Supernormal intraventricular conduction

J. ELECTROCARDIOLOGY, 4 (3) 240-248, 1971

Supernormal Intraventricular Conduction BY IVAN A. D'CRUZ, M.D., M.R.C.P, (LONDON), M.R.C.P. (EDINBURGH)

SUMMARY The supernormal phase of intraventricular conduction was diagnosed in two patients with atrial fibrillation. In one of these cases, the predominant QRS pattern was that of right bundle-branch block; detailed study of this case (1) provided a convincing demonstration of the occurrence of supernormal conduction through the right bundle-branch, (2) showed that supernormal conduction could follow both normal and aberrant beats, (3) showed that the supernormal phase of conduction became gradually more delayed with reference to the previous QRS complex as the preceding R-R interval progressively increased in length, and (4) permitted certain deductions about probable retrograde activation of the right bundle-branch during aberrant beats. Supernormal conduction was diagnosed in a second case, presenting a predominant QRS pattern of left bundle-branch block type, but detailed analysis was not possible since the ECG recording was not sufficiently long. INTRODUCTION Supernormal conduction is a rare phenomenon wherein a short phase of unexpectedly improved conduction occurs early in the diastolic period of the cardiac cycle. It is a paradoxical situation where "the second of two consecutive impulses reaching damaged tissue during the presumably unresponsive period is more effective than the preceding one that arrived later in the cardiac cycle''1. Supernormal, in this context, does not imply "better than normal"; it merely means a *Honorary Physician and Professor of Medicine, Lokmanya Tilak Municipal General Hospital, & Lokmanya Tilak Municipal Medical College Sion, Bombay - 22, India.

relative improvement of subnormal conduction and always occurs on a background of impaired A-V or intraventricular conduction. Over 50 instances of supernormal A-V conduction have been reported and analysed in detail by Pick et al. a. However, only about a dozen cases of supernormal intraventricular conduction have been described, and some of these are open to an alternative diagnosis 2"8. The essential problem in these cases has been to explain why some very prematurelyoccurring beats show normal conduction while other beats in the same strip, occurring later in the cardiac cycle, show aberrant conduction. When this phenomenon is observed in the presence of atrial fibrillation, the diagnosis of supernormal intraventricular conduction is on firmer ground, since normally conducted beats occur both early (supernormal phase) and late in the cardiac cycle, and aberrantly conducted beats during an intermediate period. This was demonstrated in 2 cases of atrial fibrillation by Schamroth 9 and earlier by Katz and Pick x~ Two further such cases were recently reported by Wellens z~ The following two cases demonstrate the supernormal phase of intraventricular conduction in association with atrial fibrillation. Detailed study of one of these cases provided information about certain aspects of aberrant and supernormal intraventricular conduction which have apparently escaped the notice of previous authors. CASE R E P O R T S A review of the ECG records of 585 patients of atrial fibrillation seen at the Lokmanya Tilak Municipal General Hospital over the last 20 years revealed 60 tracings showing phasic aberrant conduction. The supernormal phase of conduction was diagnosed in only two of them.

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Patient No. 1 was studied and treated personally by the author. The diagnosis in patient No. 2 was made only long after she had been lost to observation, so that a similar detailed study was not possible in this case. Patient No. 1, M. K., a 45-year-old woman, presented with severe anemia (haemoglobin 7 gins), congestive heart failure and a fast irregular pulse. Her anemia was of the iron deficiency type secondary to hookworm infestation and subsequently responded to iron therapy. There was neither auscuhatory nor radiological evidence of valvular heart disease. Cardiomegaly and cardiac decompensation were attributed to the combined effects of anemia and uncontrolled atrial fibrillation, although ischemic heart disease or cardiomyopathy could not be completely excluded. T h e electrocardiogram showed fibrillatory atrial activity and an irregular spacing of the ventricular complexes, consistent with a diagnosis of atrial fibrillation. She was digitalised, and over the next few weeks several continuous long strips of the ECG containing 158, 254, 172, 234 and 1540 ventricular complexes, respectively, were recorded. In each recording the QRS complexes were either of normal configuration and duration S

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Fig. 3. Patient No. 1. As in Fig 2. Note that the late normal beats which follow normal beats (dot within circle) are situated more leftward than other late normal beats. cardiac conducting tissue is expected to be m o r e refractory in these instances. I n other words, one would expect normally conducted beats to be represented in the r i g h t - h a n d lower area of the graph, all the space above a n d to the left of this a r e a being occupied by points representing a b e r r a n t Q R S complexes. As a general rule, this has been found to hold true whenever atrial fibrillation is compli-

cated by phasic a b e r r a n t conduction 12. Q R S complexes of n o r m a l d u r a t i o n a n d configuration are accordingly noted to the right of a n d below the m a i n body of a b e r r a n t complexes (Figs. 2, 3, a n d 4). However, there is in a d d i t i o n a group of normally conducted beats represented in a relatively localised area n e a r the left b o r d e r of the graph. T h e m a j o r i t y of a b e r r a n t l y conducted beats J. E L E C T R O C A R D I O L O G Y .

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Fig. 4. Patient No, 1. As in Fig. 3. The R-R intervals between 500 and 750 millisec were all terminated by aberrant QRS complexes and those over 900 millisec were all terminated by normal QRS complexes. Therefore, only the QRS complexes terminating R-R intervals less than 500 millisec, and R-R intervals more than 750 millisec, are represented in the graph. This continuous ECG strip contained 1540 QRS complexes. are represented below and to the right of these normal complexes. The paradox of unexpectedly better intraventricular conduction in these very premature yet normal beats can be explained only on the basis of the supernormal phase of conduction. These ventricular complexes exhibiting supernormal intraventricular conduction number 24, 25 and 69, respectively, in Figs. 2, 3 and 4. Closer observation of these complexes reveals that they occupy a rather narrow area in the graph, corresponding to R-R intervals within a relatively short range. Another observation is that, as the R-R interval of the preceding cardiac cycle lengthens, the supernormal phase shifts rightward to a slight but definite extent. For example, in Fig. 4, the supernormal phase extends over the range 400 to 440 millisec when the preceding cardiac cycles (R-R intervals) are shortest, but is in the range 430 to 480 millisec after the longest cardiac cycles. When two normally conducted beats occurred in succession, the first of these two beats was usually an instance of supernormal J, E L E C T R O C A R D I O L O G Y , V O L . 4, NO. 3, 1971

conduction and the second a "late normal" beat. Ventricular complexes of the latter type (dot within circle) are seen to occupy a more leftward position than other "late normal" QRS complexes which followed aberrant beats (Figs. 3 and 4). At first sight this appears a contradiction of the general rule that aberrant beats should always be represented above and to the left of normally conducted beats (excluding supernormally conducted beats). This apparent discrepancy can be explained if one takes into account the physiological difference between (a) the R-R interval as measured from the commencement of a normal beat, and (b) the same R-R interval as measured from the commencement of an aberrant beat (see discussion below). Comparison of successive tracings, recorded over a period of several weeks, showed that the time-range of the supernormal period with reference to the preceding QRS complex varied from one tracing to another. On some occasions, spontaneous improvement in right bundle-branch conduction to an almost normal level was noted, so that only the most

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Fig. 5. Patient No. 1 during a phase when spontaneous improvement of intraventricular conduction had occurred. Only two aberrant QRS c o m plexes, terminating the shortest R - R intervals, are seen. All the other QRS complexes show normal conduction. premature ventricular complexes were aberrant (Fig. 5).

Patient No. 2, R. S. P., a 61 year-old woman, had mitral stenosis with regurgitation. The electrocardiogram showed atrial fibrillation. The longest tracin.g available in this case contained 27 consecutive ventricular complexes (Figs. 6 and 7). The predominant QRS pattern was that of left bundle branch block (duration 0.14 see) but some ventricular complexes of normal duration (0.09 see) and configuration were also present, and these terminated R-R intervals of either very long or very short duration. Only two QRS complexes fell into the latter category, one of which (No. 27) was identical to the "Late normal" QRS complexes, while the other (No. 9) was only slightly different. The supernormal phase of conduction provides the most probable explanation for the unex-

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Fig. 6. Patient No. 2. Continuous strip (Lead 2) showing atrial fibrillation. Long R-K intervals are terminated by normal QRS complexes while shorter R - R intervals are terminated by aberrant QRS complexes. The ninth and twenty-seventh beats are exceptions. They are normal in duration in spite of being premature, presumably because of supernormal intraventricular conduction.

pectedly good conduction in these two very premature beats (R-R intervals 430 and 420 millisec, respectively). A less likely possibility is that they are ventricular premature beats arising from such a location in the upper ventricular septum that both bundle branches (the left one below the site of the block) -were activated in a manner simulating normal spread of the cardiac impulse. One ventricular complex (No. 20) which terminated the shortest R-R interval was of intermediate duration (0.11 see) between normal and aberrant beats. It seems possible that supernormal conduction did occur in this beat, which was nevertheless somewhat aberrant because of its extreme prematurity. DISCUSSION Although extremely rare, the supernormal phase of intraventricular conduction has been described in association with a variety of arrhythmias. An underlying impairment of intraventricular conduction existed in all instances, and supernormal conduction was proposed as a probr/ble or possible explanation for the paradoxical occurrence of premature ventricular complexes of normal contour and duration. Thus, in the cases of Contro, Magri and NatalP and that of Simon and Langendorf 2, premature QRS complexes of normal contour interrupted a regular basic rhythm consisting of widened QRS complexes of bundle-branch block configuration. Partial A-V block of Wenckebach type was present in Scherf and Scharf's case 3, the unusual feature (explained on the basis of supernormal conduction) being the bundle-branch block configuration of the first beat in each Wenckebach period, all the other vent~icular being normal. Pick and Fishman's casC was one of nodal rhythm and right bundle-branch block, complicated by premature capture beats of normal contour which presumably fell within the supernormal phase of conduction through the right bundle branch. Supernormal conduction provides a likely explanation for the unusual finding of bradycardia-dependent bundle-branch block 7,s. Tachycardia-dependent aberrant QRS complexes are frequently encountered in atrial J. E L E C T R O C A R D I O L O G Y ,

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Fig. 7. Patient No. 2. Every R-R interval in the strip shown in Fig. 6 has been plotted against its preceding R-R interval. The two QRS complexes exhibiting probable supernormal conduction are at the left end of the graph, while the three late normal QRS complexes are near the rightward end. The QRS eompiexes numbered 1 and 2 (open circles) are of different configurations from the other QRS complexes and from each other. Their nature remains uncertain. fibrillation le-14. Ventricular complexes which terminate short R-R intervals tend to be aberrant, especially if the preceding cardiac cycle (R-R interval) has been long; conversely, ventricular complexes which terminate long R-R intervals tend to be of normal configuration, particularly if the preceding R-R interval has been short. When there are, in addition, some very premature QRS complexes of normal contour identical in appearance to the latter type of "late normal" ventricular complexes, these can be adequately explained only by postulating a supernormal phase of intraventricular conduction. Alternative interpretations of normally conducted premature beats which interrupt a basic bundle-branch block pattern, in conditions other than atrial fibrillation, include the septal origin (below the level of the blocked bundle-branch) of ventricular ectopic beats, and the conduction of premature ectopic impulses (arising from A-V junctional tissue) through accessory pathways. Such theories could hardly explain the occurrence of identical normal QRS complexes both (a) after varying long R-R intervals, and (b) within a circumscribed range of short R-R intervals. Most authors of previous reports on supernormal intraventricular conduction did not J. E L E C T R O C A R D [ O L O G Y , V O L , 4 . NO, 3, 1971

try to measure the duration of the supernormal phase. Such an estimation was attempted by Contro, Magri and Natali e and by Scherf and ScharP, but they did not take into account the effect of the length of the preceding R-R interval. The former authors estimated the phase of supernorrnal conduction in their two cases as 60 and 100 millisec, respectively, while in Scherf's patient a value of 90 millisec was reported. When the duration of the preceding R-R interval is taken into account as in our first patient (Fig. 4), it is seen that the duration of the supernormal phase of conduction, for any particular length of the previous cardiac cycle, remains more or less constant at 40 to 50 millisec. However, as the duration of the previous R-R interval increases, the time range occupied by the supernormal period shifts gradually to the right - - it becomes progressively more delayed with reference to the previous QRS complex. This is perhaps not surprising since the duration of the refractory period of cardiac conducting tissue has long been known to vary directly with the length of the preceding R-R interval 11,15. This "shift to the right" has already been described in respect to the supernormal phase of excitability16 and has been reported with regard to the super-

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normal phase of intraventricular conduction only by Wellens 2~ Few previous authors have commented upon the electrical activation of the affected bundle-branch distal to the site of block, in patients with phasic bundle-branch block (aberrant conduction). Presumably this distal portion of the affected bundle (usually the right) does get depolarised in every cardiac cycle; otherwise it would be difficult to explain why the bundle-branch block pattern persists in many consecutive heats, whereas "late normal" QRS complexes, terminating long R-R intervals, are normal in contour and duration. It has recently been demonstrated by direct His bundle recordings, that retrograde activation of the His bundle occurs immediately following an aberrant beat of right bundle-branch block configurationlL In all likelihood, retrograde activation of the His bundle occurred in that case through retrograde activation of the right bundle branch via its ramifications. It is, therefore, probable that every aberrant beat is accompanied by retrograde activation of the "blocked" bundle-branch - - a relatively unnoticed variety of concealed conduction. When a normally conducted premature beat (exhibiting supernormal conduction) is preceded by an aberrant beat, it would appear that antegrade conduction through the affected bundle-branch was facilitated by retrograde conduction during the previous beat. Thus it is akin to the "Bahnung phenomenon ''1~ also known as type B supernormal A-V conduction of Pick et al. 1 who described it thus: "following concealed retrograde conduction the region of unidirectional block becomes the region of supernormal forward conduction." It has been shown that the supernormal phase of A-V conduction can interrupt the refractory period following both antegrade and retrograde conduction, in the same patientL Fig. 1 B demonstrates that the supernormal phase of intraventricular conduction can likewise follow both antegrade and retrograde (aberrant) activation of the right bundle branch, an observation not reported hitherto.

It is not yet known at which precise moment retrograde activation of the critical segment of the "blocked" bundle branch occurs, with reference to the inscription of the QRS complex in the conventional ECG. Such information may soon be available as a result of direct intracardiac recordings, since right bundle-branch potentials have already been recorded 18. It seems reasonable to suppose that the site of impaired antegrade conduction (and supernormal conduction) in the affected bundle-branch undergoes activation while the latter portion of the QRS complex is being inscribed in the conventional electrocardiogram during an aberrant beat. In a normally conducted beat, the bundle branch is activated very shortly before the beginning of the QRS. Damato et al. 18 and Narula and Samet 19 have actually measured the interval between activation of the right bundlebranch and that of the ventricles (R.B.- Q interval) in normal beats and found it to be of the order of 12 to 90 millisec. Assuming retrograde activation of the "blocked" bundle-branch during aberrant beats, it would follow that the R-R interval as measured from the commencement of a normally conducted beat to that of an identical normal beat, or from the commencement of an aberrant beat to that of a similarly aberrant beat, would correspond to the actual interval between successive activations of the abnormal segment of the affected bundlebranch. However, the R-R interval as measured from the beginning of an aberrant beat to that of a normal beat would give an erroneously high value for the r-r interval of the abnormal bundle-branch, while the R-R interval as measured from the commencement of a normal beat to that of an aberrant beat would give a fallaciously low value for this parameter (Fig. 8). Figs. 3 and 4 provide certain observations which support our hypothesis that retrograde activation of the right bundle-branch took place in every aberrant beat, and even allow a rough estimation of the delay in activation of the right bundle. The "late normal" beats terminating the shortest R-R intervals (excluding supernormally conducted beats) have J. E L E C T R O C A R D I O L O G Y ,

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all followed normally "conducted beats, while those "late normal" beats which followed aberrant beats have terminated longer R-R intervals. The reason for this appears to be that the true r-r interval of the abnormal segment of the right bundle-branch is equal to the measured R-R interval in the former beats but is shorter than the measured R-R interval in the latter beats by an extent equal to the delay in activation of the abnormal right bundle-branch segment, when conduction is aberrant. This statement presupposes that the refractory period of the right bundle branch after retrograde activation is the same as that after antegrade activation, an assumption that has not yet been proven. It can be seen in Fig. 4 that the shortest R-R interval terminated by "late normal" beats is 750 millisec but, if one considers only those "late normal" beats which follow aberrant beats, the shortest R-R interval terminated by such J. E L E C T R O C A R D I O L O G Y ,

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beats is 820 millisec. The difference between the two values (70 millisec) may be taken as approximately equal to the delay in activation (retrograde) of the right bundle branch in aberrant beats, as compared with normal (antegrade) activation of the same bundlebranch. In Fig. 3, the corresponding value (100 millisec) is slightly higher, perhaps because a sufficiently large number of ventricular complexes is not available.

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The supernormal phase of intraventricular conduction was demonstrated in a case of atrial fibrillation by Katz and Pick 1~ Schamroth 9 reported two further cases of this type, but it is possible that Schamroth's second case is not a true instance of supernormal intraventricular conduction. The three normallyconducted QRS complexes labelled, a, b and c in his Figs. 4 and 5 terminate R-R intervals that are only slightly shorter than those terminated by the "late normal" QRS complexes in the same strip. All these three beats (a, b and c) follow normally conducted beats. The discrepancy between the R-R interval as measured from the beginning of a normal beat to that of a normal beat, and the same R-R interval as measured from the beginning of an aberrant beat to that of a normal beat, is sufficient to explain the marginally shorter R-R intervals terminated by the three QRS complexes a, b and c. O n the other hand, Schamroth's first case is a very convincing example of supernormal conduction in the right bundle-branch, since the two beats designated as exhibiting supernormal conduction (Schamroth's Fig. 1) terminate much shorter R-R intervals than those terminated by "late normal" QRS complexes. The wide separation between these supernormally conducted beats and the "late normal" beats is also very evident on graphical representation (Schamroth's Fig. 3). Two well-studied instances of supernormal conduction associated with atrial fibrillation were reported by Wellens 2~ Acknowledgement: I am indebted to Dr. V. N. Panse, Dean, Lokmanya Tilak Municipal General Hospital and Medical College, for permission to use hospital records.

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REFERENCES 1. Pick, A., Langendorf, R., and Katz, L. N.: The supernormal phase of atrioventricular conduction. 1. Fundamental mechanisms. Circulation 26:388, 1962. 2. Simon, A. J., and Langendorf, R. : Intraventricular block with ectopic beats approaching normal QRS duration. Am. Heart J. 27:345, 1944. 3. Seherf, D., and Scharf, M. M.: Supernormal phase of intraventricular conduction. Am. Heart J. 36:621, 1948. 4. Burchell, H. B.: Sino-anricular block, interference dissociation, and different recovery rates of excitation in the bundle branches. Brit. Heart J. i 1:230, 1949. 5. Pick, A., and Fishman, A. P. : Observation in heart block. Supernormality of A-V and intraventricular conduction and ventricular parasystole under the influence of epinephrine. Acta Cardiol. (Brux) 5:270, 1950. 6. Contro, S., Magri, G., and Natali, G.: Premature beats overcoming impaired intraventricular conduction. Supernormal phase of intraventricular conduction. Am. Heart J. 51:378, 1956. 7. Massumi, R. A.: Bradycardia - - dependent bundle-branch block. Circulation 38:1066, 1968. 8. Sarachek, N. S.: Bradycardia - - dependent bundle-branch block. Relation to supernormal conduction and phase - - 4 depolarization. Am. J. Cardiol. 25:727, 1970. 9. Schamroth, L. : The supernormal phase of intraventricular conduction. Brit. Heart J. 31:337, 1969. 10. Katz, L. N., and Pick, A.: Clinical Electrocardiography. 1. The Arrhythmias. Philadelphia, Lea and Febiger, 1956, p. 471. 11. Gouaux, J. L., and Ashman, R.: Auricular fibrillation with aberration simulating ventric-

12.

13.

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15.

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ular paroxysmal tachycardia. Am. Heart J. 34:366, 1947. D'Cruz, I. A., Cooverji, N. D., and Deshmukh, S. D. : Anomalies of intraventricular conduction in atrial fibrillation. In press, Ind. Heart J. 1971. Schamroth, L., and Chesler, E.: Phasic aberrant ventricular conduction. Brit. Heart J. 25:217, 1963. Marriott, H. J. L., and Sandier, I. A.: Criteria, old and new, for differentiating between ectopic ventricular beats and aberrant ventricular conduction in the presence of" atrial fibrillation. Progress Cardiovasc. Dis. 9:18, 1966. Lewis, T., Drury, A. N., and Bulger, H. A.: Observations upon flutter and fibrillation VI. The refractory period and rate of propagation in the auricle. Heart, 8:83, 1921. Walker, W. J.: Factors affecting supernormal period and threshold of the ventricle, in Mechanisms and Therapy of Cardiac Arrhythmias. Dreifus, L. S., Likoff, W., and Moyer, J. H., New York, Grune and Stratton, 1966. Cohen, S. I., Lan, S. N., Scherlag, B. J., and Damato, A. N.: Alternate patterns of premature ventricular excitation during induced atrial bigeminy. Circulation 39:819, 1969. Damato, A. N., Lau, S. H., Berkowitz, W. D., Rosen, K. M., and Lisi, K. R.: Recording of specialised conducting fibres (AV Nodal, His Bundle and Right Bundle Branch) in man using an electrode catheter technic. Circulation 39:435, 1969. Narula, O. S., and Samet, P. : Wenckebach and Mobitz type II A-V block due to block within the His Bundle and bundle branches. Circulation 41:947, 1970. Wellens, H.: Unusual occurrence of nonaberrant conduction in patients with atrial fibrillation and aberrant conduction. Am. Heart J. 77:158, 1969.

J. E L E C T R O C A R D I O L O G Y . V O L . 4 , NO. 3, 1971