Electrophysiologic mapping during open heart surgery

Progress

in

Cardiovascular VOL.

XIX,

Diseases NOVEMBER/DECEMBER

NO. 3

Electrophysiologic

Mapping

During

Open Heart

1976

Surgery

Joel Kupersmith

E

mapping during LECTROPHYSIOLOGIC open heart surgery is a technique that hasbecome increasingly popular in recent years both in clinical and experimental use.rm7For certain open heart procedures, such as repair of complex congenital anomalies,8’9the technique may be required for successfuloutcome. In other instances, such as in studies on the human atrium6 and specializedconduction system,4data derived from mappinghave contributed to knowledge of human cardiac electrophysiology. This review will be concerned with the various clinical uses of electrophysiologic mapping during open heart surgery, as well aswith the experimental work that has been performed with this technique. GENERAL

METHODOLOGY

Types of Recordings By electrophysiologic mapping is meant the direct recording of electrical activity of the heart. Such direct recordings are termed “electrograms” in contrast to “electrocardiograms,” which are recorded from the body surface.” Electrograms may be recorded from endocardial, epicardial, or transmural sites and may be either bipolar or uniFrom the Division of Cardiology, Department of Medicine, Mt. Sinai School of Medicine of the City University of New York, New York, N. Y. Supported in part by Grants HL 10833-02 and HL 18801 of the National Heart and LungInstitute, USPHS. Some of the studies described in this review were supported in part by Grant HL 12138-04 of the National Heart and Lung Institute, U.S. Public Health Service and were performed during Dr. Kupersmith’s tenure as a Fellow of the New York Heart Association. Reprint requests should be addressed to Joel Kupersmith, M.D., Director of Electrocardiography and Clinical Electrophysiology, hit. Sinai School of Medicine, 5th Avenue and 100th Street, New York, N. Y. 10029. 0 1976 by Grune & Stratton, Inc. Progress

in Cardiovascular

Diseases,

Vol.

XIX,

No.

polar. Bipolar electrogramsare recordingsof potential differences between two electrodes, both placed directly on the heart usually l-10 mm apart. Unipolar electrogramsare recordings of potential differences between one active electrode placed on the heart and a distant reference electrode, i.e., either a Wilson type central terminal such as in a standardECG machineor an electrode on the body surface. Bipolar and unipolar electrogramseachhave specific characteristicsand specific uses.l”-14 Bipolar electrograms are primarily recordingsof local activity at the electrode site with little contribution of distant cardiac electrical events.“-r2 For this reasonthey are most suitable for timing of local activation, for determining the sequence of activation,roYr3 and for precisely delineating the location of the specializedconduction system.4”4 Unipolar electrograms, on. the other hand, record a combination of local and distant electrical events with the contribution of distant events decreasing in proportion to’ the squareof the distance from the unipolar electrode l/r2~10,1s The large contribution of distant electrical events interferes with the usefulnessof unipolar eIectrogramsfor determining the timing of local activation,‘23’6 though they have at times been used for this purpose.l’s’* Unipolar electrodes are most suitablefor recording ST segments and T waves1o’19and for determining the general direction of activation relative to the position of the recording electrode; direction is indicated by the polarity of the recording.” Waveformsof QRS complexes in unipolar recordings may also yield important information regarding bundle branch block and ventricular hypertrophy.20-22 In bipolar electrogramsthe time of local activation is representedby the major or maximum deflection.” In unipolar electrogramsthe so-called “intrinsic deflection” is either a notched or rapid

3 (November/December).

1976

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deflection, which has been said to represent the time of local activation at the recording site.‘0317 Though in some instances this deflection is reliable for timing, in general it is less so than the major deflection of bipolar electrograms.123’6 Figure 1 shows the recording of bipolar and unipolar electrograms from a canine heart. The top trace of Fig. 1 is a surface ECG lead, the second trace is a bipolar electrogram recorded from the anterior left ventricular epicardium, and the third and fourth traces are unipolar electrograms recorded from each of the electrodes used to record the bipolar electrogram in the second trace. The vertical line

S

ECG-rrJdI

I

I

I

I

I

EGBip

EGUni

-~-B+m

!,mvT ’ , 500

msec

Fig. 1. Electrograms recorded from the anterior left ventricular epicardium of a dog during a conducted atrial rhythm produced by atrial pacing. The top trace (EGG1 is ECG lead II: the second trace (EG-BIP) is a bipolar elec trogram recorded with electrodes 1.5 mm apart; the third and fourth traces (EG-UNI) are unipolar electrograms. The active electrodes for each of the recorded unipolar electrograms were those used for the bipolar electrogram in the second trace and the reference electrode was placed in the hindlimb. The vertical line represents the time of the major deflection in the bipolar electrogram and thus the time of local activation. The ECG lead and unipolar electrograms were recorded at l-500 Hz while the bipolar electrogram was recorded at 12-500 Hz. Note that it may be difficult to determine the precise time of local activation using the intrinsic deflection in the unipolar electrograms. Also note that the P wave and T wave are much more apparent on the unipolar than on the bipolar electrograms. The reasons for this difference are that low frequency components (T wave) were filtered out in the bipolar electrogram, slow components are more difficult to record with closely spaced bipolar electrodes, and the contribution of distant electrical events (P wave) was greater in the unipolar recording. Voltage calibration is for unipolar electrograms. See text for further explanation. S = stimulus artifact.

KUPERSMITH

shows the major deflection of the bipolar electro-’ gram and thus the time of local activation. In this example, one might approximate the time of local activation from the intrinsic deflection of the unipolar electrogram (fast portion of the recording), though less precisely than from the major deflection of bipolar electrograms. At times the intrinsic deflection of unipolar electrograms is not nearly as well defined as it is in Fig. 1. A few technical details about both bipolar and unipolar recordings are worth remembering to better understand their uses. The closer the distance between bipolar electrodes, the more exact is the recording for timing of local activation and the less of distant events are recorded. Therefore, closely spaced bipolar electrodes, i.e., 1 or 2 mm apart, are usually employed for this purpose during open heart surgery. Generally, greater electrical potential differences are recorded by unipolar than by bipolar electrodes since the former record potential differences.between a point on the heart and a reference electrode, while the latter record potential differences between contiguous portions of the heart.” With bipolar electrodes, particularly those that are closely spaced, it may be difficult to detect small differences in potential between electrodes in instances when conduction velocity is low and the wavelength of activation proceeds over a considerable length, such as during repolarization. For this reason bipolar electrodes are not ordinarily suitable for recording T waves.i’ Also, when recording bipolar electrograms for timing of local activation, one adjusts the gain settings so that an easily measureable major deflection is recorded, and generally little attention is paid to the precise voltage of the recordings. The position of both the bipolar and unipolar electrodes with reference to the spread of activation also influences the recording. With bipolar recordings, if activation proceeds parallel to the electrodes, there is a maximum potential difference between the electrodes with the polarity of the recording indicating the direction of activation. However, if the spread of activation is perpendicular to the electrodes, theoretically, no deflection is recorded since there would be no potential difference between e1ectrodes.i’ For this reason, a tripolar electrode with a triangular arrangement of the electrodes (Fig. 2) is most suitable for recording. With such an electrode, one

ELECTROPHYSIOLOGIC

Fig. 2. Recording end trophysiologic mapping. 1.5 mm between pairs, electrograms. The probe facilitate placement in minimal injury to underlying

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MAPPING

of electrode probe used in elecThe three electrodes, which are are used to record three bipolar has a partially flexible shaft to difficult locations and to assure tissues.

records three bipolar electrograms at 60” angles, thus eliminating the possibility of recording an electrogram of low or indetectible amplitude due to the passage of wave of activation perpendicular to one electrode pair. In the case of unipolar recordings, the position of the active electrode with reference to the spread of activation also influences the polarity of the recording. If the electrode is at the point of origin of cardiac activation, it will record a completely negative potential or a potential with a predominately negative component indicating that cardiac activation is proceeding in a direction away from the recording electrode. lo If the active electrode is away from the point of origin of activation, the polarity of the recording will depend on the electrode position relative to the point of origin and direction of activation. The relationship between the timing of surface bipolar electrograms to that of intracellular action potentials recorded at the same site has been determined. In general, there is good correlation between surface and intracellular recordings,11’12 though exceptions may occur during premature excitation when the failure to record a surface electrogram, while indicating depression of underlying tissue, may not necessarily reflect complete absence of activation, when the timing of the surface electrogram is not necessarily accurate, and when polarity reversal of the surface electrogram

may not mean reversal in the direction of activation.rr These inconsistencies with prematurity are probably due to nonuniform arrival of excitation at the surface recording site.‘r The use of filters to eliminate low frequency components from the recorded electrograms is important in electrophysiologic mapping.4>14 Cardiac impulses are complex electrical signals that cover a broad range of frequencies ranging from zero l(i.e., dc) to several thousand cycles per second (or Herz). Low-frequency components are prominent during depolarization of the sinus and AV nodes and during repolarization (ST segment and T wave) of all cardiac tissues. 4~14High-frequency components are prominent during depolarization of the His bundle and bundle branches and also of atria1 and ventricular muscle.i4 In general, the frequency range of the signal correlates with the rate of conduction of the particular impulse. When mapping during surgery for timing of myocardial activation or for delineation of the His bundle or bundle branches, low-frequency components are omitted with frequency limits set between 12 to 200 or 500 Hz4 (in cardiac catheter recordings from the specialized conduction system, limits are set at 40-500 Hz).~~ The use of low limit filters increases baseline stability and accentuates the myocardial, His bundle, or bundle branch transients.14 W’hen recordings of ST segments are made, low limit filters are set (0.1 to 500 Hz) allowing for reclording of low-frequency components that are prominent during repolarization. Surface ECG leads are also recorded at 0.1-200 or 0.1-500 Hz so that all components may be recorded. Intraoperative

Techniques

Specific methods of approach in electrophysiologic mapping depend on both the goals of mapping and the nature of the requirements of the surgical procedure. Mapping is performed with varying kinds of electrode probes, some of them fashioned for a specific use in a specific study.3-5*8 Most commonly employed for mapping is a handheld probe with three silver electrodes in a triangular arrangement at the distal end (Fig. 2). ‘The distal portion of the shaft of the probe is best made flexible to avoid placing inordinate pressure on the heart, particularly when recording from the specialized conduction system, and to facilitate placing the probe in difficult regions. Most regions of the heart are accessible with such a probe, de-

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pending, of course, on the surgical approach, except for the posterior basal right and left ventricles. Here, ring-like electrodes that can be placed on the examiner’s finger or electrodes placed on flexible catheters have been employed. For recording intramyocardial electrograms, needle electrodes consisting of several electrodes placed along the shaft of a small gauge needle are employed. 3Y24925Though these electrodes cause temporary local injury, the electrophysiologic effects of such injury are reversed within a few minutes.26 Suction electrodes that record monophasic action potentials have been used in electrophysiologic studies during cardiac catheterization, but have thus far not been employed intraoperatively .27-29 The feasibility of recording human transmembrane potentials in situ with microelectrodes have also been demonstrated.30 Certain kinds of recordings are made during cardiopulmonary bypass and surgery, while others are made before or after cardiopulmonary bypass. 47598Recordings made to determine the sequence of and characteristics of epicardial activation and recordings of transmural electrograms using plunge electrodes have been generally made off cardiopulmonary bypass; in fact, many such studies have been made on patients who are not destined to undergo cardiopulmonary bypass, but in whom access to the heart was made possible by thoracotomy for other reasons.3Y10-22 Recordings of endocardial activation and of the specialized conduction system are of course made during cardiopulmonary bypass,418 as are recordings made to localize zones of damaged myocardium.2 The time taken to record and to evaluate electrograms is most crucial, especially when mapping is performed during cardiopulmonary bypass. During mapping, surface ECG leads and, in some instances, intraventricular cavity potentials are recorded simultaneously with cardiac electrograms for use as reference recordings.3-5 Atria1 and/or ventricular electrodes sutured to the heart may also be employed as reference recordings.5 Most studies require a supraventricular rhythm and a normal antegrade sequence of His-Purkinje and ventricular activation during mapping. To assure a normal antegrade sequence of activation, atrial pacing is often performed to suppress arrhythmias,4*8 and to facilitate detection of abrupt changes in AV conduction due to surgical manipu-

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lation.’ Pacing is not required when mapping to delineate zone of damaged myocardium since such studies can be performed in any rhythm including ventricular fibrillation.2 Certain precautions must be taken both in recording and interpreting electrograms during open heart surgery. Firstly, because of the great variety of electrical equipment used in the modern cardiac operating room, ac (60 cycle) interference in the recordings is often a problem. Particular attention to detail in connecting all equipment to a central ground and care to assure proper function of equipment will minimize the effects of such interference. Motion artifacts may occur when making recordings with hand-held electrodes, but they are prevented by good technique and experience. Pressure of the electrode on the heart surface may also cause ST segment shifts that make interpretation of recordings for this purpose difficult unless proper precautions are taken. Changes in serum concentration of potassium, which can occur during surgery, influence the recordings. For recordings made during cardiopulmonary bypass, hypothermia may cause depression of conduction. Deep hypothermia (less than about 25°C) may so markedly depress conduction that electrophysiologic mapping cannot be performed. lo Less severe grades of hypothermia (32”-35°C) may influence conduction so little that His-Purkinje and intraventricular conduction intervals are virtually unaffected.4 Though intracardiac conduction intervals may be prolonged during hypothermia, mapping to delineate the locations of the specialized conduction system can still be performed, providing that activation is not so depressed as to render recordings completely uninterpretable. However, recordings cannot be made during ischemic arrest induced by cross-clamping of the aorta unless coronary perfusion is performed, and even then conduction is usually depressed. Certain peculiarities in the open chested situation should be kept in mind when interpreting recordings made during surgery. The configuration of the QRS complex in standard ECG leads may vary when the chest and pericardium are opened due to change in cardiac position. However, the polarity of the P wave seems to be the same and the P wave morphology similar whether the chest is open or closed.6 Voltage of canine epicardial electrograms

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MAPPING

was reported to be greater when the chest was opened because of the lack of shunting effect of contiguous lung.31 MAPPING

OF THE

ATRIUM

Atrial-mapping studies in humans have dealt with various kinds of problems: the nature of P wave morphology and polarity with rhythms originating from various ectopic atria1sites(studied by pacing the atria at various sites);6t32the nature of atria1 activation during spontaneousarrhythmias;33,34and the nature of atria1activation in certain congenital anomalies, most notably endocardial cushiondefect.35 Although both specialized and working myocardial tissuesare present in the atrium, recordings cannot be made from all atria1 tissues.Recordings can of course be made from atria1myocardium and the atria1portion of the His bundle, but they cannot ordinarily be made directly from the sinusor AV node4 nor can discrete recordings ordinarily be made from the specialized internodal tracts.36,37The nature and timing of conduction in the sinusnode, AV node, and internodal tracts are inferred from atria1myocardial or His bundle recordings. In this section, studiesof atria1 activation and pacing will be considered;studiesbasedon recordingsmadefrom the atria1portion of the His bundle will be considered separately (seeMAPPING OF THE SPECIALIZED CONDUCTION SYSTEM); and microelectrode studies of atria1 tissue in vitro,38 though most interesting, will not be considered.

formed during open heart surgery and during the postoperative period. During open heart surgery, Waldo et aL6 found the following: (1) Pacing of the posterior right and left atria1 epicardium resulted in negative P wavesin ECGleadsII, III, and AVF. (2) Pacing at the head of the sinus node causedpositive P waves and pacing at the mid1and posterior sulcusterminalis causedflat P waves in leadsII, III, and AVF. (3) Pacingat the coronary sinus ostium causednegative P waves in leadsII, III, and AVF. When the pacing site was moved more medial parallel to the margin of the AV groove (and in the vicinity of the AV node and His bundle) (Fig. 3), resulting P waves were first biphasic (-, +) and with even more medial sites (now in the vicinity of the anterior internodal tract) (Fig. 3) P waveswere positive in the inferior leads. (4) The P-R intervals resulting from pacing of atria1epicardial sitesin the sulcusterminalis and

P WaveMorphology and Polarity Electrocardiographershave always paid closeattention to the morphology and polarity of the P wave when determining the origin of atria1 arrhythmias. 3g-41For example, upright P waves in ECG leads II, III, and AVF are thought to represent antegradeatria1activation with rhythms originating in the sinusnode vicinity, while inverted P waves in these inferior leadsare thought to represent retrograde atria1 activation from impulses originating in the lower atrium AV junction or ventricle. 3g-42 Characteristic P wave morphology has also been attributed to rhythms originating from the left atrium and coronary sinus.42-44To examine some of these electrocardiographic concepts, studiesof P wave morphology and polarity with atrial pacing in various regions were per-

Fig. 3. Schematic diagram of cross-section of right atrium and ventricle showing the specialized condu’ction system. From the sinus node at the junction of the superior vena cava and right atrium, the internodal tracts pass anterior to the fossa ovalis (anterior and middle tracts) and along the crista terminalis (posterior iract) to the AV node. From the AV node the His bundle continues to the membranous septum (MS) where it bifurcates into the right and left bundle branches. CS = coronary sinus, pH = proximal His bundle, dH = distal His bundle. (Reproduced by permission of Circ~larion.~)

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posterior right and left atria always exceeded 0.12 set, and P-R intervals with pacing at the endocardial sites noted above were almost always less than 0.12 sec. Also, there was always an isoelectric interval between the pacing stimulus artifact and the onset of the P wave usually of 0.01 to 0.025 set but up to 0.059 sec. In a study in which various sites in the right and left atria were stimulated at various rates in the postoperative period using electrodes previously implanted during surgery, McLean et a1.32 found the following: (1) Negative P waves in standard ECG lead I (thought to indicate left atria1 rhythm)44 occurred only when certain left atria1 sites in the region of the pulmonary vein were paced and never when right atria1 sites were paced. Positive P waves in lead I occurred with either right or left atria1 pacing. (2) Negative P waves in inferior leads II, III, and AVF with P-R intervals both greater and less than 0.12 set (previously attributed to “coronary sinus” and “upper nodal” rhythms respectively)39-41 occurred when various sites in the lower right and left atria were paced.32 (3) Negative P waves in lead V, (thought to indicate left atria1 rhythms exclusively)‘@’ occurred when either right or left atria1 sites were paced. A positive bifid P wave in VI, similar to the “domedart” P wave that has been attributed to left atria1 rhythm,44 was in fact produced by pacing of the posterior inferior left atrium near the coronary sinus but not when other left or right atria1 sites were paced. (4) P-R intervals were highly variable but in certain instances were less than 0.12 set both when sites relatively close to and distant from the AV node were paced. There was usually an isoelectric interval between the stimulus artifact and the onset of the P wave in this study of O.Ol0.054 sec. From these studies one can reach certain conclusions that in part confirm and in part argue against previously held electrocardiographic concepts and terminology. So-called “upper nodal” rhythm (negative P waves in inferior leads and P-R interval less than 0.12 sec)39-42 could be produced by pacing in the region of the coronary sinus ostium and other sites away from the AV node. So-called “coronary nodal” rhythm (positive P waves in inferior leads and P-R intervals less than 0.12 sec)39-42 was produced by pacing near the AV groove and anterior internodal tract. So-called “coronary sinus” rhythm (negative P waves in in-

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ferior leads and P-R interval greater than 0.12 set) 39-42 was produced by pacing in the posterior right and left atrial regions and not by pacing in the region of the coronary sinus ostium where P-R intervals were always less than 0.12 sec. Thus the terms “upper nodal,” “coronary nodal,” and “coronary sinus” rhythm as commonly applied may not be accurate representations of rhythms arising in these regions.6 Of the ECG patterns considered to indicate left atrial rhythm,32 $43-4s negative P waves in ECG lead I only occurred with, but were not the exclusive pattern of, left atria1 stimulation, while negative P waves in lead V6 occurred with either right or left atria1 stimulation. The “dome-dart” P wave in lead V 1, 44,45 on the other hand, occurred only with pacing of one specific left atria1 site in the posterior inferior region. With regard to retrograde activation of the atria, pacing of the lower right atrium in the region of the AV node or His bundle could produce bifid of even upright P waves in inferior ECG leads suggesting that retrograde activation of the atrium is not necessarily associated with negative P waves in these leads as had previously been thought.39-42 Also it is of interest that there was usually an isoelectric interval between the stimulus artifact and onset of the P wave signifying that the latter may not necessarily indicate the onset of atria1 activation. It should be noted that there was left atiral enlargement in some of the patients studied, which may have influenced P wave morphology.42 Further, the findings of these studies may not be applicable to hearts with atria1 abnormalities or conduction defects that may alter P wave morphology and/or polarity during either sinus or ectopic atria1 rhythms.42y46 Significance of Internodal Tracts The results of these studies relate to a problem of atrial conduction that has intrigued anatomists and electrophysiologists for many years, i.e., is the spread of atria1 activation uniform in all directions through atria1 muscle or do the specialized internodal tracts modify the sequence of atria1 activation?36,37y47-51 Figure 3 shows the location of the anterior, middle, and posterior internodal tracts. All three structures originate in the sinus node vicinity and pass via the atrial septum to the AV

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MAPPING

node.4794g,s0 The anterior and middle internodal tracts both pass anteriorly to the fossa ovalis and are rather direct routes from sinus to the AV node,47,4g7s0 while the posterior tract has a longer and more circuitous course along the crista terminalis.47~4g3so Bachman’s bundle, which is not shown in the diagram, originates with the anterior internodal tract at the sinus node but continues into the left atrium.4g Histologically, these tracts contain specialized cells (Purkinje cells) but differ from other portions of the specialized conduction system in that they are not surrounded by collagen sheaths and the specialized cells are mixed in with working atria1 myocardium.‘* Much has been written in evidence both for and against a functional role for the internodal tracts, and these observations will not be reviewed here.36y 37,47-54 However, certain of the findings described above regarding P waves morphology and polarity in humans are best explained by functionally important internodal tracts.6,32 For one, P wave polarity in inferior ECG leads seemed to depend on the relationship of the pacing electrodes to the anterior internodal tract or Bachman’s bundle.6 When the pacing electrodes were close to one of these tracts, as in the inferior right or anterior inferior left atrium, positive or biphasic P waves occurred in inferior ECG leads.6 When the pacing electrodes were more distant from these tracts, e.g., at the coronary sinus ostium or in the posterior inferior left atrium, negative P waves occurred in inferior ECG leads.’ Furthermore, moving the pacing electrode just a few millimeters could markedly change P wave polarity.6 An explanation for these findings is as follows: Retrograde conduction through the anterior and middle internodal tracts and Bachman’s bundle to the sinus node vicinity is relatively rapid. Thus,when the anterior internodal tract or Bachman’s bundle is activated, conduction proceeds quickly and preferentially retrograde via these tracts to the sinus node vicinity and from there spreads out in an antegrade direction over the atria1 myocardium, causing positive P waves or P waves with a large positive component to occur in inferior leads. Exclusive retrograde activation of the atria1 myocardium with inverted P waves in inferior leads will occur only when the atrium is paced at sites distant from the anterior internodal tract or Bachman’s bundle.6,32 The precise sequence of atria1 activation that was responsible for these negative P waves is not clear, though

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they seemed to occur when early activation of the posterior inferior left atrium was likely, e.g., pacing of the coronary sinus ostium. Thus, negative P waves or the negative component of biphasic P waves in inferior leads6’32 during ectopic atria1 rhythms may result from retrograde activation of the left atrium. An example of distortion of the internodal tracts due to congenital displacement may occur in endocardial cushion defect. In this abnormality, the defect is located along the usual route of the anterior and middle internodal tracts and may thus disturb the normal course of these tracts?5355 P-R interval prolongation also occurs in endocardial &rshion defect56 and may be related to interatrial conduction delay resulting from distortion of these tracts. To examine this postulate, Waldo et al. performed studies of atria1 pacing and mapping in a group of patients with endocardial cushion defect, both incomplete (ostium primum ASD) and complete (AV canal),35 and found the following: With low right atria1 pacing in the region of the AV node and anterior internodal tract, P-R intervals were always less than 0.12 set, indicating no overall conduction delay in the AV node or more distally, and P waves were always negative in inferior ECG leads.3s Similar pacing in control patients, both with and without other forms of ASD, also resulted in P-R intervals less than 0.12 set:, but P waves in inferior leads were upright or biphasic as in previous atrial studies.6 When the sinus node vicinity was paced, conduction from the high to the low right atrium seemed to be delayed only in cases of endocardial cushion defect.35 Taken together, these findings suggest that interatrial delay and not delay in the AV nodes7 cause the P-R interval to be prolonged in endocardial cushion defects. The intraatrial delay might be explained by disruption of the anterior and middle internodal tracts caused by the defect. Disruption of the anterior tract might also explain why negative rather than positive or biphasic P waves occurred with pacing of the right atrium in the region of the AV node and anterior internodal tract, i.e., preferential and rapid conduction along the anterior tract retrograde to the region of the sinus node was no longer possible. %” Although each of the findings in endocardial cushion defect could alternatively be explained by right atria1 dilatation with. resulting prolongation of intraatrial conduction,s9 no similar conduction delays or results of right atria1

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pacing occurred in ostium secundum ASD where the right atrium is also dilated. However, in a study of atria1 conduction using catheter electrodes, ostium secundum ASD was associated with intraatria1 conduction delays and slight prolongation of the P-R interval that was not in the abnormal range .59 Interruption of the internodal tracts due to surgical injury rather than anatomic displacement may occur during operative repair of transposition of the great arteries (d-TGA) by Mustard technique. 6oy61Here an extensive atria1 incision is made that may interrupt the anterior and/or middle tracts 6oy62,63though the posterior tract, which is thought to be less important in modifying atria1 conduction because of its more circuitous course,6 is spared. Various atria1 arrhythmias occur following the Mustard procedure and are thought by some to relate to injury to the internodal tracts.62 However, operative injury to the sinus and AV nodes also occur and may be more important in the genesis of postoperative arrhythmias.64 One of the reasons that the functional importance of the internodal tracts has not been fully clarified is that the sequence of atrial activation in humans has not been clearly determined in situ. In an in vitro study of human atrial epicardial excitation, Durrer et al. found a uniform spread of atria1 excitation, an atria1 conduction velocity of 1 M/set, and no indication of preferential conduction except perhaps in the region of Bachman’s bundle in one heart. However, in this study, there may have been injury to the heart on removal as evidenced in part by the inability to localize the sinus nodess3

Excitation of the Great Veins One electrophysiologic-mapping study has examined the spread of activation from the atria into the muscle of the superior vena cava and pulmonary veins. ” From the right atrium activation spread into the superior vena cava for 4 to 6 cm but not into the inferior vena cava, and from the left atrium, activation spread into the right pulmonary veins, occasionally past the pericardial reflections. Double deflections were often recorded in the region of the superior vena cava and pulmonary veins and were attributed to superimposition of recordings of activation in both veins and nearby atria.65 Because activation readily spread into the superior vena cava, this vein could not be considered a barrier predisposing to circus movement

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around it as had been proposed by Lewis to explain atria1 flutter.66 What other significance there is to the finding of the spread of cardiac excitation into the great veins is not yet clear.

Atria1 Mapping During Arrhythmias Electrophysiologic mapping of the atrium has been performed in various atria1 as well as other types of arrhythmias.33’65’67 Lister et al. studied AV and VA conduction during rhythms originating in the atrium, AV junction, and ventricle by means of electrodes sutured to the right and left atrium and the right ventricle. 67 In this study, with pacing of the atrium or ventricle, unidirectional antegrade or retrograde AV block was not common, and the fastest pacemaker of the heart, whether atrial, junctional, or ventricular, usually caused activation of the entire heart.67 Studies of mapping and pacing have also been performed in isoarrhythmic AV dissociation.% In this arrhythmia there is independent activity in the atrium and ventricle or AV junction (dissociation), but there are periods of synchronization or acchrochage between the atrium and ventricle with merging of the P wave and QRS complex of the ECG. 34&8-7o A common ECG pattern is for the P wave to follow the QRS at a fixed interval for a brief (acchrochage) or long (synchronization) period of time in which the P wave is or appears to be upright in inferior leads, which, as noted above, has been thought to indicate an antegrade sequence of atria1 activation.39’40’67 The dissociation may or may not be due to complete block between atrium and ventricle. 7o Though many authors reserve the term “dissociation” for instances in which there is no complete block, 7oY71this distinction is at times difficult to make in individual ECGs. The mechanism of isoarrhythmic AV dissociation in the absence of complete block was studied in a group of patients undergoing open heart surgery.34 Atria1 and ventricular electrograms were recorded during spontaneously dissociated rhythms in which there was independent activity originating in the atrium and AV junction. When synchronization of atria1 and junctional activity occurred with the P wave following the QRS by a fixed interval, the sequence of atria1 activation and thus the site of origin of the atria1 impulse changed though P waves in inferior leads were biphasic or in one case remained positive in polarity.% This change in the sequence of atria1 activation during “synchroniza-

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MAPPING

tion” was presumably caused by a change from antegrade to retrograde activation of the atrium in spite of the fact that P waves in inferior leads did not remain completely negative in polarity.34 Additional evidence for this interpretation was the fact that P waves were also positive in these leads when selective pacing of the His bundle or ventricles was performed in some cases. Thus, the mechanism of apparent “synchronization” during AV dissociation was in reality a change in rhythm from AV dissociation with independent activity originating in the atrium and AV junction to junctional rhythm with retrograde atria1 capture. Further, during the spontaneously “synchronized” rhythm or during ventricular or His bundle pacing, P waves still were or appeared to be predominantly positive in inferior leads, particularly when obscured or modified by the QRS complex, ST segment, or T wave. 34 This finding is consonant with the observation concerning P wave polarity and morphology with antegrade and retrograde atria1 conduction described above.6 On the other hand, synchronization occurring in the presence of complete AV block has also been studied and seems to be related to a reflex mechanism.” The sequence of atria1 excitation has been determined in two cases of atria1 flutter during surgery.33 $72 In one case, in which recordings were made at five atria1 epicardial sites, the mechanism of flutter was attributed to circus movement because continuous atria1 activation was recorded for over half the atria1 cycle.” In the other case, 37 atria1 epicardial sites were mapped, and atria1 flutter was attributed to an ectopic atria1 focus originating in the midright atria1 appendage near the aortic root. However, continuous activity of the atria1 epicardium was recorded for over half the atrial cycle in this case as in the other, but was attributed to delays of atria1 conduction in part due to atria1 disease and not circus movement.33 Thus, in spite of these mapping studies, the mechanism of atria1 flutter has yet to be clearly determined. Atria1 epicardial mapping has also been performed in two patients with atrial tachycardia. In both, double excitation waves approaching one another from the upper and lower region of the sulcus terminalis and colliding in mid-right atrium were found, the significance of which for the mechanism of the arrhythmia is unclear.65 Atria1 recordings were also made in one interesting patient of apparent atria1 fibrillation as determined

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by surface ECG leads. Atria1 fibrillation was found in the left atrium, while atrial tachycardia (rate 210 beats/min) was found in the right atrium.65 Ten similar cases had previously been briefly described by Nelson et al.73 MAPPING OF THE CONDUCTION

SPECIALIZED SYSTEM

Prevention of the Heart Block One of the significant contributions of the mapping technique hasbeen in the prevention of postoperative heart block due to injury of the specialized conduction system.8.99NStuckey et a1.74and, somewhatlater, Giraud et a1.75first demonstrated the feasibility of recording human His bundle and bundle branch electrograms during open heart surgery. The former authors and, jater, Kaiser letal. suggestedthe use of this technique to locate the specialized conduction system in congenital abnormalities and thereby avoid surgically induced complete heart block. The techniquesfor mapping of the specializedconduction systemwere further refined by the samegroup at Columbia University. In the early years of surgery for repair 6f congenital defects, the overall incidence of postoperative permanent complete heart block wassaid to be lo%-12% or more.76-79However, with increasingknowledge of the anatomy of the specialized conduction systemin congenital heart disease,, the incidence of this complication was reduced to below l%-2%. 78 Still, repair of certain abnormalities such as endocardial cushion defectso9” have a significant incidence of postoperative complete heart block making it important to have availablea technique of identification of the specializedconduction systemduring surgery.8 AV block due to injury to the AV conduction system during surgery may have various causes, i.e., hemmorhage,necrosis,interruption or inflammation, at or adjacent to suture sites,79980*83y87 or interruption of blood supply to the conduction system.88 Complete heart block can also result from injury to the right bundle branch sincelocal hemmorhage or edema may dissect proximally along the plane of the bundle branch to involve a much greater portion of the specializedconduction system.89Late complete heart block following surgery could result from injury to a portion of the specializedconduction system with organization and reactive fibrosis, which progressto invade

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a much greater proportion of the conduction system.77~85Y90For these reasons, mapping of the specialized conduction system in most congenital defects should include the His bundle and as much of the ipselateral bundle branch as possible, and sutures placed for surgical repair should avoid all these portions of the specialized conduction system if possible. Techniques The technique used in mapping of the specialized conduction system using electrode probes, such as illustrated in Fig. 2, has been in part described above. A logical sequence to follow in mapping the atrium is as follows. First one places the probe in the region of the coronary sinus ostium (Fig. 3) and records electrograms.4,90p91 One then moves the probe in the direction of the membranous septum and records electrograms along the AV ring (the usual location of the AV node and His bundle) (Fig. 3), and further on one records from the ventricular portion of the membranous septum where bifurcation of the His bundle to the bundle branches occurs. In the ventricle, the probe is placed in relation to whatever defect is present, and the sites and sequence of mapping are also otherwise determined by the nature of the abnormalities present and the surgical approach. Some sort of grid diagram of the heart is helpful to use during mapping so that the findings can be efficiently recorded.4y8>N’91 Mapping of the specialized conduction system can be performed quickly and usually requires less than S-10 min of cardiopulmonary bypass time (exceptions to this may occur with complex congenital anomalies such as single ventricle). His bundle and bundle branch electrograms are easily recognized by their characteristic appearance as fast deflections of simple contour occurring within the P-R segment of the ECG.14 AV node potentials are not recorded by this technique (see the following), but the location of the AV node may be inferred from the location of the His bundle.p2 The technique of mapping of the specialized conduction system has a very low morbidity. Conduction disturbances are unusual but rarely include varying degrees of transient heart block lasting a few minutes.” Use of an electrode probe with a flexible shaft (Fig. 2) and care by the surgeon to apply the probe gently avoids this complication.

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The presence of moderate hypothermia (28°C or above) does not interfere with the recording of specialized fiber electrograms though it may cause a degree of depression of conduction within the specialized conduction system and the prolongation of His bundle and bundle branch to QRS intervals.4’9’p2 In contrast, deep hypothermia of about 25°C or less may make it impossible to record specialized fiber electrograms.” This drawback will be more important if complete repair of congenital defects in infancy under deep hypothermia becomes a widespread practice.% Location of the Specialized Conduction System in Congenital Heart Disease The location of the specialized conduction system as determined by electrophysiologic mapping is consistent with pathologic studies of the specialized conduction in congenital heart disease.76383> W~81y95His bundle electrograms in the atrium are recorded along the margin of the tricuspid ring for variable distances, and shifts in location of the atria1 portion of the His bundle occur in endocardial cushion defects (see below) but not in ostium secundum ASD, dextro-transposition of the great arteries (d-TGA), VSD (including supracristal VSD and tetralogy of Fallot), and doublechambered right ventricle.” Although the AV node cannot be precisely localized by mapping due to inability to record AV nodal electrograms, numerous anatomic studies have shown it to be just proximal (i.e., toward the coronary sinus) or slightly inferior to the His bundle.p2 Therefore, the location of the AV node can be inferred by mapping the His bundle and the repair should avoid a zone about 8 mm proximal to the structure,g2 depending o n the size of the heart. In the ventricle the location of the specialized conduction system depends on the nature of the defect.75~76Y83@,87Figure 4 shows the location of specialized conduction system recording sites in the right ventricle (filled circles, Fig. 4) in membranous VSD. Specialized conduction system electrograms are recorded at the membranous septum (most proximal filled circle in Fig. 4) and then along the posterior inferior margin of the defect, coursing for a variable distance around the defect and then in some instances arriving as far as the papillary muscle of the conus and less commonly the moderator band. 83@,87191 Since the membranous septum is the site of bifurcation of the

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these defects has been well described and is relatively constant. 78 However, in some defects the location of the specialized conduction system is unusual, variable, or unknown and postoperative complete heart block is still a problem. Surgery for these defects should not be undertaken without availability of the mapping technique.

Corrected Transposition of the Great Arteries

Fig. 4. Schematic diagram of cross-section of right atrium and ventricle in a heart with a membranous VSD showing sites (filled circles) where specialized conduction system electrograms are recorded at the posterior and inferior margin of the VSD.

His bundle, recordings of specialized fiber electrograms distal to this site in the right ventricle are recorded from the right bundle branch.92 In patients with subpulmonic or pulmonic stenosis and in patients with subaortic obstruction, it may be difficult or impossible to record specialized fiber electrograms in the involved ventricle. This may be due to the fact that severe muscle hypertrophy causes the specialized conduction system to be buried beneath the endocardial surface.” In some instances, the distal His bundle and all or part of the proximal right bundle branch course in the ventricle towards the left rather than the right side of the interventricular septum and follow an intramyocardial course. 84Y96This location, which is more common in double outlet right ventricle and in tetralogy of Fallot,% may cause a discontinuity in recording or rarely a failure to record distal His bundle and bundle branch electrograms in the right ventricle. 91 Knowledge of this sometimes altered location is important for avoidance of injury to the specialized conduction system with sutures placed in an intramyocardial position. At present, there is a minimal risk of postoperative complete heart block in surgery for most congenital defects without mapping, because the location of the specialized conduction system in

One of the defects in which mapping is both important and of interest is corrected transposition of the great arteries (1-TGA).9 In this defect there is ventricular inversion and levotransposition of the great arteries often associated with other anomalies including VSD, subpulmonic stenosis, and Ebsteinlike abnormalities of the systemic AV valve. 1-TGA is also frequently associated with conduction abnormalities including first, second, and third degree AV block.97 Postoperative complete heart block, following repair of the associated abnormalities, is a particularly common occurrence.” The location of the specialized conduction system in l-TGA in association with membranous VSD has been studied with mapping techniques and found to be markedly different from that of hearts with normally related ventricles.’ The heart of one of the patients studied in which there was l-TGA, membranous VSD, and subvalvar pulmonic stenosis is shown in Fig. 5. Here the right atrium and morphologic left ventricle (which is rightsided) are in cross-section and the circles show the only sites where specialized conduction system electrograms were recorded, i.e., at the anterior and superior VSD margin. This location of the specialized conduction system is far different from that of VSD with normally related ventricles (Fig. 4). The insert of Fig. 5 shows an example of the specialized fiber electrogram, in this case that of the His bundle, recorded at the most proximal specialized conduction system recording site. In four other patients with I-TGA and membranous VSD studied by mapping, the location of the specialized conduction system was also anterior and superior to the VSD. In one patient, I-TGA was associated with an Ebstein-like abnormality of the systemic AV valve, and mapping of the “atrialized ventricle” and true AV ring facilitated placement of a valve prosthesis.’ Since I-TGA is associated with spontaneously occurring first, second, or third degree heart block, it is of interest to determine the site of block. In IWO

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Fig. 5. Schematic diagram of a heart with I-TGA, membranous VSD, and subvalvar pulmonary stenosis. The right atrium and morphologic left ventricle (which isrightsided) are shown. The pulmonary artery arose from the morphologic left ventricle. The circles show the only sites where specialized conduction system electrograms were recorded anterior and superior to the VSD. The inset shows the most proximally recorded specialized conduction system electrogram, which was probably recorded from the His bundle adjacent to the AV ring. The lower traces are ECG leads I, II, Ill. The interval from the specialized fiber electrogram to the QRS at this site was 41 msec. S = stimulus artifact. (Reproduced by permission of Circulation. 91

patients studied with l-TGA, first degree AV block was present preoperatively and was correlated during surgery with delay proximal to the bifurcation of the bundle branches and thus in the AV node or His bundle.” Both the location of the conduction system and the site of block observed in this study were consistent with pathologic studies of l-TGA with membranous VSD.98-‘00 In these studies two AV node-like structures have been found, one located anteriorly, and the other posteriorly. The posterior node ends blindly while the anterior node gives rise to the His bundle at the AV ring. The latter then passes directly into the ventricle and bifurcates at the anterior superior margin of the VSD 98-*oo consistent with what was found in the mapiing study.’ Spontaneous heart block in l-TGA is probably related to this AV node abnormality and also to fibrosis or interruption of the His bundle that has been found in some instances.98 Postoperative heart block in l-TGA with membranous VSD8* is undoubtedly related to the unusual location of the specialized conduction system

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anterior and superior to the VSD rather than posterior and inferior to the defects as in VSD with normally related ventricles (Fig. 4). The sites where specialized conduction system electrograms were recorded in l-TGA are sites where sutures are commonly placed for VSD closure’ and are also close to the pulmonic subvalvar region that may be stenotic in l-TGA and may require resection.“’ For these reasons, open heart surgery in l-TGA should not be performed without availability of the mapping technique, particularly since in some instances the location of the specialized conduction system may be variable with portions of it not in proximity to the VSD.98 Unfortunately, as shown in a subsequent study, an occasional case of I-TGA may have a zone of specialized tissue that is so broad and sheet-like as to fill the region between the VSD and pulmonary artery making adequate closure of the VSD without injury to a portion of the specialized conduction system impossible with an approach from the morphologic left ventricle.g8*101 However, closure of the VSD from the morphologic right ventricle should have a lesser risk of complete heart block. Other Congenital Abnormalities When operative repair of single ventricle is undertaken, mapping of the specialized conduction system is most important.my’m In the group of abnormalities comprising single ventricle, the location of the specialized conduction system is highly variable and unpredictable and often close to sites where sutures are placed for repair.g0’102 Postoperative complete heart block has occurred frequently when single ventricle defects are repaired.Im When attempting valve replacement for Ebstein’s abnormality of the tricuspid valve, specialized conduction-system mapping may be helpful in delineating its location at the AV ring, permitting valve replacement without complete heart block.4’90 Where widening of a VSD is to be done for repair, such as in double outlet right ventricle, identification of the specialized conduction system, which is in close proximity to the VSD (Fig. 4), is necessary. Mapping of the specialized conduction system may also be helpful in an occasional case of muscular VSD. Unlike membranous VSDs, small muscular VSDs usually do not have a close relationship to the specialized conduction system.96

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However, if the muscular defects are large or multiple, they may be close to the specialized conduction system, with the latter passing antero-superior or infero-posterior to a muscular defect or between two defects.96 In repair of d-TGA, by Mustard Technique, an extensive incision is made in the right atrium that may interrupt the intranodal tracts. In some instances the atrial incision is close to the AV node and inferring the location of the AV node by mapping of the His bundle may be of help in avoiding injury to the node. In asymmetric septal hypertrophy when surgery is performed to abolish the subaortic gradient, complete heart block may occur postoperatively.lo3 Specialized conduction-system mapping in the left ventricle may be of help in this procedure though it has not yet been reported. However, in one case of VSD associated with asymmetric septal hypertrophy, specialized conduction system electrograms were recorded in the right ventricle and were situated away from the margin of the VSD. 91 Therefore, sutures for VSD closure were placed at the margin rather than away from the margin of the defect as is usual, to avoid injury to the conduction system.”

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Endocardial Cushion Defect In endocardial cushion defects studies of specialized conduction system,79*84Y90y104 as well as of atrial and ventricular activation,‘05,106 have helped to prevent postoperative heart block and have also increased our understanding of the electrophysiologic abnormalities that characterize this defect. In the ECG of endocardial cushion defect there is first degree AV block, left axis deviation, and right ventricular conduction delay;‘05”0” and the vectorcardiogram shows a superior axis, counterclockwise rotation and a right ventricular conduction delay. 105,107These ECG findings could be ascribed to severe conduction defects.“’ Mowever, mapping and histologic studies have made it clear that the abnormalities result from the particular relationship of the specialized conduction system to the defect.‘05-107 Studies of atria1 activation in endocardial cushion defect were described earlier. The location of the AV node, His bundle, and bundle branches as determined by both mapping” and histologic 7g784P87P104 studies in endocardial cushion defect is shown in Fig. 6. The AV node is situated at the floor of the coronary sinus between the coronary

Fig. 6. Schematic diagram of heart with endocardial cushion defect as seen from the right (A) and left (6) sides showing location of the AV node, His bundle, and bundle branches, which are all displaced by and in close proximity to the defect. The AV node is at the floor of the coronary sinus, and the His bundle and bundle branches are displaced posteroinferiorly. Of particular note is the short length of the fibers of the inferior portion of the left bundle branch and the much greater length of the fibers of the anterior portion.

1x0

sinus and the defect. The most proximal His bundle electrogram recording site is also relatively close to the coronary sinus. The His bundle is displaced posteriorly and inferiorly, courses along the inferior margin of the defect, and then bifurcates into the left and right bundle branches (Fig. 6). Thus, a significant portion of the specialized conduction system is both displaced by and in close proximity to the endocardial cushion defect, and the findings are similar whether the defect is partial (ostium primum ASD) or complete (AV canal). 79~84~87~104 Of particular interest is the displacement of the left bundle branch inferiorly (Fig. 6). Note that fibers of the inferior portion of the left bundle branch begin to separate from the His bundle at a short distance from the inferior left ventricular wall, while those of the anterior portion have a much greater distance to travel to reach the anterior wall.79>84’87Y94 The significance of this anatomic observation will be discussed below. The precarious location of such a large portion of the specialized conduction system at the rim of endocardial cushion defects is probably responsible for the still significant incidence (2%-20%) of complete heart block following repair.‘l The availability of the mapping technique should lower the frequency of this complication since the surgeon can repair the defect with interrupted sutures and avoid those sites where specialized conduction system electrograms are recorded.” When correlated with studies of ventricular activation, studies of the location of the specialized conduction system in endocardial cushion defect help explain the associated ECG abnormalities. Burchell et al. in 1960 in a preliminary observation of two cases found what appeared to be delayed activation of the anterior left ventricular wall in patients with ostium primum ASD when compared to normal controls. 56 Later, Durrer et al. in mapping studies of ostium primum ASD in which both epicardial and transmural electrodes were used found the following: lo5 Epicardial activation of the inferior wall of the left ventricle appeared to be earlier than in normal controls and there was late activation of the right ventricular and anterior left ventricular wall.‘05 At the anterior portion of the interventricular septum, activation of the right and left ventricles on either side was almost simultaneous and late while at the inferior portion of the septum, activation of the left ventricle occurred much earlier than activation of the right

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ventricle, also suggesting a peculiarly early onset of activation of the inferior left ventric1e.i” (See MAPPING OF VENTRICULAR ACTIVATION for sequence of ventricular activation in normals.) In agreement with these observations, Kupersmith et al.;’ in operative studies, and Goodman et a1.,ro9 in cardiac catheterization studies, found normal, or occasionally shorter than normal, His bundle electrogram to QRS intervals in patients with endocardial cushion defect indicating no overall slowing of His-Purkinje conduction. Boineau et al. studied the specialized conduction system and ventricular activation in a dog with ostium primum ASD associated with the characteristic ECG and VCG findings and correlated these to studies of ventricular activation in four patients with the same defect.lo6 In both man and dog with ostium primum ASD, the sequence of ventricular activation was similar to that found by Durrer et al., with relatively early activation of the inferior left ventricle and late activation of the right and anterior left ventricles.lo6 In the dog, conduction velocity in the Purkinje system was normal where determined and there were no signs of delay or block. Anatomic examination of the dog’s left ventricle revealed that as in humans there was inferior posterior displacement of the specialized conduction system with a short inferior division and a relatively long anterior division of the left bundle branch. lo6 Measurements of specialized conduction system length in the dog correlated with the activation times of the right and left ventricular endocardium when a uniform conduction velocity in all areas of the His-Purkinje system was assumed, again suggesting no true His-Purkinje delay or block.lo6 In commonly used ECG criteria, the pattern of right ventricular conduction delay with left axis deviation is labelled partial bilateral bundle branch block, i.e., right bundle branch block (RBBB) with left anterior hemiblock and presumed to be associated with specific lesions of the right bundle branch and anterior division of the left bundle branch.‘08~“0 The association of the prolonged P-R interval suggests an additional conduction delay either in the AV node or in the posterior division of the left bundle branch. However, electrophysiologic-mapping studies show that such terminology is not appropriate in describing or explaining the ECG pattern of endocardial cushion defect.

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By correlating studies of atrial activation, specialized conduction system anatomy, and ventricular activation, the ECG abnormalities of endocardial cushion defect can be explained differently. The first degree AV block in endocardial cushion defect is apparently due to displacement or disruption of the internodal tracts (see Significance of Internodal Tracts) and not an AV nodal abnormality, which would have a much different significance. The sequence of ventricular activation and the associated left axis deviation in standard ECG leads in the defect are due to anatomic displacement of the left bundle branch inferiorly causing impulses to have less distance to travel to reach the inferior left ventricle (via the inferior division of the left bundle branch) and more distance to reach the anterior left ventricle (via the anterior division) (Fig. 6). There is no block or anatomic disruption of the anterior division of the left bundle branch per se, though in an occasional case of endocardial cushion defect there is slight hypoplasia. The right ventricular conduction delay, often in the pattern of incomplete rather than complete RBBB,ro7 may also be relative and due to earlier than normal left ventricular activation’06 or it may be due to right ventricular enlargement as it is in ostium secundum ASD.42 Thus, the characteristic ECG of endocardial cushion defect is explained by the anatomy of the defect rather than by specific lesions of the specialized conduction system. However, it is also true that in certain patients with this defect, complete heart block occurs spontaneous1y.i” Anatomic studies of some of these cases have shown fibrosis of the AV node, His bundle, and/or bundle branches. These changes may be due to turbulence and trauma at the margin of the defect. Thus the intimate association of a considerable portion of the specialized conduction system with the margin of the endocardial cushion defect explain both this rare instance of spontaneous complete heart block”i and the occasional incidence of postoperative heart block.‘i Postoperative Right Bundle Branch Block The characteristic ECG pattern induced by repair of congenital defects that require right ventriculotomy is RBBB.1’2’1’3,‘14 The precise mechanism for this pattern may be one or more of several, i.e., physical disruption of the distal right ventricular conduction system due to the ventric-

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ulotomy incision, proximal disruption of the right bundle branch due to placement of patch for VSD repair, or resection of the right ventricular outflow tract for repair of subvalvar pulmonic stenosis. 82,112,117There is practical importance to d.istinguishing between these mechanisms since if the interruption of the right bundle branch is proximal and complete, a future or accompanying injury to the left bundle branch would cause complete heart block. However, if the injury to the right bundle branch is distal and partial, the addition of a left bundle branch (LBBB) might not cause complete heart block. To distinguish between these mechanisms of postoperative RBBB, Gelband et al. studied the right ventricular epicardial activation sequence in a group of patients undergoing repair for VSD, tetralogy of Fallot, and pulmonic stenosis.‘12 Following right ventriculotomy, marked delays in right ventricular epicardial activation occurred at sites distal to the ventriculotomy but no delays occurred proximal to the ventriculotomy. Subsequent VSD closure and/or subpulmonic resection caused no further delays in right ventricular activation.“’ In one patient the VSD repair was performed by an atria1 approach and was not accompanied by epicardial activation delay in the right ventricle or postoperative RBBB. Review of postoperative ECGs of all patients who had repair of VSD, tetralogy of Fallot, or pulmonic stenosis over a four-year period revealed that postoperative RBBB occurred when vertical right ventriculotomy was performed and never when the particular repair was via right atria1 or main pulmonary artery approach. These results suggest that postoperative RBBB is due to interruption of the peripheral right ventricular conduction system induced by right ventriculotomy and not due to interruption of the proximal right bundle branch.“’ In a subsequent study right ventriculotomy was performed in stepwise l-cm increments in patients undergoing surgery for various congenital cardiac abnormalities.“’ In 12 of 15 patients studied, RBBB occurred abruptly with one of the incremental l-cm incisions rather than gradually with each increment. In the other patients, RBBB never occurred. Thus, peripheral disruption of a m.ajor segment or arborization seems responsible for ventriculotomy-induced RBBB rather than continuous and partial disruptions of individual Purkinje fibers. In the three patients in whom RBBB did not

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occur, the ventriculotomy incision apparently did not extend into the crucial site of the peripheral right ventricular conduction system. This crucial site was examined and found to be at the moderator band proximal to the base of the anterior papillary muscle in some instances and distal to the base of the muscle band in others.‘r* With the former all of the fibers of the peripheral right ventricular conducting system are probably involved while in the latter some conducting tissue may be spared.“s~“8 However, in spite of these studies, it is also clear that injury to the proximal right bundle branch can at times occur due to sutures placed for repair of VSD.8J Thus postoperative RBBB can have different causes, each with its own particular significance. Injury to the proximal right bundle branch at the margin of a VSD and injury to the distal right bundle branch at the moderator band (in which no conducting tissue is spared) may have a similar functional significance in that an accompanying LBBB will cause complete heart block.“’ With injury distal to the moderator band, some right ventricular conducting fibers may be spared and accompanying or subsequent LBBB might not cause complete heart block though in this instance the safety factor for AV conduction might be low.‘r5 Finally, in an occasional instance the right ventriculotomy is not of sufficient length to inter= rupt any portion of the right bundle branch.“’ One postoperative ECG pattern that has been considered significant for prognosis is RBBB with left axis deviation.116~120-122 In this case, unlike in endocardial cushion defects, the pattern signifies injury to the anterior division of the left as well as the right bundle branch. It would appear that this pattern results from a combined injury to the proximal portion of both bundle branches, particularly in the case of tetralogy of Fallot where there is a frequent leftward and intramyocardial route of the proximal right bundle branch causing it to be in close proximity to the left ventricular conduction system for some distance.” However, separate lesions of the left and distal right bundle branch may also occur. Follow-up studies of postoperative RBBB with left axis deviation have shown a highly variable incidence of heart block and other problems.‘20-122 Recording of a postoperative His bundle electrogram by catheter technique in these patients is helpful since a prolonged His bundle to QRS inter-

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val suggests a more widespread conduction defect and a higher risk. rz3 Patients with transient complete heart block in the immediate postoperative period would appear to be at the greatest risk for the same reason.120T123 Electrophysiologic Studies of the Human Specialized Conduction System Open heart surgery allows for direct studies of human cardiac specialized conduction system that provide interesting basic information and relate to other cardiac electrophysiologic techniques. Such studies have been performed by Kupersmith et al. to examine various aspects of human cardiac conduction, to determine human His bundle conduction velocity, to determine normal conduction intervals from the His bundle and bundle branches to the ventricle, and to determine if there are any reliable methods for localizing the site of origin of specialized fiber electrograms without direct visualization of the heart.4 Some of these observations relate to the cardiac catheterization technique of recording electrograms from the His bundle and bundle branches. In this technique, electrograms are recorded via catheters placed transvenously, or occasionally transarterially, and anatomic localization of specialized fiber electograms is made indirectly via fluoroscopic visualization and/or specialized fiber to QRS intervals.lz4 In studies during open heart surgery, specialized conduction system electrograms were recorded from the following sites: proximal His bundle in the atrium; distal His bundle at the ventricular portion of the membranous septum (the distal-most portion of the His bundle where bifurcation OCcurs); and the right and left bundle branches, distal to the membranous septum (Fig. 3). These electrograms were recorded simultaneously with three standard ECG leads, one of which had been shown to display the earliest recordable QRS reflection. In this study, it was found that normal proximal His bundle to QRS (pH-Q) intervals varied with age. For patients 15 yr of age and older, the normal range of pH-Q intervals was 35 to 54 msec.4 For patients below 15 yr of age, there was an agerelated, exponential variation in pH-Q intervals such that at 3 mo of age, the normal range of pH-Q interval was 13-27 msec and at age 14 it was 32 to 54 msec (Fig. 7). Various congenital and acquired abnormalities present in the patients studied did not influence these intervals.4 The

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p=
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6 El 7 Age (yn)

9

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Fig. 7. Relationship of pH-Q interval and age. The black dots (a) represent the measured pH-Q intervals in patients below 15 years of age. The solid lines (----I represent the 95% confidence limits of the normal agerelated pH-Q interval. There is an age-related exponential variation in pH-Q intervals such that at age 3 mo the normal range is 13-27 msec and at age 14 yr it is 32-54 msec. See text for further discussion.4 (Reproduced by permission of Circ*/ation.4)

ranges of pH-Q interval in both children and adults are similar to normal H-Q intervals reported by almost all investigators using catheterization technique, 57P125-127suggesting that most His bundle electrograms recorded by catheter technique are in fact recorded from the proximal His bundle. Recordings from the distal His bundle and bundle branches yielded the following information: distal His bundle electrogram to QRS intervals ranged from 18 to 35 msec, right bundle branch electrogram to QRS intervals ranged from 18 to 30 msec, and left bundle branch to QRS intervals ranged from 20 to 39 msec. Thus overlaps existed between the normal ranges of His bundle and bundle branch electrogram to QRS intervals4 and timing of the specialized fiber electrogram did not necessarily reflect its site of origin. This finding is an important consideration for cardiac catheterization techniques where timing is a major method of localizing the site of origin of specialized fiber electrograms.124-127 Ho wever, of some help was the fact that recordings with specialized fiber electrogram to QRS intervals of 20 msec or less were thought almost surely to originate in the bundle branches (unless of course preexcitation is present).4 It was also noted that distinct atrial electro-

grams were invariably recorded when recordings were made from the proximal His bundle im the atrium. However, when recordings were made from the distal His bundle in the ventricle, either a poor or no atria1 electrogram was recorded. When recordings were made from the bundle branches, atrial electrograms were never recorded. Conduction velocity in the His bundle, determined by a specially designed electrode probe, ranged from 1.3 to 1.7 misec (mean 1.5 m/set) similar to that of experimental animals.4 His bundle conduction velocity did not vary with age and the age related increase in pH-Q intervals seemed to be due to growth of the heart and a consequent longer pathway over which impulses had to travel in a larger heart. The conduction interval from the proximal to the distal His bundle recording site ranged from 6 to 10 msec (this interval may be of some interest when evaluating specialized conduction system recordings during rhythms thought to arise at the AV junction or bundle branches). Finally, AV node electrograms were never recorded though the electrode probe was placed over the known anatomic location of the AV node in almost every patient studied. One method of localizing the site of origin of specialized conduction system electrograms is pacing of the specialized fiber-recording site,93 socalled “validation” of His bundle recordings.1”8-131 TO determine if this technique is of aid in localizing the site of origin of specialized fiber electrograms, pacing12’-131 of specialized fiber-recording sites was performed in a group of patients during open heart surgery. When stimuli were applied to the proximal His bundle recording site, characteristic His bundle pacing with the following features always occurred: stimulus artifact to QRS interval was equal to or nearly equal to the previous His bundle electrogram to QRS interval, and no change in QRS waveform from that recorded during a conducted atria1 beat was noted. When stimuli were applied to the distal His bundle recording site, the results varied and depended in part on stimulus amplitude. g3 In some instances, ventricular pacing occurred; in other instances, characteristic His bundle pacing occurred; and in still other instances, ventricular pacing occurred with high stimulus amplitudes while His bundle pacing occurred when the stimulus amplitudes were reduced below a range of 0.5 to 3.5 mA (Fig. 8).g3 Overall, thresholds for characteristic proximal or distal

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Fig. 8. Examples of pacing that resulted from stimulation of the distal His bundle recording site. (A) Records obtained during a conducted atrial rhythm produced by atrial pacing. intervals: distal His bundle electrogram-toQRS &H-Q) = 37 msec; QRS = 67 msec. (B) Records obtained while applying stimuli of decreasing amplitude to the distal His bundle recording site in the right ventricle. In the first and second beats, with stimulus amplitudes above 3 mA, right ventricular pacing occurred. Between the second and third beats, the stimulus amplitude fell below 3 mA and in the third and fourth beats, His bundle pacing occurred. In all four beats, the stimulus artifact to atrial electrogram interval (S-A) remained 120 msec, indicating that in the first and second beats pacing of the His bundle occurred simultaneously with ventricular pacing. Intervals in the first and second beats: S-A = 120 msec; QRS = 94 msec; S-Q = 39 msec; intervals in the third and fourth beats: S-A = 120 msec; QRS = 67 msec; S-Q = 39 msec. A = atrial electrogram (panel A) or stimulus delivered through atrial electrodes (panel B); HB = His bundle electrogram (panel A) or stimulus delivered to the distal His bundle recording site (panel B); I. II, III =standard ECG leads I, II, and III, respectively.g3 (Reproduced by permission of Circu/ation.93)

His bundle pacing ranged from 0.1 to 3.5 mA. When stimuli were applied to the right or left bundle branch recording sites, ventricular pacing invariably occurred.93 From these results, one may conclude that when stimuli are applied to the specialized fiber-recording sites and characteristic His bundle pacing occurs, the site of origin of the previously recorded specialized fiber electrogram is the proximal or distal His bundle. However, when ventricular pacing occurs, the site of origin of the previously recorded specialized fiber electrogram could be the distal His bundle or the bundle branches. In this instance, lowering of stimulus amplitude may be helpful since in some instances it resulted in characteristic His bundle pacing when the recording site was the distal His bundle (Fig. 8). It is also of

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interest that thresholds for His bundle pacing were far lower (0.1-3.5 mA) with electrodes placed directly on the heart than were the stimulus amplitudes reportedly used for similar pacing in the catheter technique (15 mA) where electrodes may not have been in direct contact with the surface of the heart.g3”2g Based on the previous studies of His bundle and bundle branch conduction and pacing, one can make observations that may be of value when trying to IocaIize the site of origin of catheter recorded specialized fiber electrograms. Since overlaps exist between the intervals from His bundle and bundle branch electrograms to the QRS, these intervals are ordinarily not helpful in localizing the site of recorded origin of specialized fiber electrograms. However, the recording of a distinct atria1 electrogram signifies that the recording electrode is at the atria1 and more proximal portion of the His bundle.4 Based on these conclusions certain maneuvers would appear helpful when using the catheter technique to record His bundle and bundle branch electrograms, particularly when the precise site of origin of the recorded electrogram is important, e.g., as when trying to determine the site of complete heart block. 132 In this as in most instances, it is desirable to place the recording electrode at the most proximal His bundle recording site possible. Therefore, after recording a specialized fiber electrogram with catheter technique, one should slowly withdraw the catheter until a distinct atria1 electrogram is recorded, signifying that the recording is from the atria1 portion of the His bundle, and then continue to withdraw until the longest possible H-Q interval is recorded, indicating that the electrodes are at the most proximal recording site possible. Finally, pacing via the recording electrodes may be helpful in localizing the site of origin of the recorded specialized fiber electrogram provided the limitations noted above are kept in mind.g3 It is important to note that the above observations were made with closely spaced bipolar electrodes that were 1 or 2 mm apart. With more widely spaced electrodes, e.g., 1 cm apart as is commonly used in the catheter technique,‘23’1249 132,133one electrode may be recording from the atrium while the other is in the ventricle, or an atrial electrogram may be recorded even when the catheter position is strictly ventricular particularly

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if recordings are made at high gain. Therefore, a catheter with closely spaced electrodes, i.e., 1 or 2 mm apart, should be used4Y134 since precise localization is impossible with widely spaced electrodes. However, in certain instances, more widely spaced electrodes may be useful, such as when attempting to record a “split-His” potential in second degree AV block.133 It is also of interest that in these studies AV node electrograms were not recorded, suggesting that AV node electrograms recorded by catheter technique do not necessarily represent conduction in the AV node.4 This finding is not surprising since in the catheter technique and in the technique used in the mapping studies low-frequency signals, i.e., those below 40 Hz in catheter studies and those below 12 Hz in open heart studies, are filtered out.14 This procedure would likely eliminate any recorded AV node potentials because of the slow conduction in the AV node and the slow rate of rise of phase “0” of AV node action potential. A possible method of successfully recording AV node electrograms would be to use unipolar or widely spaced bipolar electrodes to record unfiltered signals and possibly to use signal averaging methods. MAPPING

OF VENTRICULAR

ACTIVATION

The earliest studiesperformed using the electrophysiologic-mapping technique were attempts to determine the normal sequenceof ventricular activation and the waveform of epicardial electrograms recorded from the human heart.‘35-‘37 In 1930, Barker, McCleod, and Alexander recorded the first direct cardiac electrograms in a patient undergoing pericardiotomy for suppurative pericarditis. They found early activation in the high anterior right ventricle and the outflow tract, a finding that has not been confirmed in later studies.135Besides recording epicardial electrogramsfrom various sitesthey paced from both the right and left ventricles and, based on this, were able to extrapolate the characteristicsin standard ECG leadsof right and left bundle branch block.135 Previously, several authors had confused the pattern of right with left bundle branch block because of misinterpretation of studiesin dogs.135 Later mapping studieswere concernedwith comparing unipolar epicardial electrocardiograms recorded from the heart with those recorded in precordial ECG leads.7,21~18~136~138 They were per-

formed mainly in patients undergoingthoracotomy for extracardiac problems. Attempts were also made to precisely determine the sequenceof human ventricular activation,3,7,20-22’138but they were hampered by the lack of time during surgery, by the inadvisability of completely recording endocardial, epicardial, and multiple transmuralsites during surgery, and by the relative inaccessibility of certain regions of the heart, e.g., posterolbasal regionsof the left ventricle. Even when recordings were made at multiple sites in normal hearts, 3a20-22,138 the number of points explored were always inadequate to give a complete picture of the pattern of human cardiac excitation. To perform more complete studies,Durrer et al. recorded electrograms at multiple epicardial and transmural sites in revived human hearts in Tyrode’s solution. 53Caninestudieshad showngenerally good correlation between the sequenceof activation in vitro and in situ. However, in the human studies there may have been injury to the heart in removal and revival as evidenced by the lack of ability to find the sinusnode region.53Also conduction velocity of both human and canine ventricular musclewas more rapid in vitro than in situ and, becauseof this occurrence, QRS duration was shorter in vitro than it had been in the same patients antemortem. However, we can probably draw a reasonably close approximation of the normal sequenceof ventricular activation in the human heart from these in vitro studies with certain aspectsconfirmed by in situ studies.3,7,22J138 Activation of the heart is by double envelopment of both ventricles with initial activation in the endocardiums3 due to the endocardial location of the Purkinje system.84 Earliest ventricular activation occurs at three left ventricular endocardial sites: the region of the base of the anterior papillary muscle and paraseptalarea; a central area in the interventricular septum; the region of the baseof the posterior papillary muscle,including the paraseptalareaposteroinferiorly.53 Activation then spreadsout from these regions becoming confluent within 20 msec and rapidly spreadingfurther (due to rapid conduction via the Purkinje system) over the entire left ventricular endocardium except for the posterobasalor occasionally posterolateral area where Purkinje fibers are sparse. 841g2Earliest right ventricular activation is later than that of the left ventricle by 10 msec

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or so and occurs in the region of insertion of the anterior papillary muscle. Right ventricular activation then spreads over the endocardium to the septum and adjacent right ventricular wall and later to the area of the conus supraventricularis in the outflow tract. Activation of the intraventricular septum occurs mainly in a left to right direction and from apex (i.e., the region of the papillary muscles) to base, with excitation of the entire septum occurring rather rapidly and well before the end of ventricular free wall activation.53 Some activation of the septum in a right to left direction may occur from the region of the anterior papillary muscle and the middle third of the septum anteriorly, but the remainder of the septum is activated entirely in a left to right direction. The spread of excitation from endocardium to epicardium varies to some extent in the left and right ventricles because of the difference of the thickness of the walls and distribution of the Purkinje system. In the right ventricle activation spreads rapidly from endocardium to epicardium, and the breakthrough of epicardial activation in the heart occurs earliest in the mid-anterior right ventricle near the septum, i.e., the trabecular reand shortly thereafter over the engion, 7J22~53Y183 tire anterior right ventricular epicardium.7~22J3*138 From there activation spreads to the right ventricular outflow tract where it is tangential in direction with simultaneous activation of both endocardium and epicardium.53 The late and tangential activation of the outflow tract of the right ventricle is due to the lack of Purkinje fibers in this region.84,g2 Activation of the left ventricle occurs in an almost strictly endocardial to epicardial direction with earliest epicardial breakthrough in the anterobasal and posteromedial paraseptal areas7Y22v53,‘38 and in one study at the apex as well.38 The last area of the heart to be activated is the left ventricular posterobasal paraseptal area, though in some studies the last area is somewhat more lateral or even anterolateral in the left ventricle.7’22’53’138 Ventricular muscle conduction velocity determined by the rate of endocardial to epicardial conduction was approximately 30 cm/sec3 in situ and 45 cm/set in vitro, 53 slightly less than that of canines in some studiess3 but much less than in others.139 A conduction velocity of 1.3 m/set was found in one microelectrode study of human ventricular muscle in vitro, but this is much higher than values

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in other studies of canines or humans.r4* Calculations of muscle conduction velocity in situ are in any case subject to error, because of possible nonlinear spread of activation and because of changes in velocity with varying degrees of muscle stretch in vitro. A number of points about normal human ventricular activation deserve comment. (1) Earliest activation in all regions of the heart except for the outflow tract of the right ventricle occurs strictly at the endocardium. This observation is consistent with the fact that the Purkinje system is strictly endocardial in location in humans and penetrates minimally into the myocardium.3 In dogs where the Purkinje system is much more extensive and penetrates well into the left ventricular wall, earliest activation may be within the wall;26 m goats where the Purkinje system penetrates through the entire myocardial wall, earliest activation in a given region may be endocardial or anywhere within the myocardial wall.r41 (2) The rapid endocardial spread of activation is of course due to Purkinje fiber conduction. In areas where the Purkinje system is sparse, such as the outflow tract of the right ventricle and the posterobasal left ventricle, endocardial activation occurs relatively late.52,84 In fact, in the former region, endocardial and epicardial activation are virtually simultaneous. (3) Left ventricular activation begins earlier and ends later than right ventricular activation. The latest right ventricular activation occurs in the outflow tract, and it occurs earlier than the latest left ventricular activation in the posterobasal paraseptal region.53 Also septal activation is complete well before the completion of activation of the free ventricular wall.53 Some confusion on these points has existed in the past.42 The reason for activation to be latest in the left ventricle is probably the greater thickness of the left than the right ventricular wall, In hearts with right ventricular hypertrophy latest cardiac activation may occur in the right ventricle. 142 (4) The regions of the papillary muscles are activated very earlys3 and for good teleological reasons since proper ventricular function is associated with early papillary muscle contraction to close the mitral and tricuspid valves. (5) The earliest activation of the ventricle occurs mainly in the septum, suggesting that the earliest portion of the QRS complex in surface ECG leads

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represents mainly septal activation as commonly thought. 42 However, the bases of the papillary muscles are probably activated early53 and may also contribute slightly to the earliest portion of the QRS complex; there is also some early activation of the left ventricular wall adjacent to the septum.53 (6) Controversy exists over the anatomy of the divisions of the left bundle branch. It has been stated that fibers of the left bundle branch fan out in all directions’* rather than bifurcating into anterior and posterior hemibundles.84’143 A finding of two discrete sites of early left ventricular activation would be consistent with the presence of two discrete hemibundles. However, in the in vitro study of Durrer et al., initial activation occurred at three sites, i.e., the regions of the anterior and posterior papillary muscles and a middle region of the septum. 53 This finding was thought to be consistent with the presence of two left hemibundles with further branching of the anterior hemibundle.53 However, other interpretations are equally or more likely, and more detailed explorations of human endocardial excitation are needed to resolve this problem from a functional standpoint. Several differences between ventricular activation in canines and humans are evident and deserve comment if only because much has been made of canine studies, particularly in interpretation of human surface ECGs. As noted above, in dogs the Purkinje system is much more extensive than in humans, so that in the left ventricle earliest activation is not strictly endocardial, but extends into the ventricular wail for a variable distance.26 Also, there is a more extensive network of Purkinje fiber ramifications spreading out from the left bundle branch in dogs, causing widespread activation of the middle region of the interventricular septum both in the vicinity of the base of the papillary muscles and between them.lM The contribution to activation of the interventricular septum from the right bundle branch in dogs has varied in different studies but, in all, the contribution appears to be greater than in humans.17~13p~145In dogs there is activation of the septum from both sides, although earliest activity of the right septal surface starts later than on the left and some parts may be activated entirely from the left side. 17*13p2145In humans, on the other hand, activation of the septum is predominantly from the left side.s3

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Fig. 9. Schematic diagram of epicardium of heart as seen from anterior (upper left) and lateral (upper right) aspects. Shown are schematic examples of epicardial unipolar electrograms that were recorded from various sites in normal hearts.13’139,146 See text for further explanation.

Waveforms of Unipolar Epicardial Electrograms Waveforms of unipolar epicardial electrograms recorded from various regions of the normal human right and left ventricles have been determined in a number of studies and have been compared to waveformsrecordedin surface ECG leads.7~21~22~138 A composite of the results of such studies is shown in Fig. 9. Complexes with rS waveforms are recorded from most of the right ventricular epicardium, i.e., in the trabecular region anteriorly and in the lateral and paraseptal regions.7$21’221138Occasionally, relatively large R waves and Rs complexes are recorded from the trabecular region and posterior right ventricle. 13’ Superiorly, complexes recorded from the epicardium of the right ventricular outflow region are variable and rS (some with notching of r and/or S), rSr‘, rsr’S’; and rarely qRS complexes may be recorded (Fig. 9)’ Adjacent to the interventricular septum small notched, sometimes broad, r waves (called “v” waves) followed by relatively large S waves an: recorded from the epicardium of both ventricles anteriorly and posteriorly. ** On the left ventricular epicardium away from the interventricular septum anteriorly and inferiorly, q waves and qrS complexes are recorded, and as one proceeds leftward and posteriorly R waves become larger and S waves smaller to form qRs complexes in these regions. 71213223138 Also RS or Rs complexes may be recorded from the left ventricular epicardium posteriorly (Fig. 9)’ There are several interesting features concerning waveforms of epicardial unipolar electrograms that deserve comment: (1) The waveform of epicardial

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complexes recorded from the normal heart are similar to those recorded in overlying or nearby precordial or standard ECG leads in spite of the distorting effects of intervening body tissues2r (2) Very small and notched waves may be recorded from the epicardium adjacent to the interventricular septum and probably represent septal excitation (Fig. 9). 22 Therefore, r wave size may be smaller adjacent to the septum than it is in the right ventricle and the paraseptal r wave may also be notched. These findings should speak for a cautious interpretation of “poor r wave progression” in overlying precordial ECG leads often attributed to anterior myocardial infarction and explain why this pattern is so nonspecific. (3) The rS complexes recorded over most of the right ventricle suggest that right ventricular excitation contributes little to the QRS complex in surface ECG leads, since the same rS complexes are recorded in the right ventricular cavity and they reflect mainly left ventricular activation.’ (4) The variable complexes recorded from the epicardium of the right ventricular outflow tract are not ordinarily recorded in standard or precordial ECG leads, but may be recorded by leads placed in higher intercostal spaces, i.e., the second or third intercostal space.’ The notching of epicardial unipolar complexes in this region probably reflects tangential activation.

Ventricular Activation in Abnormal States Studies of ventricular activation and of the waveform of unipolar epicardial complexes have also been made in certain abnormal states. In right ventricular hypertrophy (RVH) due to “systolic overload,” epicardial electrograms display Rs, qR, rR’, rsR’ waveforms at the outflow tract and lateral right ventricle, rS waveforms at the trabecular region of the right ventricle, and qRs (i.e., normal) waveforms at the anterior and lateral left ventric1e.18y20~22~142~145 Right-sided precordial and standard ECG leads in RVH display similar waveforms as those recorded directly from the right ventricle. 18s22,142However, left-sided ECG leads display rS complexes similar to those recorded from the trabecular region of the right ventricle and not the left ventricle’8~22~142 perhaps because the former assumes a more leftward position due to hypertrophy. In mild hypertrophy due to systolic overload, there is moderate delay of right ventricular epicardial activation in all regions with little change in

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the normal sequence of activation, but in severe hypertrophy there is delayed activation which is greatest in the outflow tract.22,‘45 Right ventricular Purkinje fiber activation is not delayed in this form of RVH and conduction velocity in right ventricular muscle has been estimated to be 30 cm/ set, similar to that found in normal hearts.146 Thus the delay of epicardial activation in this state seems to be due to increased thickness of the myocardium and not to decreased conduction velocity of hypertrophied muscle.‘46 The greater delay of activation and the more prominent R waves recorded from the epicardium of the right ventricular outflow tract are consistent with pathologic studies that show more severe involvement of this region in RVH.g2 In “diastolic overload” of the right ventricle, with either incomplete or complete RBBB patterns on surface ECG leads, rSr’ patterns are recorded from the epicardium of the right ventricular outflow tract, and there is abnormal delay of activation in this region.148,‘4g Delays also occur in other regions of the right ventricle but are less consistent even in cases of RVH with complete RBBB.14’ The ECG pattern of diastolic overload of the right ventricle has been attributed to either localized outflow tract hypertrophy20,‘48,‘4g or injury to the conduction system due to stretch,15’ but in any case the term does not necessarily reflect the underlying pathophysiology. For example, it can occur in pulmonic stenosis and merely represent a less severe form of RVH than the “systolic overload” pattern.14’ In left ventricular hypertrophy, there are generalized delays of activation, and abnormally large unipolar complexes are recorded over all accessible regions of the left ventricular epicardium.18’22 In one case of the Sr , S2, S3 ECG pattern, polyphasic QRS complexes and delay of activation were found in the basal and lateral right ventricle, suggesting that this pattern is due to abnormal right ventricular activation and not abnormal position of the heart. r3’ A case of asymmetric septal hypertrophy displayed no abnormality in the sequence and time course of activation except for slightly greater delay in the posterobasal right ventricle.417 Also, in another case of cardiomyopathy (perhaps of the hypertrophic type, though not indicated) with deep Q waves in left-sided leads, simultaneous activation of the septum in all regions was found rather than the normal left to

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right sequence of septal activation, suggesting that the Q waves were due to cancellation of septal forces.3 Mapping of Infarcted Zones The effects of infarction on the shape and amplitude of locally recorded electrograms and on the sequence of myocardial activation have been studied both in humans and in experimental animals. Bipolar electrograms recorded from chronically infarcted myocardium display loss of amplitude, delay of activation, and fragmentation.2>15124>151The degree of reduction in amplitude of bipolar recordings varies depending on the severity of infarction. In zones of completely nonviable tissue, as in ventricular aneurysm, there is complete loss of local electrical activity,2,‘51 while in small zones of infarction there may be little change in the amplitude of these recordings.15>i52 Considerable delay in the normal endocardial to epicardial spread of activation occurs in chronically infarcted zones causing activation of infarcted epicardium to proceed mainly in a tangential direction from adjacent normal myocardium. 15,24 However, there may also be some delays of activation in normal myocardium immediately adjacent to the infarcted zone when the spread of activation to these normal zones was previously through the now infarcted myocardium.‘52 Because of its proximity to oxygenated blood of the left ventricular cavity and its lower oxygen requirement, the Purkinje system is relatively resistant to the effects of ischemia’53 and may be less involved than ventricular muscle in chronic infarction.15,241’52 In canines, partly or completely normal Purkinje system activation has been demonstrated in chronically infarcted zones,15r24a152but in humans complete studies have not as yet been performed. Histologically a rim of viable endocardial tissue often remains in infarcted zones of humans, suggesting that the Purkinje system might be sparedI except perhaps in cases with generalized conduction defects, such as RBBB with left axis deviation. l5 Abnormal Q waves or loss of R wave voltage are recorded in epicardial and intramural unipolar electrograms from chronically infarcted zones and also from a rim of normal tissue adjacent to these zones.24 Subendocardial as well as transmural infarctions may display Q waves in electrograms recorded from overlying epicardium.24’152 The size

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of the Q wave generally correlates with the size of the infarct15 except perhaps when it is subendocardial or located in the interventricular septum.15 Q waves also occur normally in certain areas of the ventricular epicardium and Daniel et al.ls found normal epicardial values for Q wave dluration to be as follows: Q waves of O-27 msec in duration occurred in the outflow tract of the right ventricle, in the anterolateral left ventricle, and in the inferior paraseptal regions of both ventricles adjacent to the posterior descending coronary artery; Q waves of 4-32 msec in duration occurred in the lateral and most of the posterior left ventricle; no Q waves occurred in the remainder of the right and left ventricles. In the acute state of myocardial infarction, local bipolar recordings of ventricular muscle display delay of activation and fragmentation2’152 and also ST segment elevation when low frequency recordings are not filtered out.‘54 Unipolar recordings from acutely infarcted zones display abnormally large Q waves and ST segment elevation.‘55 During open heart surgery epicardial mapping has been used to delineate zones of damaged myocardium to facilitate the removal of such zones. The method commonly employed is to record bipolar electrograms from the epicardium and identify zones where loss of amplitude and desynchronization of electrograms occur, indicating nonviable myocardium. 2Y151 The technique during mapping is to first record from a zone of normal tissue for standardization of recordings and then to go on and record from expected nonviable zones.2 Closely spaced bipolar electrograms should be used for more precise localization of damaged zones because the electrodes are placed over a smaller area, and because there is a lesser contribution of distant electrical events than with widely spaced electrodes. Mapping of Q waves with unipolar electrodes does not allow for precise localization of damaged zones since abnormal Q waves may be recorded from normal tissue adjacent to the infarcted zone.152 Nonviable myocardium is reliably identified by the loss of amplitude and fragmentation of the bipolar electrograms in such tissue. Differences of amplitude between electrograms recorded in infarcted and normal zones occur both during conducted atria1 rhythms and during ventricular fibrillation.2 Figure 10 shows an example of bipolar electrograms recorded simultaneously from normal

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INF mV

T

Fig. 10. Bipolar electrograms recorded from normal right ventricular myocardium (NL) and an infarcted zone in the left ventricle (INF) along with a surface ECG lead II. Recordings were made 3 hr after coronary artery occlusion. The rhythm is ventricular fibrillation but in spite of this, the nonviable tissue in the infarcted zone can be clearly distinguished from normal myocardium. See text for further discussion.

canine myocardium in the right ventricle and from an infarcted zone in the left ventricle 3 hr after coronary artery occlusion. Recordingswere made during ventricular fibrillation and show that a nonviable zone was easily identifiable during the arrhythmia. Neither epicardial adhesionsnor epicardial fat pads interfere with reliable epicardial mapping to localize damaged myocardium2 as they do with dye techniques used for the same purpose.‘56 The technique of mapping nonviable myocardium has been most commonly used to delineate the marginsof ventricular aneurysms,the borders of which are electrically well demarcated.2,151 However, the borders of ventricular aneurysmsare also clearly visualized without mapping and the limits of the resection are governed by technical factors, rather than the results of mapping. Electrophysiologic mapping may also be helpful in deciding whether to excise akinetic zones that are not aneurysmalper se and in delineating the margins of such zones though they may be neither electrically nor visually distinct.151 Mapping has also been used to determine if injury to left ventricular papillary muscleshas in fact occurred in casesof mitral regurgitation due to suspectedpapillary muscledysfunction or fibrosis.2 Where the technique of mapping zones of damaged myocardium may be of most benefit is in surgery for acute myocardial infarction. Here the surgeoncannot visualize the extent of injury or in

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some casesthe sites of injury without mapping.2 Also in this instanceleaving the nonviable and still acutely infarcted tissuein place and using this tissue for suture placement would causea tendency towards postoperative myocardial rupture. However, in this instance, asin others, the periphery of the infarct may not be well demarcated electrically, and even in mapping there may be diffculties in deciding the extent of resection, though any information on the status of the myocardium at the line of resectionis helpful. There is alsopotential useof the mapping technique to delineateischemit zones when choosing sites for placement of saphenousvein coronary artery bypassgraft and in determining whether after graft implacement the ischemia was reversed at the siteschosen. In such cases, ST segment mapping would be required since depolarization (QRS) abnormalities due to chronic ischemiaare ordinarily permanent.i5’ WOLFF-PARKINSON-WHITE

SYNDROME

One of the more important applications of the mapping technique has been in the surgical treatment of the Wolff-Parkinson-White (WPW) syndrome.‘Y5~2511589159Y160 A complete discussionof the diagnosisof WPW and managementof arrhythmias in WPWnjl are beyond the scope of this review. Cardiac catheterization techniques in delineating various functional and anatomical characteristics of WPW have also been described elsewhere.5~‘58~161~‘62 This review will deal with electrophysiologic mapping and surgical techniques, touching on other aspects only where pertinent.

Characteristics of WPW The WPW syndrome is characterized by an ECG in which there is a short P-R interval (less than 0.12 set) and a widened QRS with initial slurring (delta wave). 163Though WPW is often asymptomatic, there is a propensity to various arrhythmias, most commonly atrial tachycardia often at very rapid rates and also atria1 flutter and atrial fibrillation with rapid ventricular responses.‘@Variants of WPW occur, including those with normal P-R internal and delta wave and those with a short P-R interval and normal QRS (Lown-Ganong-Levine syndrome), and these may also be associatedwith arrhythmias. “i It has been thought that the characteristic ECG of WPW and also the arrhythmias result from ac-

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cessory pathways that conduct impulses from the atrium or parts of the specialized conduction system directly to the ventricle, thus bypassing the normal AV conduction pathways. The ECG of WPW is thought to be a fusion beat between impulses conducted via the accessory pathways and those via the normal AV pathway.161 The presence of accessory pathways also explains the arrhythmias in WPW. the atria1 tachycardias are mediated by reentrant cycles that include the normal AV conduction pathway in one direction and the accessory pathway in the other direction. A typical example of such a reentrant pathway is atriumAV node-His bundle-bundle branch-ventricleaccessory pathway-atrium. Various other reentrant pathways may also OCCUT. Atria1 flutter and fibrillation are due to a reentrant atria1 echo beat conducted via the accessory pathway arriving back in the atrium during the vulnerable period causing atrial flutter or fibrillation.161 An alternate hypothesis for WPW, that of James,16’ is that preexcitation is due to longitudinal dissociation within the His bundle or to strictly septal accessory pathways in and around the AV node, and arrhythmias occur because of reentry utilizing these pathways. Certain accessory pathways that may explain WPW have been found histologically and have been given the following eponyms: James pathway, an extension of the posterior internodal tract extending from the atrium directly into the His bundle and bundle branches bypassing the AV node;52 Mahaim pathways from the AV node or His bundle directly into the ventricle bypassing the more distal portions of the specialized conduction system;r61,‘@ and Kent pathways from the right or left atrium into the corresponding ventricle bypassing the entire specialized conduction system.161 Also septal pathways bypassing the entire conduction system may occur. In some instances the presence of these pathways histologically has been directly correlated with antemortem WPW’66-169 but in other instances no accessory pathways were found in WPW.“’ The accessory pathways ordinarily have anatomic and electrophysiologic characteristics of muscular tissue and not those of specialized tissue.1623’66-169 One or another of these pathways alone or in combination could account for WPW. For example, a Kent or septal accessory pathway could explain the ECG of WPW as could a combination of James and Mahaim pathways.i68 James pathways

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or septal accessory pathways could account for short P-R interval with normal QRS. Two forms of WPW have been classified by Rosenbaum et al., i.e., types A and B.171 In type A, the delta wave vector is anterior in direction causing an initial R wave in ECG lead Vl , while in type B the initial vector is posterior causing a Q wave in lead Vr . Type A WPW is thought to be related to a Kent pathway from the left atrium to the left ventricle, while type B is thought to be related to a Kent pathway from the right atriurn to the right ventricle.5~‘583161 Of course, other accessory pathways alone or in combination could account for either type A or B WPW and the distinction between the two is often not clear, i.e., is a delta wave with a moderately small r wave in lead V, type A or type B? WPW is confirmed by cardiac catheterization studies in which a short H-Q interval is found or the His bundle electrogram may occur after the onset of the QRS complex. During rapid atrial pacing, the His bundle electrogram is recorded progressively later with reference to the QRS because of rate-related delay of conduction in the AV node, until finally normalization of the QRS occurs, marking the refractory period of the accessory pathway. ‘lle2 This change in the His bundle electrogram to QRS relationship does not occur in the case of Mahaim type fibers or in the usual case of Lown-Ganong-Levine. Since anatomically distinct accessory pathways may account for WPW, it is logical then to attempt their surgical division, which if successful should also abolish the arrhythmias by interrupting reentrant cycles. Kent pathways would be the most amenable to division and, in fact, an anterior Kent pathway was the earliest to be divided surgically. 172 Mapping of WPW was first performed by Durrer and Roos in a patient with a coexisting ostium secundum ASD, and a Kent type accessory pathway was localized between the right atrium and ventricle anterolaterally.173 Burchell et al. were the first to try to interrupt an accessory pathway by injecting procainamide into a site in the anterolateral right ventricle where the earliest ventricular activation was localized, signifying the presence of an accessory pathway there.r The attempt was unsuccessful and the authors felt that they were “unduly timid” in not attempting transection.’ Earlier, Dreyfus et al. had successfully abolished WPW arrhythmias by dividing the His

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bundle and implanting a permanent pacemaker.174 The first successful division of an accessory pathway causing regression of WPW was reported by Cobb et al. from Duke University.‘72 The indications for surgery in WPW are the proven presence of WPW and severe and recurrent arrhythmias refractory to good medical management. Also the occurrence of syncope due to arrhythmias is considered an indication.r7’ Prior to surgery all patients should have an extensive electrophysiologic evaluation in the cardiac catheterization laboratory to confirm the. diagnosis of WPW and to localize the site of the accessory pathway as well as possible. Surgery should only be performed in centers where experience and expertise with mapping techniques exist. Recently it has become apparent that in some patients reentrant arrhythmias are caused by accessory pathways that conduct only in a retrograde direction and therefore will not have a WPW pattern on ECG.‘62t176 In one study, such pathways occurred in 5 of 54 patients with reentrant arrhythmias and no WPW on ECG.‘62 If these retrograde pathways are detected by cardiac catheterization, patients may in the future be considered for surgical correction if arrhythmias are severe and medical management is unsuccessful. Techniques of Mapping for WPW Mapping to localize the site of the accessory pathway in WPW is similar to electrophysiologic mapping for other reasons, though more precision only a few is generally required. 5,25,158,159,177-184 centers have much experience in mapping for WPW, with the Duke University group having the most experience and providing much of the known information on surgery for WPW.s~“5*y17g During surgery, a standard midline approach to the heart is used for accessory pathways thought to be rightsided or septal, but a left lateral approach is used for those thought to be left-sided.5 Mapping is performed prior to bypass and the object of mapping is, of course, to find the site of earliest ventricular activation that marks the position of the accessory bypass pathway. One cannot see the accessory pathways, and electrograms have only rarely and inconsistently been recorded directly from these pathways. 159 Bipolar electrograms are recorded over the entire ventricular epicardium usually by means of a hand-held probe to determine the timing and sequence of activation and to localize

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the site of earliest ventricular activation. Unipolar electrograms are also recorded.5~25~‘58~15g~‘77~184 A variety of procedures are used and precautions advised to assure proper localization of accessory pathways. A plaque electrode is sutured to the ventricle as close to the site of presumed preexcitation as possible to use as a reference electrode for timing and also for ventricular pacing.’ Ventricular cavity potentials have also been used as references for timing. ls4 Recordings are made with a handheld probe (e.g., as in Fig. 1) over the atria1 and ventricular epicardium at about 55 sites, including the entire circumference of the AV ring.5~‘85 A surface ECG lead with a markedly pronounced delta wave, reference electrogram and/or cavity potential, and local myocardial electrograms are all recorded simultaneously. At Duke University Hospital an analog computer device is used to display, in digital form, the interval between the onset of the delta wave and local electrograms recorded with a hand-held probe.’ (This task is performed indirectly. First the interval between the delta wave and reference electrode is determined by hand measurements; then the interval between reference electrode and local electrogram recorded with hand-held probe is determined. The slow rise time of the delta wave would not permit accurate and repeatable digital readouts by machine, and it may be so slow as to make it difficult to determine its beginning by any means.) Atria1 and ventricular pacing are performed at various rates with the use of premature stimuli at varying intervals to provoke maximum (or “total”) preexcitation, i.e., ventricular excitation that is the result solely of activation via the accessory pathway and is not a fusion beat between conduction via normal and accessory pathways. Pacing is performed at various atria1 and ventricular sites to try to pace as close to the accessory pathway as possible for better localization of the pathway. Both the earliest site of ventricular activation during atria1 pacing and the earliest site of atria1 activation during ventricular pacing are determined for greatest assurance in detecting the accessory pathway.’ Arrhythmias are provoked by atria1 or ventricular pacing or premature stimulation or sometimes by more complex trains of stimuli, so that pathways through which conduction occurs during these arrhythmias in either an antegrade or retrograde direction can be localized. When the earliest site of epicardial activation is determined, its timing with reference to

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the delta wave is important, for in the case of a free wall accessory pathway it should occur prior to the delta wave, but with a septal accessory pathway it occurs 5-15 msec after the onset of the delta wave.5’ 177 Also if earliest epicardial activation is close to the septum anteriorly or posteriorly, a septal accessory pathway should be considered. On the other hand, if the pressure of the probe on the epicardium momentarily abolishes preexcitation at a particular site, it suggests that this is the site of the accessory pathway. To detect free wall accessory pathways that are endocardial in location, intramyocardial electrodes25 are used or mapping of the endocardium is performed during cardiopulmonary bypass. Following mapping, the patient is placed on cardiopulmonary bypass. Further endocardial mapping is then performed if necessary, as for example, if a septal accessory pathway was suggested either during mapping or during previous cardiac catheterization.53 177 The heart is fibrillated and division of the pathway is then undertaken.5’1791180~183In the early operated cases of WPW, ventricular incisions were performed,180~‘83 but more recently incision of the atrium via the endocardium has been considered by Sealy et al. to be the preferred method of dividing the accessory pathways. 179 The atrium is opened, and an incision is made from its endocardial surface, using the fat pad beneath the coronary vessel to provide a safe place for separation of the atrium from tha annulus fibrosis without injury to the coronary vessels.‘79 Incisions of at least 2 cm are made, but they may be longer if necessary. Certain areas are avoided: on the left, the area between the left and right trigones where the anterior mitral leaflet attaches to the aorta and there is natural separation between atrium and ventricle; and on the right, the septal region between the coronary sinus and membranous septum, where the AV node and His bundle are located.179 Division of the accessory pathway by this atria1 endocardial approach has several advantages over incision of the ventricle since it allows access to septal pathways on the right and a safe approach to left-sided pathways where injury to the coronary vessels posteriorly and parts of the left bundle branch might occur.177,179 Also, it allows easy access to the AV node and His bundle if division of the normal AV pathways must be performed. Following atria1 incision, repeat mapping during cardiopulmonary bypass is performed and then at

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termination of cardiopulmonary bypass repeat extensive mapping is performed to assure that no accessory pathways remain intact.55”s8 When it is apparent that the accessory pathway has not been divided and the surgery is thus far unsuccessful, division of the His bundle may be performed.5,25,15871743184This form of surgery is sometimes a primary procedure in WPW and, in fact, the earliest surgery for WPW was division of normal AV conduction system.‘74 Following this procedure, there is either total preexcitation via the accessory pathway or complete heart block.i’, 2s3158Y174~184 The latter may occur because the accessory pathway was septal in location and ligated along with the His bundle, or because accessory pathways were not active at the time of division. In some instances after division of the His bundle, complete heart block was an early result but conduction via the accessory pathways recurred later.25’174 In any case, implantation of a pacemaker at the time of surgery has been advised when interrupting the normal AV conduction pathwaylsl because the accessory pathway has been considered a precarious form of AV conduction by itself, though at times unfortunately it is surprisingly resilient. To assure complete interruption of the His bundle, it has been stated that deep sutures from the coronary sinus region to the area between coronary sinus and tricuspid orifice are required. 25 Destruction of the His bundle by electrocautery has been successfully used though it has also been considered unreliable.25 Interruption of the normal AV conduction pathway will interrupt the reentrant cycles of WPW and should abolish episodes of atria1 tachycardia. Occasionally, it may abolish or diminish episodes of atria1 fibrillation that depend on a single welltimed echo beat. However, there are many disadvantages of this approach. Use of a pacemaker in young active persons is fraught with psychologic problems and many complications due to physical activity. The accessory pathway that remains still has a short refractory period, so that if atria1 fibrillation occurs, it may be accompanied by very rapid ventricular rates. Two remaining intact accessory pathways may be present and reentry via the pathways could possibly occur, providing there is sufficient conduction delay between pathways to permit reentry. For these reasons, it is still preferable to try to divide the accessory pathway or pathways rather than to create complete heart block.5~158~160

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However, when division of the accessory pathway is impossible, one should be prepared to divide the normal AV pathway, and also the latter is a more reliable and technically less difficult procedure. Division of the His bundle should be uniformly successful, while attempts to divide the accessory pathway alone are at times unsuccessful.*’ Although much success has been achieved with surgery for WPW, note should be made of the number of problems that arise when attempting this approach. In some cases, a long period of time is required for mapping, which even performed off cardiopulmonary bypass carries some risk to the patient. Certain areas of the heart where accessory pathways may occur are relatively inaccessible. The posterior surface of the heart is not easily approached for mapping and for this reason earlier operative cases of WPW were exclusively type B, where accessory pathways are anterior in location.“172 However, specially designed electrodes may be used to reach the posterior AV groove. Also the mapping of the posterior AV groove is most difficult prior to cardiopulmonary bypass, but can be performed during bypass.5$‘60 Changes in position in the heart often required during mapping of posterior accessory pathways may make standard ECG leads unrecognizable and delta waves hard to discern, thereby making evaluation of data difficult. An additional problem in dividing posterior accessory pathways is the proximity of the coronary sinus posteriorly, which makes division of the pathway technically difficult.160 However, the atria1 endocardial approach for division seems to have circumvented this problem.“’ A given accessory pathway may be endocardial rather than epicardial in location, and thus mapping of the epicardium alone may be insufficient or misleading particularly for the left ventricle where there is a relatively thick wall and thus earliest endocardial excitation could occur at some distance from the earliest epicardial site.25 Mapping of the endocardium during cardiopulmonary bypass or use of a plunge electrode can circumvent Anesthesia, premeditation, or this problem.*’ other factors during surgery may cause preexcitation and the propensity to arrhythmias to be diminished or even abolished temporarily. Also, edema and local injury due to probe placement during mapping may cause depression of conduction of the accessory pathway, which may then reestablish itself postoperatively. The incision itself

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may only cause temporary injury to the accessory pathway especially if it is made at too great a distance from the AV groove. Septal pathways are dangerous to divide because of their proximity to the AV node and His bundle.25*‘77 Multiple pathways may occur so that the division of one or two accessory pathways may only incompletely resolve the problem. 5Y182,186Combinations of Kent pathways that are relatively accessible to division with James and/or Mahaim pathways that are relatively inaccessible may occur.“’ Although localization of accessory pathways by electrophysiologic mapping techniques during cardiac catheterization is reasonably precise, it is less than perfect. 188 A particular problem may arise in placing catheters in the anterior right atrium or ventricle to detect pathways in this location. Also, rarely, it may be difficult to place a catheter in the coronary sinus for localization of posterior pathways. Multiple pathways may cause confusion in evaluation of data.5~1*2~186Also, in some patients with proven WPW, reentry entirely within the AV node seems to be the major cause of the arrhythmias as found in 8 of 71 patients with WPW studied by Wellens and Durrer162 but only 1 of 80 patients studied by Gallagher et a1.1s5 Since division of accessory pathways in these patients would not abolish the arrhythmia, one should make a careful attempt to exclude AV nodal reentry preoperatively in WPW.‘62 Finally, surgical success may only be temporary and apparent rather than real. Changes in sympathetic innervation to the heart or even psychologic factors may cause temporary regression of arrhythmias when pathways have not been completely divided, e.g., in cases where delta waves were modified.5T’58 Though it is doubtful that these factors are important in the operative success that has been achieved in WPW, the questions arise only because surgery for WPW is a form of therapy that does not lend itself to rigorous controlled trials. Results of Surgery The results of surgery for WPW in the Duke experience have been generally successful.5y’58 Data as of March 1975 are as follows:‘58 A total of 34 operations were performed of which 30 patients had one documented accessory pathway, three patients had two documented accessory pathways, and one patient had no documented accessory

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atrial crass Fig. 11. Schematic diagram of cross-section of the AV ring from above showing location of 36 accessory pathways in 33 patients who underwent surgery for W~w.158 See text for further explanation. (Reproduced by permission of Medical Clinics of North America. 158)

9 o 0 *

wall in section

DELTA GONE DELTA MODIFIED NO CHANGE BUNDLE of HIS

pathway. Figure 11 showsthe location of the 36 accessorypathways found in these patients. In 19 of thesepatients, the delta wave was abolishedand there were no further arrhythmias. One of these patients, who had coexisting cardiomyopathy, died in the postoperative period. In three patients intact retrograde conduction remained, but the delta wave and antegrade conduction via the accessory pathway were abolished(partial injury to the accessorypathway injury, but not division); in 2 of these patients His bundle division was performed, and the other patient was placed on low dose medical therapy; all became asymptomatic. In five patients the delta wave remained unchanged; three of these underwent His bundle division, and two were easily managedwith drugs so that all becameasymptomatic. In four patients the delta wave was modified (delay of conduction in accessorypathway? or multiple pathways with one or more left intact?) and all becameasymptomatic with drug therapy. In two patients the delta wave remained unchanged postoperatively and there was persistent atrial tachycardia. One further patient underwent surgery in emergency circumstances for unremitting severe atria1 arrhythmia; no delta wave had been present and no accessorypathway wasfound. The patient died and autopsy alsorevealedno accessorypathways. Overall, 18 of 34 severely symptomatic patients had complete correction of WPW arrhythmias with modification of the accessorypathway alone; another seven b,ecame asymptomatic with drug therapy following surgery; and three patients re-

quired His bundle section. There were two surgical failures and additionally two operative deaths (operative mortality, 6%). As to which pathways are more amenableto surgery, there were a total of 36 pathways in 33 patients (Fig. 11); eight of eight free wall right ventricular accessorypathways were successfullyinterrupted (including 1 that still could conduct retrograde). Also, 12 of 14 left ventricular free wall accessorypathways were successfully interrupted (including two that still could conduct retrograde) but only 5 of 14 septalaccessory pathways were successfullyinterrupted (Fig. 11). Operative studies of WPW have enabledinvestigators to examine the various hypotheses of its pathogenesis.First the existenceof Kent pathways to explain WPW has been conclusively proved by virtue of electrophysiologic localization of these pathways and abolition of WPW by their excision, at least in certain cases.However, it is also clear that Kent pathways are not the only explanation for WPW, that Jamesand Mahaim pathways also occur in WPW,l” and that longitudinal dissociation in the His bundle is still a possibleexplanation for this syndromein certain cases.165 The value of the ECG in localizing WPW pathways has also been examined. It hasbeen thought that patients with a prominent R wave in V1 and anterior direction of delta wave vector (type A of Rosenbaum) have posterior left accessory pathways, and those with initial Q wavesor very small r waveswith predominant S waves in V1 and posterior direction of delta wave vector (type I3 of

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Rosenbaum) have anterior right-sided accessory pathways.171 Of 31 patients with single accessory pathways proved by mapping at surgery, 17 patients had type A-WPW and 12 of these had left ventricular free wall accessory pathways, while 5 had septal accessory pathways. The remaining 14 patients had type B-WPW; six of these had right ventricular free wall accessory pathways, while eight had septal pathways.ls8 Thus, right ventricular free wall accessory pathways were never associated with type A ECGs while left ventricular free wall accessory pathways were never associated with type B ECGs, but septal pathways could occur with either ECG pattern.‘58 In one reported case of type B-WPW, a posterior right ventricular accessory pathway was described,rE9 but anatomic localization in this case may have been less than precise.5

Surgery for Reentrant Ventricular Tachycardia The success with surgery for abolishing accessory pathways in WPW has led to attempts to correct arrhythmias associated with other types of reentrant pathways. A number of studies have appeared in which surgery was performed in patients with refractory ventricular tachycardia in whom a reentrant mechanism was suggested by cardiac catheterization studies. r9’-rg4 In these patients, programmed ventricular premature stimulation could provoke ventricular tachycardia both during cardiac catheterization and during surgery.1y0-1y4 Epicardial mapping, combined with recording of intramyocardial electrograms in some of the patients, showed great delay of activation in certain regions of the epicardium, and in some instances latest activation occurred well after termination of the QRS complex and during inscription of the ST segment. 1y09192 Epicardial mapping during the ventricular tachycardia suggested that the arrhythmia originated in these same areas. At times a second late potential was recorded during sinus rhythm or during ventricular tachycardia suggesting the presence of a reentrant impulse, and in other instances sites of very late activation were found during tachycardia suggesting continuous electrical activity in reentrant pathways.19* Ventriculotomy incisions were made in the presumed areas of reentry with regression of arrhythmias postoperatively.190~‘92-194 Necessary to success of this form of therapy was the ability to provoke

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ventricular tachycardia by programmed premature stimulation both in the cardiac catheterization laboratory to prove the presence of reentry and on the operating table to enable mapping during the arrhythmia. Preoperatively, of course, it was not possible to determine the location of the reentrant pathway in ventricular tachycardia as well as in WPW.190-‘y4 Cases have also been reported in which incision of a bundle branch was performed for ventricular tachycardia presumed to result from macroreentry involving the same bundle branch, though the evidence for this mechanism was inconclusive.‘93 A form of control group for the above studies was provided by five patients in whom both preoperative studies and findings during mapping were consistent with an automatic ectopic focus causing ventricular tachycardia. 194 Ventriculotomy at the presumed site of the ectopic focus in these cases did not cause regression of arrhythmias postoperatively. In spite of the fact that surgical success seemed to depend on a reentrant mechanism for ventricular tachycardia, the studies thus far performed have not conclusively proved a relationship between the presumed mechanism of the arrhythmias and the treatment. Repeat mapping studies following ventriculotomy were not reported in any case.190-194 The criteria for determining that reentry is the mechanism of a given arrhythmia, i.e., provocation and termination with premature stimulation, are not necessarily valid since arrhythmias due to triggered automatic mechanisms may behave similarly. 19’ The type of the reentrant pathways causing ventricular tachycardia in the patients undergoing surgery was not always clear, i.e., were the pathways discrete isolated tracts or was there a complex mosaic of slowly conducting tissue? In either case destruction of cardiac tissue due to ventriculotomy may have made future reentrant arrhythmias impossible. Also the site of origin of the ventricular tachycardia in several of the patients could have been endocardial or subendocardial and at some distance from the site of earliest epicardial activation during tachycardia.‘y0y’y2-194 Amelioration of ventricular tachycardia postoperatively could be due to a number of factors besides interruption of reentrant pathways, i.e., loss of autonomic innervation, correction of coexisting abnormalities in some patients,lgl and psychologic factors. Also, it is possible that slowly

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conducting reentrant pathways will reestablish themselves in some fashion postoperatively due to coexisting myocardial disease or even fibrosis in the area of incision. Some of these problems, as well as others, will have to be considered if more attempts are made to approach ventricular tachycardia by mapping and surgery. It has also been well established that ventricular tachycardia as the primary manifestation of coronary artery disease and/or ventricular aneurysm can be successfully treated by correction of the underlying abnormality without benefit of mapping. lg6,1g7 Surgery in this instance is in part empirical since the precise mechanism and site

origin of the arrhythmia is unknown and perhaps for this reason surgery in such cases has not been uniformly successful. lg7 More precise delineation of the site of origin and mechanism of the arrhythmia, if possible, would probably increase the effectiveness of this form of therapy, not only when the arrhythmias are reentrant but also when they are automatic, since automatic foci could be excised. The techniques for mapping of ventricular tachycardia would appear to be a promising initial step, both for patients with and without underlying heart disease, in the future correction of a problem that is life-threatening and often not amenable to medical therapy.

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33. Wellens HJJ, Janse MJ, van Dam RT, et al: Epicardial excitation of the atria in a patient with atria1 flutter. Br Heart J 33:233-237, 1971 34. Waldo AL, Vitikainen KJ, Harris PD, et al: The mechanism of synchronization in isorhythmic A-V dissociation. Circulation 38:880-898, 1968 35. Waldo AL, Kaiser GA, Bowman FO Jr, et al: Etiology of prolongation of the P-R interval in patients with an endocardial cushion defect. Circulation 48: 19-26, 1973 36.

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James RH, Sherf L: Specialized tissues and preferential conduction in the atria of the heart. Am J Cardiol 28:414-427,197l S 1. Wagner ML, Lazzara R, Weiss RM, et al: Specialized conducting fibers in the interatrial band. Circ Res 18:502S18,1966 52. Massing GK, Liebman J, James TN: Cardiac conduction pathways in the infant and child. Cardiovas Clin 4:27-42,1972 53. Durrer

D, van Dam RT, Freud GE, et al: Total excitation of the isolated human heart. Circulation 41:899912,197o 54. Sano T, Yamagishi S: Spread of excitation from the sinus node. Circ Res 16:423-430, 1965 55. Van Mierop LHS, Alley RD, Kausel HW, et al: The anatomy and embryology of endocardial cushion defects. J Thorac Cardiovasc Surg 43:71-83, 1962 56. Burchell HB, DuShane JW, Brandenburg RO: The electrocardiogram of patients with atrioventricular cushion defects (defects of the atrioventricular canal). Am J Cardiol6:575-588, 1960 57. Narula OS, Scherlag BJ, Samet P, et al: Atrioventricular block. Am J Med 50:146-165, 1971 58. WaIdo AL, Bush HL Jr, Gelband H, et al: Effects on the canine P wave of discrete lesions in the specialized atria1 tracts. Circ Res 29:452-467, 1971 59. Anderson PAW, Rogers MC, Canent RV Jr, et al: Atrioventricular conduction in secundum atria1 septal defects. Circulation 48:27-31, 1973 60. Isaacson R, Titus JL, Merideth J, et al: Apparent interruption of atria1 conduction pathways after surgical repair of transposition of great arteries. Am J Cardiol 30: 533~535,1972

61. Waldo AL, Krongra E, Bowman FO Jr, et al: Electrophysiological considerations during total repair of transposition of the great vessels. Circulation 46 (Suppl II):34, 1972 62. Mustard WT: Successful two-stage correction of transpostion of the great vessels. Surgery 55:469-472, 1964 63. Angelini P, Sandiford FM: Functional correction of transposition of the great arteries. J Thorac Cardiovasc Surg 66:87-92,1973 64. Aberdeen E: Correction of uncomplicated cases of transposition of the great arteries. Br Heart J 33 (Suppl): 66-68,197l

65. Spadh MS, Barr RC, Jewett PH: Spread of excitation from the atrium into thoracic veins in human beings and dogs. Am J Cardiol 30: 844-854, 1972 66. Lewis T, Fell HS, Stroud WD: Observations upon flutter and fibrillation. Part 2. The nature of auricular flutter. Heart 7:191-245, 1920 67. Lister JW, Delman AJ, Stein E, et al: The dominant pacemaker of the human heart. Circulation 34:22-31, 1967 68. Marriott HJL: Atrioventricular synchronization and accrochage. Circulation 14:38-43, 1956 69. Schott A: Atrioventricular dissociation with and

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