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1、CardiovascularPathology19(2010)102–111OriginalArticleAtrialfibrillationisassociatedwithcardiachypoxiaa,⁎bbcdFelixGramley,JohannLorenzen,BrittaJedamzik,KevinGatter,EvaKoellensperger,acThomasMunzel,FrancescoPezzellaaDepartmentofCardiologyandVascularMedicine,MainzUniversity,GermanybInstitutef
2、orPathology,RWTHAachenUniversity,GermanycNuffieldDepartmentofClinicalLaboratorySciences,OxfordUniversity,UKdDepartmentforPlasticandHandSurgery,UniversityofHeidelberg,GermanyReceived8January2008;receivedinrevisedform2November2008;accepted18November2008AbstractBackground:Atrialfibrillation(A
3、F),themostcommonhumanarrhythmia,isresponsibleforsubstantialmorbidityandmortalityandmaybepromotedbyselectiveatrialischemiaandatrialfibrosis.Consequently,weinvestigatedmarkersforhypoxiaandangiogenesisinAF.Methods:Rightatrialappendages(n=158)weregroupedaccordingtoheartrhythm[sinusrhythm(SR)or
4、AF].ThedegreeoffibrosisandmicrovesseldensityofallpatientsweredeterminedmorphometricallyusingSirius-Red-andCD34/CD105-stainedsections,respectively.Next,sections(n=77)underwentimmunostainingtodetecthypoxia-andangiogenesis-relatedproteins[hypoxia-induciblefactor(HIF)1α,HIF2α,vascularendotheli
5、algrowthfactor(VEGF),VEGFreceptor2(KDR),phosphorylatedKDR(pKDR),carboanhydraseIX,platelet-derivedgrowthfactor]andtheapoptosis-relatedB-celllymphoma2protein.Results:Fibrosisprogressedsignificantlyfrom14.7±0.8%(SR)to22.3±1.4%(AF).WhilethepositivecytoplasmicstainingofHIF1α,HIF2α,VEGF,KDR,andp
6、KDRrosesignificantlyfromSRtoAF,theirnuclearfractionsfell(onlypKDRsignificantly).ThemedianCD34/CD105-positivemicrovesselsizeincreasedsignificantlyfromSRtoAF.Conclusions:AFiscloselyassociatedwithanatrialup-regulationofhypoxicandangiogenicmarkers.Whetherthisiscause,effect,orco-phenomenonoffib
7、rosisremainstobeinvestigated.ItisconceivablethatfibrosismightleadtoanincreasedO2diffusiondistanceandthusinduceischemicsignaling,which,inturn,leadstoangiogenesis.©2010ElsevierInc.Allrightsreserved.Keywords:Atrial;Hypoxia;HIF1;Fibrosis;Arrhythmia;Angiogenesis1.I
