Atorvastatin Therapy during the Peri-Infarct Period Attenuates Left Ventricular Dysfunction and Remodeling after Myocardial Infarction 英文参考文献.docVIP

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Atorvastatin Therapy during the Peri-Infarct Period Attenuates Left Ventricular Dysfunction and Remodeling after Myocardial Infarction 英文参考文献.doc

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Atorvastatin Therapy during the Peri-Infarct Period Attenuates Left Ventricular Dysfunction and Remodeling after Myocardial Infarction 英文参考文献

AtorvastatinTherapyduringthePeri-InfarctPeriod AttenuatesLeftVentricularDysfunctionandRemodeling afterMyocardialInfarction Xian-LiangTang1.,SantoshK.Sanganalmath1.,HiroshiSato1,QiuliBi1,GregHunt1,RobertJ.Vincent2, YongPeng1,GreggShirk1,BuddhadebDawn2,RobertoBolli1* 1Division of Cardiovascular Medicine and Institute of Molecular Cardiology, University of Louisville, Louisville, Kentucky, United States of America, 2Cardiovascular ResearchInstitute,KansasUniversityMedicalCenter,KansasCity,Kansas,UnitedStatesofAmerica Abstract Althoughstatinsimpartanumberofcardiovascularbenefits,whetherstatintherapyduringtheperi-infarctperiodimproves subsequentmyocardialstructureandfunctionremainsunclear.Thus,weevaluatedtheeffectsofatorvastatinoncardiac function, remodeling, fibrosis, and apoptosis after myocardial infarction (MI). Two groups of rats were subjected to permanentcoronaryocclusion.GroupII(n=14)receivedoralatorvastatin(10mg/kg/d)dailyfor3wkbeforeand4wkafter MI,whilegroupI(n=12)receivedequivalentdosesofvehicle.Infarctsize(Masson’strichrome-stainedsections)wassimilar in both groups. Compared with group I, echocardiographic left ventricular ejection fraction (LVEF) and fractional area change(FAC)werehigherwhileLVend-diastolicvolume(LVEDV)andLVend-systolicandend-diastolicdiameters(LVESD andLVEDD)werelowerintreatedrats.Hemodynamically,atorvastatin-treatedratsexhibitedsignificantlyhigherdP/dtmax , end-systolic elastance (Ees), and preload recruitable stroke work (PRSW) and lower LV end-diastolic pressure (LVEDP). Morphometrically,infarctwallthicknesswasgreaterintreatedrats.TheimprovementofLVfunctionbyatorvastatinwas associatedwithadecreaseinhydroxyprolinecontentandinthenumberofapoptoticcardiomyocytenuclei.Weconclude thatatorvastatintherapyduringtheperi-infarctperiodsignificantlyimprovesLVfunctionandlimitsadverseLVremodeling following MI independent of a reduction in infarct size. These salubrious effects may be due in part to a decrease in myocardialfibrosisandapoptosis. Citati