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Main-stem extrasystoles with aberrant ventricular conduction mimicking ventricular extrasystoles∗
Diagnostic
Shelf
Main-Stem
Extrasystoles
Ventricular
Conduction
Ventricular HENRY J.
with Aberrant
L. MARRIOTT,
Mimicking
Extrasystoles* M.D. and PIERRE M.
St. Petersburg,
A
NIZET, M.D.
Florida
VENTRICULAR extrasystole is diagnosed when a premature anomalous ventricular complex, not preceded by an ectopic P’ wave, is When a followed by a compensatory pause. premature normal ventricular complex, not preceded by an ectopic P’ wave, is followed by a compensatory pause, a main-stem extrasystole (or A-V junctional extrasystole without retrograde conduction) is diagnosed.’ It follows that, if the main-stem extrasystole is complicated by aberrant ventricular conduction, it will mimic the presumably commoner ventricular extrasystole. This problem in differentiation, not only theoretic but real, is here illustrated and poses the valid question : How many of the premature beats that we call ectopic ventricular are in reality of A-V junctional origin with aberrant ventricular, but without retrograde, conduction?
beats (two reproduced here in Fig. 1B and C) whose QRS duration is normal and whose contour suggests a supraventricular origin. They also are not preceded by a P’, do not disturb the sinus rhythm and are followed by a fully compensatory pause. They therefore qualify as main-stem extrasystoles.’ In C, with a coupling interval of 481 preceded by a cycle of 83, the QRS contour is little In changed from the pattern of the sinus beats. B, however, with a shorter coupling interval of 46, the QRS, though still of normal duration, is With the mood for aberraobviously distorted. tion thus revealed, we have further confirmation that the distortion of the beat in A is due to even greater aberration, thanks to the longer antecedent cycle of 85.
A CASE IN POINT
The recognition of ventricular arrhythmias is widely regarded as a simple matter. In 1957 we wrote, “. . . the common ventricular extrasystole can never be diagnosed with unequivocal certainty; for there is always the possibility that such a beat is a main-stem extrasystole with aberrant ventricular canduction.“l Indeed, until we have a method whereby the two can be clearly separated, we have no means of knowing the relative incidence of aberrantly conducted main-stem beats compared with ventricular prematurities. Adapting to our modern environment, we recently translated the earlier thought into “the
DISCXJSSION
Consider the premature beat in Figure 1A. The QRS is widened and bizarre; it is not preceded by a P’ wave : it does not disturb the sinus rhythm and is therefore followed by a fully compensatory pause. In short, it has all the accepted hallmarks of a ventricular premature beat. But is it one? The contour of the anomalous QRS is triphasic (rsR’), and its initial deflection is identical with that of the flanking sinus beats. By recently proposed criteria,2 this combination weighs heavily (with odds of more Elsethan 100 to 1) against ventricular ectopy. where in the tracing we find other premature
t Intervals are expressed in hundredths of a second.
* From the Rogers Heart Foundation,
VOLUME19, MAY 1967
755
St. Petersburg,
Fla.
756
Marriott
and
Nizet
Fig. 1. In A, the premature beat has the widely accepted characteristics of a ventricular extrasystole: bizarre wide complex, undisturbed sinus rhythm, compensatory pause. But it also has a triphasic (rsR’) contour and an initial deflection identical with that of the flanking sinus beats. In C, the premature beat is obviously supraventricular (with minor ventricular aberration) ; nevertheless, it does not disturb the sinus rhythm and is followed by a compensatory pause and therefore qualifies as a main-stem extrasystole. The premature beat in B shows an intermediate contour. All 3 premature beats are presumably main-stem extrasystoles with varying degrees of ventricular aberration. Note that the cycle sequences are compatible with decreasing degrees of aberration (A > B > C). (The tracing is from a 15 year old white boy with no evidence of heart disease.)
ectopic ventricular origin of an impulse can be diagnosed with reasonable certainty only in the presence of an implanted pacemaker.” The demonstrable fact that theoretic mimics have reality requires that they have an acceptSupraventricular premature beats able name. that, in common with ventricular extrasystoles, fail to disturb the sinus rhythm and are therefore followed by compensatory pauses, were called main-stem, rather than A-V nodal, on the assumption that if they arose in the A-V node they would surely activate the atria; since they did not do so, it was assumed that they arose lower in the A-V junction.3 The justification for calling such beats main-stem may well be challenged. Certainly the argument on which introduction of the term was based has lost validity since the frequency of retrograde conduction from even lower (ectopic ventricular) centers has been repeatedly demonstrated.4-6 However, Hoffman and Cranefield? were unable to find automatic cells in the A-V node proper but found them in so that it is possible that the A-V bundle; “nodal” beats in fact originate in the common bundle. If this is so, the main-stem beat may well come into its own, though not for the reason that it was originally so designated. Meanwhile, faute de mieux, the term may be conveniently
preserved for much the same reason that “ ” “mid” and “lower” nodal, though upper, their anatomic implications may not be precise, remain useful terms to avoid clumsy circumlocutions.
SUMMARY This brief exposC stresses the fact that ventricular premature beats cannot be diagnosed with certainty and illustrates the reason by presenting, perhaps for the first time, main-stem extrasystoles with aberrant ventricular conduction recognizable as such only by means of new criteria. How many of the premature beats we glibly call ectopic ventricular are in reality supraventricular-arising in the A-V junctional tissues without retrograde conduction to the atria-we at present have no means of knowing. The justification for labeling such beats main-stem is briefly discussed.
REFERENCES 1. MARRIOTT, H. J. L. and BRADLEY, S. M. Main-stem extrasystoles. Circulation, 16: 544, 1957. 2. SANDLER, I. A. and MARRIOTT, H. .I. L. The differential morphology of anomalous ventricular complexes of RBBB-type in lead VI. Circulation,
31: 551, 1965. THE AMERICAN JOURNAL OF CARDIOLOGY
Main-Stem I,I. \ws, ‘I’. l’rematurc contractions arising in the junctional tissues. Quart. J. Med., 5: 1, 1911. 4. KISTIN, \. and LANDOWNE, M. Retrograde conduction from premature ventricular contractions, J common occurrence in the human heart. Cir&zlior/, 3: ‘38, 1951.
3
VOLUME 19, MAY 1967
Extrasystoies
‘57
5. KISTIX, .2. D. Retrograde conduction to the atria in ventricular tachycardia. Circulation. 24: 236, 1961. 6. KISTIN, i\. D. Personal communication, 1965. 7. HOFEMAN, B. F. and CRANEFIELD, P. F‘. ‘l‘hc physiological basis of cardiac arrhythmias. Aw. .I. .Cfed.. 37: 670, 1964.
Shelf
Main-Stem
Extrasystoles
Ventricular
Conduction
Ventricular HENRY J.
with Aberrant
L. MARRIOTT,
Mimicking
Extrasystoles* M.D. and PIERRE M.
St. Petersburg,
A
NIZET, M.D.
Florida
VENTRICULAR extrasystole is diagnosed when a premature anomalous ventricular complex, not preceded by an ectopic P’ wave, is When a followed by a compensatory pause. premature normal ventricular complex, not preceded by an ectopic P’ wave, is followed by a compensatory pause, a main-stem extrasystole (or A-V junctional extrasystole without retrograde conduction) is diagnosed.’ It follows that, if the main-stem extrasystole is complicated by aberrant ventricular conduction, it will mimic the presumably commoner ventricular extrasystole. This problem in differentiation, not only theoretic but real, is here illustrated and poses the valid question : How many of the premature beats that we call ectopic ventricular are in reality of A-V junctional origin with aberrant ventricular, but without retrograde, conduction?
beats (two reproduced here in Fig. 1B and C) whose QRS duration is normal and whose contour suggests a supraventricular origin. They also are not preceded by a P’, do not disturb the sinus rhythm and are followed by a fully compensatory pause. They therefore qualify as main-stem extrasystoles.’ In C, with a coupling interval of 481 preceded by a cycle of 83, the QRS contour is little In changed from the pattern of the sinus beats. B, however, with a shorter coupling interval of 46, the QRS, though still of normal duration, is With the mood for aberraobviously distorted. tion thus revealed, we have further confirmation that the distortion of the beat in A is due to even greater aberration, thanks to the longer antecedent cycle of 85.
A CASE IN POINT
The recognition of ventricular arrhythmias is widely regarded as a simple matter. In 1957 we wrote, “. . . the common ventricular extrasystole can never be diagnosed with unequivocal certainty; for there is always the possibility that such a beat is a main-stem extrasystole with aberrant ventricular canduction.“l Indeed, until we have a method whereby the two can be clearly separated, we have no means of knowing the relative incidence of aberrantly conducted main-stem beats compared with ventricular prematurities. Adapting to our modern environment, we recently translated the earlier thought into “the
DISCXJSSION
Consider the premature beat in Figure 1A. The QRS is widened and bizarre; it is not preceded by a P’ wave : it does not disturb the sinus rhythm and is therefore followed by a fully compensatory pause. In short, it has all the accepted hallmarks of a ventricular premature beat. But is it one? The contour of the anomalous QRS is triphasic (rsR’), and its initial deflection is identical with that of the flanking sinus beats. By recently proposed criteria,2 this combination weighs heavily (with odds of more Elsethan 100 to 1) against ventricular ectopy. where in the tracing we find other premature
t Intervals are expressed in hundredths of a second.
* From the Rogers Heart Foundation,
VOLUME19, MAY 1967
755
St. Petersburg,
Fla.
756
Marriott
and
Nizet
Fig. 1. In A, the premature beat has the widely accepted characteristics of a ventricular extrasystole: bizarre wide complex, undisturbed sinus rhythm, compensatory pause. But it also has a triphasic (rsR’) contour and an initial deflection identical with that of the flanking sinus beats. In C, the premature beat is obviously supraventricular (with minor ventricular aberration) ; nevertheless, it does not disturb the sinus rhythm and is followed by a compensatory pause and therefore qualifies as a main-stem extrasystole. The premature beat in B shows an intermediate contour. All 3 premature beats are presumably main-stem extrasystoles with varying degrees of ventricular aberration. Note that the cycle sequences are compatible with decreasing degrees of aberration (A > B > C). (The tracing is from a 15 year old white boy with no evidence of heart disease.)
ectopic ventricular origin of an impulse can be diagnosed with reasonable certainty only in the presence of an implanted pacemaker.” The demonstrable fact that theoretic mimics have reality requires that they have an acceptSupraventricular premature beats able name. that, in common with ventricular extrasystoles, fail to disturb the sinus rhythm and are therefore followed by compensatory pauses, were called main-stem, rather than A-V nodal, on the assumption that if they arose in the A-V node they would surely activate the atria; since they did not do so, it was assumed that they arose lower in the A-V junction.3 The justification for calling such beats main-stem may well be challenged. Certainly the argument on which introduction of the term was based has lost validity since the frequency of retrograde conduction from even lower (ectopic ventricular) centers has been repeatedly demonstrated.4-6 However, Hoffman and Cranefield? were unable to find automatic cells in the A-V node proper but found them in so that it is possible that the A-V bundle; “nodal” beats in fact originate in the common bundle. If this is so, the main-stem beat may well come into its own, though not for the reason that it was originally so designated. Meanwhile, faute de mieux, the term may be conveniently
preserved for much the same reason that “ ” “mid” and “lower” nodal, though upper, their anatomic implications may not be precise, remain useful terms to avoid clumsy circumlocutions.
SUMMARY This brief exposC stresses the fact that ventricular premature beats cannot be diagnosed with certainty and illustrates the reason by presenting, perhaps for the first time, main-stem extrasystoles with aberrant ventricular conduction recognizable as such only by means of new criteria. How many of the premature beats we glibly call ectopic ventricular are in reality supraventricular-arising in the A-V junctional tissues without retrograde conduction to the atria-we at present have no means of knowing. The justification for labeling such beats main-stem is briefly discussed.
REFERENCES 1. MARRIOTT, H. J. L. and BRADLEY, S. M. Main-stem extrasystoles. Circulation, 16: 544, 1957. 2. SANDLER, I. A. and MARRIOTT, H. .I. L. The differential morphology of anomalous ventricular complexes of RBBB-type in lead VI. Circulation,
31: 551, 1965. THE AMERICAN JOURNAL OF CARDIOLOGY
Main-Stem I,I. \ws, ‘I’. l’rematurc contractions arising in the junctional tissues. Quart. J. Med., 5: 1, 1911. 4. KISTIN, \. and LANDOWNE, M. Retrograde conduction from premature ventricular contractions, J common occurrence in the human heart. Cir&zlior/, 3: ‘38, 1951.
3
VOLUME 19, MAY 1967
Extrasystoies
‘57
5. KISTIX, .2. D. Retrograde conduction to the atria in ventricular tachycardia. Circulation. 24: 236, 1961. 6. KISTIN, i\. D. Personal communication, 1965. 7. HOFEMAN, B. F. and CRANEFIELD, P. F‘. ‘l‘hc physiological basis of cardiac arrhythmias. Aw. .I. .Cfed.. 37: 670, 1964.