《應激性心肌病》課件

應激性心肌病

StressCardiomyopathy，SC

Diagnosis,Pathophysiology,Management,andPrognosis武漢亞洲心臟病醫(yī)院徐承義History1991年日本學者Dote等報道心理或軀體應激狀態(tài)可以誘發(fā)一過性左心室功能不全，由于在收縮末期左心室造影呈底部圓隆、頸部狹小的圖像，類似日本古代捉捕章魚的簍子，而被命名為“Tako-tsudo”(章魚瘺)心肌病1997年法國的心臟病學家DominiquePavin報道了2例類似的病例，指出應激狀態(tài)時兒茶酚胺水平升高和該病明顯相關(guān)，并且提出了應激性心肌病的概念2006年AHA關(guān)于心肌病的科學聲明中，將其分類為一種獨立的心肌病，正式命名為應激性心肌病DefinitionSCisareversiblecardiomyopathy,withaclinicalpresentationmimickingAcutecoronarysyndromeintheabsenceofsignificantcoronaryarterydiseaseTako-tsubocardiomyopathy,ApicalBallooningsyndrome,andampullacardiomyopathyBrokenHeartsyndrome，TransientCardiacBallooningsyndrome應激性心肌病是應激因素誘發(fā)的類似急性冠脈綜合征臨床表現(xiàn)，伴有可逆性左室收縮功能障礙的一種臨床綜合征MayoCriteriaTransienthypokinesis,akinesis,ordyskinesisintheleftventriclemidsegmentswithorwithoutapicalinvolvement,regionalwallmotionabnormalityextendingbeyondasingleepicardialvasculardistribution,thepresenceofastresstrigger

左心室心尖和中部區(qū)域室壁運動短暫、超出單一血管供血范圍的可逆性收縮功能喪失或異常，并存在應激因素CriteriaproposedbytheMayoClinicin2004andmodifiedin2008Absenceofobstructivecoronarydiseaseorangiographicevidenceofacuteplaquerupture

冠脈造影示冠狀動脈管狹窄程度＜50%，或無急性斑塊破裂證據(jù)Newelectrographicabnormalitiesand/ormodestelevationinserumcardiacenzymes

新出現(xiàn)心電圖異?；蛐募∶笇W輕度升高Absenceofpheochromocytomaormyocarditis

排除嗜鉻細胞瘤、心肌炎All4criteriamustbepresentINCIDENCETheincidenceofSCislikelyunderrecognizedApproximately1%to2%ofpatientspresentingwithaninitialdiagnosisACSactuallyhaveSC發(fā)病率不明確，1%-2%的ACS患者實為SCUnderestimatedforavarietyofreasons：nonavailabilityofcardiaccatheterizationfacilitiesinmanyregionsthepossibilityfornoncardiacpresentationlackofaconsensusofdiagnosticcriteriamaycontributetomisdiagnosisPRESENTATIONItoccursmostcommonlyinpostmenopausalWomen（90%）,

meanagebetween58and75yrsSCseemstohaveanassociationwithhypertension,COPD,andbronchialasthmaSCmimicsACSinmostpatients，acutesubsternalchestpainanddyspnea.shock,syncope,andcardiacarresthavebeenreportedrarely2/3ofpatientswithemotionalorphysicalstressECGFINDINGSSTelevationintheprecordialanddiffuseTwavearethemostcommonfindings胸前導聯(lián)ST段抬高及多導聯(lián)T波倒置最為常見DifferentiateSCfromanteriorSTEMIPresenceofSTsegmentdepressioninleadavRandabsenceofSTsegmentelevationinleadV1identifiedSCwith91%sensitivity,96%specificity,and95%predictiveaccuracyLABORATORYFINDINGSElevationsintroponinandcreatinekinaseMBaretypicallymild

SeverehemodynamiccompromiseisoutofproportionandincontrasttothedegreeofcardiacenzymeelevationTroponinTlevelsrangedfrom0.01to5.2ng/mLCARDIACCATHETERIZATIONCoronaryangiographyLeftventriculographyARAOendsystolicleftventriculogramintypicalvariant(apicalballooning)ofSC.BRAOend-diastolicventriculogramintypicalvariantofSC.CRAOend-systolicleftventriculograminatypicalvariant(basalballooning)ofSC.DRAOend-diastolicventriculograminatypicalvariantofSC.IMAGINGEchocardiographyventricularballooning，wallmotionabnormalities，decreaseinEFNuclearImagingusingTc-99m，impairmentofmyocardialperfusionMagneticResonanceImagingpatientswithSCdonotshowhyper-enhancementondelayedcontrastenhancementMRIPATHOPHYSIOLOGYThecausalmechanismsremainuncertain機制不明確Stunnedmyocardiumresultingfrombriefperiodsofischemiaowingtovasospasmisonepossibility心肌頓抑（冠脈痙攣引起短暫心肌缺血所致）是一種可能的機制Coronarymicrovasculardysfunction冠狀動脈微血管功能障礙

Increasingplasmalevelsofcatecholamines交感神經(jīng)過度興奮和血漿兒茶酚胺水平增高Reductioninestrogenlevelsfollowingmenopause雌激素水平降低MANAGEMENTThetreatmentofpatientswithSCismainlysupportive

目前尚無標準化的治療方案,去除誘發(fā)因素很關(guān)鍵,加強對癥支持治療Patientswithshock,cautioususeofinotropicagentssuchasdobutamineanddopamine

謹慎使用β受體興奮劑以及多巴胺或多巴酚丁胺，必要時可考慮IABP支持ItisreasonabletotreatSCwithβ-blocker,ACEinhibitorandifpulmonaryedemaevelops,diuretics

β受體阻滯劑、ACEI或ARB被推薦使用，β受體阻滯劑可預防2.7%-8%的病人復發(fā)PROGNOSISSChasafavorableprognosiswithin-hospitalmortality1%,withdeathmorecommoninthesettingofoutflowobstructionThe4-yearrecurrencerateofSChasbeenreportedtobe11.4%,butwithoutanysignificantdifferenceinsurvivalinanageandgender-matchedpopulationoverthesameduration

SC長期預后相對較好,避免情緒激動,在預防復發(fā)中非常重要CaseReview王得清，男/66歲，

住院號：654098主訴：胸痛2天，暈厥一次現(xiàn)病史：2013.11.2日突發(fā)胸痛，位于下段胸骨后，壓迫感，持續(xù)約半小時好轉(zhuǎn)，于當?shù)卦\所診治過程中突發(fā)黑朦、暈厥，數(shù)秒后意識恢復。11.3日14:00再發(fā)胸痛，性質(zhì)同前，程度較前劇烈伴出汗，持續(xù)不能緩解，當?shù)蒯t(yī)院診斷“AMI”，給予藥物治療（ASA300mg,波立維300mg,立普妥20mg）及杜冷丁肌注后好轉(zhuǎn)。既往史、個人史及家族史無特殊。入院查體：T36.6℃，P98bpm，R20bpm，BP140/80mmHg，肺部以及查體無陽性體征；HR104次/分，律絕對不齊，S1強弱不等，各瓣膜聽診區(qū)未聞及雜音；雙下肢無水腫院前輔助檢查：2013年11月4日我院ECG:1.心房顫動2.前壁導聯(lián)ST-T改變。UCG:1.雙房擴大室間隔,左室前壁室壁運動幅度減低,三尖瓣輕度反流,左室收縮功能稍減低,心包腔少量積液心律不齊;2.先天性心臟病：房間隔小缺損（篩孔型，左向右分流）。cTnI0.096ng/ml急診室UCG入院診斷冠狀動脈粥樣硬化性心臟病急性前壁心肌梗死心房顫動心功能I級（Killip分級）監(jiān)測ECG12013.11.04監(jiān)測ECG211.0511.06監(jiān)測cTnI冠脈CTALAD