研究資料表明Tdp發(fā)生的機制是TDR增大,而不是因為QT間期延長。長QT綜合征的病人,包括遺傳性長QT,藥物性長QT,心梗后的長QT,慢性心衰長QT,和心肌病長QT等,其TDR的增加隨QT間期的增加而增加,QT和TDR呈平行性增加;發(fā)生多型性或扭轉(zhuǎn)性室速(PVT/TdP)的二位相折返的TDR閾值(TDR threshold of reentry)比較高,通常要≥90ms,就是說TDR增加到≥90ms以上才可能發(fā)生PVT或TdP;而短QT綜合征的TDR的增加隨QT間期的縮短而增加, TDR增加和QT間期呈反向性;發(fā)生PVT/TdP的二位相折返的TDR閾值比較低,通常達(dá)50ms以上,就可能發(fā)生PVT或TdP;Brugada綜合征的TDR增加,QT間期不變化或梢短, TDR增加和QT間期長短無關(guān);發(fā)生PVT/TdP的二位相折返的TDR閾值也較低, ≥50-80ms就可發(fā)生PVT或TdP。參見圖2-3-2-6。
4.2.1.2 二位相折返的二種機制:【9,10,15-20】
心臟性猝死的2相折返的機制和類型,可按離子流機制,心電圖和臨床特點區(qū)分為QT間期病理性延長和QT間期正?;虿±硇钥s短二類:
一類是以長QT綜合征為代表的,Ikr、Iks等外向鉀電流外流減少或鈣超載,后除極觸發(fā)機制誘發(fā)的2位相折返,心電圖表現(xiàn)為QT間期延長、QT長短交替、T波交替、Tp—Te延長和QT離散度增大等,臨床常見于心室肥厚、陳舊性心梗、慢性心衰和各種藥物所致的QT間期延長等。
另一類以J綜合征為代表,心外膜瞬時外向鉀電流(Ito)增加,穹窿消失與心內(nèi)膜的電位差增大,誘發(fā)2位相折返性室速、室顫。心電圖特點是J點抬高、J波形成,ST段抬高,且與T波的上升支融合為一體弓背向下,但QT間期正?;蚩s短,可同時有T波交替、Tp—Te延長和QT離散度增大等。臨床常見于急性冠脈綜合征超急期的J波形成和Brugada綜合征、ERS和SQTS。
4.2.2 預(yù)后和預(yù)防4.2.2.1 預(yù)后 心電圖Tp-e是可以間接反映TDR變化的臨床指標(biāo)【10-31】
心臟性猝死是危害人類的最大的死亡原因,占心血管病死亡總數(shù)的64%。心臟性猝死的心電圖的高危預(yù)警指標(biāo)有:QT間期延長(≥460/480ms), QT間期縮短(≤350/330ms), QT離散度增大(≥80/100ms),T波交替(TWA),和心率變異、心室晚電位等。
近年來特別重視T波頂點(T-peak)到T波終點(T-end)間期(Tp-e)增大(≥80/120ms),和J波異常。因為Tp-e是目前唯一的心電圖可反映心室復(fù)極跨壁離散(TDR)的指標(biāo)。TDR增大是公認(rèn)的最能預(yù)警的指標(biāo),但是TDR只有在冠脈灌注的心肌組織塊的細(xì)胞電生理研究時才能獲得,因此心電圖Tp-e間接反映TDR具有十分重要的臨床意義。T波形成的離子機制決定于復(fù)極期的外向IK1、IKr、IKs和內(nèi)向INa、ICa等離子流。心電圖T波形成機制,概括一句話就是心外膜、中層和心內(nèi)膜三層細(xì)胞復(fù)極二位相-三位相電位的動態(tài)代數(shù)和。心內(nèi)膜(或/和中層)與心外膜的電位差為正,T波直立;為負(fù)T波倒置。心外膜復(fù)極先結(jié)束,相當(dāng)于T波的頂點;心內(nèi)膜梢后結(jié)束,M細(xì)胞結(jié)束最晚,相當(dāng)于T波的終點,因此T波的頂點至終點的間期(Tp-e)可以代表復(fù)極離散度(TDR) 【12-13,19-29】 。
4.2.2.2 預(yù)防 一級預(yù)防為主-輔以ICD防治VT/VF和SCD
流行病學(xué)資料顯示:心血管病死亡的64% 是SCD,其中的60%是急性缺血所致。因此積極預(yù)防冠心病和動脈硬化,以調(diào)理生活方式和藥物等一級極預(yù)為主;對有適應(yīng)癥的病人積極開展ICD防治二位相折返性VT/VF和SCD【31-45】。
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