Elevated Cardiac Troponin I in Sepsis and Septic Shock No Evidence for Thrombus Associated Myocardial Necrosis 英文参考文献.docVIP

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Elevated Cardiac Troponin I in Sepsis and Septic Shock No Evidence for Thrombus Associated Myocardial Necrosis 英文参考文献.doc

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Elevated Cardiac Troponin I in Sepsis and Septic Shock No Evidence for Thrombus Associated Myocardial Necrosis 英文参考文献

ElevatedCardiacTroponinIinSepsisandSepticShock: NoEvidenceforThrombusAssociatedMyocardial Necrosis DavidR.Altmann1,WolfgangKorte2,MichaT.Maeder3,ThomasFehr4,PhilippHaager1,HansRickli1, Gian-RetoKleger5,ReguloRodriguez6,PeterAmmann1* 1DivisionofCardiology,KantonsspitalSt.Gallen,St.Gallen,Switzerland,2InstituteforClinicalChemistryandHematology,KantonsspitalSt.Gallen,St.Gallen,Switzerland, 3BakerIDIHeartandDiabetesInstitute,Melbourne,Australia,4DivisionofNephrology,UniversityHospitalZu¨rich,Zu¨rich,Switzerland,5IntensiveCareUnit,Department ofInternalMedicine,KantonsspitalSt.Gallen,St.Gallen,Switzerland,6InstituteofPathology,KantonsspitalSt.Gallen,St.Gallen,Switzerland Abstract Background: Elevated cardiac troponin I (cTnI) is frequently observed in patients with severe sepsis and septic shock. However, the mechanisms underlying cTnI release in these patients are still unknown. To date no data regarding coagulationdisturbancesasapossiblemechanismforcTnIreleaseduringsepsisareavailable. Methodology/Principal Findings: Consecutive patients with systemic inflammatory response syndrome (SIRS), sepsis or septicshockwithoutevidenceofanacutecoronarysyndromewereanalyzed.Coagulationparameters(clottingtime(CT), clotformationtime(CFT),maximumclotfirmness(MCF),a-angle)wereassessedinnativewholebloodsamples,andusing specificactivatorstoevaluatetheextrinsicandintrinsicaswellasthefibrincomponentofthecoagulationpathwaywiththe use of rotational thrombelastometry (ROTEM). Thirty-eight patients were included and 22 (58%) were cTnI-positive. BaselinecharacteristicsbetweenTnI-positiveand-negativepatientsweresimilar.TheCT,CFT,MCFandthea-anglewere similarbetweenthegroupswithtrendstowardsshorterCTintheextrinsicandfibrinactivation. Conclusions/Significance:Wefoundnodifferencesincoagulationparametersanalyzedwithrotationalthrombelastometry between cTnI-positive and -negative patients with SIRS, severe sepsis, and septic shock. These findings suggest that pathophysiological mechanisms other than t