Isolated and complicated left anterior fascicular block: A review of suggested electrocardiographic criteria

J. ELECTROCARDIOLOGY 16 (2), 1983, 199-212

R e v i e w Article Isolated and Complicated Left Anterior Fascicular Block: A Review of Suggested Electrocardiographic Criteria BY JOIIN A. MILLIKEN, M.D., F.R.C.P.(C), F.A.C.P., F.A.C.C.*

SUMMARY The electrocardiographic criteria for isolated left anterior fascicular block are reviewed and illustrated. Left anterior fascicular block decreases the voltage in the chest leads and increases the voltage in the limb leads. The usual voltage criteria of left ventricular hypertrophy must be modified appropriately. Changes in repolarization include a decrease in the T wave of leads I and AVL and an increase in leads II, III, AVF, V 5 and V 6. Small Q waves in V 2 may simulate an anteroseptal myocardial infarction. Three criteria for the possible diagnosis of superimposed inferior myocardial infarction have been suggested. Both inferior and anterior myocardial infarctions may be masked by R wave'5 replacing Q waves. In the presence of a recent anterior infarction, right bundle branch block may also be masked. Thus, left anterior fascicular block may mask or mimic infarction and left ventricular hypertrophy and mask right bundle branch block in the setting of an acute anterior myocardial infarction.

The e l e c t r o c a r d i o g r a p h i c c r i t e r i a for the diagnosis of block in the anterior division of the left bundle branch are often confusing. Even the terminology is suspect. Literally applied, empirical textbook criteria m a y lead to obvious errors and yet the medical literature contains much information t h a t might clarify the confusion. The divisions or fascicles of the left bundle branch of the His-Purkinje network are seldom as clearly defined as the terms left anterior fascicle and left posteror fascicle would imply. Kulbertus, 1 in a careful anatomical mapping of the divisions Of the left bundle, has concluded t h a t there may Often be three main fascicles or divisions (29 of 34 had the equivalent of a third division). This suggestion of three fascicles is further supported by Durrer's 2 studies of conduction in the human heart, which showed t h a t there were three sites of initiation of depolarization of the left ventricle. These sites are a basal anteroparaseptal area, a midseptal site and a posteroparaseptal region. Each of these can be related to the terminus of a division or fascicle: i.e., left anterosuperior, left

.*Professor of Medicine, Queen's University. Kingston. Ontario, Canada. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be marked "advertisement" in accordance with 18 U.S.C:'w 1734 solely to indicate this fact. Reprint requests to: Dr. John A. Milliken, ttotel Dieu Itospital, Kingston, Ontario, Canada, K7L 3}t6.

posteroinferior and left medical (or septal) fascicles (Fig. 1). Thus the frequent presence of more than two divisions in the left bundle contradicts the implications of the term " h e m i b l o c k " . Fascicular block 3 has, therefore, been suggested as a preferable term even though less euphonious, and less appealing to physicians. Left anterior hemiblock or left anterior fascicular block is abbreviated hereafter as LAFB. Left Axis Deviation (LAD). The separation of left axis deviation from left anterior fascicular block is a major problem. 4 Although lip service is paid to the statement t h a t left anterior fascicular block and left axis deviation (LAD) are not synonymous, .little is done to clarify the two. Usually a list of causes of left axis deviation, other than fascicular block, is offered: normal variant, extensive myocardial infarction, cardiomyopathy, pulmonary emphysema, hyperkalemia, W P W syndrome, and even congenital heart disease with early activation of the posterior left ventricular wall. Left axis deviation is usually defined as a mean QRS axis t h a t lies between - 3 0 and - 9 0 degrees 9 in the frontal plane. T h i r t y years ago it was considered a useful indicator of left ventricular hypertrophy (LVH). W i t h the more widespread use of unipolar leads, it was soon obvious t h a t LVH with left axis deviation was something more -- a complication had occurred. In 1956 Grant 5 rekindled interest in left axis

199

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Fig. 1. A sketch of the Bundle of His with the right and left bundle branches. The left bundle branch is illustrated as having three divisions, an auterosuperior fascicle (AS), a septal or medial fascicle (SM), and a posteroinferior fascicle (PI).

deviation as a sign of underlying heart disease, when he reported on an a u t o p s y correlation of 672 patients who had ECGs within five weeks of death. L A D (greater than - 1 5 ) was found in 131, b u t only 54 had a myocardial infarction. In 23 of the 77 non-infarctions, the heart weight was 400 gms. and 15 of these had only "parietal block". In contrast, only 35 of the 73 with LVH had LAD. He concluded that L A D could not be explained b y an anatomical shift of the heart, b y incomplete left bundle branch block, or by LVH. Later, he suggested that it might be due to block of the anterior fibers of the left bundle branch. 6 In 1960, Davies and Evans, 7 in a discussion of the significance of deep S waves in leads II and III, noted that such a p a t t e r n suggested involvement of the anterolateral wall of the left ventricle. They quoted Grant from the Third World Congress of Cardiology, who, in turn, attributed to Manning the suggestion that such a pattern was due to a small conduction defect in the l e f t ventricular wall. Thus, more than 20 years ago, at least three cardiologists felt a non-specific conduction defect explained some cases of marked left axis deviation of the QRS complex. Left Anterior Fascicular Block (LAFB). The concept of fascicular blocks has been generally acknowledged since Rosenbaum 8"n introduced the term "hemiblock" in 1968. His concepts and terminology were. soon rapidly a n d w i d e l y accepted. The left anterior (and superior) fascicle of the left bundle branch supplies fibers to the anterosuperior and lateral wall of the,left ventricle. It has been described b y Rosenbau~n as a relatively long, narrow, superficial, outflow t r a c t structure, vulnerable to h e m o d y n a m i c

trauma and fibrous replacement. Failure of conduction or delay of conduction in the anterosuperior fascicle is called left anterior fascicular block (LAFB). This fascicle has a single arterial supply 12 via the septal branch of the left anterior descending coronary artery, which also nourishes the right bundle branch; hence right ventricular conduction delay plus L A F B is frequent. R o s e n b a u m ' s c r i t e r i a 11 for l e f t a n t e r i o r hemiblock were as follows: Frontal QRS axis of - 4 5 to - 8 0 QRS duration of ~<0.11 sacs Small septal Q wave <0.02 sec in leads I and AVL. Criteria. The use of left axis alone is inadequate to recognize L A F B since most agree that L A D and L A F B are not synonymous. 4 There are many causes other than L A F B that produce this shift of electrical forces to the left and superiorly in the frontal plane. A discrete cut-off point of - 4 5 eliminates many of these causes b u t probably misses instances of L A F B of a lesser degree. There is no certain discrete point at which L A D suddenly changes and becomes L A F B , nor is there an upper limit where it ceases. This has led some to categorize all LAD beyond --30 as L A F B . ]3,14 Das 15 and Burchel116 have both concluded that there is a continuum of dirrectional aberrations, or a continuum of L A D and its relation to the intraventricular conduction time, so that all leftward shifts of the QRS axis represent a spectrum of intraventricular conduction delay. The degree of L A D that occurs in L A F B is likely to be dependent on the original axis as well as on the extent of the delay. While it might be possible to accept a more liberal definition of the degree of L A D which constitutes LAFB, this can only be done if we have some w a y of measuring the regional delay in the left anterosuperior and basal left ventricle. Rosenbaum's second criterion of a QRS duration ~<110 msecs, is for "pure, uncomplicated" L A F B and is necessary because such complications as right bundle branch block, marked LVH, and fibrosis or scarring in the free wall of the left ventricle m a y prolong the QRS. 11 The depolarization delay of the anterosuperior left ventricle when L A F B occurs m a y cause the QRS duration to increase b y 10 to 20 msecs. 9,11,17,1s The axis shift is evident within the first 60 msecs since left ventricular conduction spreads from the left posteroinferior fascicle's termination toward the delayed area. To diagnose L A F B with a QRS durJ. ELECTROCARDIOLOGY 16 (2), 1983

ECG C R I T E R I A F O R L A F B

ation >100 msecs, one should note the axis during the first 60 msecs of the QRS complex. In contrast, right bundle branch block alters the axis of the terminal QRS. Other causes of QRS delay with L A F B should be considered clinically and excluded. The last criterion of R o s e n b a u m specifies a small septal Q wave in leads I and A V L b u t causes even more controversy. W h y should L A F B require such a Q wave? Due to the initial forces in the left ventricle coming largely from the left posteroinferior fascicle, it is readily understandable that they should be directed inferiorly, b u t w h y always to the right? W h y not to the left? In 1970 Kulbertus et al. 19 in a VCG s t u d y found that the 10 msec. vectors are nearly always directed inferiorly b u t " ~ a y be to the left in 45% and to the right in 40%. Concerned about this requirement for a Q wave in leads I and A V L before diagnosing LAFB, Jacobson et al., 2~ in 1977, reported on a critical appraisal of the initial forces in L A F B . They examined tracings with a left axis deviation of - 4 5 to - 8 0 and noted the marked variability in the Q waves. In only 30% of these is there a Q in I and AVL; 27% had neither, and 43% had it in .AVL alone. While noting that the frequency of such Q waves increased with increasing LAD, they concluded that a Q in I and A V L is not a requirement for LAFB. BurchelP 6 has also reported On the absence of a Q in I and AVL, finding that 40% of left axis deviation > - 3 0 had the initial 5 msec. vector to the left. Such Q waves appear to depend on whether the septal portion of the left ventricular conduction s y s t e m is involved and on whether or not such Q waves are present prior to the development of L A F B . Therefore, L A F B does occur without such initial Q waves, and left axis alone is sufficient to consider the possiblity of LAFB. Thus, all three criteria recommended in 1972 have been challenged to some degree. This is probably due to the fact that none of the three criteria directly measure the delay in activation of 10 to 20 msecs that results from L A F B . Animal studies, 17 direct epicardial leads, 21 body surface mapping, 22 and vectorcardiography 1s019 have all confirmed that there is a regional delay of -depolarization of the left anterosuperior wall of the left ventricle when L A F B is present. In 1972, Medrano et al., 17 from their studies in dogs and humans, suggested that additional cri-, teria involving changes in A V L and A V R are necessary to diagnose L A F B . Either of these leads m a y reflect the altered regional delay of the

J. ELECTROCARDIOLOGY 16 (2), 1983

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TABLE I Criteria for Left Anterior Fascicular Block

1. Left axis deviation beyond - 3 0 , and 2. Delayed intrinsicoid deflection in AVL >145 msecs or a slurred downstroke of R in AVL; (rarely only a slurred terminal R in AVR instead) 3. Slurred S waves in the left precordial leads

anterobasal left ventricle. According to them, there should be slurring of the downstroke of the R wave in AVL and a delayed R peak time greater than or equal to 45 msec. If these signs are absent in AVL, then a late slurred terminal R wave in A V R should be present. Slurred S waves were also seen in leads V 5 and V 6. In 1975, Horwitz et al., 23 investigated whether a delayed intrinsicoid deflection time of A V L asynchronous to V 6 would be a useful additional criterion for LAFB. Only 62% of 400 records with LAD beyond - 3 0 had such asynchronous activation. While the prevalence increased to 100% when the LAD became - 7 5 or greater, they still questioned the validity of this criterion because of the lack of correlation in so many instances. No mention was made of A V R in their study. Fisher et al., 24 in 1979, reported on the late terminal R in A V R as a

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Fig. 2. A 50 year old male with LAFB. Note the left axis deviation beyond -30, a slurred, late R AVR, a slurred terminal R in AVL and S waves in leads V 5 and V 6.

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dial T waves are only slightly affected by L A F B . The T waves of V4, V 5 and V s tend to become higher or abnormal T's tend to become less abnormal. All of these changes have been identified from repeated recordings of transient LAFB. 25,27 Though probably present in LAFB, they are not likely to be attributed to the fascicular block unless one is aware of the secondary repolarization changes t h a t such a block can induce (see Figs. 3, 4). L A F B in Combination with Other ECG Abnormalities. L A F B causes m a n y confusing changes in the ECG. 11 It may mask or mJm[c myocardial infarction and mask or mimic left ventricular hypertrophy, n.3~ I t m a y also conceal right bundle

r ~ ' ~ . ' :-~j ~7~'~L'qIT,THT=ll ,::i=:., $I!; m~[l}!{ Fig. 3. A 77 year old male with typical voltage changes of left ventricular hypertrophy in the chest leads (SV1 +RV s =48) and Q waves in II, III and AVF due to his old IMI. He later developed LAFB, as seen in Fig. 4.

manifestation of L A F B , as originally suggested by Medrano. Only three of their 47 patients with L A F B by vectorcardiography failed to have this finding and two of the three had the typical AVL alterations. Thus, if one utilizes the regional delay in depolarization t h a t can be detected, as suggested by Medrano et al., then much of the difficulty is resolved. Since we can not rely on left axis deviation alone, the criteria for L A F B should be altered (as noted in Table I) to include some measure of delayed conduction in the region of the affected fascicle. (see Figs. 2, 3, 4)

~entricular Repolarization and LAFB. Ventricular repolarization is also altered by LAFB. 25"31The T waves in leads II, I I I and AVF tend to become upright even when previously inverted. These changes in the limb leads can mask the repolarization abnormalities previously present. If the T waves in leads II, I I I and AVF remain inverted despite L A F B , then a recent inferior myocardial infarction is likely. 1L2s,3~ The 1~ wave in lead I and AVL m a y become flat' or even negative, or, if already inverted, then such inversion is deepened? 8,3~In contrast, the precor-

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Fig. 4. This record, four months later than Fig. 3, has LAFB superimposed. The Q waves in II, III and AVF have disappeared, replaced by a large R wave in lead II and smaller R waves in III and AVF. The axis is beyond - 3 0 degrees and the R in AVL is slightly slurred, with S waves in V5 and V~, indicative of the left anterior fascicular block. The voltage has decreased in the chest leads, where SV l + RVs has declined from 48mms. to 39mms. The voltage in the limb leads has increased with the R in AVL rising from 5.5 to 15rams. and the S in III from 2 to 20mms. Note also the more negative T wave in AVL and the morepositive T wave in AVF, V5 and Vs.

J. ELECTROCARDIOLOGY 16 (2), 1983

ECG C R I T E R I A FOR L A F B

2) intracardiac surgery, which provides the in vivo counterpart of animal experiments; 3) sequential ECGs, whether illustrating beatto-beat variation of transient changes; and 4) the induction of L A F B by coupled atrial pacing. Finally, one can apply the suggested 12-lead electrocardiographic criteria to cases selected by the allegedly superior VCG. Neither method has histological proof since anatomical evidence of a functional abnormality (especially if transient) is almost impossible to obtain. In 1975, Demoulin et al., 3s reported on the quantitative s t u d y of left bundle branch fibrosis in LAFB. Their detailed s t u d y of eight patients with L A F B and eight normals revealed that septal fibrosis was present in all those with fascicular block. While more fibrosis was seen in the left anterior fascicle, it was widespread in all areas of the conducting tissue. Only half the cases with L A F B had it predominantly in the left anterior and left septal fascicles. All suggested criteria for the combination of L A F B and hypertrophy of L A F B and infarction require validation b y large scale studies before the true sensitivity and specificity are known.

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Fig. 5. The possible combinations of LAFB and an IMI are illustrated by sketches of lead II. A) A typical QS complex, B) a slurred, notched, tiny R wave with a deep S, and C) a small, persistent Q wave accompanied by a deep S wave. Not shown is the completely masked infarction with an R and deep S in II. branch block] 32 particularly in the setting of an acute myocardial infarction. 33 Even more confusion arises, however, because L A F B is usually associated with some form of cardiac disease. The ECGs are frequently already altered by LVH, m y o c a r d i a l infarction, ischemia, or a complicating conduction disturbance and then L A F B is superimposed. The combined ECG changes m a y well mask one of the underlying abnormalities. There are several ways to try to prove that ECG criteria are associated with L A F B : 34 1) extrapolation from animal experiments, especially if the animal's conduction s y s t e m and E C G ' s are similar to man's (e.g. baboons};

Inferior Myocardial Infarction (IMI) and L A F B The classic diagnostic features of an inferior myocardial infarction (IMI) include Q waves in leads II, III and particularly AVF. If the IMI is fairly recent, ST-T changes are also present. In

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J. ELECTROCARDIOLOGY 16 (2), 1983

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Fig. 6. An 82 year old male with chronic coronary heart disease. Atrial fibrillation is present with right bundle branch block seen in the late R of V~ and slurred S of V 6. The LAFB is evident from the deep S II, S I I I and S AVF. The QS in lead II suggests an old IMI.

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Fig. 7. An 81 year old male with an old IMI and left anterior fascicular block. The marked left axis deviation seen in lead II, the late R wave in AVR and the delayed intrinsicoid inflection in AVL, plus the slurred S in Vs and V6 are evidence of the LAFB. The tiny, notched R wave in lead II indicates his old inferior infarction. The tiny Q in V 2 is typical of that seen with LAFB. addition, an IMI often causes left axis deviation and m a y even be complicated by LAFB. 9,11,31,36"46 ECG criteria for such a combination were initially identified by studying those cases with an IMI t h a t transiently developed L A F B , or those with L A F B who developed an IMI. 9.11,31, In 1970, Rosenbaum9.11 described the changes which may occur when an I M I is associated with L A F B and suggested three possibilities (see Figs. 5, 6, 7): 1) a QS seen in leads II, I I I and AVF, if the port i o n of the posteroinferior wall causing the initial forces of L A F B is infarcted; if it is spared, then 2) the IMI is masked by small r waves replacing Q waves in leads II, I I I and AVF. Often the r waves are small, notched and double peaked or slurred into the beginning of the S wave; and if the I M I is recent, ST-T abnormalities m a y still be present whereas the usual L A F B causes upright T waves in leads II, I I I and AVF; 3) if the area of the usual initial forces in L A F B is only partially affected, then a tiny Q wave may be seen in lead II and Q is absent in lead I. These criteria were reiterated and amplified s l i g h t l y by Castellanos 31 in 1971, when he reported the serial vectorcardiographic and

12-lead records of eight patients with abnormal axis deviation and an acute IMI. A QS in lead II developed in four of his eight patients who had a normal pre-infarction axis. He also illustrated the persisting negative T waves in leads II, I I I and AVF of a recent I M I despite LAFB. This was true even when rudimentary R waves in leads II, I I I and AVF masked the IMI. L A F B m a y correct the negative T waves of an old IMI, as he illustrated. He described these changes in one of Rosenbaum's cases where developing L A F B with beat-to-beat alternation changed lead AVF from a QS complex with a negative T wave to an rS complex with a positive T wave. Others have likewise demonstrated, in occasional case reports, the transient development of R waves t h a t mask the usual 12-lead criteria for an IMI when L A F B is superimposed. 36.4~ In one case, transient L A F B occurred during chest pain and one hour later, when it was gone, the diagnostic Q waves had r e t u r n e d Y In 1976, Guisti et al. 41 observed t h a t L A F B usually showed an increasing R wave from lead III to AVF to lead II. In contrast, there was a decreasing R wave from I I I to AVF to II when L A F B was complicated by an IMI. 3~ Recke et al. 3s studied 43 patients with a previous IMI and L A D by ECG. The IMI was often masked by the presence of an rS complex in leads II, I I I and AVF. Autopsy proof of the IMI was found in 18 of the 43 cases. The other 25 living patients were studied by vectorcardiography as well and all contributed to his criteria. He found t h a t notching and slurring of the S wave in II and AVF helps to confirm the diagnosis. These various reports lead to the suggested criteria in Table II. Sohi and Flowers 42 used body surface potential mapping to distinguish L A F B and IMI. Their 19 patients with an axis >--45 had a tiny R in leads II, I I I and AVF and a qR in leads I and AVL. Six patients with a similar axis but a QS in leads II and AVF were called uncertain examples of an TABLE II Criteria for Combined Left Anterior Fascicular Block and Inferior Myocardial Infarction (IMI) 1. QS complex in lead II 2. Small slurred initial R (
J. ELECTROCARDIOLOGY 16 (2), 1983

ECG C R I T E R I A F O R L A F B

IMI since they lacked any clinical history of myocardial infarction. One of their figures illustrates many of the criteria contained in Table II. Vectorcardiographic criteria for the diagnosis of an IMI complicated b y L A F B are reported to be superior to the standard 12-lead criteria. 3s4~ In 1965, Kohn and Harris 4a reported on the VCG a n a l y s i s of L A D in the d i f f e r e n t i a t i o n of diaphragmatic infarction and parietal block. There were 59 with an IMI b y VCG and 20 of these had as rS in A V F with a counterclockwise superiorly oriented frontal plane vector loop, i.e. "Parietal block". In 12 cases the rS complex in A V F had a "notch or slur of the r wave or downstroke of the aftercoming S V~ave". Kulbertus et al., 44 in 1971, described 30 patients with an acute I M I who, ~ h e n followed cardiographically five months to four years later, had marked left axis deviation. Seven had vectorcardiographic evidence of L A F B and the old IMI while the others had only an IMI with LAD. Two of their figures illustrate a QS in lead II. Benchimol's three cases in 1972 all had a tiny R wave in lead II or a QS in lead II. 39 He later reported 25 patients with vectorcardiographic features of L A F B and IMI. 4~ All 25 had ECG criteria of LAFB. Most examples had a QS in lead II or a rS in lead II. He noted that 14 of 25 had only an "embryonic" R wave in lead II while 11 had an RII >0.10 mV thus masking or concealing the IMI. Kourtesis et al., 45 in 1976, studied 56 patients with an acute IMI b y means of serial VCGs. L A F B by VCG criteria was present in seven (12.5%) and their clinical course was indistinguishable from the others. Their only figure that contains limb leads is an example of a tiny R wave in leads II, III and A V F with persistent T w a v e inversion, pointing to the recent IMI. The criteria in Table II are obtained from the available literature. They m a y allow one to identify an IMI masked by L A F B . However, Lopes et al. 46 found that only 3 of 15 (20%) with L A F B plus an IMI by vectorcardiographic criteria had a proven MI, thus questioning the validity of the VCG criteria. Obviously, many additional studies are needed to determine the true specificity of the criteria in Table II. Meanwhile, their critical use might well improve diagnosis. " The fact that L A F B m a y conceal an IMI is of some clinical importance. The usual IMI does not involve the left anterosuperior fascicle or the region of the myocardium supplied b y that fascicle. The presence of L A F B implies additional

d. ELECTROCARDIOLOGY 16 (2), 1983

205

disease. In 1970, Rosenbaumg, 10 maintained that in patients with angina pectoris, L A F B indicates left anterior descending coronary artery disease. McKeever et al. 47 reported a significantly greater frequency of three vessel coronary disease (78%) and a strong probabilty of left anterior descending disease (97%). Support for these concepts has recently been provided b y Levy et al.J 8 who reported on 20 patients with L A F B (7.3% of 283 consecutive patients) among those with significant coronary artery disease at angiography. All 20 had a significant lesion of the left anterior descending coronary artery and, in addition, had severe disease affecting at least 2.5 vessels per patient. Later they noted six patients with transient L A F B during angina pectoris and all six had severe disease of the left anterior descending coronary artery. 49 Therefore, L A F B may be a significant finding indicative of such stenosis if associated with anginal symptoms. Lateral Myocardial Infarction and LAFB. When a lateral MI is complicated by L A F B , the usual Q waves in leads I and AVL are enhanced and the terminal forces are directed beyond - 3 0 degrees. 9,n,3~176 All three standard limb leads have predominantly negative QRS complexes and a QS in lead I is typical for the combined diagnosis (see Fig. 8). If a terminal r in lead I is

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MILLIKEN

Alboni et al. ss They studied 1008 cases and found 139 with a qrS p a t t e r n in the V 2 and V 3 leads with small, narrow q waves. All such patients were over age 30 and had some evidence of acquired heart disease. From their data, they concluded t h a t L A F B modified septal activation by causing a posterior shift of the first vector. If there is also loss of septal electrical forces due to septal fibrosis or peripheral septal block, then the appearance of these small q waves is even more understandable. In contrast, L A F B may mask an anterior myocardial infarction by converting the QS complex into a rS pattern. In the few reported cases to date, replacement of diagnostic QS complexes by a normal looking rS and almost normal T wave makes the diagnosis of anterior infarction unlikely,s6"s9 In the case reported by Khair (see Fig. 9), both the I M I and A M I were masked and even the VCG became typical of isolated L A F B . s9 There are no criteria to detect the masked infarction -- only serial records showing transient L A F B would help. Additional cases need to be studied. Ventricular Hypertrophy and LAFB. Because of the changing QRS amplitudes t h a t occur with left anterior fascicular block, the diagnosis of LVH can be either over- or undere s t i m a t e d . 9"11,6~ L A F B i n c r e a s e s the QRS amplitudes in the frontal plane, t h a t is in the limb leads, and decreases the QRS amplitudes in the horizontal plane, or chest leads. 9"11,3~176This means t h a t R I, SIII and R-AVL all become larger, while RV 6 and RV 5 become smaller with an S wave in these latter leads tending to become deeper. Using the usual voltage criteria, L A F B

present, it will always be smaller than the terminal r in AVL. 3~ L A F B may not be recognized due to the right axis deviation associated with extensive lateral wall necrosis. In contrast, L A F B m a y enhance the normal Q waves in I and AVL, suggesting a high anterolateral MI. In such cases, the Q wave is usually less than 0.04 secs. and R II is not widened. 3~ Even if no acute ST-T changes of infarction are present, the inverted T waves in I and AVL induced by LAFB alone m a y simulate ischaemia. 3~ Anteroseptal Myocardial Infarction and LAFB. Rosenbaum first described a qrS pattern in V 2 due to LAFB. 811 In 1971, M c H e n r y et al. 51 reported five patients with L / ( F B and Q waves in the right precordial leads simulating an anteroseptal MI. There were, of course, no ST-T changes of infarction. When the V leads were recorded one interspace lower, all five developed R waves replacing the small initial Q waves. None of the five had a history suggestive of infarction or even angina. It was observed t h a t L A F B seemed to shift the electrical forces slightly, as if V 1, V 2, V 3 were recorded higher t h a n usual. Others then also noted t h a t when L A F B shifts the QRS forces into the left superior quadrant, it m a y produce changes in the horizontal plane t h a t simulate an anteroseptal infarction./~ Small q waves are occasionally seen in the right precordial leads. 3~ Lamb, s4 in a study of over 6000 normal subjects, found an incidence of 0.4% Q waves limited to V a in females. While recording V 1, V 2 and V 3 at a lower interspace m a y cause these small q waves to vanish, the significance of such a finding is uncertain. The frequency of right precordial q waves due to L A F B has been reported as 14% by

OLD

Fig. 9. A sketched reproduction of the ECGs reported by Khair et al. (redrawn With the permission of the publisher, J Electrocardiol 13:93, 1980). The old and new infarctions can be seen in the sketch of the ECG on the left, where Q waves in II, III and AVF indicate the inferior infarct and the more recent anterior infarction is seen in the rudimentary R V~ with the QS complex developing in lead Va. Two weeks later, with the occurrence of LAFB, R waves have replaced the Q in leads II, III and AVF and have also masked the anterior infarction with R waves now present in leads V2 through

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J. ELECTROCARDIOLOGY 16 (2), 1983

ECG C R I T E R I A F O R L A F B

deep S 2 >S 3 point to emphysema, whereas absence of the prominence of the P waves in II, I I I and A V F under such circumstances would favour a straight back syndrome.

TABLE III Criteria for Left Ventricular Hypertrophy in the Presence of LAFB 1. S III >`15mm 2. RIAVL >-13mm 3. SV~ + RV 5 + SV 5 > 2 5 m m

R i g h t B u n d l e B r a n c h B l o c k ( R B B B ) and L A F B .

masks LVH in the chest leads and over-diagnoses it in the limb leads. Bozzi and Figini 6~ suggest that when L A F B is present, the performance of Sokolow's index (SV 1 + RV~ or RV6 >35mm) or Grant's index (SV~ + SV2 + RV6 >40mm) is significantly improved b y adding the S wave in V~ or V6 to the sum," and" b y setting the discriminating value at 25mm for both indices. Conversely, the R wave in A V L needs to be increased to >~13mm, and the S wave in lead I I I increased to >~15mm before LVH can be diagnosed on the basis of limb lead voltage. Cohen et al. m illustrated an example of aberrant conduction inducing such voltage changes in a normal subject. Studies are required to determine the sensitivity and specificity of the suggested voltage criteria for L V H complicated by L A F B (see Table III and Figs. 3, 4, 10). When L A F B occurs in the setting of RVH, ~ it m a y also confuse the picture since moderate or slight R V H may be completely masked b y the change to a left axis in the limb leads. Only definite R V H would then still be evident in the chest leads. Rosenbaum suggests that if S 2 is >S 3, L A F B is unlikely so emphysema, straight back syndrome or other chest deformities should l~e considered. Low voltage, an absent S~ and

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In 1969, W a t t and Pruitt, 62 reviewed the character, cause and consequence of combined left axis deviation and R B B B in human ECGs. They noted that Wilson and Herrmann, in 1921, suggested the possiblity that an electrocardiographic pattern characterized by a combination of extreme L A D and R B B B might be the result of block of the anterior fascicles of the left bundle branch, plus block of the entire right bundle branch. Later, Wilson et al., s3 presented three cases of atypical R B B B with broad, terminal Sni. Similar ECGs were noted in the earlier literature and Richmond and Wolff, 6~ in 1954, termed these paradoxical tracings " L B B B masquerading as R B B B " . They were subsequently called "bilateral bundle branch block", " R B B B with left parietal block" or simply R B B B with left axis deviation.9-~ 1.32.33 R B B B plus L A F B , as an electrocardiographic entity, has been 1) produced in animals experimentally; 2) r e p r o d u c e d b y accident during surgical repair of tetralogy of Fallot; 3) induced as aberrant ventricular conduction of paced supraventricular premature beats; and 4) recorded as an intermittent, transient, or successive conduction disturbance in humans. Histologic studies have contributed little, as d e m o n s t r a t e d b y Hackel et al., 6~ who performed careful anatomic studies on 20 patients with conduction disturbances following an acute myocardial infarction.

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J. ELECTROCARDIOLOGY 16 (2), 1983

Fig. 10. A 67 year old male with LAFB, RBBB, LVH and a recent anteroseptal myocardial infarction. LAFB is seen in the deep S waves in II, III and AVF. There is RBBB with a slurred, late RV 1 and SV 6. The deep SIII of 21.5 mms and the tall R in AVL of 16 mms suggests LVH. A recent anteroseptal infarction is seen in the Q waves and typical elevated ST segments of V 1 to V 3.

208

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Fig. 11. A 70 year old male with LAFB and a recent anterior infarction concealing right bundle branch block. The LAFB can be seen in the deep S wave of lead II and the slurred late terminal R in AVL. The anterior infarction is evident from the Q waves and the elevated ST segments of leads V 1 through V4. The concealed RBBB is identified by the slurred, terminal S in Vs and the slurred, late upstroke of the S wave in V r Probable LVH is suggested by the deep S in III of 19 mms.

In 12 there was no apparent morphologic injury to the conducting fibres and in five of the remaining eight with focal necrosis of the conducting tissue, the involvement was relatively minor. The conduction failure was attributed to possible focal effects on conduction tissue from the metabolites produced by infarction of neighbouring muscle. L A F B prolongs the QRS duration by only 10 20 msecs so when a QRS duration of 0.11 secs or more is seen, some complication p r o b a b l y exists. 911 Under these circumstances, one should consider LVH, focal fibrosis, infarction or bundle branch blockJ 1 RBBB is diagnosed from the chest leads by noting a slurred, late R wave in V 1 and a slurred S wave in V 6. The addition of L A F B with delay in the depolarization of the anterosuperior left ventricle is readily identified by noting the axis of the first 60 msecs. Since RBBB affects mainly the terminal vectors, the ~ardiographic evidence of L A F B should be obvious (see Fig. 10}. A small or absent S 1 of L A F B m a y be superim-

posed on the slurred S 1 of RBBB. 11 The result is a small or absent slurred S 1 despite the RBBB, and leads to the term 'masquerading BBB' since the record has clearly evident RBBB in the chest leads yet the limb leads suggest LBBB. Since most electrocardiographers currently rely largely on the chest leads to identify the presence of right or left BBB, it is much less likely to be considered a problem. I t is disturbing, therefore, to learn t h a t L A F B m a y even conceal RBBB in the chest leads. I t was first noted by Rosenbaum when a p a t i e n t w i t h R B B B developed i n t e r m i t t e n t LAFB. 3e He later reported three cases. The S waves in I and AVL become obliterated as the S in II and I I I becomes deeper. A t times the S in V 5 and V 6 also disappears as the R" sinks into the S wave in V I. Focal block, LVH or even the heart position in relation to the electrodes m a y also be factors in this masquerading effect. By placing the electrodes higher on the chest, the classical RBBB pattern is seen. It is suggested t h a t concealed RBBB be considered in cases of L A F B with a QRS duration of 0.11 secs or more, especially if terminal slurring of the S upstroke in V 1 is present. If this is done, then masked or concealed RBBB m a y be identified (see Fig. 11). In 1979, Sclarovsky et al. 33 reported 34 patients with L A F B obscuring the diagnosis of RBBB in the setting of acute myocardial infarction. The L A F B occurred soon after the acute event and lasted 1 - 7 days. High or right sided chest leads were needed to show RBBB at such times. Although it occurred in 12% of 249 infarctions, it had a transient benign course with a mortality rate of 6.7%. While intracavitary recordings in the right ventricle are the best method of establishing the diagnosis of concealment of RBBB by L A F B , as suggested by MayorgaCortes, 66 a careful s t u d y of Sclarovsky's illustration shows a slurred terminal upstroke of the S wave in V 1 and a slurred S in V 6. These cases support Rosenbaum's observations " t h a t a high degree of L A H m a y conceal a small degree of RBBB by making a tiny late R' to sink within a much deeper S wave in lead VI". Until these reports, it was felt t h a t anterior infarction with RBBB and L A F B was readily recognized. The effect of L A F B on an IMI has already been detailed and described. For the most part, RBBB modifies the terminal half of the QRS and causes little confusion. Its effects are only superimposed on the L A F B plus I M I criteria of Table II. Emphysema, straight-back syndrome and other chest deformities m a y all cause a superior axis to

J. ELECTROCARDIOLOGY 16 (2), 1983

ECG CRITERIA FOR LAFB

accompany the RBBB. 11 If S H is deeper than SH[, L A F B is unlikely and one of these chest conditions is probably present. Also, if S H and SHI are very deep, then L A F B is supported since it tends to cause larger QRS voltage in the limb leads, unlike the above chest Conditions, which usually have a small QRS voltage. If RVH is marked, RBBB plus L A F B may have a mean electrical axis directed to the right and superiorly, or even to the right (i.e. no left axis deviation). Under these conditions, L A F B would be likely to go unrecognized despite Rosenbaum's example. H

5.

6.

7. 8. 9.

Conclusion.

T h e e l e c t r o c a r d i o g r a p h i c , c r i t e r i a for the diagnosis of L A F B m u s t include some measure of the delay in conduction to the myocardium supplied by th~ ;left anterosuperior fascicle. Such a delay may be identified by a late R in AVR or a slurred terminal R in AVL. In addition to the shift in QRS axis to the left to greater than - 3 0 , depolarization and repolarization are also affected. The limb lead voltage increases and the chest lead voltage decreases with S waves appear in leads V s and V 6. The T waves in leads II, III A V F and V 5 and V s tend to become more upright while the T wave in AVL is reduced. The QRS changes of L A F B can mask or mimic LVH and mask or mimic myocardial infarction. They may even obscure RBBB, particularly in the setting of an acute myocardial infarction. Awareness of these multifacetcd aspects of L A F B will lead to more accurate electrocardiographic diagnosis. Several tables outlining suggested electrocardiographic criteria for L A F B alone or complicated by IMI and/or LVH are provided. The sensitivity and specificity of these criteria require independent confirmation. Meanwhile, awareness of such possibilities m a y confirm their clinical Utility.

10.

11.

12.

13.

14.

15. 16.

17.

18. 1. 2.

3.

4.

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37. CR1STAL,N, Ho, W AND GUERON, M: Left anterior

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49.

50.

51.

52.

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ECG CRITERIA FOR LAFB

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55.

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59.

qrs or qRS patterns in right precordial leads. Adv Cardiol 16:507, 1976 FAaNHAM, D J AND SIiAII, P M: Left anterior hemiblock simulating anteroseptal myocardial infarction. Am Heart J 92:363, 1976 LAMB,L E: Electrocardiography and Vectorcardiography. Instrumentation, Fundamentals and Clinical Applications. W B Saunders Company, Philadelphia, 1965 ALBONI,P, MALACARNE,C, DE LOBENZhE, PIRANI, R, BALDASSARRI, F AND MASONI, A: Right precordial q waves due to anterior fascicular block. Clinical and vectorcardiographic study. J Electrocardiol 12:41, 1979 KULnEaTUS, H E: Electrocardiographic recognition of anterior infarction in leftanterior fascicularblock: A diagnostic challenge. Chest 62:91, 1972 ALTmRI,;xP AND SCIIAAL, S F: Inferior and anteroseptal myocardial infarction concealed by transient left anterior hemiblock. J Electrocardiol 6:257, 1973 ALBINADER, E G AND NASCIIITZ, I-" Left anterior hemiblock modifying anteroseptal myocardial infarction. Ir J Med Sci 147:97, 1978 KtIA1R, G Z, TRISTANI, E AND BROOKS, H L: Recognition of myocardial infarction complicated by

d. ELECTROCARDIOLOGY 16 (2), 1983

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left anterior hemiblock: A diagnostic dilemma. J Electrocardiol 13:93, 1980 Bozzl, G AND FIGINI, A: LAFB and the ECG diagnosis of LVH. Adv Cardiol 16:495, 1976 COIIEN,S I, LAU, S H, STEIN, E, YOUNG,M W AND DAMATO, A N: Variations of aberrant ventricular conduction in man: Evidence of isolated and combined block within the specialized conduction system. Circulation 38:899, 1968 WATT, T B AND PRUITT, R D: Character, cause and consequence of combined left axis deviation and right bundle branch block in human electrocardiograms. Am Heart J 77:460, 1969 WILSON, F N, JOIINSTON, F D AND BARKER, P S: Electrocardiograms of an unusual type in right bundle branch block. Am Heart J 9:472, 1934 RICHMOND,J L AND WOLFF, L: Left bundle branch block masquerading as right bundle branch block. Am Heart J 47:383, 1954 HACKEL, D B, WAGNER, G, RATLIF, N B, CIES, A ANDESTES, E H, JR: Anatomic studies of the cardiac conduction system in acute myocardial infarction. Am Heart J 83:77, 1972

66. MAYORGACORTES, A, CASTELLANOS,h AND MYER-

Buao, R J: LAHB obscuring RBBB, Circulation 61:866, 1980