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The term atrial abnormalities encompasses atrial enlargement, atrial blocks, and abnormalities of atrial repolarization. The following general principles should be emphasized 2:
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Atria become dilated rather than hypertrophied.
P-wave voltage is influenced by extracardiac factors that increase it (eg, hypoxia, increased sympathetic tone) or decrease it (eg, emphysema, atrial fibrosis).
The atrial repolarization wave is usually hidden within the QRS complex (see Fig. 12–1).
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Right Atrial Enlargement
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Right atrial enlargement (RAE) is mainly present in patients with congenital and valvular heart diseases affecting the right side of the heart and in patients with cor pulmonale (see Fig. 12–23B and C) (Figs. 12–22 and 12–23). Typically, the P wave is increased in voltage but not in length.
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The diagnostic criteria of RAE are based on P-wave abnormalities (positive voltage of P ≥ 2.5 mm in II and/or positive voltage > 1.5 mm in V1). These criteria have low sensitivity and somewhat higher specificity.2
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Left Atrial Enlargement
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Left atrial enlargement (LAE) is seen in patients with mitral and aortic valvular disease, IHD, hypertension and some cardiomyopathies (see Figs. 12–22C and 12–23D). Typically, the P wave is bimodal in some leads and +/– in V1 with evident final negative deflection.
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The diagnostic criteria of LAE are as follows2: (1) P wave with a duration 0.12 second or longer, especially seen in leads I or II, generally bimodal, but with normal height, and (2) diphasic P wave in V1 with evident final negative deflection of at least 0.04 second of duration because the second part of the loop is directed backward due to LAE (see Fig. 12–23D, horizontal plane). These two criteria have good specificity (close to 90%; few false-positive cases) but discrete sensitivity (< 60%; more false-negative cases). The +/– P-wave morphology in II, III, and VF with a P of at least 0.12 second is a very specific criterion and has a high positive predictive value (100% in valvular heart disease and cardiomyopathies). However, it has a low sensitivity and low negative predictive value for LAE.
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The most important diagnostic criteria of biatrial enlargement are the following (see Fig. 12–23E)2: (1) P wave in lead II that is taller (≥ 2.5 mm) and wider (≥ 0.12 s) than normal, (2) first part of P wave that is positive and peaked in V1-V2 (positive mode > 1.5 mm) with a slow negative deflection (width ≥ 4 mm), (3) signs of LAE with right ÂP; the opposite case is not valid because the ÂP can be on the left side in isolated RAE of patients with congenital heart diseases, and (4) presence of atrial fibrillation (AF) along with QRS changes suggestive of RAE. Frequently, more than one criterion is found (P ≥ 120 ms in FP + P± in V1 with first part peaked and a slow negative mode).
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The concept of a block means that in a certain part of the heart (sinoatrial junction, atria, AV junction, or ventricles), the electrical stimulus encounters overall significant difficulties for its conduction. A first-degree or partial block (P-IAB) occurs when conduction is slow but the stimulus passes through the area but with slow conduction. A third-degree or advanced block (A-IAB) is when the stimulus does not pass completely through the zone but perhaps could pass at a very slower heart rate; therefore, we call it advanced, not complete. A second-degree block is when the stimulus sometimes passes and sometimes does not2.
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The conduction delay in interatrial block occurs between the right and left atria (Fig. 12–24). Although usually associated with LAE, it may also exist as an isolated finding in cases of pericarditis, IHD, old age, and other conditions.22
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In P-IAB, the stimulus reaches the left atrium via the normal pathway, but with certain delay. The diagnostic criterion of P-IAB is a P wave with a duration at least 0.12 second in the frontal plane.26,27,28 The P-wave length and, consequently, the bimodal morphology of the P wave seen in lead II (which is the most typical lead to detect an isolated P-IAB) are similar to the P wave occurring in LAE. In fact, the delay in interatrial conduction, rather than the left atrium dilation, generally explains the morphology observed with an LAE. However, the morphology of the P wave in the horizontal plane, especially in V1, is usually different. In case of isolated interatrial block (eg, pericarditis), the second part of the loop is not directed so much backward because there is no LAE, and consequently, the P-wave morphology in V1 is positive or only presents a small negative part.
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In A-IAB (see Fig. 12–24),27,28 the stimulus does not reach the left atrium via the normal path but by retrograde left atrial activation.28 The diagnostic criteria of A-IAB are as follows27: (1) P wave with a duration of at least 0.12 second and +/– in II, III, and VF, and (2) often, P wave +/– in V1 to V3 or V4. The prevalence of A-IAB increases with age, being very low before 50 years of age and approaching 25% in centenarians in whom an increase of dementia and stroke associated with A-IAB has been detected.22 This type of block is frequently accompanied, especially when it is present in patients with advanced heart disease, by supraventricular arrhythmias, particularly AF and/or atrial flutter (Bayes syndrome).29,30,31
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Abnormalities of Atrial Repolarization
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The atrial repolarization wave (ST-Ta) usually has a polarity opposed to the P wave and is not visible because it is hidden within the QRS complex. In cases of great sympathetic overdrive in normal individuals, an ST-Ta depression may be seen (see Fig. 12–17C). Moreover, in some cases of remarkable atrial enlargement, pericarditis, or atrial infarction, especially in the presence of a long PR interval, shifts of ST-Ta may be observed (Fig. 12–25).
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Ventricular Enlargement
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Morphologies of ventricular enlargement are secondary to a hypertrophy rather than to dilatation, unlike what occurs in the atria. Slight or even moderate degrees of enlargement of either of the ventricles, mainly the right, or of both at the same time, may not produce abnormalities in the ECG.
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The superiority of echocardiography over the ECG for the diagnosis of ventricular enlargement, mainly of the left ventricle, is evident (the sensitivity is much higher, and the specificity is similar). However, when a ventricular enlargement is diagnosed with an ECG, the accuracy of the ECG is greater than that of the echocardiogram in predicting heart disease evolution and prognosis.
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For details on the diagnosis of RVE and/or left ventricular enlargement (LVE) combined with ventricular block (QRS complex duration > 120 milliseconds), the reader is referred to Bayés de Luna2 and McFarlane and Lawrie.14
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Right Ventricular Enlargement
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RVE is found especially in congenital heart diseases, valvular heart diseases, and cor pulmonale. The changes produced by RVE move the loop rightward and either frontward or backward. This is more a result of a delay of activation of the right ventricle, rather than an increase of the right ventricle mass (which generally never overcomes the mass of the left ventricle). Figure 12–26 shows the changes that RVE may produce in ventricular activation expressed as ventricular loops and how these changes may explain the different ECG patterns. Basically, a large part of the QRS loop is going to the right (presence of S in V6) but sometimes with an anterior loop (R or RS in V1) and occasionally with a posterior loop (rS or QS in V1).
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The lower part of Fig. 12–26 shows three cases of RVE of different etiologies (see legend) in which the ECG pattern in V1 (with more or less R wave) is related more to RVE degree than to RVE etiology.
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The ECG criteria (low sensitivity, high specificity) most frequently used for the diagnosis of RVE are shown in Table 12–1.
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Morphology of V1: (1) Morphologies with dominant or exclusive R wave in V1 are very specific but not very sensitive (< 10%) for the diagnosis of RVE because the loop that gives rise to them (anterior and to the right; see Fig. 12–26B–D) is observed in a small number of cases with RVE (especially in some congenital heart diseases such as pulmonary stenosis). In these cases, the prominent R in V1 is also seen in V2 and V3. Moreover, the repolarization presents an ST-segment depression and a negative and asymmetric T wave (strain pattern; Fig. 12–26, Fig. 12–27A), except in newborns because they may present with an exclusive R wave with a positive T wave. On the contrary, in cases of pulmonary stenosis from tetralogy of Fallot, the morphology in V1 is similar to that in isolated pulmonary stenosis, but in V2, there is an rS morphology. Other causes that may present a dominant R pattern in V1 must be ruled out (Table 12–2). (2) The presence of rsR′ is especially typical of atrial septal defect and sometimes may also be seen in moderate pulmonary stenosis. (3) The rS or even the QS morphology in V1, with RS in V6, may often be observed in the early phases of RVE, or with rS in V6 in advanced cases of chronic cor pulmonale (see Fig. 12–26B).
Morphology of V6. The presence of evident forces directed to the right, which are expressed as an evident S wave in V5 to V6, is one of the most important ECG diagnostic criteria (see Figs. 12–26 and 12–27; see Table 12–1).
SI, SII, SIII. This morphology is frequently seen in chronic cor pulmonale with QS pattern in V1 and RS pattern in V6. Note that this pattern may be secondary to positional changes or it may simply be a normal variant.2 Nonetheless, an abnormal P wave favors the diagnosis of RVE (see Fig. 12–27B).
Electrical axis: ÂQRS of at least +110°. Inferoposterior hemiblock, vertical heart, and lateral infarction must be ruled out. This criterion is quite specific (> 95%) but relays low sensitivity.
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++
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The combination of more than one of these criteria increases the diagnostic possibilities. The differential diagnosis of exclusive or predominant R wave in V1(R, Rs, or RSR′ pattern) is shown in Table 12–2.
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++
The ECG signs indicative of right ventricle acute overload (decompensation of cor pulmonale or pulmonary embolism) are as follows32:
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Change in the ÂQRS (> 30° to the right of its usual position)
Transient negative T waves, sometimes very evident in the right precordial leads
SI, QIII with negative TIII pattern (McGinn-White pattern) in the frontal plane and an RS or rS pattern in V6 (Fig. 12–28)
Appearance of a complete right bundle branch block morphology, often with ST-segment elevation
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++
The latter two criteria are highly specific but have low sensitivity for important pulmonary embolism (see Cor Pulmonale). Nevertheless, the clinical setting and comparison with previous ECGs are important to make a differential diagnosis of both processes.
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Left Ventricular Enlargement
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LVE is found in hypertension, IHD, valvular heart disease, cardiomyopathies, and some congenital heart diseases. In general, in patients with LVE, the maximum QRS vector of the loop increases its voltage and is directed more posteriorly than normal (Fig. 12–29). This explains why the QRS complex negativity predominates in the right precordial leads (see Fig. 12–29A–C). Occasionally, the maximum vector is not directed posteriorly (it is located close to 0°). This implies a tall R wave that is seen even in V2, especially in cases of apical hypertrophic cardiomyopathy (see Fig. 12–29E).
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The ECG pattern changes during disease evolution. The pattern of “strain” appears more in relation with the duration of the disease than with the presence of different types of hemodynamic overload. However, in aortic valve disease, a q wave in V5 to V6 is found more frequently in long-standing aortic regurgitation than in aortic stenosis (Fig. 12–30). The disappearance of the q wave in V6 is probably more related to interstitial septal fibrosis, a substrate of partial left bundle branch block, than to hemodynamic overload31 (see Figs. 12–29 and 12–30).
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The presence of noticeable signs that are suggestive of LVE (high voltage of the QRS together with inverted ST-T wave—strain pattern) in an asymptomatic patient without heart murmur or hypertension suggests hypertrophic cardiomyopathy. The ECG does not correlate with the gene mutation,33 but there are two at least ECG changes suggestive of hypertrophic cardiomyopathy: (1) the striking negative T waves (see Fig. 12–29E) and (2) the presence of a deep and narrow q waves (see Fig. 12–29D).
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Sometimes the LVE pattern, at least partially, and especially the changes in ST-T may be resolved in a few months with pharmacologic treatment, as occurs in hypertension or after surgery (valvular heart disease).
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Various diagnostic criteria exist for LVE,34,35,36,37 with varying sensitivity and specificity, as shown in Table 12–3. It is usually possible to diagnose an LVE through an ECG in patients with severe hypertension, whereas this diagnosis is difficult in asymptomatic normotensive adults. However, the value of the ECG diagnostic criteria shown in Table 12–3 is lower in hypertensive patients. For these patients, the following criterion is useful: sum of the QRS voltage of 12 ECG leads greater than 120 mm.37
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Biventricular Enlargement
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The ECG diagnosis of biventricular enlargement is even more difficult than that of the enlargement of just one ventricle. This is true because the increased opposing forces of both ventricles often counterbalance each other or the notable predominance of the enlargement of one ventricle completely masks the enlargement of the other. Therefore, even those criteria that have fair specificity only have a moderate sensitivity.38
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The following ECG patterns are used for the diagnosis of biventricular enlargement:
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Tall R wave with s in V5 and V6, rSR′ pattern in V1, and P wave of biatrial enlargement
Tall R wave in V5 and V6, with an ÂQRS shifted to the right (≥ 90°). The presence of an inferoposterior hemiblock associated with LVE and an asthenic body build must be ruled out.
Small S wave in V1, deep S wave in V2, predominant R wave in V5 and V6, and an ÂQRS shifted to the right in the frontal plane or an SI–, SII–, SIII–type morphology
The presence, especially in the elderly, of QRS complexes within normal limits but with significant repolarization abnormalities (negative T wave and depression of the ST segment), mainly when the patient presents with AF. This type of ECG can be found in the elderly with advanced heart diseases and biventricular enlargement.
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Blocks at the ventricular level can occur on the right side (Table 12–4) or on the left side (Table 12–5). They can affect the entire ventricle (global block) or only part of it (zonal or divisional block). The blockage of electrical impulses, in the ventricles or in the whole heart (see interatrial blocks) is called a first-degree (partial) block when the impulses pass through the area but with a delay; second-degree block when the stimulus sometimes passes and sometimes does not; and third-degree (advanced) block when the passage of stimulus is blocked.2 The term advanced is preferred over complete, because one can not know whether the stimulus would pass at a very lower heart rate. Second-degree block is known as aberrancy of conduction and is explained in Section 6).
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In global ventricular block, the conduction delay usually occurs in the proximal part of the right or left branches. For this reason, the global ventricular block is known as bundle branch block.
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Advanced or third-degree bundle branch blocks, both right and left, have the following characteristics2,13:
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Depolarization of the ventricle corresponding to the blocked branch that occurs transseptally, beginning at the contralateral ventricle. This phenomenon explains the QRS complex widening (≥ 0.12 second) caused by a small number of Purkinje fibers in the septum and the peculiar QRS complex morphology, both in right and left bundle branch blocks, caused by the loop-hemifield correlation (Figs. 12–31, 12–32, and 12–33).
Diagnosis is mainly based on data provided by the horizontal plane leads V1 and V6 and the frontal plane lead VR.
Slurring at the end of the small of the QRS is usually opposed to the T wave.
Septal repolarization dominates over that of the left ventricular free wall and is responsible for the ST-T changes.
In general, the anatomic changes are more diffuse than the ECG expression.
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Partial or first-degree bundle branch block presents a QRS complex with a duration less than 120 milliseconds, which gives rise to morphologies that are sometimes indistinguishable from some patterns seen in homolateral ventricular enlargement (see Fig. 12–32).
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Zonal or divisional left blocks (hemiblocks) have been studied more in depth, both from the anatomic and electrophysiologic viewpoints, compared with right zonal blocks.
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There are four intraventricular fascicles: right bundle branch, trunk of the left bundle branch, and the superoanterior and inferoposterior divisions of the left bundle. A block of the middle fibers (septal fascicle) of the left bundle can probably also occur (see later). Therefore, in addition to the block of one fascicle, blocks of two fascicles (bifascicular block) or three fascicles (trifascicular) may occur.
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Advanced or Third-Degree Right Bundle Branch Block
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In third-degree right bundle branch block (RBBB), the depolarization of the right ventricle occurs entirely through the septum from the left side, originating the formation of vectors 3 and 4 and causing the global change in QRS loop. The classic ECG morphologies, which result from the loop-hemifield correlation in the frontal and horizontal planes, are shown in Fig. 12–31. The repolarization is from right to left at septal level in case of proximal RBBB or at peripheral level in case of peripheral block. Consequently, the T wave is negative in V1 and positive in V6.
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The blockade location, both in advanced and partial block, is usually proximal. Nevertheless, a block located in the distal part of the branch or in the right ventricle Purkinje network is often seen in some congenital heart diseases (eg, Ebstein anomaly, atrial septal defect, following surgery for tetralogy of Fallot) and in some cardiomyopathies (eg, arrhythmogenic right ventricular cardiomyopathy), giving rise to morphologies similar to those of classic complete or partial bundle branch block but with some specific patterns. See Table 12–2 concerning the differential diagnosis of tall R wave in V1.
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The presence of advanced RBBB does not usually represent a poor prognosis in the absence of overt heart disease. However, it predicts an adverse outcome if it appears after acute MI, concomitantly with acute dyspnea (resulting from probable pulmonary embolism) or during an ACS caused by occlusion of the left anterior descending coronary artery (LAD) proximal to the first septal branch, which is the branch perfusing the right bundle.2
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The ECG diagnostic criteria are as follows (see Fig. 12–31 and Table 12–4):
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QRS of at least 0.12 second with midfinal slurring
V1: rSR′ with slurred R wave and a negative T wave
V6: qRS with evident S wave slurring and positive T wave
VR: QR with evident R wave slurring and negative T wave
T wave with its polarity opposed to QRS slurring
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Partial or First-Degree Right Bundle Branch Block
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In first-degree RBBB, the delay of the activation in the entire ventricle is less important. This explains why the QRS is narrower and the morphology shows less prominent forces to the right (see Fig. 12–32).
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The ECG diagnostic criteria are as follows:
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QRS complex duration less than 0.12 second
Morphology with rsR′ or rsr′ pattern or even rs (RS) in V1, final r in VR, and s wave in VL and V6, but with fewer notches and slurring2
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A similar pattern may be seen in some cases of RVE, as in atrial septal defect, because of a delay of activation of some parts of the right ventricle as a result of the enlargement (see Fig. 12–26C).
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Experimentally,23,39 the injury of the fibers of the superoanterior zone of the right ventricle often causes ECG morphologies of the SI, SII, SIII types.23 Less frequently, the injury of the inferoposterior zone may originate SI RII RIII pattern. In clinical practice, these morphologies are difficult to differentiate from normal variants or RVE.2 The changes in P and T waves may help in the differential diagnosis. The SI, RII, RIII morphology must also be found in the inferoposterior hemiblock.
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Advanced or Third-Degree Left Bundle Branch Block
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In third-degree left bundle branch block (LBBB), the left ventricle activation is through the septum from the right side and differs completely from normal activation. This transseptal activation causes the formation of four vectors, which are characteristic of this type of block and explain the global change in the QRS loop. The classic ECG morphologies, caused by the loop-hemifield correlation in the frontal and horizontal planes, are shown in Fig. 12–33. The repolarization in case of more advanced LBBB is directed from left to right with the T loop opposite in direction to QRS (discordant LBBB).40 This explains the negativity of T wave in leads I, V5, and V6. The T wave is normally located opposite slurring and dominant deflection of the QRS complex. In cases of less advanced LBBB, the T wave is often concordant with the QRS (T-wave positive in leads I, V5, and V6). Also, the concordant repolarization may be explained, in a few cases, by associated IHD.
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The morphology of the distal blocks is similar to that of the classic proximal complete left ventricular block but with more significant final slurrings of the QRS complex. Wherever the global block is located (proximal or distal), when the delay is significant, an R-wave morphology in V6 and a QS complex in V1, with a QRS of at least 0.12 second, are generated.
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The presence of LBBB by itself necessitates the exclusion of heart disease and periodic surveillance. In the acute and chronic phase of IHD, as happens with RBBB,2 LBBB is a marker of poor outcomes. The polarity of T wave concordant with QRS is associated with better prognosis and less comorbidity.40 The presence of LBBB pattern after acute infarction41 or that appears with exercise has worse prognosis.42 Also associated with a worse prognosis is the LBBB that appears after transaortic valve implantation,43 and in heart failure, especially, if associated with AF.44,45 Finally, the morphology of QRS in V3 may help to diagnose the etiology of LBBB.46
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The diagnostic criteria of third-degree LBBB are as follows (see Fig. 12–33 and Table 12–5):
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QRS of at least 0.12 second, sometimes greater than 0.16 second, especially with midportion slurring
V1: QS or rS with a tiny r wave and positive T wave
I and V6: single R with its peak after the initial 0.06 second
VR: QS with positive T wave
T-wave polarity is opposed to the QRS complex slurrings in more than two-thirds of cases (discordant LBBB)
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Partial or First-Degree Left Bundle Branch Block
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In first-degree LBBB, the activation delay in the entire ventricle is less significant (see Fig. 12–32) but is sufficient to conceal the first vector responsible for formation of r in V1 and q in V6. Because of this delay, this first vector is counteracted by the initial activation vector of RV and is not formed. The presence of septal fibrosis, demonstrated by biopsy in patients with aortic valve replacement also explains the lack of first vector (q wave) in left ventricular leads (I, VL, V6).2
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The ECG diagnostic criteria are as follows:
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QRS complex duration less than 0.12 second
A QS complex or a tiny r wave in V1 and a single R wave in I and V6
A similar morphology with disappearance of q in V6, which may be seen because of the presence of septal fibrosis31
Often present in LVE
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Zonal (Divisional) Left Ventricular Block: Hemiblocks
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These zonal blocks are much more known and well studied than the zonal blocks of the right ventricle, especially after the studies of Rosenbaum school.47,48 In zonal (divisional) left ventricular block, the stimulus is blocked in either the superoanterior or inferoposterior division of the left branch (hemiblocks) (Figs. 12–34 and 12–35; see also Fig. 12–13C). Only the ECG criteria of well-established (advanced) superoanterior and inferoposterior division of the left branch (superoanterior or inferoposterior hemiblocks according to Rosenbaum) will be discussed.
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A change in left intraventricular activation occurs in both hemiblocks. As a consequence, the blocked area is depolarized with certain delay, which explains the typical ECG changes that can be seen.
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Superoanterior Hemiblock
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Figure 12–34A shows the activation of the left ventricle in superoanterior hemiblock (SAH) or superoanterior divisional block, and the loop-hemifield correlation in the frontal and horizontal planes. In Fig. 12–34B, a typical example of an SAH is depicted, as well as differences with the SI, SII, SIII pattern (see legend for Fig. 12–34). The diagnosis of SAH may be made only using the ECG criteria.
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The diagnostic criteria are as follows:
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RS complex duration less than 0.12 second
ÂQRS deviated to the left (mainly between –45° and –75°). For the differential diagnosis, it is necessary to rule out other diseases with leftward ÂQRS, such as inferior necrosis, type II Wolff-Parkinson-White (WPW) syndrome, pacemaker implant, and SI, SII, SIII pattern (see Fig. 12–34B)
I and VL: qR; in advanced cases with slurring, especially in the descending part of the R wave
II, III and VF: rS with SIII > SII and RII > RII.
An S wave seen up to V6, with intrinsic deflection in V6 less than VL
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Inferoposterior Hemiblock
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In inferoposterior hemiblock (IPH) or divisional block, typical ECG morphology and clinical conditions, mainly the absence of RVE and asthenic habit, have to be present. It is also usually considered that evidence of left ventricular abnormalities must exist. Figure 12–35A shows the location of the block and the activation of the left ventricle in the case of an IPH or inferoposterior divisional block. In this figure, the typical ECG morphology, in frontal and horizontal planes, explained by the loop-hemifield correlation, can also be observed. In this case, the diagnosis is assured if the ECG pattern appeared abruptly, in the absence of another possible explanation (see Fig. 12–35B and legend).
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The diagnostic criteria are as follows:
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QRS complex duration less than 0.12 second
ÂQRS shifted to the right (between +90° and 110° or more for some authors and +140° for others)
I and VL: RS or rS
II, III, and VF: qR; in advanced cases with slurring, especially in the descending part of the R wave
Precordial leads: S wave up to V6, with an intrinsic deflection time in V6 less than VF
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Block of the middle fibers, called septal block by the Brazilian school, probably produces RS morphology often with slurrings in S in V2 and a prominent R wave in V1. To confirm this diagnosis, the ECG pattern has to be transient. However, this intermittent RS pattern may be also recorded in the evolutive pattern of progressive RBBB.2
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In this section, the ECG criteria of the three most characteristic bifascicular blocks—complete (or advanced) RBBB plus SAH, complete RBBB plus IPH, and bilateral bundle branch block—are discussed.
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The diagnostic criteria of advanced RBBB plus SAH are as follows (Fig. 12–36A and B):
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QRS complex duration greater than 0.12 second
QRS complex morphology: The first portion is directed as in SAH, upward and toward the left, whereas the second portion is directed as in complete global RBBB, anteriorly and toward the right (see Fig. 12–45A). If there is a significant left delay, it can counteract the right forces, giving rise to anterior but left final forces. Therefore, a tall R wave can be seen in V1, but without an S wave in I and, occasionally, also in V6. In this case, a complete LBBB appears to exist in the frontal plane and a complete RBBB in the horizontal plane (“masked” block)49 (see Fig. 12–36B). Sometimes this pattern may be transient.50 A masked bifascicular block usually indicates a worse outcome, even if a pacemaker is implanted.2
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The diagnostic criteria of advanced RBBB plus IPH (Fig. 12–36C) are as follows:
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QRS complex duration greater than 0.12 second
QRS complex morphology: The first portion of the QRS complex is directed downward, as in IPH, whereas the second portion is directed anteriorly and toward the right, as in complete RBBB. This diagnosis requires the presence of some clinical conditions, as occurs in isolated IPH (see Inferoposterior Hemiblock section).
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In bilateral bundle branch block, there is an alternation of complete RBBB and LBBB morphologies in the ECG. This diagnosis requires a pacemaker to be implanted.
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There are several types of trifascicular blocks, but their coverage is beyond the scope of this chapter (see Bayés de Luna2). The most frequent features are as follows:
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RBBB alternating with the block of one of two left bundle branch divisions (Rosenbaum-Elizari syndrome)2,47 (Fig. 12–37)
Once the block of three fascicles has been confirmed by an ECG (RBBB alternating with superoanterior and inferoposterior fascicle blocks) (see Fig. 12–37), a pacemaker should be implanted as soon as possible because the patient may suddenly develop a paroxysmal AV block.2
Bifascicular blocks with a long PR segment. Note that a long PR segment may also be caused by a block at a proximal location (bundle of His); thus, electrophysiologic studies are required to confirm their occurrence.
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Ventricular Preexcitation
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Ventricular preexcitation is considered to exist when the electric stimulus reaches the ventricles earlier (early excitation) than via the normal conduction system.2 Early excitation can be explained by the presence of Kent bundles, which are accessory pathways with accelerated conduction that connect the atria with the ventricles (WPW-type preexcitation).51 The conduction through the Kent bundles may be anterograde, retrograde, or in both directions. In rare cases, there are also other anomalous bundles (atypical preexcitation). In more than 80% of these cases, they consist of long slowly conducting atriofascicular or AV bypass tracts. Other rare anomalous bundles are the fasciculoventricular and nodofascicular tracts, which include the formerly named Mahaim fiber.52 In addition, the presence of an accelerated AV conduction or the rare occurrence of an atrio-His bundle may cause a short PR-type preexcitation.53
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The clinical importance of preexcitation lies in its association with supraventricular tachycardias; its potential to trigger malignant ventricular arrhythmia; and the risk of being confounded with other processes, especially in case of a WPW preexcitation (see the following section).
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Wolff-Parkinson-White–Type Preexcitation
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WPW-type preexcitation is diagnosed by an ECG that shows a short PR interval plus QRS-T abnormalities, primarily caused by a slurred upstroke at the beginning of the QRS complex known as the delta wave (Fig. 12–38).
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Short PR interval: The PR interval generally lasts between 0.08 and 0.11 second. However, a WPW-type preexcitation may also occur with a normal PR interval in the following instances: (1) conduction block in the anomalous pathway; (2) preexcitation far from the sinus node (left side), frequently with a long anomalous pathway; and (3) atypical preexcitation presenting normal PR intervals. The only way to corroborate that the PR interval is shorter, in order to confirm the diagnosis, is by making a comparison with the baseline ECG tracing without preexcitation.
QRS-T abnormalities (Figs. 12–39 and 12–40): The QRS complexes show an abnormal morphology with a width greater than the baseline QRS complex (often > 0.11 second) and a characteristic initial slurring (delta wave). These features are secondary to the initial activation through the contractile myocardium where there are few Purkinje fibers. Different degrees of preexcitation (or delta wave) may be observed (see Fig. 12–38A–C).
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The QRS complex morphology in the different surface ECG leads depends on the location of the epicardial zone of earlier excitation. The vector of the first 20 milliseconds on the ECG (first vector of the delta wave, which can be measured in the ECG) is located at different sites on the frontal plane according to where the earlier ventricular epicardial excitation occurred first (see Fig. 12–39). As a result, the WPW-type preexcitation may be divided into four types (see Fig. 12–39A–D).2 Examples of these four types are displayed in Fig. 12–40.
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Different algorithms have been proposed to predict the location of the anomalous pathway.54 One of the most popular was published by Milstein et al.55
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Repolarization is altered except in cases with minor preexcitation. Repolarization abnormalities are secondary to the alteration in depolarization, and the pathology is more severe when the T-wave polarity opposes that of the preexcited R wave, as when the preexcitation is greater (see Fig. 12–38A–C).
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Changes in the degree of preexcitation are frequent, and they may be abrupt or progressive (Fig. 12–41). Preexcitation can increase if the conduction of the stimulus through the AV node is depressed (eg, vagal maneuvers, drugs), or in contrast, preexcitation can decrease if the AV node conduction is enhanced (eg, physical exercise).
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Regarding the differential diagnosis of WPW-type preexcitation, type-A and type-B preexcitations (see Fig. 12–39) should be differentiated with LBBB (see Fig. 12–40A and B); type-C preexcitation (see Fig. 12–39) with inferolateral infarction, RBBB, or RVE (see Fig. 12–40C); and type-D preexcitation (see Fig. 12–39) with lateral infarction or RVE (see Fig. 12–40D). In all of these cases, the short PR interval and the presence of a delta wave are decisive data for the diagnosis of WPW-type preexcitation.
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Paroxysmal arrhythmias in patients with a WPW ECG pattern constitute the WPW syndrome. Patients with WPW preexcitation frequently present macro-reentrant paroxysmal tachycardia. They show a narrow QRS because the stimulus is activating the ventricles via normal AV conduction and a QRS-P′ less than P′-QRS (orthodromic tachycardia) (Fig. 12–42D). In cases of paroxysmal reentrant tachycardia exclusively resulting from the intranodal (junctional) circuit, the P′ mimics the end of QRS or is hidden within it (see Chap. 84). Indeed, approximately 40% to 50% of paroxysmal tachycardias are attributed to a reentry, including an accessory pathway. In a few cases, the anterograde arm of the circuit is via the anomalous Kent bundle, and the QRS complex is wide during the tachycardia (antidromic tachycardia) (see Chap. 84).
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AF and flutter episodes are also more frequent than in the general population. This is attributed to the rapid retrograde conduction, via the abnormal pathway, of a ventricular premature complex that may reach the atria during a vulnerable atrial period. Another possibility is that paroxysmal tachycardia triggers other arrhythmias, such as AF/flutter. The risk of these arrhythmias is two-fold. First, AF/flutter in patients with an ECG pattern of WPW can be mistaken for sustained ventricular tachycardia, with the associated consequences (Fig. 12–42A and B). Indeed, the differential diagnosis by surface ECG between atrial flutter in WPW syndrome and ventricular tachycardia is especially difficult (see Fig. 12–42B) The second potential risk, in the presence of AF/flutter, is that the accessory pathway may transmit to the ventricle more stimuli than normal, facilitating the possibility of reaching the ventricle in its vulnerable period. Consequently, this can result in ventricular fibrillation and sudden death (Fig. 12–42C).56,57
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Atypical Preexcitation
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In general, the atypical preexcitation that presents reentrant arrhythmias occurs through a long atriofascicular or AV pathway. The other bundles, which include the classic Mahaim fiber, are general bystanders and do not participate in the circuit in reentrant tachycardia.
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The ECG in normal sinus rhythm is normal in the majority of cases or presents minimal preexcitation (absence of q wave in leads I and V6 and rS morphology in lead III).58
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The arrhythmias are less frequent and usually of reentrant junctional type. During preexcited tachycardia, the anterograde conduction is through an atypical bundle (antidromic tachycardia) with retrograde conduction by right bundle branch. Therefore, the morphology is usually of LBBB with left ÂQRS. Generally, there is a late R/S precordial transition zone (at V4 to V6), and in the cases of antidromic tachycardia through Kent bundle and LBBB pattern, the transition zone occurs earlier (R/S in V2 to V3) (see Chap. 84).
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Short PR-Type Preexcitation
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Short PR-type preexcitation, described by Lown et al,53 is evidenced by a short PR interval without changes in QRS morphology (see Fig. 12–38).
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By a surface ECG, it is impossible to differentiate between a hyperconductive AV node, the most frequent, and preexcitation occurring via an atrio-His bundle, which bypasses the AV node slow conduction area and, therefore, does not modify the QRS complex morphology. However, it is easy to differentiate them by intracavitary ECG because this will show a short AV interval in case of a hyperconductive AV node and a short HV interval or even an absent H deflection in the presence of an atrio-hisian tract.
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The association with arrhythmias and sudden death is less frequent in short PR-type preexcitation than in the WPW-type preexcitation. Nevertheless, in case of AF, the ventricular response may be very fast because of the presence of a short PR-type preexcitation, and this can be a problematic situation.
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From the electrophysiologic point of view, according to the importance and duration of ischemia, the TAPs of myocardial cells present the following changes: (1) delay of the repolarization that corresponds to primary T-wave changes, (2) formation of “low-quality” TAP (change in shape) that corresponds to changes of ST, and (3) lack of formation of TAP that explains the presence of the Q wave.
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From the surface ECG point of view, the most typical ECG changes resulting from ischemia are as follows2,59,60,61,62,63,64,65,66: (1) primary T-wave changes that include T waves that are wider, peaked, and/or taller and T-wave flat or negative; (2) primary ST deviations, including ST segment shifts (up and down) from baseline; and (3) changes of QRS (Q wave of necrosis and reciprocal patterns) and changes in the mid-late part of QRS (fractionated QRS).
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However, ischemia may induce many other changes, including the following:
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Prolongation of QT interval that may be considered a part of the changes in the T wave. It is present in the first moments of acute transmural ischemia when there is an increase in duration of TAP of the endocardium, making the T wave wider and taller and lengthening the QT interval.67
Changes in P wave, especially in atrial infarction60
Distortion of QRS complex, especially in very severe ischemia59,60,61,68,69
Appearance of different types of bradyarrhythmias (sinus bradycardia and AV block); tachyarrhythmias (especially AF and premature ventricular contractions, which may lead to ventricular tachycardia and unfortunately to ventricular fibrillation); and intraventricular block (eg, RBBB when the LAD occlusion is proximal to the first septal branch that perfuses the right bundle)60
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First, we will explain how the different models of experimental occlusion of the coronary artery produce different ECG changes. Then, discussion will focus on the changes in T wave, ST segment, and QRS complex that are induced by experimental and clinical ischemia and their electrophysiologic mechanisms. Finally, the ECG changes that appear during the evolution of different clinical settings of IHD, their diagnostic criteria, and the most important clinical and prognostic implications of these ECG changes will be discussed.
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Changes in Electrocardiography under Different Models of Experimental Ischemia Caused by Coronary Occlusion
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After experimental coronary occlusion of the LAD in dogs, performed with an open chest and with the electrodes located in the pericardial sac, Bailey and La Due70 found (Fig. 12–43, 1) that the first ECG change induced by ischemia was negativity of the T wave, which was called ECG pattern of ischemia. This was followed by an ST-segment elevation that he called ECG pattern of injury, and finally, a Q wave appeared, which was called ECG pattern of necrosis (see Fig. 12–43, 1). This terminology was accepted by several groups.13 Thus, it was considered that in patients with IHD, the presence of a negative T wave represented a grade of acute ischemia that was less severe than an ST-segment elevation.
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However, when the experiment to occlude the artery was performed in awake dogs with an unopened chest,71 the changes in the ECG were similar to the ECG changes that occurred in coronary spasm or transmural MI in humans (Fig. 12–43, 2). The negative T wave only appeared as a late manifestation, when the acute ischemia was already vanishing or had already disappeared. Therefore, a flat or negative T wave represents postischemic changes rather than the first phase of acute ischemia. Thus, it is a frequent mistake to consider the presence of a negative T wave as an indicator of active ischemia.
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Morphology of T-Wave Changes and Electrophysiologic Experimental Mechanisms
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It has been demonstrated by different experimental open chest methods that when ischemia or similar effect is induced (eg, by cooling the tissue)7,8,72 in the epicardium or in a part of tissue close to the recording electrode, the TAP of this zone presents a delay of repolarization without changing its shape, and a flat or negative T wave appears (Fig. 12–44B). When the same procedure is performed in the endocardium or in a part of tissue far from the electrode, a delay of repolarization is induced in this zone, and a peaked and usually taller T wave appears (Fig. 12–44A).
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The electrophysiologic explanation of these changes in T wave (more positive T wave and flat or negative T wave) caused by experimental subendocardial and subepicardial ischemia, that are found in these areas that present delay of repolarization (prolonged TAP), may be explained (see Fig. 12–44) by two concepts: the summation of TAPs of subendocardium and subepicardium (the longer is located in the ischemic zone), and the concept of ischemic vector. According to these concepts, the area with delayed TAP (named ischemic area), either in the subendocardium or in the subepicardium, was not fully repolarized at the time when the other area was already repolarized. Therefore, it still presents negative charges. As repolarization starts in the zone that is more perfused, the sense of repolarization (see Fig. 12–44) will face the ischemic zone. However, as this zone presents more negative changes, a flow of current having a vectorial expression is generated, going from more ischemic to less ischemic zones. Then, the vector of ischemia with the positive change in the head is directed away from the ischemic area and originates a more positive T wave in experimental subendocardial ischemia and a flat or negative T wave in experimental subepicardial ischemia. Note that the vector of necrosis is also directed away from the necrosis area (see Fig. 12–46), but on the contrary, the vector of the area with greater ischemia (injury area) is directed toward this area (see Figs. 12-49 and 12–50).
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T-Wave Changes in Patients with Ischemic Heart Disease
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In clinical settings, the explanation of T-wave changes caused by ischemia is in some aspects different (see Electrocardiography in Ischemic Heart Disease).72,73
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Peaked, symmetrical, wider, and/or taller T wave. This morphology, accompanied by a lengthening of the QT interval, appears in the beginning of acute transmural ischemia resulting from total coronary occlusion, sometimes accompanied by slight ST depression. As a consequence of the occlusion, there is first subendocardial involvement. Different factors explain the susceptibility of the subendocardium to the development of ischemia. These include the greater dependence of this region on diastole perfusion and the greater degree of energy expenditure of this area during systole.60
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This initial subendocardial ischemia, also demonstrated by contrast-enhanced cardiovascular magnetic resonance (CE-CMR),74 produces a delay of repolarization in this area and, as a result, a lengthening of the TAP of the subendocardium, explaining the increase of the QT interval and usually also the presence of wider, peaked, symmetric, and/or taller T waves (see Fig. 12–44A; Fig. 12–45).
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As mentioned earlier, the results of animal experiments performed with unopened chest71 coincide with the ECG changes that often appear in different clinical settings of transmural or near-transmural ischemia that are the consequence of total or near-total coronary occlusion, such as coronary spasm (see Fig. 12–45),75,76 hyperacute phase of ST-segment elevation ACS (STE-ACS; see Fig. 12–60A), and percutaneous coronary intervention (PCI).63 In the majority of cases, after a short period of peaked T wave with QT prolongation, an evident ST-segment elevation appears (see Fig. 12–60A). Later on, if ischemia persists, the ECG pattern may evolve to Q-wave MI.
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In addition, a tall, positive, and symmetrical T wave is frequently seen in a chronic phase of Q-wave MI. This is the expression of the mirror image of a negative T wave. The most frequent leads where this is seen are I, VL, and V1 to V3 as mirror images of inferolateral involvement (Fig. 12–46, 2).
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None of these clinical situations represents acute active ischemia. Rather, they indicate postischemic changes.
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The involvement of the left ventricle wall is usually transmural in the presence of a flat/negative T wave. No clinical situation caused by ischemia presents exclusively with subepicardial involvement. Therefore, the theories that explain the presence of flat/negative T waves in experimental clinical ischemia (see Fig. 12–44B) are not useful in the clinical setting. Probably, the negative T wave seen in these clinical cases, associated with acute transmural ischemia (ST↑) that has subsided, may be explained by the mechanisms shown in Fig. 12–47.
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Differential Diagnosis
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A long list of conditions, apart from IHD, may present with changes in the T wave (symmetric-wide and/or taller than normal, flat, or negative).2,60 Tables 12–6 and 12–7 summarize the most important conditions, and Fig. 12–48 presents some of the most striking examples.
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Notably, taller T waves of ischemic origin are very transient (see Figs. 12–45 and 12–60A). The persistent high-voltage T wave, seen in V1 to V2 in cases of chronic lateral infarction (see Fig. 12–46B), is an indirect (mirror) pattern, rather than a direct pattern, of tall T wave caused by ischemia.
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In cases with a negative T wave, chronic pericarditis is the most important condition for a clinical differential diagnosis because this disease also presents with pain in the acute phase. The negative T wave of pericarditis (see Fig. 12–77) is usually more extensive, does not present mirror pattern in the frontal plane, and is less intensive (negative) than in cases of IHD, especially in post–Q-wave MI (see Fig. 12–46).
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Changes in ST Segment
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Morphologies of ST Deviations and Electrophysiologic Experimental Mechanism
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The area of the myocardium with significant and persistent ischemia (called the area of injury) presents an evident diastolic depolarization. From an experimental point of view, two injury currents are generated as a consequence of an important ischemia—one occurring during systole and the other during diastole. However, the injury current generated during systole is the only one considered because the ECG equipment is adjusted by alternating current amplifiers to maintain a stable isoelectric baseline during diastole, despite the existence of diastolic depolarization that would change the QT interval. The area with systolic injury current presents a “low-quality” TAP (eg, slower upstroke, lower voltage, smaller area).
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The ECG pattern of the ST segment during an important diastolic depolarization caused by an experimental injury induced in open chest animals varies depending on the location of the injury. Thus, an ST-segment depression is observed if the injury affects the subendocardium, whereas an ST-segment elevation is recorded if the experimental injury is transmural. These two situations may be explained considering the concepts of TAP summation and the vector of severe ischemia.2,14,72,73
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Figure 12–49 shows how the sum of the TAPs of the subendocardium and the subepicardium with a TAP of subendocardium with slower upstroke and smaller size may explain the presence of ST-segment depression following a subendocardial injury (ECG pattern of subendocardial injury; see Fig. 12–49A) or of ST-segment elevation after transmural injury (ECG pattern of transmural ischemia that is known as ECG pattern of injury).
On the other hand, according to the concept of severe ischemia (injury vector) when the zone with low-quality TAP (injured zone) is on the subendocardium (Fig. 12–50A), at the end of depolarization (end of systole), this zone presents fewer negative charges. Consequently, a flow of current exists from the zone with more negative charges to the low-quality TAP zone with fewer negative charges. This originates an injury vector with fewer negative charges (relatively positive) in the head, which points to the zone with low-quality TAP, or the injured zone. If this zone is limited to subendocardium, therefore, the injury vector points toward the subendocardium (injured zone) and is expressed as an ST-segment depression in the surface leads (see Fig. 12–50A). Likewise, when the injured zone is more important and becomes transmural, this zone is relatively less negative (relatively positive), and the injury vector that starts in the subendocardium points toward this zone and is recorded in the surface lead as an ST-segment elevation (Fig. 12–50B).
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ST-Segment Deviations in Patients with Ischemic Heart Disease
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See also Electrocardiography in Ischemic Heart Disease. ST-segment depression appears in the following circumstances:
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In patients usually with preexistent IHD who present with NSTE-ACS without total occlusion of the artery. In these cases, there is important involvement of subendocardial flow, as a consequence of sudden but not total cessation of blood flow. The ST-segment depression tends to normalize from the acute to the subacute phases (Fig. 12–51A; see legend).
In patients with IHD who, as a consequence of exercise or stress, have an increased demand for flow, but where it cannot be supplied because there is a fixed stenosis and a decrease in subendocardial flow. In these cases, different types of ST-segment depression may appear (Fig. 12–51B). As the stenosis is fixed, there is no total occlusion and thus no transmural ischemia.
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ST-segment depression in clinical practice usually appears because the subendocardium is more vulnerable to ischemic damage than the rest of the ventricular wall, and thus, it may be affected without transmural involvement if the occlusion is subtotal. When the subendocardial/subepicardial ratio is reduced to approximately 40%, the flow ratio decreases dramatically. This occurs during exercise and mental stress and also when there is an increased left ventricle end-diastolic pressure.63 In these cases, the TAP of the subendocardium resulting from extensive and already existent ischemia shows a change in its shape but not a prolongation of the TAP duration, as happens in the first minutes of total occlusion in patients usually without previous ischemia. This explains why, in one case, a taller T wave appears (see Fig. 12–44B), whereas in the other case, an ST-segment depression occurs (see Fig. 12–49B).
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ST-segment elevation appears in transmural ischemia, often after a period of taller and wider T wave (STE-ACS). Usually, these patients do not present with a previous important ischemia. The ST-segment elevation tends to normalize from the acute to the chronic phases (Figs. 12–52 and 12–53) (see Acute Coronary Syndrome with Narrow QRS: Evolutionary Changes).
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To explain the appearance of this pattern, we have to consider that even the injured zone is transmural and the surface electrodes located closer to the epicardium are recording the ECG pattern as in the case of the experimental subepicardial injury that presented a change of the TAP shape in the subepicardial layers and a less negative charge (relatively positive) (see Fig. 12–50B, right).
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Because the injury patterns develop at the end of the depolarization, which corresponds to the end of generation of QRS at the beginning of repolarization, the ECG expression of injury starts during the first part of the ST segment. Therefore, in cases of relevant injury, there is an elevation of the S wave, which persists along the whole ST segment and usually encompasses a T wave that becomes negative (see Electrocardiogram in Acute Coronary Syndrome with ST-Segment Elevation).
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An ST-segment elevation may also be recorded in other clinical settings that are not related to atherothrombosis, such as isolated coronary spasm75,76 and Takotsubo syndrome (TTS)60,78,79 (see Electrocardiographic Changes in Ischemia Not Related to Atherothrombosis).
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The leads that face the head of the vector of injury in transmural acute ischemia record an ST-segment elevation, whereas the leads facing the tail of the injury vector record an ST-segment depression. The global study of direct and mirror images of the ST deviations in different leads is crucial to correctly diagnosis the location of the injury and to understand the corresponding prognostic implications (see Fig. 12–53 and Electrocardiogram in Acute Coronary Syndrome with ST-Segment Elevation).
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Differential Diagnosis
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The list of conditions that, apart from IHD, may present an ST-segment elevation or depression is large.2,60
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Tables 12–8 and 12–9 summarize the most important conditions of ST-segment depression and elevation not caused by IHD. On the other hand, Fig. 12–54 shows the most typical variants that present with ST-segment elevation or depression. In the first phase of pericarditis, a disease that also presents with chest pain, the most striking change is an elevation of the ST segment. Many conditions can also present with ST-segment depression, although usually small. The most important factor to take into account is the correlation of the clinical symptoms with the deviations of the ST segment. The diagnostic criteria for considering the deviations (ups and downs) of ST suggestive of ACS and all their prognostic implications will be discussed later (see Acute Coronary Syndrome with Narrow QRS: Evolutionary Changes).
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Q Wave of Necrosis: Electrophysiologic Mechanisms
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The activation of the subendocardial area is very fast because the density of Purkinje fibers is so great that the electrodes located in this area do not record any positive deflection (1 and 2 in Fig. 12–55A). Later on, the subsequent activation of the other part of the left ventricle wall records progressively greater R waves until a unique R wave is recorded from the epicardium (5 in Fig. 12–55A).
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In the presence of MI, the diastolic depolarization in the infarcted area is so important that it cannot be excited and does not originate a TAP. Therefore, a Q wave is generated when the infarcted area surpasses the subendocardium and affects part of the myocardium that is depolarized within the first 40 to 50 milliseconds64 (Fig. 12–55B and C).
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The Q wave of necrosis may be explained by two theories. The first theory is the theory of the electrical window of Wilson. According to this theory, the transmural infarcted area acts as an electrical window and, consequently, the electrode that faces that area records the negativity of the intracavitary QRS (Q wave of necrosis) (see Fig. 12–55B).
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The second theory is the theory of the infarction vector. This theory proposes that the infarcted area generates a vector (infarction vector) that has the same magnitude, but opposite direction, to the one that would have been generated at the same zone in the absence of infarction. Therefore, the infarction vector moves away from the infarcted area (see Fig. 12–46). As we have stated, the ventricular depolarization changes that originate the Q wave occur when the infarction area is depolarized within the first 40 milliseconds of ventricular activation.
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Anomalies in the mid-to-late part of QRS, such as slurring, rsr′, and low voltage in the left precordial leads (Fig. 12–55D), are called fractioned QRS.65,66 Fractioned QRS may occur as a consequence of alterations of ventricular activation after 40 to 50 milliseconds (basal segments according to standardized myocardial segmentation nomenclature by Cerqueira et al80). The fractioned QRS may appear either isolated or with a Q wave. It may be caused by a necrotic area that does not involve the whole wall (see Fig. 12–55D).
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The MI with fractioned QRS forms part of the non–Q-wave MI, which will be discussed later (see Myocardial Infarction Without Q Wave or Equivalent).
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Changes in QRS in Patients with Ischemic Heart Disease
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The appearance of the Q wave of necrosis in the evolutionary changes of STE-ACS is evidence that the patient has evolved to MI, involving an area that surpasses the subendocardium (see Fig. 12–55B). However, this is not an irreversible pattern. In fact, in a few cases, such as aborted MI and Prinzmetal angina, the presence of Q waves may be transient (see Electrocardiography in Ischemic Heart Disease).
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The criteria to diagnose a Q wave as abnormal and the location of MI, according to the presence of the Q wave in different leads, are discussed later in Q-Wave Myocardial Infarction (see Table 12–11).
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As with changes in the T-wave and ST-segment deviations, the presence of a mirror image of the Q wave of necrosis is also very important for diagnostic purposes. It is especially evident that, in patients with IHD, the presence of a prominent R wave in V1 may be the only manifestation of abnormality. It is currently known that this R wave result from a lateral, not a posterior, MI (see Q-Wave Myocardial Infarction).81,82
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Recently, it has been reported that the presence of fractioned QRS provides a more accurate criterion for the diagnosis of necrosis than the existence of a Q wave.65 However, it is necessary to match these morphologies with the clinical setting because they may also be seen in normal subjects.
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The fractioned QRS also arises in other diseases or circumstances, such as ventricular aneurysm83 and Brugada syndrome.84
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Differential Diagnosis
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The specificity of the pathologic Q wave (Table 12–10) for diagnosing myocardial necrosis is relatively high. However, it must be noted that similar “Q” waves are seen in other processes. The diagnosis of acute MI is based not only on ECG findings, but also on the clinical setting, as well as on enzymatic changes. The presence of ST-T alterations accompanying a pathologic Q wave gives support to an IHD as the cause for this ECG pattern. However, as indicated later, in 5% to 25% of infarctions (higher incidence in inferior infarction), the Q wave disappears with time; thus, the sensitivity of the ECG for detecting old infarction is not very high (Fig. 12–56).
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The principal causes of the pathologic Q wave, other than myocardial necrosis, are listed in Table 12–10.
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As already stated, there are many other changes in the ECG parameters that are induced by ischemia. Some of them, such as lengthening of the QT interval, have already been discussed. For more information on other ECG changes, such as for instance those of the P wave in case of atrial infarction consult Bayés de Luna,2 Surawicz,12 and Bayés de Luna and Fiol-Sala.60