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1、1,急性心肌梗死病理、病理生理及臨床,,2,【急性心肌梗塞(AMI)】定 義,梗死:血管閉塞引起的組織壞死。AMI是急性心肌缺血性壞死,大多是在冠狀動(dòng)脈病變的基礎(chǔ)上發(fā)生冠狀動(dòng)脈血供急劇減少或中斷,使相應(yīng)的心肌嚴(yán)重而持久地急性缺血所致,3,Coronary Artery,,Blood Clot (Thrombus),,,,,,Unstable Plaque Rupture,Coronary Artery,,,Infarcted (dea

2、d) or injured (dying) tissue,Healthy Heart Muscle (Myocardium),Myocardial Infarction,,,原因通常是在冠狀動(dòng)脈粥樣硬化不穩(wěn)定斑塊病變的基礎(chǔ)上繼發(fā)血栓形成導(dǎo)致冠脈持續(xù)、完全阻塞,4,【急性心肌梗塞(AMI)】定 義,臨床診斷要求有病史和應(yīng)用生化方法、心電圖和顯像方法的得到心肌壞死間接證據(jù)綜合評定病理診斷要求有心肌細(xì)胞壞死的證據(jù),壞死是缺血時(shí)間過長導(dǎo)致的。

3、細(xì)胞壞死的特征性表現(xiàn)包括細(xì)胞凝固性壞死和(或)收縮帶的壞死,常伴有梗死灶周圍的斑片狀心肌細(xì)胞溶解區(qū)。,5,急性心肌梗死的新定義,(1)典型的心肌壞死生物標(biāo)志物濃度升高(肌鈣蛋白)超過參考值上限(URL)99百分位值并有動(dòng)態(tài)變化,同時(shí)伴有以下一項(xiàng)心肌缺血的證據(jù):缺血性癥狀ECG提示新發(fā)的缺血性改變(新發(fā)的ST段變化或左束支傳導(dǎo)阻滯[LBBB])心電圖提示病理性Q波形成影像學(xué)證據(jù)提示新發(fā)的節(jié)段性室壁運(yùn)動(dòng)異?;虼婊钚募G失,6,新定義

4、,;(2)突發(fā)的心源性死亡(包括心臟停搏),通常伴有心肌缺血的癥狀新發(fā)ECG缺血性改變或LBBB和(或)經(jīng)冠狀動(dòng)脈(冠脈)造影(或尸檢)證實(shí)的新發(fā)血栓證據(jù),但死亡常常發(fā)生在獲取血標(biāo)本或發(fā)現(xiàn)心肌酶學(xué)標(biāo)志物升高之前;,7,新定義,(3)基線cTn水平正常者接受經(jīng)皮冠狀動(dòng)脈介入治療(PCI)后,如果心臟標(biāo)志物水平升高超過URL99百分位值,則提示圍手術(shù)期心肌壞死;如果心臟標(biāo)志物水平超過URL99百分位值的3倍,則定義為與PCI相關(guān)的心肌

5、梗死;,8,新定義,(4)基線cTn水平正常者接受冠狀動(dòng)脈旁路移植術(shù)(CABG)后,如果心臟標(biāo)志物水平升高超過URL99百分位值,則提示圍手術(shù)期心肌壞死;如果心臟標(biāo)志物水平超過URL99百分位值的5倍,同時(shí)伴有以下任何一項(xiàng):新發(fā)的病理性Q波、新發(fā)的LBBB、冠脈造影證實(shí)新發(fā)橋血管或自身冠脈閉塞、新出現(xiàn)的存活心肌丟失的影像學(xué)證據(jù),則定義為與CABG相關(guān)的心肌梗死;(5)病理檢查時(shí)發(fā)現(xiàn)急性心肌梗死。,9,心肌壞死生化標(biāo)志物,新定義建議采用c

6、Tn,即在癥狀發(fā)生后24小時(shí)內(nèi),cTn的峰值超過正常對照值的99百分位。因?yàn)閏TnI或cTnT具有高度的心肌組織特異性和敏感性,即使心肌組織發(fā)生微小區(qū)域的壞死也能檢查到cTn的升高,因此是評價(jià)心肌壞死的首選標(biāo)志物。如果沒有條件檢測cTn,也可以采用CK-MB mass作為最佳替換指標(biāo),診斷標(biāo)準(zhǔn)與cTn相同。由于CK廣泛分布于骨骼肌,缺乏特異性,因此不再推薦用于診斷心肌梗死。,10,,在cTn升高但缺少心肌缺血臨床證據(jù)時(shí),應(yīng)尋

7、找其他可能導(dǎo)致心肌壞死的病因,包括急性和慢性充血性心力衰竭、腎功能衰竭、快速性或緩慢性心律失常、急性神經(jīng)系統(tǒng)疾病、肺栓塞和肺動(dòng)脈高壓、心臟挫傷/消融/起搏/復(fù)律、浸潤性心臟疾?。ㄈ绲矸蹣幼冃院陀财げ。?、炎性疾?。ㄈ缧募⊙祝?、藥物毒性、主動(dòng)脈夾層、肥厚型心肌病、甲狀腺功能減退、心尖球型綜合征、橫紋肌溶解伴心肌損傷、敗血癥等嚴(yán)重全身性疾病等。,11,按病因?qū)⑿募」K婪譃?型,1型:自發(fā)性心肌梗死,由于原發(fā)的冠狀動(dòng)脈事件如斑塊破裂等引起的心肌

8、缺血;2型:心肌梗死繼發(fā)于心肌的供氧和耗氧不平衡所導(dǎo)致的心肌缺血,如冠狀動(dòng)脈痙攣、貧血、冠狀動(dòng)脈栓塞、心律失?;虻脱獕旱龋?型:心源性猝死,有心肌缺血的癥狀和新出現(xiàn)的ST段抬高或新的LBBB,但未及采集血樣之前就死亡;4型:與因缺血性冠脈事件而進(jìn)行的PCI相關(guān)的心肌梗死;4a 4b5型:與因缺血性冠脈事件而進(jìn)行的CABG相關(guān)的心肌梗死。,12,60% Narrowing of Coronary Artery,13,痙攣Norm

9、al Coronary Artery Cross Section,14,Coronary Artery Thrombus,Source: University of Utah WebPath,The external anterior view of the heart shows a dark clot formation in this artery,15,,16,,陳舊性心肌梗死的定義標(biāo)準(zhǔn)為:(1)新出現(xiàn)的病理性Q波,伴或不伴癥

10、狀;(2)影像學(xué)證據(jù)提示心肌變薄或瘢痕化,失去收縮力或無存活性;(3)病理檢查時(shí)發(fā)現(xiàn)已經(jīng)或正在愈合的心肌梗死。,17,,18,,19,【發(fā)病機(jī)理】,20,,冠狀動(dòng)脈粥樣硬化造成管腔狹窄和心肌供血不足,而側(cè)支循環(huán)尚未建立時(shí),下列原因加重心肌缺血即可發(fā)生心肌梗塞。一、 冠狀動(dòng)脈完全閉塞二、心排血量驟降三、心肌需氧需血量猛增,21,一、冠狀動(dòng)脈完全閉塞,1、病變血管粥樣斑塊內(nèi)或內(nèi)膜下出血,2、血小板聚集管腔內(nèi)血栓形成,3、動(dòng)脈持久性

11、痙攣。,22,二、心排血量驟降,休克、脫水、出血、嚴(yán)重的心律失?;蛲饪剖中g(shù)等引起心排出量驟降,23,三、心肌需氧需血量猛增,重度體力勞動(dòng)、情緒激動(dòng)或血壓劇升時(shí),左心室負(fù)荷劇增,兒茶酚胺分泌增多,心肌需氧需血量增加。,24,誘因:,1、 飽餐(尤其是進(jìn)食大量脂肪) 因餐后血脂增高,血液粘稠度也高,血小板粘附性增強(qiáng),局部血流緩慢,血小板易于聚集以致血栓形成;2、睡眠 迷走神經(jīng)張力增高,易引起冠狀動(dòng)脈痙攣;3、用力大便 增加心臟

12、負(fù)荷。心肌梗塞后發(fā)生的嚴(yán)重心律失常,休克或心力衰竭,均可使冠狀動(dòng)脈灌流量進(jìn)一步降低,心肌壞死范圍擴(kuò)大。,25,【病理】,26,Coronary Artery With Plaque and Thrombus Formation,A - Coronary Artery cross-sectionB - LumenC - Fissured Plaque w/o CapD - Acute thrombus,Source: Em

13、ergency Cardiovascular Care Library (CD-ROM), American Heart Association, Dallas 1997,27,,,28,Thrombus Causing MI,“Needle-Like” white spots are cholesterol crystals,,,Thrombus ocluding artery,,,Likely site of plaque rupt

14、ure,29,,高倍鏡下可見粥樣斑塊中有許多泡沫細(xì)胞(即吞噬大量脂質(zhì)的巨噬細(xì)胞)和膽固醇結(jié)晶。,30,,,動(dòng)脈粥樣斑塊比右邊殘存的動(dòng)脈中膜要厚。可見大量針狀的膽固醇結(jié)晶(針狀空隙),左邊有新鮮出血,血栓可在這樣的斑塊頂部形成。,31,31,Myocardial Ischemia,Myocardial cell metabolic demands not metTime frame of coronary blockage:10 se

15、conds following coronary blockDecreased strength of contractionsAbnormal hemodynamics See a shift in metabolism, so within minutes: Anaerobic metabolism takes overGet build-up of lactic acid, which is toxic within t

16、he cellElectrolyte imbalancesLoss of contractibility,32,32,20 minutes after blockageMyocytes are still viable, soIf blood flow is restored, and increased aerobic metabolism, and cell repair, →Increased contractilit

17、yAbout 30-45 minutes after blockage, if no reliefCardiac infarct & cell death,33,,20-30分鐘,心肌即可有少數(shù)壞死,1-12小時(shí),絕大部分心肌呈凝固性壞死,心肌間質(zhì)充血、水腫、伴有多量炎癥細(xì)胞浸潤。1-2周后開始溶解吸收,逐漸纖維化,6-8周形成疤痕而愈合→陳舊性心梗。,34,,3小時(shí)在壞死邊緣有波狀肌纖維3-6小時(shí) 凝固性壞死;水

18、腫;局部出血;中性粒細(xì)胞浸潤開始壞死開始后6-12小時(shí)肉眼檢查心肌難于確定心肌改變。但多種組織化學(xué)染色方法在3小時(shí)即可辨認(rèn)。,35,,6-12小時(shí) 凝固性壞死繼續(xù),間質(zhì)水腫明顯,胞漿呈嗜酸性,核固縮,核溶解,小血管壞死 心肌組織完全喪失活力18-36小時(shí) 壞死細(xì)胞核丟失 中性粒細(xì)胞浸潤 心肌呈棕紅色或紫紅色(因紅細(xì)胞進(jìn)入)透壁性心肌梗死的外膜有漿液纖維蛋白性滲出物,持續(xù)至48小時(shí),心肌梗死區(qū)轉(zhuǎn)為灰色,伴梗死邊緣有繼發(fā)于中性粒

19、細(xì)胞浸潤形成的黃色細(xì)線條,,36,,急性心肌梗塞第一天最初的明顯表現(xiàn)是收縮帶壞死。在大多數(shù)可見細(xì)胞中,心肌纖維的橫紋丟失,細(xì)胞核模糊。注意在纖維上有許多無規(guī)律暗紅的呈波浪狀的收縮帶經(jīng)過。,37,,心肌梗塞已發(fā)生了大約1到2天時(shí)間。在心肌纖維上有暗紅的收縮帶經(jīng)過,心肌細(xì)胞核有幾乎全部消失,有急性炎癥開始的跡象,急性心肌梗塞在臨床上表現(xiàn)為心電圖改變以及肌酸激酶同功酶部分的升高。,38,39,,圖為急性心肌梗死的受損心肌,石蠟切片。上圖是HE

20、染色,下圖是PTX3蛋白免疫組化。 HE染色結(jié)果顯示,受損心肌有大片壞死,周圍有炎癥細(xì)胞集中。 PTX3免疫組化結(jié)果,炎癥細(xì)胞呈現(xiàn)陽性反應(yīng),為深棕色。 正五聚蛋白(pentraxins, PTX3),40,再灌注損傷,壞死,出血,凝固性壞死和收縮帶壞死等混合表現(xiàn),酶峰前移,41,,圖示心肌梗死:凝固性壞死。中性粒細(xì)胞廣泛浸潤,核溶解、胞漿減少,是典型的急性心肌梗死的1-4天的表現(xiàn)。心肌梗死常發(fā)生于冠狀動(dòng)脈粥樣硬化閉塞。雖然側(cè)支循

21、環(huán)形成能夠有效應(yīng)對缺血,但不能阻止壞死的發(fā)生。,42,3-7天 中性粒細(xì)胞浸潤逐漸變寬,延伸至整個(gè)梗死區(qū),肌纖維破壞,被吞噬細(xì)胞吞噬 梗死灶變軟,呈淡黃色或黃褐色,梗死灶外周出現(xiàn)充血出血帶。光鏡下,心肌纖維腫脹、空泡變,胞漿內(nèi)出現(xiàn)顆粒及不規(guī)則橫帶(收縮帶),在梗死灶周邊帶開始肉芽組織增生,梗死區(qū)開始機(jī)化。間質(zhì)水腫,常見出血。,43,,This myocardial infarction is about 3 to 4 days o

22、ld. There is an extensive acute inflammatory cell infiltrate and the myocardial fibers are so necrotic that the outlines of them are only barely visible,44,,45,,8-10天 單核細(xì)胞清除壞死心肌,壞死心肌細(xì)胞開始溶解,梗死區(qū)心室壁變薄,梗死區(qū)切割面呈黃色,周圍有紅紫色的肉芽組織帶

23、,46,Myocardial Infarction Histology,normal muscle cells remaining,macrophages and the beginnings of scar tissue,,,,47,,3-4周時(shí)肉芽組織帶伸展入壞死組織3-4周至2-3個(gè)月內(nèi)心肌壞死區(qū)的質(zhì)地逐漸成為明膠狀,呈毛玻璃樣灰色,再逐漸變白,質(zhì)地變硬,成為縮小的薄而硬的瘢痕,48,,,49,,心肌梗死的分期在病理學(xué)上可分為急

24、性期、愈合期和陳舊期,而臨床上則分為進(jìn)展期(<6小時(shí))、急性期(6小時(shí)~7天)、愈合期(7天~28天)和陳舊期(≥29天)。應(yīng)當(dāng)注意,根據(jù)臨床和心電圖確定急性缺血事件的時(shí)間,與根據(jù)病理學(xué)確定急性心肌梗死的時(shí)間并不一定相同。,50,,51,〖病理類型〗,透壁性心肌梗塞:心肌梗塞累及心室壁厚度的全層或大部分。心內(nèi)膜下心肌梗塞:梗塞呈灶性分布累及心室壁的內(nèi)層,不到心室壁厚度的一半。心室腔內(nèi)附壁血栓:波及心內(nèi)膜導(dǎo)致形成。,52,,根據(jù)面積將

25、心肌梗死分為顯微鏡下梗死(局灶性壞死)、小面積(<10%左室心?。?、中等面積(10%~30%左室心?。┐竺娣e(>30%左室心?。?53,【病理生理】,54,一、收縮功能損害:,梗死區(qū)四種異常形式的心肌收縮運(yùn)動(dòng):  (1)非同步收縮運(yùn)動(dòng):即缺血或壞死心肌與其附近的正常心肌收縮的時(shí)間不一致; ?。?)運(yùn)動(dòng)機(jī)能減退:即心肌纖維縮短程度降低; ?。?)不能運(yùn)動(dòng):即心肌纖維縮短停滯; ?。?)反常運(yùn)動(dòng):即壞死心肌完全喪失收縮功能,

26、于心肌收縮相呈收縮期外突狀態(tài),故又稱矛盾性膨脹運(yùn)動(dòng)?! 》枪K绤^(qū)心肌運(yùn)動(dòng)則通過frank—starling機(jī)制和血循環(huán)中兒茶酚胺類物質(zhì)的增加而代償性增強(qiáng),即呈高動(dòng)力性收縮狀態(tài)。ACEI心肌異常收縮范圍25 %心衰,40%心源性休克,55,二、舒張功能損害:,急性心肌梗死不僅使左心室收縮功能下降,同樣亦造成左心室舒張功能下降。最初可出現(xiàn)左心室舒張期順應(yīng)性增加,而后因左心室舒張末期壓力的過度升高而下降。急性心肌梗死的恢復(fù)期,由于左心室纖

27、維性瘢痕的存在,左心室順應(yīng)性仍表現(xiàn)為低下。,56,三、血流動(dòng)力學(xué)的改變:,梗死面積達(dá)一定程度,則左心室功能抑制,每搏量降低,充盈壓升高。若同時(shí)有房室傳導(dǎo)阻滯、二尖瓣關(guān)閉不全或室間隔破裂,血液動(dòng)力學(xué)更趨惡化。左心室每搏量明顯下降,使主動(dòng)脈壓降低致冠狀動(dòng)脈血液灌注減少,加重心肌缺血,引起惡性循環(huán)。左室排空障礙亦導(dǎo)致前負(fù)荷增加,左心室容積和壓力增加,心室壁張力增大,心室后負(fù)荷也增加。心室后負(fù)荷增加,不僅阻礙左心室射血排空,亦可使心肌耗氧量增加

28、,更加重心肌缺血。,57,四、病理性心室結(jié)構(gòu)改變:,梗死壁擴(kuò)展(infarct expansion)梗死節(jié)段擴(kuò)大稱為“梗死膨展”,以室壁變薄和顯著的心室腔擴(kuò)大為特征,這由于增加局部長度和曲率半徑所致。梗死膨展的程度似乎與梗死前壁的厚度有關(guān),肥厚者可能不會(huì)出現(xiàn)梗死區(qū)變薄。明顯的梗死膨展可伴發(fā)梗死節(jié)段破裂。梗死區(qū)延展(infarct extension)左室重構(gòu)  在急性心肌梗死早期正常地收縮的心室壁也有心內(nèi)膜周邊的節(jié)段性延長,稱為心

29、室擴(kuò)張。有些患者,此過程可持續(xù)幾個(gè)月。非梗死節(jié)段的延長似乎不伴區(qū)域性的壁變?。灰虼朔枪K拦?jié)段可增大。早期III型膠原,晚期I型膠原,早期室壁瘤,后期心臟僵硬度增加。,58,,59,五、其他組織器官的功能變化,肺功能改變:急性心肌??梢鸱瓮狻Q氣功能障礙和氣體交換異常。此外,低氧血癥亦可造成一氧化碳的彌散能力下降。某些心肌梗死病人尤其是劇烈胸痛伴有煩躁不安、焦慮者,可出現(xiàn)過度通氣,引起低碳酸血癥和呼吸性堿中毒。,60,,內(nèi)分泌功能改變

30、:  (1)胰腺:急性心肌梗死時(shí),可出現(xiàn)內(nèi)臟血管收縮,胰腺血流量減少,胰島素分泌功能障礙而產(chǎn)生高血糖血癥和葡萄糖耐量降低。此外,交感神經(jīng)系統(tǒng)活性增加,兒茶酚胺類物質(zhì)分泌增加,抑制胰島素的分泌和促進(jìn)糖原降解,亦使血糖增高。,61,,(2)腎上腺髓質(zhì):分泌兒茶酚胺過多導(dǎo)致許多急性心肌梗死的特征性癥狀和體征。在胸痛發(fā)作初24小時(shí),血漿和尿的兒茶酚胺水平最高。血漿兒茶酚胺分泌在梗死后1小時(shí)上升最快。在急性心肌梗死患者中,高兒茶酚胺血癥可引起嚴(yán)

31、重的心律失常,增加心肌耗氧量和血液中游離脂肪酸濃度,導(dǎo)致心肌廣泛性損害、心源性休克,引起早期和晚期死亡率增高。,62,,(3)腎上腺皮質(zhì):急性心肌梗死時(shí),血漿與尿液中17—羥類固醇、17—酮類固醇和醛固酮亦明顯增加,其濃度與血漿谷草轉(zhuǎn)氨酶和血清肌酸激酶的峰值水平直接相關(guān),說明心肌梗死可促進(jìn)腎上腺糖皮質(zhì)激素的分泌。,63,,(4)甲狀腺:急性心肌梗死時(shí),血清T3,可呈明顯的短暫性降低,并伴有反T3水平的升高,T4和TSH水平無變化。,64

32、,,血液系統(tǒng)功能改變: ?。?)血小板:急性心肌梗死患者,血小板均有高度聚集現(xiàn)象,且大約1/3的病人其血小板存活時(shí)間縮短。此外,血小板的功能亦發(fā)生異常,其血栓素a2的含量明顯增加?! ?2)凝血功能:血小板被激活后,血栓的終末產(chǎn)物如纖維蛋白原降解產(chǎn)物增加,凝血功能增強(qiáng)。,65,,(3)白細(xì)胞:急性心肌梗死常伴有白細(xì)胞增加,增加程度與心肌壞死的程度有關(guān)。目前認(rèn)為白細(xì)胞參與了血栓形成過程。嗜中性白細(xì)胞可產(chǎn)生白三烯b4和氧自由基等中介物,

33、對微循環(huán)功能產(chǎn)生重要影響?! ?4)血粘度:急性心肌梗死患者的血粘度均有不同程度的增加,可能與血清α球蛋白和纖維蛋白原濃度的增高致紅細(xì)胞聚集有關(guān)。,66,,腎功能損害:急性心肌梗死并發(fā)心源性休克,心輸量降低,均可導(dǎo)致氮質(zhì)血癥和腎功能不全。,67,〖六、電生理學(xué)改變:〗,梗塞區(qū)心電圖的特異性變化及各種心律失常。(一)特征性改變(二)動(dòng)態(tài)性改變(三)判斷部位和范圍,68,(一)特征性改變,69,(一)特征性改變,70,(二)動(dòng)態(tài)性改

34、變,1.超急性期 發(fā)病數(shù)小時(shí)內(nèi),異常高大兩肢不對稱的T波。2.急性期 數(shù)小時(shí)后,ST段明顯抬高,弓背向上,直立的T波,形成單向曲線,1-2日內(nèi)出現(xiàn)病理性Q波,同時(shí)R波減低,病理性Q波或QS波常持久不退。3.亞急性期 ST段抬高持續(xù)數(shù)日于兩周左右,逐漸回到基線水平,T波變?yōu)槠教够虻怪谩?.恢復(fù)期 數(shù)周至數(shù)月后,T波呈V形對稱性倒置,可永久存在,或在數(shù)月至數(shù)年后恢復(fù)。,71,(三)判斷部位和范圍,可根據(jù)出現(xiàn)特征性改變的導(dǎo)聯(lián)來判斷心肌梗

35、塞的部位。如V1、V2、V3反映左心室前壁和側(cè)壁,Ⅱ、Ⅲ、aVF反映下壁。Ⅰ、avF反映左心室高側(cè)壁病變。,72,肢體導(dǎo)聯(lián),,73,Correlation of ECG Changes and Areas of Damage,74,Acute Anterior MI,左冠狀動(dòng)脈前降支閉塞,梗塞區(qū)在左心室前壁、心尖部、下側(cè)壁、室間隔前部。,左冠狀動(dòng)脈前降支閉塞,梗塞區(qū)在左心室前壁、心尖部、下側(cè)壁、室間隔前部。,75,Acute Anter

36、ior Wall MI,76,Acute Anterior Wall MI,77,Acute Inferior MI,右冠狀動(dòng)脈閉塞,梗塞區(qū)在左心室膈面(右冠狀動(dòng)脈占優(yōu)勢時(shí))、室間隔后部、和右心室,并可累及竇房結(jié)和房室結(jié)。,,78,Acute Inferior Wall MI,79,Acute Posterior MI,左冠狀動(dòng)脈回旋支閉塞,梗塞區(qū)在左心室高側(cè)壁、膈面(左冠狀動(dòng)脈占優(yōu)勢時(shí)),和左心房,可累及房室結(jié)。,,80,Acute

37、Inferior Wall MI with Posterior Extension,81,Right Ventricular Infarction,ST segment elevation V4R highly predictive of RV infarctHigher in-hospital mortalityHigher incidence of in-hospital complicationsNEJM 199

38、3(APR);328:981-8.,82,Acute Right Ventricular Wall MIRight Sided Leads,83,〖七、生物標(biāo)志物濃度的改變:〗,,,Shapiro BP, Jaffe AS. Cardiac biomarkers. In: Murphy JG, Lloyd MA, editors. Mayo Clinic Cardiology: Concise Textbook. 3rd ed. Ro

39、chester, MN: Mayo Clinic Scientific Press and New York: Informa Healthcare USA, 2007:773–80. Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 5.,84,Non ACS causes of Troponin Elevation,Trauma (including con

40、tusion; ablation; pacing; ICD firings,, endomyocardial biopsy, cardiac surgery, after-interventional closure of ASDs)Congestive heart failure (acute and chronic)Aortic valve disease and HOCM with significant LVHHypert

41、ensionHypotension, often with arrhythmiasNoncardiac surgery Renal failureCritically ill patients, especially with diabetes, respiratory failureDrug toxicity (eg, adriamycin, 5 FU, herceptin, snake venoms)Hypothyroi

42、dismCoronary vasospasm, including apical ballooning syndromeInflammatory diseases (eg, myocarditis, Kawasaki disease, smallpox vaccination, Post-PCI Pulmonary embolism, severe pulmonary hypertensionSepsisBurns, esp

43、ecially if TBSA greater than 30%Infiltrative diseases: amyloidosis, hemachromatosis, sarcoidosis, and sclerodermaAcute neurologic disease, including CVA, subarchnoid bleedsRhabdomyolysis with cardiac injuryTransplant

44、 vasculopathyVital exhaustion,Modified from Apple FS, et al Heart J. 2002;144:981-986.,85,并發(fā)癥,86,Acute Myocardial InfarctionComplications,Death (18% within 1 hour, 36% within 24 hours)Non-fatal arrhythmiaAcute left v

45、entricular failureCardiogenic shockPapillary muscle rupture and mitral regurgitationMyocardial rupture and tamponadeVentricular aneurysm and thrombus,87,Acute MI: Acute Complications,Postinfarction VSDFree wall rup

46、turePostinfarction ventricular aneurysm associated with ventricular tachyarrhythmias/CHF,88,Complications of MI,Cardiac Tamponade: Fluid between pericardium/myocardiumPericarditis: Inflammation of the pericardiumEmbol

47、i: From either MI thrombus or atrial clots formed with atrial pooling,89,,90,,91,,92,Most Common Complications:,Congestive Heart Failure:75% of MI’s experience overt CHF Fluid backs up…25% of MI’s experience

48、“compensated” CHF reduced perfusion to “vital organs”?Dysrhythmias: The importance of ECG monitoring post-MI,93,Cyanosis (blue fingernails &lips),Clubbing of the fingers,Pitting Edema (note handprint),,Maj

49、or Physical Signs Suggestive of Cardiopulmonary Disease,Ascites (fluid in the peritoneum),Xanthelasma,,,94,治療,95,MANAGEMENT OF ACUTE MYOCARDIAL INFARCTION AND THE RATIONALE FOR EARLY EPERFUSION,Aims:Prevent death Limi

50、t the extent of myocardial damageMinimise patient´s discomfort and distress,“TIME IS MUSCLE!”,Strategy:Re-establish myocardial reperfusion before irreversible damage occurs:mechanically (PCI)pharmacologically (i

51、nduction of thrombolysis by thrombolytic agent),Van de Werf et al. Eur Heart J 2003; 24: 28–66.,96,目的,97,原則,如果開始PCI治療的時(shí)間要比開始藥物纖溶的時(shí)間延遲60分鐘以上,那么PCI治療可能并不能降低死亡率及時(shí)采用合適的再灌注治療比選擇治療方式更重要,98,Ischemic Coronary Syndromes,“Ischemi

52、c and injured tissue have reduced blood flow but may be salvaged. The area of the Penumbra may be viable for several hours after onset of occlusion.”Source: Emergency Cardiovascular Care Library (CD-ROM), American Hea

53、rt Association, Dallas, 1997,99,Treatment of Acute MISummary,100,,INFLUENCE OF TIME-TO-TREATMENT ON THE ODDS RATIO (OR) OF MORTALITY,Boersma et al. Lancet 1996; 348: 771–775.,ABSOLUTE BENEFIT PER 1,000 TREATED PATIENTS

54、,TREATMENT DELAY IN HOURS,,,,,,,,,,0,3,6,9,12,15,18,21,24,0,20,40,60,80,,,,,,,The “golden hour”: 65 lives are saved for every 1,000 patients treated when the treatment is initiated within the first hour of symptom onset!

55、,,,,101,,IMPACT OF TIME-TO-TREATMENT AND 30-DAY MORTALITY PCI VS. THROMBOLYSIS,30-35-DAY MORTALITY (%),Thrombolysis,,PCI,,Cannon et al. J Thromb Thrombol 1994; 1: 27–34.Cannon et al. JAMA 2000; 283: 2941–2947. Huber et

56、al. Eur Heart J 2005; 26: 1063–1074.,TIME FROM ONSET OF PAIN TO THERAPY IN HOURS,,0,6,12,2,4,2,4,6,8,10,8,0,1,3,5,7,,,,102,102,ESC STEMI GUIDELINES 2008: REPERFUSION STRATEGIES,Van de Werf et al. Eur Heart J 2008; 29: 29

57、09-2945..,Ambulance,First Medical Contact (FMC),,PCI-capable hospital?,Non-PCI-capable hospital,primary PCI,rescue PCI,angiography§,Pre-, in-hospital fibrinolysis,,2h,12h,24h,Time Limits,* Time FMC to first balloon

58、 inflation must be shorter than 90 min in patients presenting early (< 2 h after symptom onset), with large amount of viable myocardium and low risk of bleeding.,#If PCI is not possible < 2 h of FMC, start fibrinol

59、ytic therapy as soon as possible.,§Not earlier than 3h after start fibrinolysis.,?24/7 service,successful,failed,PCI < 2h possible*PCI < 2h not possible#.,,,,,,,,103,Specifics of Early Hospital Care,Anti-I

60、schemic TherapyAnti-Platelet TherapyAnticoagulant Therapy,104,Early Hospital CareAnti-Ischemic Therapy,Class IBed/Chair rest and TelemetryOxygen (maintain saturation >90%)Nitrates (SLx3 Oral/topical. IV for ongo

61、ing iscemia, heart failure, hypertension)Oral B-blockers in First 24-hours if no contraindications. (IV B-blockers class IIa indication)Non-dihydropyridine Ca-channel blockers for those with contraindication fo B-block

62、ersACE inhibitors in first 24-hours for heart failure or EF<40% (Class IIa for all other pts) (ARBs for those intolerant)Statins,105,,Early Hospital CareAnti-Ischemic Therapy,Class IIINitrates if BP0.24 sec, 2nd o

63、r 3rd degree heart block, active asthma, or reactive airway diseaseNSAIDS and Cox-2 inhibitors,106,Early Hospital CareAnti-Platelet Therapy,Class IAspirin (162-325 mg), non enteric coatedClopidogrel for those with As

64、pirin allergy/intolerance (300-600 mg load and 75 mg/d)GI prophylaxis if a Hx of GI bleedGP IIb/IIIa inhibitors should be evaluated based on whether an invasive or conservative strategy is usedGP IIb/IIIa inhibitors r

65、ecommended for all diabetics and all patient in early invasive arm,107,Early Hospital CareAnticoagulant Therapy,Class IUnfractionated HeparinEnoxaparinBivalarudinFondaparinuxRelative choice depends on invasive vs

66、conservative strategy and bleeding risk,108,8,16,32,40,48,56,72,隨機(jī)后小時(shí),Antman EM, et al. Circulation 1999;100:1593-1601,TIMI - 11B 研究依諾肝素的顯著優(yōu)勢在早期(48小時(shí))就顯示出來,急性期(48小時(shí)) 依諾肝素組事件發(fā)生率顯著低于普通肝素,,10 –,8 –,6 –,4 –,2 –,0,,普通肝素,依諾肝

67、素,發(fā)生事件病人%,7.3%,5.5%,,,,,,RRR = 23.8%P=0.029,,,109,Cohen M, et al. N Engl J Med. 1997;337:447-52.,ESSENCE 研究依諾肝素與普通肝素相比,顯著降低30天終點(diǎn)事件(死亡、MI和復(fù)發(fā)心絞痛),且14天時(shí)就已顯現(xiàn)其優(yōu)勢,110,依諾肝素是唯一被證實(shí)優(yōu)于UFH的LMWH,也是唯一被ACC/AHA UA/NSTEMI治療指南推薦的LMWH,美國

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