特殊STEMI-協和病例討論-楊明

CaseSharing:

BrokenHeartSyndrome北京協和醫(yī)院

楊明病例1高某，女，67歲，病案號：C767493入院日期：2011-3-30主訴：

心悸、胸悶3h入院情況心電圖既往史

個人史、月經婚育史、家族史無殊

入院查體

T36.8℃、HR117bpm、BP110/80mmHg，

SpO2100%（3L/min）

精神煩躁，時間及空間定向力準確，對答切題，言語欠清，雙側瞳孔等大，對光反射靈敏，鼻膽管引流通暢、可見墨綠色膽汁、無異常臭味，心肺腹未見明顯異常，四肢肌力肌張力正常，雙側病理征及腦膜刺激征陰性。

入院診斷STEMI!

急診冠脈造影病例1冠脈造影病例1冠脈造影病例1冠脈造影病例1冠脈造影病例1冠脈造影心臟超聲(入院當天3-30)：心尖部心肌運動明顯減弱，EF41%心臟超聲(入院當天3-30)：入院后治療可達龍艾司洛爾2d倍他樂克至今心肌酶變化表心電圖變化入院一周后一周后心臟超聲：

心尖部及左室余室壁運動未見異常,EF73%

入院當天一周后心臟超聲入院當天一周后心臟超聲病例2韓某某，女，72歲

病案號1681545

主訴：胸悶10小時

入院日期：2010-11-30

入院情況胸痛時ECG

II，III，AVF，V2,V3,V4導聯ST段抬高我院急診搶救室（發(fā)病4h）

I，AVL，V2-4導聯ST抬高，V2呈QS型，V3rS型1：15pm（起病5h）：我院急診查心肌酶：CK97U/l、CKMB9.5ug/l、cTnI2.51ug/l。

床旁UCG：室間隔中下段無運動、心尖部、前壁運動減低，EF單平面50%既往史：否認高血壓、糖尿病、高血脂病史。個人史、月經婚育史、家族史無特殊，不嗜煙酒。入院查體：HR100bpm，BP108/63mmHg，雙肺呼吸音低，雙下肺可及細濕羅音，左肺為著。心律齊，全腹韌，叩診實音，中下腹可及不規(guī)則包塊，質韌，壓痛（+），無反跳痛、肌緊張，肝脾肋下未及，肝脾區(qū)無叩痛，移動性濁音（+），腸鳴音正常。雙下肢無水腫，雙足背動脈正常。左胸可見穿刺引流管通暢。入院診斷：冠狀動脈粥樣硬化性心臟病

急性ST段抬高性心肌梗死（前壁）心功能1級（Killip）盆腔占位卵巢癌可能性大雙側胸腔積液腹腔積液

STEMI!

病例2冠脈造影病例2冠脈造影病例2冠脈造影病例2冠脈造影病例2冠脈造影病例2冠脈造影病例2冠脈造影病例2冠脈造影診治經過心肌酶發(fā)病12h達峰：cTnI4.87ug/l，CKMB28.1ug/l，CK239U/l，之后逐漸回落至正常床旁心臟超聲：室壁運動及左室收縮功能逐漸恢復正常血脂:TC:3.57mmol/l,TG:1.24mmol/lLDL:1.83mmol/l,HDL:1.18mmol/l發(fā)病24h

I，AVLST段抬高，V2-4ST段抬高，V3R波恢復12月6日（發(fā)病7天）

V2-4T波雙向，R波恢復正常入院ECHO1周后ECHO入院ECHO1周后ECHO2個病例與常見的STEMI不同：STEMI？MyocardialinfarctionwithnormalcoronaryarteriesPathogeneticmechanisms正向重構負向重構IVUS纖維帽破口OCT能敏銳發(fā)現斑塊破裂OCTOCT能敏銳發(fā)現內膜撕裂MisdiagnosesTako-tsubo-likesyndromeTako-tsubo-likesyndromeThisraresyndrome,?rstdescribedinJapanesepatientsin1991,consistsoftransientleftventriculardysfunctionwithchestsymptoms,electrocardiographicchangesandminimalmyocardialenzymereleasemimickingAMI,butwithoutsigni?cantCAD.stresscardiomyopathy“ampulla”cardiomyopathytransientleftventricularapicalballooningsyndrome“brokenheartsyndrome”neurogenicmyocardialstunning

In2006,underthename“stresscardiomyopathy”,itwasclassifiedwithinthegroupofacquiredcardiomyopathiesItwasnamedTako-tsubo-likesyndromebecauseoftheend-systolicshapeoftheleftventricleatventriculography,withapicalballooning,whichresemblesatako-tsubo,i.e.,theJapanesedeviceusedfortrappingoctopuses.EpidemiologyTheprevalenceofthediseaseisunknown.InJapanitisestimatedtobeashighas1-2%ofhospitaladmissionsforchestpainandacutedynamicST-segmentelectrocardiographicchanges.IntheUnitedStates

2-2.2%ofthepatientspresentingwiththeclinicalpictureofanST-segmentelevationacutemyocardialinfarction(STEMI)orunstableanginaareultimatelydiagnosedwithTTC.EpidemiologyStudiesinspecificpopulationshaveshownamuchhigherincidence.1/3ofthepatientstheystudied,whowereadmittedtoamedicalICUwithanon-cardiacdiagnosis(respiratoryfailureorsepsis),sufferedfromtransientleftventricularapicalballooning.AnincreasedincidenceofchronicobstructivepulmonarydiseaseorbronchialasthmawasfoundbyHerttingetalin32patientsdiagnosedretrospectivelywithTTC.Allthesefindingsoffersomeevidencesupportingthehypothesisthatcatecholaminesurgemayplayanimportantroleinthepathogenesisofthesyndrome.Triggeringconditions：psychologicaltrigger：unexpectedlossofacloserelative,confrontationwithanotherperson,devastatingfinancialloss,fearpriortoamedicalprocedure,etc.physicalstress

：pulmonarydisease,sepsis,trauma,cerebrovascularaccidentPathogenesisUnknownSeveraltheoriesCatecholaminesurgeoccultcoronaryatherosclerosiswithplaquerupturecoronaryspasmMicrovasculardysfunctionandspasmClinicalcharacteristicsChestpain（100%）ECG：56%ST-segmentelevation17%T-waveinversions10%Q-wavesorabnormalR-waveprogression.17%non-specificchangesornochangesatall.ECGdifferencearetoosubtletobehelpfulinthedifferentialdiagnosisbetweenTTCandanACSineverydayclinicalpractice.ThetimecourseoftheseECGchangesinTTCseemssimilartothatobservedinpatientswithearlyreperfusedST-elevationacutemyocardialinfarction,withT-waveinversionpersistingforatleast2-3weeksMinimallyelevatedcardiacmarkersCardiacimagingstudiesusuallyrevealextensiveapicaland/ormid-ventricularakinesisorhypokinesiswithbasalsparing,discordantwiththeminimallyincreasedcardiacenzymes.Thesewallmotionabnormalitiestypicallyextendbeyondthevascularterritoryofasinglecoronaryartery,suggestingthatmyocardialstunningratherthannecrosisistheunderlyingmechanismoftheacuteleftventriculardysfunction.冠脈造影Thetypicalfindingistheabsenceofobstructivecoronaryarterydisease.However,Ibanezetalwereabletodescribethepresenceofrupturedatheroscleroticplaquesinsomepatientswiththeuseofintravascularultrasound.Whetherthisfindingisofanypathophysiologicrelevanceremainscurrentlyunknown.左室造影MRITreatmentTheoptimaltreatmentforTTCremainsunknown.

Initialmanagementshouldbethetreatmentofmyocardialischemia（aspirin,clopidogrel,nitrates,intravenousheparinandβ-blockers）sendthepatientimmediatelytothecatheterizationlaboratoryClosemonitoringforthedevelopmentofheartfailure,cardiogenicshockormalignantarrhythmiasAfterthediagnosisofTTChasbeenestablished,antiplateletagentsandnitratesshouldbediscontinued.Ontheotherhand,sincethisiscatecholamine-inducedclinicalsyndrome,β-blockersshouldbekeptonboardandACEIshouldalsobestarteduntiltherecoveryofcardiacfunction.Diureticsareappropriateinthecasethatcongestiveheartfailuredevelops.Anticoagulationshouldalsobeconsideredinthecaseofseveresystolicdysfunctiontoreducetheriskofthromboembolism.PrognosisTTCusuallyhasabenigncoursewithfullrecoveryofleftventricularfunctionwithin2-4week