conventional balloon angioplasty or coronary stent placement) in the setting of ST elevation MI (STEMI) without antecedent treatment with a fibrinolytic agent. (wikidoc.org)
  • The preclinical work focuses on animal models of myocardial ischemia-reperfusion injury, which is an experimental model for STEMI, as well as ex-vivo models of myocardial ischemia. (gu.se)
  • Sixty-five patients with acute STEMI (mean age 60 ± 11 years) underwent CMR at 1-3 days post-reperfusion (baseline) and at 4 months. (biomedcentral.com)
  • It is uncommon in the age of reperfusion therapy, as most STEMI get treated reasonably early, before transmural infarct. (blogspot.com)
  • We tested the feasibility, safety and potential utility of FDY-5301 as a treatment to limit ischemia-reperfusion injury, in patients with first-time STEMI undergoing emergency PPCI. (ox.ac.uk)
  • METHODS: STEMI patients (n = 120, median 62 years) presenting within 12 h of chest pain onset were randomized at 20 PPCI centers, in a double blind Phase 2 clinical trial, to receive FDY-5301 (0.5, 1.0 or 2.0 mg/kg) or placebo prior to reperfusion, to evaluate the feasibility endpoints. (ox.ac.uk)
  • Achieving the shortest possible delay between symptom onset and reperfusion is therefore one of the most critical factors in the management of STEMI. (tci-thaijo.org)
Percutaneous coronary int5
  • Primary percutaneous coronary intervention (PCI) is the preferred method of reperfusion if this can be performed within recommended time frames. (dovepress.com)
  • This treatment strategy refers to the pre-PCI administration of pharmacologic reperfusion followed by planned diagnostic catheterization and immediate Percutaneous Coronary Intervention. (wikidoc.org)
  • Objectives Percutaneous coronary intervention (PCI) for acute coronary syndromes frequently fails to restore myocardial perfusion despite establishing epicardial vessel patency. (bmj.com)
  • Following percutaneous coronary intervention (PCI) for acute coronary syndromes, rise in endothelin-1 (ET-1) levels, a potent vasoconstrictor produced by the vascular endothelium, has been proposed as a potential mediator of reperfusion injury and 'no reflow' phenomenon. (bmj.com)
  • An IABP may be placed in the emergency department (ED) as a bridge to percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG), to decrease myocardial workload, and to improve end-organ perfusion. (medscape.com)
Necrosis8
  • Venous thrombosis (sometimes called DVT, deep vein thrombosis) leads to a blood clot in the affected part of the body, while arterial thrombosis (and, rarely, severe venous thrombosis) affects the blood supply and leads to damage of the tissue supplied by that artery (ischemia and necrosis). (wikipedia.org)
  • For the end point infarct size, estimated by biomarkers of myocardial necrosis, an overall pooled effect was SMD =−0.58, 95% CI: −0.96 to −0.19. (dovepress.com)
  • w3 The associated ischaemic injury and subsequent myocardial necrosis spreads from the subendocardial to the subepicardial myocardium in a time span of several hours. (bmj.com)
  • The differential diagnosis of a small amount of cardiomyocyte necrosis and, therefore, mild elevation of cTn, is broad and includes acute and chronic disorders. (radcliffecardiology.com)
  • The differential diagnosis of more extensive cardiomyocyte necrosis, and therefore substantial elevation of cTn, is much smaller and largely restricted to AMI, myocarditis and Tako-Tsubo cardiomyopathy. (radcliffecardiology.com)
  • and release of BIOMARKERS of myocardial NECROSIS (e.g., elevated TROPONIN levels). (nih.gov)
  • Additionally, it may clinically manifest with myocardial necrosis, cardiac arrhythmia, myocardial stunning and microvascular dysfunction ( 5 ). (spandidos-publications.com)
  • Rapid restoration of coronary blood flow is essential in preventing myocardial necrosis. (tci-thaijo.org)
Myocardium7
  • This coupled comorbidity of pathological ischemia and therapeutic reinjury of infarcted myocardium, namely, myocardial ischemia-reperfusion injury (MIRI), is particularly refractory to treatment [ 4 , 5 ]. (hindawi.com)
  • Coronary thrombolysis and mechanical revascularization have revolutionized the primary treatment of acute MI, largely because they allow salvage of the myocardium when implemented early after the onset of ischemia. (medscape.com)
  • The modest prognostic benefit of an opened infarct-related artery may be realized even when recanalization is induced only 6 hours or later after the onset of symptoms, that is, when the salvaging of substantial amounts of jeopardized ischemic myocardium is no longer likely. (medscape.com)
  • Here we show, using large animal models of reperfused MI, that intramyocardial hemorrhage - the most damaging form of reperfusion injury (evident in nearly 40% of reperfused ST-elevation MI patients) - drives delayed infarct healing and is centrally responsible for continuous fatty degeneration of the infarcted myocardium contributing to adverse remodeling of the heart. (nature.com)
  • Ischemia-reperfusion injury (IRI) is a syndrome affecting the myocardium upon blood flow restoration following a sufficiently long interruption, such as encountered in a coronary thrombosis or heart surgery [1,2]. (justia.com)
  • and is an intrinsic process through which repeated short episodes of ischemia are instituted to protect the myocardium against subsequent ischemic insults [ 7 ]. (biomedcentral.com)
  • In the situation of acute coronary occlusion, the myocardium supplied by the occluded vessel is subject to ischemia and is referred to as the myocardium at risk (MaR). Single photon emission computed tomography has previously been used for quantitative assessment of the MaR. It is, however, associated with considerable logistic challenges for employment in clinical routine. (biomedcentral.com)
Perfusion9
  • Myocardial salvage depends on the prompt, complete, and sustained restoration of myocardial perfusion. (bmj.com)
  • At present, this can only be obtained by re-establishing coronary flow, although coronary reperfusion does not necessarily imply myocardial perfusion. (bmj.com)
  • In this study, we aim to define the role of endothelin in regulating coronary microvascular blood flow and myocardial perfusion following PCI in patients with non-ST elevation acute coronary syndromes (NSTACS), by assessing whether adjunctive therapy with a selective endothelin A (ET A ) receptor antagonist acutely improves postprocedural coronary microvascular blood flow. (bmj.com)
  • Post-PCI coronary microvascular blood flow and myocardial perfusion were assessed by measuring Doppler-derived average peak velocity (APV), and cardiac biomarker levels were quantified. (bmj.com)
  • Conclusions Endothelin is a mediator of microvascular dysfunction during PCI in NSTACS, and adjunctive selective ET A antagonist may augment myocardial perfusion during PCI. (bmj.com)
  • Gibson invented several of the measures of coronary blood flow that are widely used today (the TIMI frame count and the TIMI myocardial perfusion grade). (wikidoc.org)
  • Currently, the most widely used method to determine myocardial perfusion defects is myocardial perfusion single photon emission computed tomography (SPECT). (biomedcentral.com)
  • However, this approach has limitations in the clinical setting since the patient needs to have the perfusion tracer injected prior to reperfusion and undergo imaging in a gamma camera within approximately 3 hours. (biomedcentral.com)
  • Thus, using myocardial perfusion SPECT for determination of MaR in patients with acute coronary occlusion is a major logistic challenge not possible at many hospitals[ 6 ]. (biomedcentral.com)
Acute ischemia-reperfusion injury3
  • Oral dosing of rats with SCN-, before acute ischemia-reperfusion injury (30 min occlusion, 24 h or 4 week recovery), significantly reduced the infarct size as a percentage of the total reperfused area (54% versus 74%), and increased the salvageable area (46% versus 26%) as determined by MRI imaging. (ku.dk)
  • These data indicate that elevated levels of the MPO substrate SCN-, which can be readily modulated by dietary means, can protect against acute ischemia-reperfusion injury. (ku.dk)
  • A larger trial is justified to test the effects of FDY-5301 on acute ischemia-reperfusion injury and clinical outcomes. (ox.ac.uk)
Early reperfusion2
  • While effective early reperfusion of the criminal coronary artery after a confirmed AMI is the typical treatment at present, collateral myocardial ischemia-reperfusion injury (MIRI) and pertinent cardioprotection are still challenging to address and have inadequately understood mechanisms. (hindawi.com)
  • Early reperfusion of the infarct-related artery limits infarct size and improves outcome. (tci-thaijo.org)
Ischemic5
Thrombolysis2
  • A vast number of trials have consistently and unequivocally proven that thrombolysis reduces infarct size and mortality and improves long term outcome. (bmj.com)
  • Thrombolysis can also play an important part in reperfusion therapy that deals specifically with blocked arteries . (wikimili.com)
Thrombolytic therapy2
Artery6
  • The pathophysiological nature of MIRI is the short-term disturbance of myocardial energy and metabolism caused by reflow after ischemia and hypoxia in the coronary artery and the dynamic changes in apoptosis and the prosurvival signaling pathways in response to related injury factors. (hindawi.com)
  • If there are clinical signs and symptoms of failure of the fibrinolytic agent to achieve reperfusion, then rescue PCI is performed to open the totally occluded artery. (wikidoc.org)
  • If there are clinical signs and symptoms of incomplete reperfusion, then adjunctive PCI is performed to further open a patent artery (one with TIMI grade 2 or 3 flow). (wikidoc.org)
  • The opening of an infarct-related artery may improve ventricular function, collateral blood flow, and ventricular remodeling, and it may decrease infarct expansion, ventricular aneurysm formation, left ventricular (LV) dilatation, late arrhythmia associated with ventricular aneurysms, and mortality. (medscape.com)
  • RESULTS: Intravenous FDY-5301 was delivered before re-opening of the infarct-related artery in 97% participants and increased plasma iodide levels ~1000-fold within 2 min. (ox.ac.uk)
  • Importance of early and complete infarct artery reperfusion. (tci-thaijo.org)
Hypoxia6
  • However, in spite of their resistance to hypoxia only a small portion of cells survive when transplanted into an infarct scar (6). (escardio.org)
  • We aimed to investigate the effect of PLCA on hypoxia/reoxygenation (H/R) in neonatal rat ventricular myocytes (NRVM) and on myocardial I/R in rats. (biomedcentral.com)
  • Cardiomyocytes were isolated and subjected to 6 h hypoxia followed by 18 h reperfusion. (biomedcentral.com)
  • H9c2 cells were subjected to 3‑h hypoxia, followed by 1‑h reperfusion. (spandidos-publications.com)
  • Increases in knowledge have revealed that the common pathophysiological scenario, myocardial ischemia reperfusion injury, including ischemia/reperfusion (I/R) and hypoxia/reoxygenation (H/R) forms of injury, results in depressed myocardial function and harmful morphological alterations, which may lead to heart failure ( 4 ). (spandidos-publications.com)
  • Ischemia/reperfusion (I/R) in mouse hearts and hypoxia/oxidative stress in neonatal rat cardiomyocytes have been associated with a downregulation of MG53. (biomedcentral.com)
Injury24
  • 2 Paradoxically, reperfusion itself can enlarge the infarct size, by complex mechanisms collectively termed ischemia/reperfusion injury. (dovepress.com)
  • 3 In a previous study, different pharmacological principles that aimed to reduce ischemia/reperfusion injury failed to show effect. (dovepress.com)
  • These device-based therapies can be categorized according to the pathophysiological pathways they target: (i) techniques to prevent distal atherothrombotic embolization, (ii) techniques to prevent or mitigate ischaemia/reperfusion injury, and (iii) techniques to enhance coronary microvascular function/integrity. (ox.ac.uk)
  • However, while myocardial reperfusion is well established, the process itself can trigger myocardial reperfusion injury by causing further cardiomyocyte death through multiple pathophysiological mechanisms [ 3 - 5 ]. (hindawi.com)
  • Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
  • However, whether the increase in DJ-1 expression mediates protection against ischemia/reperfusion (I/R) injury in vivo during the late phase of IPC remains to be determined. (spandidos-publications.com)
  • We have recently shown that postischemic administration of intralipid protects the heart against ischemia-reperfusion injury. (silverchair.com)
  • oxidative stress that occurs during reperfusion injury has been shown to induce apoptosis, over and above that induced by ischemia. (latestfashiontips.com)
  • The uncoupling of glycolysis and glucose oxidation induces lactate accumulation during myocardial ischemia/reperfusion (I/R) injury. (biomedcentral.com)
  • We provide a new insight into this potential drug for the treatment of myocardial I/R injury. (biomedcentral.com)
  • A therapeutic drug that targets ischemia reperfusion (I/R) injury is needed and has yet to be developed. (biomedcentral.com)
  • Short-term cardiac stress, induced by ischemia-reperfusion (I/R) injury resulted in impaired left ventricular (LV) recovery and increased infarct size in heterozygous Hmox1-deficient (Hmox1 +/− ) mice [ 55 ]. (springer.com)
  • It has previously been demonstrated that phosphatidylinositol‑3‑kinase (PI3K)/Akt and cleaved caspase‑3 serve critical roles in the apoptosis of cardiac myocytes following ischemia/reperfusion injury. (spandidos-publications.com)
  • The invention pertains to a polypeptide for the protection against heart ischemia-reperfusion injury. (justia.com)
  • This is called reperfusion injury. (justia.com)
  • One object of the present invention is to provide a therapy of heart ischemia-reperfusion injury by applying GLP-1 analogues which can be administered as single component and avoiding administration of the drug with a second compound. (justia.com)
  • The present invention is based on the surprising finding that the peptides of the invention have protective cardiovascular effects without simultaneous administration of other compounds, specifically they have protective effects on the heart against ischemia-reperfusion injury. (justia.com)
  • Postconditioning using N-Ac-GLP-1(7-34)amide N-terminally blocked and C-terminally truncated results in a limitation of ischemia-reperfusion injury in an isolated rat heart. (justia.com)
  • However, accumulating evidence suggests that MG53 has a potentially protective role in heart tissue, including in ischemia/reperfusion injury of the heart, cardiomyocyte membrane injury repair, and atrial fibrosis. (biomedcentral.com)
  • IPC activates the reperfusion injury salvage kinase (RISK) and survivor activating factor enhancement (SAFE) pathways to protect the heart against IR injury. (biomedcentral.com)
  • Current methods of cold static storage have reached their limits in storage time due to the extent of ischemia-reperfusion (I/R) injury induced during static cold storage. (gotomydoctor.com)
  • The extent of reperfusion injury is directly proportional to preservation time in cold storage, and research has shown that with static storage methods, heart storage time will not exceed six hours. (gotomydoctor.com)
  • Additionally, machine reperfusion induces the production of ROS, which results in I/R injury to the heart. (gotomydoctor.com)
  • There are no effective therapies to limit ischemia-reperfusion injury, which is caused by multiple pathways activated by rapid tissue reoxygenation and the generation of reactive oxygen species (ROS). (ox.ac.uk)
Oxidative stress1
Fibrinolytic1
  • The strategy differs from facilitated PCI, a strategy in which the intent is to administer a fibrinolytic agent, and routinely perform PCI in the majority of patients even in the presence of or irrespective of signs and symptoms of successful fibrinolytic reperfusion. (wikidoc.org)
Segment elevation1
  • Consequences depend on degree and location of obstruction and range from unstable angina to non-ST-segment elevation. (msdmanuals.com)
Final infarct1
  • MRI at 3 months revealed median final infarct sizes in placebo vs. 2.0 mg/kg FDY-5301-treated patients of 14.9% vs. 8.5%, and LV ejection fractions of 53.9% vs. 63.2%, respectively, although the study was not powered to detect statistical significance. (ox.ac.uk)
Ventricular1
  • Given that a study on Novartis' Galvus (vildagliptin) found that the drug had an effect on ventricular size, Dr. Sattar noted that a class-wide effect cannot be ruled out. (closeconcerns.com)
Mortality2
  • While high levels of overall cardiac sympathetic drive are a negative prognostic indicator of mortality following MI and during heart failure, β-adrenergic receptor stimulation in the infarct border zone reduced spatially heterogeneous alternans, and prevented conduction block and propagation of extrasystoles. (frontiersin.org)
  • Link between the angiographic substudy and mortality outcomes in a large randomized trial of myocardial reperfusion. (tci-thaijo.org)
Patients5
  • Despite a technically successful PPCI procedure, a variable proportion of patients experience suboptimal myocardial reperfusion. (ox.ac.uk)
  • These include the inability of fibrinolysis to restore normal TIMI flow grade 3 in 50-60% of patients, the occurrence of intracerebral hemorrhage in 0.9% of cases [3] and recurrent ischemia and reinfarction in 3-5% cases. (wikidoc.org)
  • However, a significant number of patients receiving PCI fail to achieve complete and sustained myocardial reperfusion and therefore remain at risk of developing large infarcts ( 1 ). (spandidos-publications.com)
  • These findings suggest that a combination of canagliflozin or sotagliflozin and a DPP4 inhibitor can provide a beneficial effect associated with elevation of circulating active GLP-1 and may serve as a treatment for patients with type 2 diabetes. (omicsdi.org)
  • 2007 Focused update of the ACC/AHA 2004 Guidelines for the Man agement of Patients With ST-Elevation Myocardial In farction. (tci-thaijo.org)
Infarctions occur2
  • More than two thirds of myocardial infarctions occur in lesions that are less than 60% severe. (medscape.com)
  • In the US, about 1.0 million myocardial infarctions occur annually. (msdmanuals.com)
Reflow2
  • 12. Galiuto L. Optimal therapeutic strategies in the setting of post-infarct no reflow: the need for a pathogenetic classification. (razavihospital.ir)
  • The major components of this syndrome include cardiomyocyte death, myocardial stunning, arrhythmias and no-reflow [1]. (justia.com)
Vivo1
  • In vivo rat hearts or isolated Langendorff-perfused mouse hearts were subjected to ischemia followed by reperfusion with intralipid (0.5%, 1% and 2% ex-vivo, and 20% in vivo), cyclosporine-A (0.2 μM, 0.8 μM, and 1.5 μM ex- vivo and 10 mg/kg in vivo), or vehicle. (silverchair.com)
Symptoms2
  • Initial symptoms, comorbidities, and localization of cerebral ischemia were recorded. (istanbulmedicaljournal.org)
  • Acute coronary syndrome (ACS) is a cardiovascular disease, which describes any condition characterized by signs and symptoms of sudden myocardial ischaemia and reduction in blood flow to the heart [ 1 ]. (hindawi.com)
Cardioprotection1
  • MG53 KO mice lack IPC-mediated cardioprotection as evidenced by a failure of IPC to reduce IR-induced myocardial infarct size. (biomedcentral.com)
Therapeutic1
  • Collectively, our findings elucidate why some, but not all, MIs are destined to CHF and help define a potential therapeutic strategy to mitigate post-MI CHF independent of MI size. (nature.com)
Heart5
  • The resistant state of skeletal myoblasts to ischemia renders these cells suitable candidates for repair of chronically infracted and failing heart (5). (escardio.org)
  • 1├óÔé¼ÔÇ£3 cTns, structural proteins unique to the heart, are sensitive and specific biochemical markers of myocardial damage. (radcliffecardiology.com)
  • With ischemia in coronary heart disease, impairment of the oxygen supply and metabolic disorder both occur [ 2 ]. (biomedcentral.com)
  • Facilitation of glucose utilization contributes to the protective effect of AKT signaling to reduce infarct size and improve myocardial function in a heart subjected to I/R [ 15 ]. (biomedcentral.com)
  • The cAMP analogue 8-Br-cAMP-AM (8-Br) confers marked protection against global ischaemia/reperfusion of isolated perfused heart. (mdpi.com)
Decrease2
  • The increase in HOMA-IR was associated with a progressive decrease in myocardial uptake (P (bvsalud.org)
  • In addition, IPC reduced LDH and CK‑MB release, attenuated myocardial infarct size, improved cardiac function following I/R, and inhibited the elevation of ROS and MDA and the decrease in activities of the antioxidant enzymes SOD, CAT and GPx. (spandidos-publications.com)
Left ventricle1
  • Prompt restoration of blood flow through the epicardial arteries (reperfusion) during the acute phase of MI (lasting hours to days: Fig. 1a ) has been a major advance and has reduced immediate death from acute MI with partial recovery of left ventricle function during the sub-acute phase of MI (lasting days to weeks: Fig. 1a ). (nature.com)
Atherosclerosis3
  • Absence of myocardial uptake was associated with higher prevalence of early atherosclerosis (i.e., arterial 18F-FDG uptake, P = 0.004). (bvsalud.org)
  • The physiopathological process of ACS is the atherosclerosis, the build-up of an atherosclerotic plaque starts at lesion-prone areas in large- and medium-sized arteries where the endothelium is dysfunctional, induced by cardiovascular risk factors like chronic smoking, hypertension, and permeation of macromolecules such as lipoproteins to the intima layer [ 6 , 7 ]. (hindawi.com)
  • In this review, we focus on the role of cardiomyocyte-derived and cardiac fibroblast-derived microRNAs that are involved in the regulation of genes associated with cardiomyocyte and fibroblast function and in atherosclerosis-related cardiac ischemia. (archivesofmedicalscience.com)
Occurs1
  • This effect probably occurs partly via inhibition of intestinal SGLT1, and the elevation of active GLP-1 levels is especially apparent when these drugs are co-administered with dipeptidyl peptidase 4 (DPP4) inhibitors. (omicsdi.org)
Phenomenon2
  • Although the phenomenon of ischaemic preconditioning (IPC) is associated with the desired protective capacity, the necessity of its application before sustained ischaemia limits its clinical potential. (sun.ac.za)
  • Thereafter, the infarcted area will increase by transmural progression from the endocardium to the epicardium with increasing duration of ischemia, referred to as the wavefront phenomenon[ 11 ]. (biomedcentral.com)
TROPONIN1
  • One would think that such a high troponin would be correlated with very poor ejection fraction, but as I explain below, peak troponin is not a reliable indicator of infarct size. (blogspot.com)
Outcome1
  • The random effects model pooled estimate for the outcome infarct size assessed by cardiac magnetic resonance was estimated by the standardized mean difference (SMD) =−0.06, 95% confidence interval (CI): −0.34 to 0.21, ie, no effect of IPost. (dovepress.com)
Subsequent1
Tissue1
  • We hypothesized that elevation of thiocyanate ions (SCN-), a competitive MPO substrate, would modulate tissue damage. (ku.dk)