（童鴻）

Classic definition of the term cardiac memory(CM)refers to the persistent T-wave changes on the ECG after a period of wide QRS rhythms that become evident once normal ventricular activation pattern is restored.It is related to the term ventricular electric remodeling sometimes used in basic science literature.Although CM itself is considered as an adaptive reaction to the change in the ventricular activation sequence,its manifestations (usually T-wave inversions,TWIs)are often confused with pathological conditions manifesting with TWI,such as myocardial ischemia or infarction.

In 1982,Rosenbaum et al introduced the term heart memory and presented the first unified hypothesis of how abnormal ventricular activation could lead to the development of T-wave abnormalities regardless of the wide QRS cause by a process he referred to as electrotonic modulation.In this seminal article,3 principles of CM were formulated:(1)the direction of the T waves in sinus rhythm follows (remembers)the direction of the QRS complex during preceding episode of abnormal activation;(2)the amplitude of memory T waves increases the longer abnormalconduction continues,and (3)repeatepisodesofabnormal activation after complete normalization of T waves result in more rapid and prominent accumulation of T-wave changes(hence the term memory).

Molecular Mechanisms

In brief,CM comprises a spectrum of 2 distinct but overlapping phenomena which differ in the mechanisms by which repolarization changes are achieved:shortterm and long-term CM.Short-term CM observed within minutes of ventricular pacing is thought to occur from modulation and modification of existing proteins and channel trafficking.It is relatively short-lived and dissipates within minutes.Long-term CM is seen after longer periods of abnormal activation and is longer lasting (days to weeks).It includes changes in gene transcription and protein synthesis.Molecular changes observed in the setting of CM include alterations of multiple ion channels,receptors,and cell coupling,including the transient outward current,Ito,IKr,ICa,Na/Ca exchanger,AT1 receptors,stretch-activated receptors,and gap junction redistribution.

Triggers of CM

Perhaps the most important discovery in the physiology of CM was establishing its relationship to the mechanical function of the heart.The notion that it is the change in ventricular contraction pattern and local ventricular wall stress (as opposed to electrotonic modulation originally proposed by M.Rosenbaum)that triggers CM was first made on the basis of CM inhibition by the renin-angiotensin system blockade.It was later confirmed in elegant experiments with excitation-contraction uncoupling demonstrating that pacing-induced CM only develops if the change in the electric activation sequence is accompanied by the active mechanical contraction, whereas CM-like changes can develop as the result of local mechanical myocardial stretching alone without electric activation change.

Role of Vectorcardiography in Evaluation of CM

As originally noted by Rosenbaum et al,not only the T waves follow the direction of the wide QRS complex in each ECG lead,but also the whole T-wave 3-dimensional vector aligns with the wide QRS vector when assessed using vectorcardiography.

This3-dimensionalnature ofrepolarization changes in CM made vectorcardiography a preferred tool of its assessment so that instead of tracking disparate T-wave polarities and amplitudes in individual leads the change in the whole T-wave vector can be observed and measured. The vectorcardiography-based measurement of CM,T-vector peak displacement was developed.It allowed to express CM magnitude as a single numeric value and track its changes under different experimental conditions.

Why was CM Initially Described only during Normal Ventricular Activation

Traditionally,CM has been associated with TWI during sinus rhythm with narrow QRS for several reasons:

First,normal T waves during sinus rhythm are positive in mostleads,whereasTWIisusually associated with pathological conditions (eg,ischemia,strain, cerebral hemorrhage). Therefore, T-wave changes are more likely to be noticed when TWI is present.Second,in the most common situations leading to CM development (LBBB,right ventricular apical pacing),wide QRS deflections initiating CM are negative in the majority of the leads and therefore produce TWI.Third,large secondary repolarization changes during wide QRS rhythms mask CM until the QRS becomes narrow(Figure 1).

Figure 1 ECG during narrow (AAI pacing,A)and wide QRS(DDD pacing,B)before (baseline)and after cardiac memory(CM)induction(day 7).A,At baseline,the T waves during AAI pacing are positive in most leads.On day 7 during AAI pacing,inverted T waves in multiple leads assume the polarity of the paced QRS complex consistent with CM.B,During wide QRS rhythm,CM manifests as a decrease in the T-wave amplitude with no change in polarity on day 7 compared with the baseline. Unless quantitative vectorcardiography methods are used to measure the T-wave loop,this change usually goes unnoticed on a 12-lead ECG.

Distin guishing between TWI from CM and Ischemia

Since the time CM was first described,its similarity to ischemic TWI made it a significant confounder in the diagnosis of myocardial ischemia often resulting in excessive cardiac testing.In particular,precordial TWI because of intermittent right ventricular pacing or LBBB(by farthe mostcommon presentationsofCM encountered in clinical practice)can be easily confused with the Wellens'syndrome2characteristic of transient proximalleftanteriordescending coronary artery occlusion,a condition requiring promptcoronary intervention.

In general,the direction of the ischemic T-waves points away from the area of ischemia.Because the ischemic region attributable to the proximal left anterior descending coronary artery lesion involves the left ventricle,the ischemic precordial TWI has a rightward axis in the frontal plane and is characterized by TWI in leads I and aVL.The rare cases of right coronary artery ischemia producing precordial TWI with the leftward axis have deeper TWI in inferior leads than that in the precordial leads.However,right ventricular apical pacing and LBBB produce QRS vectors positive in leads I and aVL resulting in positive T waves in these leads on resumption of normal conduction consistent with CM principles.It also produces precordial TWI deeper than the inferior TWI.

The combination of positive T in lead aVL and positive/isoelectric T in lead I,and precordial TWI＞inferior TWI produces a unique pacing induced CM signature that was 92%sensitive and 100%specific in differentiating pacing-induced TWI from ischemia in a retrospective study.

Figure2 Vectorcardiogram of the patient in Figure 1 during AAI and DDD pacing in frontal (A)and transverse(B)projections before(baseline)and after the induction of cardiac memory (CM;day 7).On day 7 during AAI pacing,the T vector assumes the direction of the paced QRS complex while increasing in magnitude.At the same time in DDD mode,the T-vector magnitude decreases with no change in direction.Black arrows indicate the direction and magnitude of the projection of T-peak displacement as the result of CM and are similar in AAI and DDD modes.

Cardiac Memory in Wide QRS Rhythms

Despite the fact that processes underlying CM do not develop suddenly on QRS normalization but rather progress gradually during abnormal ventricular activation,for a long time it was thought that CM cannot be detected until QRS becomes narrow.Secondary T-wave changes in wide QRS rhythms occur immediately and are dominant,whereas CM-induced T-wave changes are initially subtle and while gradually increasing over time are obscured by the secondary changes.The assessment of CM by surface ECG in the setting of wide QRS is limited because of the dominance ofthesecondaryT-wave changes.Repolarization changes because of CM in this situation have been largely overlooked,being masked by the large discordant T waves.Nevertheless,vectorcardiogram can readily detect CM in this situation.Figure 2 presents the vectorcardiogram of the patient shown in Figure 1 demonstrating the 3-dimensional T-vector displacement after 7 days of right ventricular pacing during the narrow(AAI pacing)and wide(DDD pacing)QRS.The actual T-vector change (T peak displacement)in the narrow and wide QRS is nearly identical in both magnitude and direction.As seen on both Figures 1 and 2,CM in wide QRS rhythms presents as a decrease in T-vector magnitude without directional change (another reason why they are usually missed)in contrast to the narrow QRS rhythm,where T vector becomes larger and rotates toward the paced QRS. Using quantitative vectorcardiograpic analysis,CM can be detected in paced rhythm within minutes after the onset of pacing.

Clinical Application of CM in Wide QRS:Age Determination of LBBB

The finding that CM decreases discordant T-wave amplitude in wide QRS rhythms has important clinical implications.For example,it can be used to determine whether LBBB is old or new which becomes valuable in the setting of chest pain.

The criterion for LBBB age determination was developed on the premise that new LBBB would have larger T vector(and taller T waves on a 12-lead ECG)compared with the old one in accordance with CM development in wide QRS rhythm (Figure 3).As the duration of LBBB increases the discordant secondary T waves become smaller (Figure 3A).A retrospective analysis＞1700 LBBB ECGs showed that indeed the new onset LBBB (defined as＜24-hour duration)was rare(3%)and had significantly larger T waves(as well as smaller QRS vector magnitude)compared with the chronic LBBB (Figure 3B and 3C).Although the best results in LBBB age determination were achieved using quantitative vectorcardiography technique,a simplified 12-lead ECG criterion using the ratio of the maximal precordial S wave/maximal precordial T-wave amplitude(asapproximationsofthe QRS and T vectors,respectively)was also developed.A conservative cutoff of S/T＜2.5 allowed to detect 100%of the new LBBBs.

Figure 3 Use of the maximal precordial S/T ratio in left bundle branch block (LBBB)age determination.S/T represents the ratio of the maximal precordial S wave/maximal precordial T-wave amplitude.A,As the duration of LBBB increases,the maximal precordial S/T ratio increases from 1.64 at 6 hours(=new)to 3.22 at 15 days(=old).B,A typical example of resolution of a new LBBB (＜8-hour duration).S/T ratio is 1.61.Resolution of LBBB results in no apparent T-wave abnormalities during narrow QRS.C,A typical example of resolution of an old LBBB (＞3-day duration).S/T ratio is 2.93.Typical changes of cardiac memory with precordial TWI are evident during narrow QRS.D,A new onset LBBB (＜75 minutes)in a setting of an acute left anterior descending coronary artery thrombosis.S/T ratio is 1.68 consistent with the new LBBB.Note ST segment changes in the baseline tracing consistent with ischemia and loss of R waves after resolution of LBBB.

TheT-vectormagnitudein LBBB changes significantly during the first 24 hours.In cases of painful LBBB syndrome when ECG isrecorded within seconds/minutes of symptoms onset (often during an exercise stress test),S/T ratio can be as low as 1.4.The majority of the T-wave changes occur within the first 24 hours of LBBB persistence when it assumes chronic QRST configuration.In the true chronic LBBB,the S/T ratio is close to≥3.0 (Figure 3A and 3C).It is important to recognize that LBBB is often a dynamic phenomenon and can be intermittent or rate-dependent.Repeated episodes of intermittent LBBB can cause accumulation of CM-related T-wave changes,sometimes making the distinction between new and old LBBB difficult.

The new LBBB S/T criterion held true in a small subgroup of patients with acute coronary syndrome(Figure 3D)but needs to be confirmed in larger clinical trials.

詞 匯

seminal adj.精液的,繁殖的,種子的

trafficking n.非法買賣

dissipate v.驅(qū)散,使……消散,消散,使...散放,放蕩,耗散,浪費(fèi),使……耗散

synthesis n.綜合,合成,合題

elegant adj.雅致,優(yōu)美的,精確的,上等的

vectorcardiography n.心電向量測定法

disparate adj.全異的

displacement n.移位,位移,撤換

confounder n.混亂者

resumption n.重新開始,恢復(fù)

obscure adj.&v.晦澀的,無名的,隱藏的；使……變暗,遮住,使……難解

premise n.假定,前提;v.引出

土壤消毒的方法有：高溫消毒和藥物消毒，高溫消毒就是把整個(gè)大棚密閉，高溫悶棚7～8天。藥物消毒就是把多菌靈與濕潤細(xì)土按1∶25的比例拌勻后與基肥均撒在地面上，同時(shí)用辛硫磷（500克/畝）對水噴霧，然后進(jìn)行深翻，既滅菌又滅地下害蟲。種子處理的做法有：將備足的種子用兩份開水對一份涼溫水（55℃）浸種10分鐘，邊浸邊攪動(dòng)，先用30℃溫水浸種3～4小時(shí)，再用高錳酸鉀1000倍液浸泡15分鐘，隨即將種子用清水洗凈，包好放入盆內(nèi)，置于25～30℃處進(jìn)行催芽，種子有半數(shù)露白時(shí)即可播種。

conservative adj.&n.保守,保守的,保守黨,穩(wěn)當(dāng)?shù)?保守者,防腐劑

注 釋

1.in the making指“正在興起、正在形成、策劃中、醞釀中”等，如A stem cell that loses its immunoprotection over time is a time bomb in the making.隨著時(shí)間推移，失去免疫保護(hù)的干細(xì)胞是潛在的定時(shí)炸彈。

2.Wellens'syndrome是De Zwaan等于80年代首先描述的一種綜合征，患者胸痛時(shí)心電圖表現(xiàn)為V2、V3T波深倒（＞5mm）或雙向，ST段不抬高或輕度抬高，是冠狀動(dòng)脈前降支近端嚴(yán)重狹窄的特征性改變，預(yù)示前壁大面積梗死的危險(xiǎn)，而當(dāng)患者來急診時(shí)通常已無胸痛癥狀，心肌酶正常或僅輕度增高，如果單純藥物治療，75%會在數(shù)周內(nèi)發(fā)生急性心肌梗死。

參考譯文

第83課心臟記憶：新興的診斷工具

術(shù)語心臟記憶的經(jīng)典定義是指一段時(shí)間寬QRS節(jié)律后心電圖上出現(xiàn)的持續(xù)性T波變化，一旦恢復(fù)正常心室激動(dòng)圖形后，這種T波變化就變得顯而易見。這與有時(shí)用于基礎(chǔ)科學(xué)文獻(xiàn)中的術(shù)語心室電調(diào)節(jié)相關(guān)。雖認(rèn)為心臟記憶本身是對心室激動(dòng)順序變化的適應(yīng)性反應(yīng)，其表現(xiàn)（通常為T波倒置，T-wave inversion，TWI）經(jīng)常與呈現(xiàn)TWI的病理狀態(tài)如心肌缺血或梗死相混。

1982年，Rosenbaum等引入術(shù)語心臟記憶，并首次提出，無論寬QRS波群的原因是什么，異常心室激動(dòng)通過他稱作電張調(diào)節(jié)的過程如何導(dǎo)致T波異常的統(tǒng)一假設(shè)。在這一開創(chuàng)性文章中，規(guī)定了心臟記憶的三原則：（1）竇性節(jié)律的T波方向追隨其前一陣異常激動(dòng)的QRS波群方向；（2）記憶T波振幅隨異常傳導(dǎo)持續(xù)時(shí)間延長而增大；（3）T波完全正?；?，重復(fù)一陣異常激動(dòng)導(dǎo)致更快速和明顯的T波變化累積。

分子機(jī)制

簡言之，心臟記憶由兩種復(fù)極機(jī)制明顯不同但卻重疊的一組現(xiàn)象構(gòu)成，即短期和長期心臟記憶。短期心臟記憶見于心室起搏后數(shù)分鐘內(nèi)，認(rèn)為與現(xiàn)存的蛋白調(diào)節(jié)和修飾以及通道的異常通行有關(guān)。持續(xù)時(shí)間短，數(shù)分鐘內(nèi)消失。長期心臟記憶見于較長時(shí)間的異常激動(dòng)后，持續(xù)時(shí)間較長（數(shù)天到數(shù)周）。涉及基因轉(zhuǎn)錄和蛋白合成的變化。心臟記憶研究觀察到的分子變化包括多個(gè)離子通道、受體、細(xì)胞偶聯(lián)的改變，包含短暫外向電流、Ito,IKr,ICa,Na/Ca交換蛋白,AT1受體,伸拉活化受體和間隙連接再分布。

心臟記憶的促發(fā)因素

心臟記憶電生理學(xué)中最為重要的發(fā)現(xiàn)也許是正在建立起其與心臟機(jī)械功能的關(guān)系?；谘芫o張素系統(tǒng)抑制劑對心臟記憶的抑制，首次提出促發(fā)心臟記憶的是心室收縮類型與局部室壁應(yīng)力變化這一概念（與Rosenbaum最初假設(shè)的電張調(diào)節(jié)相對立）。這在以后興奮-收縮解偶聯(lián)的精準(zhǔn)實(shí)驗(yàn)中得以證實(shí)，起搏誘發(fā)的心臟記憶只發(fā)生于電激動(dòng)順序變化伴隨主動(dòng)機(jī)械收縮時(shí)，而不伴電激動(dòng)變化的局部機(jī)械性伸展會產(chǎn)生心臟記憶樣變化。

心電向量在評價(jià)心臟記憶中的作用

正如Rosenbaum最初觀察到的，采用向量圖分析顯示，不僅每個(gè)心電圖導(dǎo)聯(lián)上的T波追隨寬QRS波群方向，整個(gè)T波三維向量與寬QRS波群向量相一致。

心臟記憶中復(fù)極變化的三維特性，使得心電向量圖成為復(fù)極變化分析的優(yōu)選工具，以致取代追蹤各個(gè)心電圖導(dǎo)聯(lián)上T波反向極性和振幅，從而觀察和測量整個(gè)T波向量的變化。已形成以心電向量圖為基礎(chǔ)的心臟記憶測定，即T波-向量峰值位移。這使得心臟記憶幅度可用單個(gè)數(shù)值表達(dá)，并可追蹤不同實(shí)驗(yàn)條件下的變化。

為什么最初描述的心臟記憶只出現(xiàn)于正常心室激動(dòng)期間

傳統(tǒng)意義上，竇性節(jié)律窄QRS波群時(shí)心臟記憶總與TWI聯(lián)系在一起有幾個(gè)原因：

首先，竇性節(jié)律時(shí)的正常T波在多數(shù)導(dǎo)聯(lián)呈正向，而TWI通常與病理狀態(tài)（如缺血、勞損、腦出血）相關(guān)。因此，當(dāng)出現(xiàn)TWI時(shí)更易觀察到T波的變化。其次，在最常導(dǎo)致心臟記憶發(fā)生的狀態(tài) [左束支傳導(dǎo)阻滯（LBBB），右心室心尖起搏]，引發(fā)心臟記憶的寬QRS波群在多數(shù)心電圖導(dǎo)聯(lián)上是負(fù)向的，因此而產(chǎn)生TWI。第三，寬QRS節(jié)律時(shí)大的繼發(fā)性復(fù)極變化掩蓋了心臟記憶，直至QRS波群變窄（圖1）。

心臟記憶與缺血所致TWI的鑒別

自從心臟記憶首次提出那一刻開始，它與缺血性TWI的相似性使得其成為心肌缺血診斷的重要鑒別對象，經(jīng)常導(dǎo)致過度的心臟檢測。特別一提的是源于間歇右心室起搏或LBBB（至今臨床實(shí)踐中最常遇見的心臟記憶）的胸導(dǎo)聯(lián)TWI，易與冠狀動(dòng)脈前降支近端短暫阻塞引起的Wellans'綜合征相混，后者需要緊急冠狀動(dòng)脈介入治療。

通常，缺血性T波的方向背離缺血區(qū)。因前降支冠狀動(dòng)脈近端病變引起的缺血累及左心室，額面上缺血性胸導(dǎo)聯(lián)TWI電軸右偏，特征表現(xiàn)為Ⅰ和aVL TWI。右冠狀動(dòng)脈缺血引起電軸左偏、胸導(dǎo)聯(lián)TWI的罕見病例，下壁導(dǎo)聯(lián)的TWI較胸導(dǎo)聯(lián)深。然而，右心室心尖起搏和LBBB產(chǎn)生I和aVL QRS波向量向上，基于重新開始的正常傳導(dǎo)與心臟記憶一致的原理，導(dǎo)致這些導(dǎo)聯(lián)T波向上，這也導(dǎo)致胸導(dǎo)聯(lián)TWI深度超過下壁TWI。

一項(xiàng)回顧性研究顯示，結(jié)合aVL T波直立和ⅠT波直立/等電位線，以及胸導(dǎo)聯(lián)TWI＞下壁TWI，產(chǎn)生獨(dú)特的起搏誘發(fā)心臟記憶特征，這對鑒別起搏和缺血誘發(fā)的TWI的敏感性和特異性分別達(dá)92%和100%。

寬QRS波群節(jié)律心臟記憶

盡管心臟記憶的過程并非突發(fā)于QRS波群正常化，而是在異常心室激動(dòng)過程中逐漸進(jìn)展，在很長一段時(shí)間內(nèi)認(rèn)為，除非QRS波群變窄，否則，不能探及心臟記憶。寬QRS節(jié)律時(shí)即刻發(fā)生繼發(fā)性T變化且明顯，而心臟記憶誘發(fā)的T波變化初始細(xì)微，隨著時(shí)間推移逐漸增大卻被繼發(fā)性變化所掩蓋。因?yàn)槔^發(fā)性T波變化明顯，在寬QRS波群情況下通過體表心電圖分析心臟記憶受限。在這種情況下，心臟記憶引起的復(fù)極變化多被忽視，因?yàn)槭艿酱蠖聪虻腡波掩蓋。盡管如此，心電向量圖能隨意檢測到此時(shí)的心臟記憶。圖2呈現(xiàn)的是圖1的心電向量圖，證實(shí)7d起搏后窄QRS波群（AAI起搏）和寬QRS（DDD起搏）波時(shí)的三維T-向量位移。窄和寬QRS波時(shí)實(shí)際T-向量變化（T波移位）的量和方向近乎一致。正如圖1和圖2所示，寬QRS節(jié)律時(shí)心臟記憶呈現(xiàn)T-向量降低而方向不變（這是為什么常被遺漏的另一原因），而窄QRS波群節(jié)律時(shí)，T向量增大并且旋轉(zhuǎn)指向起搏QRS波群方向。采用定量心電向量圖分析，于起搏后數(shù)分鐘內(nèi)即可探及起搏節(jié)律的心臟記憶。

寬QRS波群時(shí)心臟記憶的應(yīng)用：LBBB時(shí)間的確定

心臟記憶降低寬QRS節(jié)律時(shí)反向T波幅度具有重要臨床意義。例如，它可用于確定LBBB是陳舊的或新發(fā)的，這在胸痛時(shí)顯得很重要。

根據(jù)寬QRS節(jié)律時(shí)心臟記憶的形成（圖3），與陳舊的LBBB相比，新發(fā)LBBB T向量較大（12導(dǎo)聯(lián)心電圖上T波高尖），以此為前提，形成鑒別LBBB發(fā)生時(shí)間的標(biāo)準(zhǔn)。隨著LBBB持續(xù)時(shí)間延長，反向的繼發(fā)性T波變小（圖3A）?；仡櫡治觯? 700例LBBB心電圖發(fā)現(xiàn)，新發(fā)LBBB（定義為＜24h）極少見 （3%），與慢性LBBB比較具有明顯高尖T波（而QRS向量較?。▓D3B和3C）。雖然采用定量心電向量圖技術(shù)確定LBBB時(shí)間能達(dá)到最佳結(jié)果，但采用胸導(dǎo)聯(lián)最大S波與最大T波振幅比值的簡單12導(dǎo)聯(lián)心電圖標(biāo)準(zhǔn)已經(jīng)形成。取S/T＜2.5的保守截點(diǎn)，能100%診斷新發(fā)LBBB。

LBBB時(shí)T-向量幅度最初24h變化明顯。在疼痛性LBBB綜合征，于癥狀發(fā)作的數(shù)秒或數(shù)分鐘內(nèi)記錄到的心電圖（常在運(yùn)動(dòng)負(fù)荷試驗(yàn)時(shí)），S/T比值可低至1.4。大多數(shù)T波變化發(fā)生于LBBB持續(xù)的最初24h內(nèi)，其時(shí)表現(xiàn)為慢性QRST圖形。對于真正的慢性LBBB，S/T比值≥3（圖3A和3C）。重要的是應(yīng)該認(rèn)識到LBBB常呈動(dòng)態(tài)變化，可呈間歇性或頻率依賴。反復(fù)間歇性LBBB可引起心臟記憶相關(guān)T-波變化的累積，有時(shí)使得新發(fā)與陳舊LBBB難以鑒別。

新的LBBB S/T標(biāo)準(zhǔn)在小樣本急性冠脈綜合征亞組患者中保持準(zhǔn)確性（圖3D），但需在較大的臨床試驗(yàn)中加以證實(shí)。

圖1 誘發(fā)心臟記憶前（基礎(chǔ)）后（第7天）窄（AAI起搏，A）和寬（DDD起搏，B）QRS心電圖。A：基礎(chǔ)狀態(tài)下，AAI起搏期間T波多數(shù)導(dǎo)聯(lián)直立。AAI起搏第7天，多個(gè)導(dǎo)聯(lián)T波倒置，呈現(xiàn)起搏QRS綜合波極性與心臟記憶的一致。B：寬QRS波群節(jié)律期間，與基礎(chǔ)狀態(tài)比較，第7天心臟記憶表現(xiàn)為T-波振幅降低而極性不變。除非采用定量心電向量圖方法測定T-波環(huán)，否則，12-導(dǎo)聯(lián)心電圖上這種變化通常被忽視。

圖2 圖1患者AAI和DDD起搏期間誘發(fā)心臟記憶前（基礎(chǔ)）后（第7天）的額面（A）和橫面（B）心電向量圖。AAI起搏第7天，T向量與起搏QRS波群方向一致，而振幅增大。DDD模式的同一時(shí)間，T-向量振幅減小而方向不變。黑色箭頭標(biāo)明因心臟記憶產(chǎn)生的T-峰位移突起的方向和幅度，AAI和DDD模式下相似。

圖3 胸導(dǎo)聯(lián)最大S/T比值在LBBB時(shí)間判斷中的應(yīng)用。S/T代表最大胸導(dǎo)聯(lián)S波/最大胸導(dǎo)聯(lián)T-波振幅。A：隨著LBBB時(shí)間延長，最大胸導(dǎo)聯(lián)S/T比值從6h（=新發(fā)）的1.64增至15d（=陳舊）的3.22。B：新發(fā)LBBB（＜8h）緩解的典型病例。S/T比值是1.61，LBBB緩解致使窄QRS期間無明顯T-波異常。C：陳舊LBBB（＞3d）緩解的典型病例。S/T比值2.93，窄QRS波群期間呈典型的心臟記憶胸導(dǎo)聯(lián)TWI變化。D：急性左前降支冠狀動(dòng)脈血栓導(dǎo)致的新發(fā)LBBB（＜75min）。S/T比值1.68與新發(fā)LBBB相一致。注意基礎(chǔ)狀態(tài)下ST段變化與缺血相符，LBBB緩解后R波消失。

[1]Shvilkin A,Huang HD,Josephson ME.Cardiac Memory-Diagnostic Tool in the Making.Circ Arrhythm Electrophysiol.2015;8:475-482.