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28. McCammon RW: A longitudinal study of electrocardiographic intervals in healthy children. Acta Paediatr Scand (Uppsala) (suppl) 126, 1961 29. Simonson E, Cady LD Jr, Woodbury M: The normal QT interval. Am Heart J 63: 747, 1962 30. Fraser GR, Froggatt P, James TN: Congenital deafness associated with electrocardiographic abnormalities, fainting attacks and sudden death. A recessive syndrome. Quart J Med (New Series) 33: 361, 1964 31. Fraser GR, Froggatt P, Murphy T: Genetical aspects of the cardioauditory syndrome of Jervell and Lange-Nielsen (congenital deafness and electrocardiographic abnormalities). Ann Hum Genet (London) 28: 133, 1964 32. Alimurung MM, Joseph LG, Craige E, Massell BF: The QT interval in normal infants and children. Circulation 1: 1329, 1950 33. Lepeschkin E, Surawicz B: The measurement of the Q-T interval of the electrocardiogram. Circulation 6: 378, 1953 34. Bazett HC: An analysis of the time-relations of electrocardiograms. Heart 7: 353, 1920 35. Friedman ME, Geidel S, Havens B, Hoppenbrouwers T, Hodgman JE: Near-miss for sudden infant death syndrome. Clin Res 23: 142A, 1975 36. Ferrer PL, Talner NS: Changes in the QT index with sleep in young mammals. Pediatr Res 8: 349/75, 1974 37. Schwartz PJ, Malliani A: Electrical alternation of the T-wave: Clinical and experimental evidence of its relationship with the sympathetic nervous system and with the long Q-T syndrome. Am Heart J 89: 45, 1975 38. Jervell A, Lange-Nielsen F: Congenital deaf-mutism, functional heart disease with prolongation of the Q-T interval, and sudden death. Am Heart J 54: 59, 1957 39. James TN: Congenital deafness and cardiac arrhythmias. Am J Cardiol 19: 627, 1967 40. Olley PM, Fowler RS: The surdo-cardiac syndrome and therapeutic observations. Br Heart J 32: 467, 1970 41. Garza LA, Vick RL, Nora JJ, McNamara DG: Heritable Q-T prolonga-
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tion without deafness. Circulation 41: 30, 1970 42. Ratshin RA, Hunt D, Russell RO Jr, Rackley CE: QT interval prolongation, paroxysmal ventricular arrhythmias, and convulsive syncope. Ann Intern Med 75: 919, 1971 43. Froggatt P, James TN: Sudden unexpected death in infants. Evidence of a lethal cardiac arrhythmia. Ulster Med J 42: 136, 1973 44. Schwartz PJ: Cardiac sympathetic innervation and the sudden infant death syndrome. A possible pathogenetic link. Am J Med 60: 167, 1976 45. Fraser GR, Froggatt P: Unexpected cot deaths. Lancet 2: 56, 1966 46. Mathews EC Jr, Blount AW Jr, Townsend JI: Q-T prolongation and ventricular arrhythmias, with and without deafness, in the same family. Am J Cardiol 29: 702, 1972 47. Hanazono N, Ando Y, Ohnishi M, Oda H, Yuhara N, Nishio T, Ishida H, Takeuchi A, Kohashi K: Heritable QT prolongation without deafness: The Romano-Ward syndrome. Jap Heart J 14: 479, 1973 48. Hugenholtz PG: Electrocardiographic abnormalities in cerebral disorders. Report of six cases and review of the literature. Am Heart J 63: 451, 1962 49. Burch GE, Meyers R, Abildskov JA: A new electrocardiographic pattern observed in cerebrovascular accidents. Circulation 9: 719, 1954 50. Yanowitz F, Preston JB, Abildskov JA: Functional distribution of right and left stellate innervation to the ventricles: Production of neurogenic electrocardiographic changes by unilateral alteration of sympathetic tone. Circ Res 18: 416, 1966 51. Moss AJ, McDonald J: Unilateral cervicothoracic sympathetic ganglionectomy for the treatment of long QT interval syndrome. N Engl J Med 285: 903, 1971 52. Schwartz PJ, Snebold NG, Brown AM: Effects of unilateral cardiac sympathetic denervation on the ventricular fibrillation threshold. Am J Cardiol 35: 169, 1975 53. Simonson E, Brozek J, Keys A: Variability of the electrocardiogram in normal young men. Am Heart J 38: 407, 1949
Paroxysmal Supraventricular Tachycardia Is
the Atrium
a
MARK E. JOSEPHSON, M.D.,
Necessary Link? AND
JOHN A. KASTOR, M.D.
SUMMARY Whether or not the atrium plays an essential role in initiating and/or sustaining atrioventricular (A-V) nodal re-entrant tachycardia was evaluated in eight patients. In all eight patients, the atrium could be rendered refractory to retrograde atriai echoes during the tachycardia without interrupting the arrhythmia. This was accomplished by introducing atrial premature depolarizations prior to the time the atrium would normally be retrogradely depolarized by
atrial echoes. In one patient, two atrial premature depolarizations could be introduced, producing A-V dissociation, without termatig the tachycardia. In another patient, the tachycardia could be initiated without an atrial echo. Our data suggest that most, if not all of the atrium is unnecessary for the initiation and maintenance of A-V nodal re-entrant supraventricular tachycardia.
MOST CASES of paroxysmal supraventricular tachycardia are initiated and sustained through re-entry within the atrioventricular (A-V) node.' Whether or not the atria form a portion of the re-entrant pathway remains unsettled. The present investigation of eight patients demonstrated that in each case no portion of the atrium recorded by our electrode catheters was required to sustain A-V nodal re-
entrant supraventricular tachycardia and in one the atrium did not play an essential role in initiating the arrhythmia.
From the Cardiac Clinical Electrophysiology Laboratory, Hospital of the University of Pennsylvania; the Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania. Presented at the 25th Annual Scientific Session of the American College of Cardiology, February 24, 1976, New Orleans, Louisiana. Supported in part by grants from the USPHS, NIH, HL 14807, and the American Heart Association, Southeastern Pennsylvania Affiliate. Address for reprints: Dr. Mark E. Josephson, Director, Electrophysiology Laboratories, 669 White Building, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, Pennsylvania 19104. Received March 5, 1975; revision accepted March 29, 1976.
Methods, Materials, and Clinical Patient Information Eight patients were studied in the nonsedated postabsorptive state after informed consent was obtained (table 1). All had symptomatic supraventricular tachycardia (SVT), and none demonstrated evidence of pre-excitation. No patient was taking antiarrhythmic drugs at the time of the study. A quadripolar electrode catheter was introduced percutaneously into an antecubital and/or femoral vein and positioned under fluoroscopic control against the lateral wall of the high right atrium and/or the coronary sinus. The proximal pair of electrodes was used to record a high right atrial or coronary sinus electrogram, while the distal pair was used for atrial stimulation. A bipolar electrode catheter
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SUPRAVENTRICULAR TACHYCARDIA/Josephson, Kastor was similarly introduced into another antecubital vein and positioned in the right ventricular apex for stimulation. A His bundle electrogram was obtained using a tripolar electrode catheter introduced percutaneously into the right femoral vein.4 The intracardiac electrograms were filtered at 40 and 500 Hz and were simultaneously displayed with at least three surface ECG leads and timelines generated at 10 and 100 msec on a multichannel oscilloscope (Electronics for Medicine DR-16). Rectangular impulses of I msec duration and at approximately twice diastolic threshold were delivered by a specially designed programmed digital stimulator (Murray Bloom, Narberth, Pa.). All data were stored on magnetic tape (Honeywell 14 channel recorder) and later retrieved on photographic paper at speeds of 150 to 200 mm/sec. In each patient, after initiation of A-V nodal re-entrant tachycardia, atrial premature depolarizations were introduced to activate the atria prior to the time they would have been retrogradely activated by atrial echoes during the tachycardia. In addition, refractory periods were determined by the extrastimulus method. Results All patients were in sinus rhythm at the beginning of the study and no abnormalities of conduction were present (table 1). In each patient, single atrial premature beats at coupling intervals ranging from 255-380 msec initiated the tachycardia. The echo zones1 2 were 10 to 120 msec in duration. The critical A-H interval required for the initiation of the tachycardia ranged between 140 and 400 msec.3 The tachycardia could also be started in each patient during Wenckebach cycles produced by rapid atrial pacing,3 and in two patients (E.H. and H.H.), by one or more ventricular premature beats. In all patients, atrial premature depolarizations could be introduced at intervals resulting in atrial depolarizations 10 to 130 msec prior to the time of spontaneous retrograde atrial activation without interrupting the tachycardia or altering its cycle length. In three patients, both right and left atrial (coronary sinus) sites were prematurely depolarized without influencing the tachycardia. Examples are shown in
TABLE 1. Clinical Data PR* QRS* AH*
HV*
A-H required to initiate SVT*
125 140
75 90
70 95
50 35
400 170
165 160 135 ASHD 155 None 148 ASHD 160
65 82 86 88 90 90
90 78 50 85 80 92
40 45 50 48 45 45
145 140 295 195 250 290
Pt/Age/Sex
Dx
K.M./27/F H.H./66/M
MVP ASHD IMI MVP ASHD MVP
M.B./17/F W.P./56/M E.H./37/F
M.U./55/M L.R./18/F C.N./72/F
*All values are given in msec. Abbreviations: ASHD = atherosclerotic heart disease; MVP = mitral valve prolapse; IMI = inferior myocardial infarction.
figures 1-3. Note in particular that the low right atrium is depolarized: a) 30 and 20 msec early in beats 2 and 4 of figure 1; b) 25 msec early in beat 3 of figure 2; c) 70 msec early in beat 3 of figure 3A and 100 msec early in beat 3 of figure 3B. Furthermore, the coronary sinus is depolarized 120 msec early in figure 3A and 55 msec early in figure 3B. The configuration of the high and low atrial electrograms were different in the atrial premature depolarizations (Ap) when compared to the atrial echoes (Ae). In addition, the atrial electrograms of the premature depolarizations introduced from the right or left atrium were recorded before the onset of the His bundle deflection in the patient illustrated in figure 3. Thus in each of these three cases, that part of the atria giving rise to the high right atrial electrogram, low right atrial electrogram (in the His bundle recording), and in one case the coronary sinus electrogram, could be prematurely depolarized without interrupting the tachycardia. Since the atrial refractory periods of our patients were 210-300 msec, the atria would have been refractory for at least 200 msec after Ap, during which time Ae would have appeared (10 to 130 msec after the atrium was prematurely
depolarized). In patient K.M., two premature atrial depolarizations (Ap) could be introduced which depolarized both the high and low right atrium without terminating the tachycardia (fig. 4). In addition, after the two stimulated atrial FIGURE 1. A trial stimulation during supraventricular tachycardia in patient K.M. This figure and all subsequent intracardiac recordings are similarly organized. From top to bottom are ECG leads I, II, III, V1; high right atrial electrogram (HRA), His bundle electrogram (HBE), and timelines (T) generated at 10 and 100 msec. During supraventricular tachycardia (SVT), which has a stable cycle length of 340 msec, each QRS is associated with atrial echoes (Ae) reflecting retrograde depolarization of the atria. Note that the atrial electrogram of the A e in the HBE precedes that in the HRA. A trial premature beats (Ap) are introduced at a coupling interval of 22S msec after thefirst and third QRS complexes. In the Ap, the HRA precedes the atrial electrogram in the HBE and both occur earlier than they would during the tachycardia. Despite the fact that the atrium is depolarized prior to the time the Ae would normally occur. the tachycardia continues its cycle length unaffected by the stimulated atrial beats. S represents the stimulus artifact.
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FIGURE 2. A trial stimulation during supraventricular tachycardia in patient M.B. The panel is organized as in figure 1. Supraventricular tachycardia is present at a cycle length of 470 msec. After the third QRS an atrial premature beat (Ap) is introduced at a coupling interval of 400 msec. In the Ap, the HRA precedes the atrial depolarization in the His bundle electrogram (JIBE), a reversal of the sequence of the atrial echo (A e). Despite this, the tachycardia is unaffected. Also note the change in the atrial electrograms produced by Ap.
finilli
tiated in the absence of an atrial echo (Ae) (fig. 5). On other occasions, an atrial echo was seen following the stimulated atrial premature depolarization (A2) if the resulting A2H interval exceeded 200 msec. This was the only patient we observed in whom no atrial echo followed the atrial premature depolarizations initiating the tachycardia. In two of the eight patients, A-V nodal refractory curves were consistent with "dual pathways."5
premature depolarizations, there is a pause in atrial activity followed by what appears to be a sinus P wave (A.). A8 does not conduct because the A.H interval of 40 msec is too short (AH during sinus rhythm was 70 msec). Thus a period of A-V dissociation resulted without termirnating the tachycardia. That A8 arises in the area of the sinus is supported by: a) the sequence of atrial activation (high right atrium activated prior to low right atrium), and b) the normal appearance of the P wave seen in the surface ECG (heavy arrow, fig. 4). The pause and transient change in ventricular cycle length developed because the first Ap penetrated the A-V node and depolarized the ventricles while the second Ap did not penetrate the A-V node. The tachycardia continued even though no atrial echoes (Ae) were seen following the fifth and sixth QRS complexes. In patient W.P., supraventricular tachycardia was ini-
A
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Discussion The purpose of these studies was to determine whether the atria form part of the re-entrant circuit in patients with A-V nodal re-entrant tachycardia.1 3 In an attempt to answer this question, premature atrial depolarizations were introduced during the tachycardia prior to the time the atria would have been retrogradely activated during the tachycardia. Per-
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FIGURE 3. A trial stimulation during supraventricular tachycardia in patient E.H. Panels A and B are organized from top to bottom leads I, aVF, V1, high right atrial electrogram (HRA), coronary sinus electrogram (CS), His bundle electrogram (HBE) and timelines (T). Supraventricular tachycardia (SVT) is present at a cycle length of 370 msec in each panel. Note that during supraventricular tachycardia, the atrial electrograms in the JBE, HRA and CS follow the onset of the His deflection. In panel A, an atrial premature beat (Ap) is stimulated from a catheter in the distal coronary sinus 250 msec after the prior CS electrogram. This results in depolarization of both the high and low atrium, as well as that part of the left atrium recorded by the CS electrogram prior to the inscription of the His bundle, without altering the H-H interval or cycle length of the supraventricular tachycardia. Thus both atria were depolarized 70-120 msec prior to the time Ae would have occurred without altering the SVT. In panel B, an Ap from the high right atrium is introduced 240 msec after the prior high right atrial electrogram. The high and low right atrial and coronary sinus electrograms appear 130, 100, and 55 msec premature respectively without altering the SVT.
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FIGURE 4. A trial premature beats causing A- Vdissociation during supraventricular tachycardia in patient K.M. During SVT, two Ap's are introduced depolarizing both the high and low atrium prematurely without terminating the tachycardia. The next spontaneous atrial depolarization (As) has the appearance of a sinus beat both by its surface ECG appearance (heavy arrow) and the sequence of atrial activation. Clearly the HRA precedes the atrial electrogram in the HBE as it does in sinus beats. A period of A-V dissociation is present since As occurs almost simultaneously with the His deflection and could therefore not be responsible for it. Thus, no Ae is seen after the fifth and sixth QRS complexes, and in spite of transient A-V dissociation, the SVT continues.
sistence of the tachycardia without change of cycle length in the face of atrial capture was considered presumptive evidence that the recorded atrium did not form part of the re-entrant circuit. This technique of atrial "pre-excitation" has been previously utilized in an effort to determine the role of the atrium in the production of ventricular echoes.6' The role of the atrium in the initiation and maintenance of A-V nodal re-entrant tachycardia has not yet been evaluated in
arrhythmia. If any atrial tissue is necessary, it may be a very small rim immediately adjacent to the A-V node that was not recorded by our catheters. Resolution of this question must come from appropriate intra-atrial mapping and stimulation during open heart surgery in patients with A-V nodal re-entrant tachycardia.
man.
One could postulate that each premature atrial depolarization was conducted down the antegrade limb of the re-entrant circuit and fortuitously failed to alter the cycle length of the tachycardia due to an exact "compensatory" delay of conduction down that limb. However, premature atrial depolarizations could be delivered over a range of 20-50 msec without changing the tachycardia. Some irregularity of cycle length should have been noted during the scanning interval. Furthermore, in the presence of premature capture of the low right atrium by as much as 100 msec (fig. 3B), it seems very unlikely that the impulse would not have altered the cycle length of the tachycardia. Fortuitous atrial participation certainly could not explain the findings noted in figure 4 in which two successive premature depolarizations capture the atrium without interrupting the tachycardia. Although the first Ap could have and probably did capture the ventricle, the second could not possibly have penetrated the re-entrant circuit since it had just been depolarized by the first Ap and would have been refractory. The persistence of the tachycardia after two Ap's, despite the altered cycle length, the absence of echoes, and subsequent period of A-V dissociation, argues strongly against fortuitous atrial participation. In one patient, W.P., the tachycardia was initiated in the absence of an atrial echo following the premature beat (fig. 5). This phenomenon, not previously described, strongly implies that the atrium was not necessary to initiate the tachycardia. Superficial examination of the record might lead one to suggest that retrograde atrial depolarization did
The Route of A-V Nodal Re-entry
The physiologic basis of A-V nodal re-entry depends on the presence of longitudinal dissociation of the A-V node into two pathways: one with fast conduction and a long refractory period (beta pathway), and the other with slower conduction but shorter refractoriness (alpha pathway). Sustained tachycardias develop when atrial premature depolarizations are blocked in the beta pathway but conduct sufficiently slowly down the alpha pathway so that the impulse can retrogradely activate the previously refractory beta pathway returning through atrial tissue back to the alpha pathway to complete the circuit. This concept proposed by Moe and Mendez8 I included the atrium as a necessary link in the re-entrant circuit. The data obtained in this study suggest that most, if not all, of the atria are uninvolved in the re-entrant circuit. In each case, both the high and low right atrium could be depolarized without altering the tachycardia. In addition, the left atrium could be "captured" without influencing the tachycardia in three cases, suggesting that the demonstration of atrial "capture" without altering the tachycardia was unrelated to the direction of the wavefront of the premature atrial depolarization. Furthermore, A-V dissociation during the tachycardia was produced in one patient (fig. 4), and an atrial echo was not required to initiate the tachycardia in another (fig. 5). These findings suggest that none of the recorded atrial tissue was required to sustain the
Alternative Explanations
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occur but that the atrial electrogram was "buried" in the ventricular electrogram. This conclusion is unlikely for three reasons. First, during the tachycardia the atrial electrogram clearly appears before each QRS, and would therefore certainly be present in that position for the initiation. Second, if atrial depolarization did occur and was buried within the ventricular electrogram, one would have to assume simultaneous intra-atrial block preventing it from propagating to the high right atrium since there is no evidence of activity at that site. No intra-atrial block or latency was seen at similar coupling intervals during premature stimulation and these phenomena are less likely to occur in this situation since the introduction of A2 would shorten atrial refractoriness for the subsequent beat. Third, with a greater increase in the A2H interval, the atria had time to recover and an Ae was demonstrated at the onset of the tachycardia. Thus evidence for "hidden" atrial depolarization after A2 is lacking.
V
V
FIGURE 5. Initiation of supraventricular tachycardia without a critical atrial echo. The panels are organized as in figure 1, but in addition, the top panel has a ladder diagram underneath depicting the mechanism of the arrhythmia. In the ladder diagram and top panel, A, is eighth of a series ofpaced atrial beats at a cycle length of 700 msec. A, represents the premature beat. In the ladder diagram, A is atrium, A VN is A - V node, HPS is His-Purkinje, and V is ventricle. A, is introduced at a coupling interval of 300 msec and SVT is initiated. However, no atrial echo is seen during or after the stimulated beat, but is present in subsequent beats of the SVT. As depicted in the ladder diagram, re-entry occurs within the A - V node; the atrium is not depolarized initially because it is still refractory. The lack of an initial Ae strongly suggests that the Ae is not necessary to initiate SVT. In panel opposite, A2 is delivered at a coupling interval of 300 msec after the eighth paced beat at a cycle length of 600 msec. The resulting A2H of 220 msec is long enough to allow atrial refractoriness to recover and atrial echo to resume.
Therapeutic Implications
Clinical practice has established that drugs and maneuvers which prolong A-V nodal conduction can interrupt and prevent episodes of supraventricular tachycardia. Electrophysiologic studies have demonstrated that digitalis,10 propranolol,'1 Valsalva maneuver,'2 and carotid sinus pressure2' 13 prolong A-V nodal conduction and refractoriness, thereby altering the temporal relationships within the A-V node that must be established to initiate and sustain supraventricular tachycardia. Quinidine and procainamide, which are less useful in the treatment of supraventricular tachycardia, have minimal effects on A-V nodal conduction and tend to shorten A-V nodal refractoriness by their vagolytic properties.'4' '5 Similarly, because of its lack of effect on the A-V node, lidocaine is of little value in the management of supraventricular tachycardia. However, quinidine and procainamide are useful in preventing supraventricular tachycardia by suppressing the atrial or ventric-
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SUPRAVENTRICULAR TACHYCARDIA/Josephson, Kastor
ular premature beats that initiate the arrhythmia. It has been recently demonstrated that extra-nodal bypass tracts exist and can function as part of the retrograde limb of the re-entrant circuit, even in the absence of their utilization in an antegrade fashion.'6"'i Demonstration that the atrium is not required to sustain supraventricular tachycardia argues against the presence of functional bypass tracts during the tachycardia. From a pharmacologic standpoint, if such retrograde bypass tracts and atrial tissue formed part of the re-entrant pathway, drugs affecting atrial and bypass conduction and refractoriness, i.e., quinidine and procainamide, would be useful.", "I Occasionally, permanent atrial or ventricular pacing is employed to treat patients whose supraventricular tachycardia is refractory to drug therapy.2" 22 The success of pacemaker therapy in supraventricular tachycardia depends on the ability of the induced atrial or ventricular beat to penetrate the re-entrant circuit and interrupt the arrhythmia. Infrequently, the use of single atrial beats is ineffective; the atrium may be depolarized without terminating the arrhythmia. In such cases, lack of atrial requirement during supraventricular tachycardia may explain the lack of success. Evidence from Animal Experiments
Whether or not the atrium forms a requisite link in sustaining atrial echoes, supraventricular tachycardia, or ventricular echoes has not been resolved in the animal laboratory. The original mechanism of supraventricular tachycardia described by Moe and Mendez", I included the atrium and a longitudinally dissociated A-V node to form the re-entrant circuit. More recently, Wit et al.23 showed that in the isolated rabbit heart, a small but significant portion of the right atrium was required to sustain supraventricular tachycardia. However, Janse and co-workers,2' using a similar preparation with a plaque electrode over the A-V node, came to the opposite conclusion, i.e., that reentry was entirely subatrial, located entirely in the A-V node. Both these latter studies demonstrated that infranodal structures were unnecessary to sustain supraventricular tachycardia. Findings in studies attempting to evaluate the role of the atrium in the production of ventricular echoes have contributed to the controversy. Using the technique of "atrial pre-excitation," Mignone and Wallace25 found that ventricular echoes resulted from re-entry within the A-V node and did not require the atrium. Mendez and Moe' came to the opposite conclusion in the isolated rabbit heart. Thus, several carefully designed animal studies have failed to resolve the question of atrial requirement in these reentrant arrhythmias. Conclusion Our data strongly suggest that in certain patients with A-V nodal re-entrant supraventricular tachycardia, no part of the recorded atrium is required to sustain or initiate A-V nodal re-entrant tachycardia. The demonstration of lack of the atrial requirement could be shown in the absence of A-V nodal refractory curves demonstrating "sdual pathways."5 It therefore seems likely that, in these cases, the basic re-entrant circuit is limited to the A-V node and that the atrial and ventricular responses during supraventricular
435
tachycardia are "secondary" phenomena. The finding of lack of atrial requirement in a patient with paroxysmal supraventricular tachycardia suggests the absence of a functional extranodal bypass tract and directs pharmacologic therapy toward those drugs which have a major action on A-V nodal conduction and/or refractoriness. Since the atria can be captured without terminating the tachycardia, an explanation is now available for the occasional inability to terminate supraventricular tachycardia with induced atrial premature beats. References 1. Bigger JT, Goldreyer BN: The mechanism of supraventricular tachycardia. Circulation 42: 673, 1970 2. Goldreyer BN, Bigger JT Jr: Site of re-entry in paroxysmal supraventricular tachycardia. Circulation 43: 15, 1971 3. Goldreyer BN, Damato AN: The essential role of atrioventricular conduction delay in the initiation of paroxysmal supraventricular tachycardia. Circulation 43: 679, 1971 4. Scherlag BJ, Lau SH, Helfant RH, Berkowitz WD, Stein E, Damato AN: Catheter technique for recording His bundle activity in man. Circulation 39: 13, 1969 5. Denes P, Wu D, Dhingra R, Chuguimia R, Rosen KM: Demonstration of dual A-V nodal pathways in patients with paroxysmal supraventricular tachycardia. Circulation 48: 549, 1973 6. Schuilenburg RM, Durrer D: Further observations on the ventricular echo phenomenon elicited in the human heart. Circulation 45: 629, 1972 7. Narula OS: Ventricular echoes without atrial participation. (abstr) Am J Cardiol 35: 160, 1975 8. Moe GK, Mendez C: The physiologic basis of reciprocal rhythms. Prog Cardiovasc Dis 8: 461, 1966 9. Mendez C, Moe GK: Demonstration of a dual A-V nodal conduction system in the isolated rabbit heart. Circ Res 19: 378, 1966 10. Przybyla AC, Paulay KL, Stein E, Damato AN: Effects of digoxin on atrioventricular conduction patterns in man. Am J Cardiol 33: 344, 1974 11. Seides SF, Josephson ME, Batsford WP, Weisfogel GM, Lau SH, Damato AN: The electrophysiology of propranolol in man. Am Heart J 88: 733, 1974 12. Josephson ME, Seides SF, Batsford WP, Caracta AR, Damato AN, Kastor JA: The effects of carotid sinus pressure in re-entrant paroxysmal supraventricular tachycardia. Am Heart J 88: 694, 1974 13. Goldreyer BN: Mechanisms of supraventricular tachycardia. Ann Rev Med 26: 219, 1975 14. Josephson ME, Seides SF, Batsford WP, Weisfogel GM, Akhtar M, Caracta AR, Lau SH, Damato AN: The electrophysiological effects of intramuscular quinidine on the atrioventricular conduction system in man. Am Heart J 87: 55, 1974 15. Josephson ME, Caracta AR, Ricciutti MA, Lau SH, Damato AN: Electrophysiologic properties of procainamide in man. Am J Cardiol 33: 596, 1974 16. Spurrel RAK, Krickler DM, Sowton E: Concealed bypass of the atrioventricular node in patients with paroxysmal supraventricular tachycardia revealed by intracardiac electrical stimulation and verapamil. Am J Cardiol 33: 590, 1974 17. Coumel P, Barold SS: Mechanisms of supraventricular tachycardia. In Clinical His Bundle Electrocardiography and Clinical Electrophysiology, edited by Narula OS. Philadelphia, F. A. Davis, 1975, pp 205-241 18. Coumel P, Attuel P: Localization of the circus movement of reciprocating tachycardia in Wolff-Parkinson-White syndrome. In Clinical His Bundle Electrography and Clinical Electrophysiology, edited by Narula OS. Philadelphia, F. A. Davis, 1975, pp 343-366 19. Zipes DP, DeJoseph RL, Rothbaum DA: Unusual properties of accessory pathways. Circulation 49: 1200, 1974 20. Wellens HJJ, Durrer D: Effect of procainamide, quinidine, and ajmaline in the Wolff-Parkinson-White syndrome. Circulation 50: 114, 1974 21. Schnitzler RN, Goldreyer BN, Westura EE, Damato AN: Demand coronary vein pacemakers for drug-resistant supraventricular tachycardia. (abstr) Circulation 44: 97, 1971 22. Kitchen JG III, Goldreyer BN: Demand pacemaker for refractory supraventricular tachycardia. N Engl J Med 287: 596, 1972 23. Wit AL, Goldreyer BN, Damato AN: An in vitro model of paroxysmal supraventricular tachycardia. Circulation 43: 862, 1971 24. Janse MJ, van Capelle FJL, Freud GE, Durrer D: Circus movement within the A-V node as a basis for supraventricular tachycardia as shown by multiple microelectrode recordings in the isolated rabbit heart. Circ Res 28: 403, 1971 25. Mignone RJ, Wallace AG: Ventricular echoes. Evidence for dissociation of conduction and reentry within the A-V node. Circ Res 19: 638, 1966
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Paroxysmal supraventricular tachycardia: is the atrium a necessary link? M E Josephson and J A Kastor Circulation. 1976;54:430-435 doi: 10.1161/01.CIR.54.3.430 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1976 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539
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28. McCammon RW: A longitudinal study of electrocardiographic intervals in healthy children. Acta Paediatr Scand (Uppsala) (suppl) 126, 1961 29. Simonson E, Cady LD Jr, Woodbury M: The normal QT interval. Am Heart J 63: 747, 1962 30. Fraser GR, Froggatt P, James TN: Congenital deafness associated with electrocardiographic abnormalities, fainting attacks and sudden death. A recessive syndrome. Quart J Med (New Series) 33: 361, 1964 31. Fraser GR, Froggatt P, Murphy T: Genetical aspects of the cardioauditory syndrome of Jervell and Lange-Nielsen (congenital deafness and electrocardiographic abnormalities). Ann Hum Genet (London) 28: 133, 1964 32. Alimurung MM, Joseph LG, Craige E, Massell BF: The QT interval in normal infants and children. Circulation 1: 1329, 1950 33. Lepeschkin E, Surawicz B: The measurement of the Q-T interval of the electrocardiogram. Circulation 6: 378, 1953 34. Bazett HC: An analysis of the time-relations of electrocardiograms. Heart 7: 353, 1920 35. Friedman ME, Geidel S, Havens B, Hoppenbrouwers T, Hodgman JE: Near-miss for sudden infant death syndrome. Clin Res 23: 142A, 1975 36. Ferrer PL, Talner NS: Changes in the QT index with sleep in young mammals. Pediatr Res 8: 349/75, 1974 37. Schwartz PJ, Malliani A: Electrical alternation of the T-wave: Clinical and experimental evidence of its relationship with the sympathetic nervous system and with the long Q-T syndrome. Am Heart J 89: 45, 1975 38. Jervell A, Lange-Nielsen F: Congenital deaf-mutism, functional heart disease with prolongation of the Q-T interval, and sudden death. Am Heart J 54: 59, 1957 39. James TN: Congenital deafness and cardiac arrhythmias. Am J Cardiol 19: 627, 1967 40. Olley PM, Fowler RS: The surdo-cardiac syndrome and therapeutic observations. Br Heart J 32: 467, 1970 41. Garza LA, Vick RL, Nora JJ, McNamara DG: Heritable Q-T prolonga-
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tion without deafness. Circulation 41: 30, 1970 42. Ratshin RA, Hunt D, Russell RO Jr, Rackley CE: QT interval prolongation, paroxysmal ventricular arrhythmias, and convulsive syncope. Ann Intern Med 75: 919, 1971 43. Froggatt P, James TN: Sudden unexpected death in infants. Evidence of a lethal cardiac arrhythmia. Ulster Med J 42: 136, 1973 44. Schwartz PJ: Cardiac sympathetic innervation and the sudden infant death syndrome. A possible pathogenetic link. Am J Med 60: 167, 1976 45. Fraser GR, Froggatt P: Unexpected cot deaths. Lancet 2: 56, 1966 46. Mathews EC Jr, Blount AW Jr, Townsend JI: Q-T prolongation and ventricular arrhythmias, with and without deafness, in the same family. Am J Cardiol 29: 702, 1972 47. Hanazono N, Ando Y, Ohnishi M, Oda H, Yuhara N, Nishio T, Ishida H, Takeuchi A, Kohashi K: Heritable QT prolongation without deafness: The Romano-Ward syndrome. Jap Heart J 14: 479, 1973 48. Hugenholtz PG: Electrocardiographic abnormalities in cerebral disorders. Report of six cases and review of the literature. Am Heart J 63: 451, 1962 49. Burch GE, Meyers R, Abildskov JA: A new electrocardiographic pattern observed in cerebrovascular accidents. Circulation 9: 719, 1954 50. Yanowitz F, Preston JB, Abildskov JA: Functional distribution of right and left stellate innervation to the ventricles: Production of neurogenic electrocardiographic changes by unilateral alteration of sympathetic tone. Circ Res 18: 416, 1966 51. Moss AJ, McDonald J: Unilateral cervicothoracic sympathetic ganglionectomy for the treatment of long QT interval syndrome. N Engl J Med 285: 903, 1971 52. Schwartz PJ, Snebold NG, Brown AM: Effects of unilateral cardiac sympathetic denervation on the ventricular fibrillation threshold. Am J Cardiol 35: 169, 1975 53. Simonson E, Brozek J, Keys A: Variability of the electrocardiogram in normal young men. Am Heart J 38: 407, 1949
Paroxysmal Supraventricular Tachycardia Is
the Atrium
a
MARK E. JOSEPHSON, M.D.,
Necessary Link? AND
JOHN A. KASTOR, M.D.
SUMMARY Whether or not the atrium plays an essential role in initiating and/or sustaining atrioventricular (A-V) nodal re-entrant tachycardia was evaluated in eight patients. In all eight patients, the atrium could be rendered refractory to retrograde atriai echoes during the tachycardia without interrupting the arrhythmia. This was accomplished by introducing atrial premature depolarizations prior to the time the atrium would normally be retrogradely depolarized by
atrial echoes. In one patient, two atrial premature depolarizations could be introduced, producing A-V dissociation, without termatig the tachycardia. In another patient, the tachycardia could be initiated without an atrial echo. Our data suggest that most, if not all of the atrium is unnecessary for the initiation and maintenance of A-V nodal re-entrant supraventricular tachycardia.
MOST CASES of paroxysmal supraventricular tachycardia are initiated and sustained through re-entry within the atrioventricular (A-V) node.' Whether or not the atria form a portion of the re-entrant pathway remains unsettled. The present investigation of eight patients demonstrated that in each case no portion of the atrium recorded by our electrode catheters was required to sustain A-V nodal re-
entrant supraventricular tachycardia and in one the atrium did not play an essential role in initiating the arrhythmia.
From the Cardiac Clinical Electrophysiology Laboratory, Hospital of the University of Pennsylvania; the Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania. Presented at the 25th Annual Scientific Session of the American College of Cardiology, February 24, 1976, New Orleans, Louisiana. Supported in part by grants from the USPHS, NIH, HL 14807, and the American Heart Association, Southeastern Pennsylvania Affiliate. Address for reprints: Dr. Mark E. Josephson, Director, Electrophysiology Laboratories, 669 White Building, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, Pennsylvania 19104. Received March 5, 1975; revision accepted March 29, 1976.
Methods, Materials, and Clinical Patient Information Eight patients were studied in the nonsedated postabsorptive state after informed consent was obtained (table 1). All had symptomatic supraventricular tachycardia (SVT), and none demonstrated evidence of pre-excitation. No patient was taking antiarrhythmic drugs at the time of the study. A quadripolar electrode catheter was introduced percutaneously into an antecubital and/or femoral vein and positioned under fluoroscopic control against the lateral wall of the high right atrium and/or the coronary sinus. The proximal pair of electrodes was used to record a high right atrial or coronary sinus electrogram, while the distal pair was used for atrial stimulation. A bipolar electrode catheter
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SUPRAVENTRICULAR TACHYCARDIA/Josephson, Kastor was similarly introduced into another antecubital vein and positioned in the right ventricular apex for stimulation. A His bundle electrogram was obtained using a tripolar electrode catheter introduced percutaneously into the right femoral vein.4 The intracardiac electrograms were filtered at 40 and 500 Hz and were simultaneously displayed with at least three surface ECG leads and timelines generated at 10 and 100 msec on a multichannel oscilloscope (Electronics for Medicine DR-16). Rectangular impulses of I msec duration and at approximately twice diastolic threshold were delivered by a specially designed programmed digital stimulator (Murray Bloom, Narberth, Pa.). All data were stored on magnetic tape (Honeywell 14 channel recorder) and later retrieved on photographic paper at speeds of 150 to 200 mm/sec. In each patient, after initiation of A-V nodal re-entrant tachycardia, atrial premature depolarizations were introduced to activate the atria prior to the time they would have been retrogradely activated by atrial echoes during the tachycardia. In addition, refractory periods were determined by the extrastimulus method. Results All patients were in sinus rhythm at the beginning of the study and no abnormalities of conduction were present (table 1). In each patient, single atrial premature beats at coupling intervals ranging from 255-380 msec initiated the tachycardia. The echo zones1 2 were 10 to 120 msec in duration. The critical A-H interval required for the initiation of the tachycardia ranged between 140 and 400 msec.3 The tachycardia could also be started in each patient during Wenckebach cycles produced by rapid atrial pacing,3 and in two patients (E.H. and H.H.), by one or more ventricular premature beats. In all patients, atrial premature depolarizations could be introduced at intervals resulting in atrial depolarizations 10 to 130 msec prior to the time of spontaneous retrograde atrial activation without interrupting the tachycardia or altering its cycle length. In three patients, both right and left atrial (coronary sinus) sites were prematurely depolarized without influencing the tachycardia. Examples are shown in
TABLE 1. Clinical Data PR* QRS* AH*
HV*
A-H required to initiate SVT*
125 140
75 90
70 95
50 35
400 170
165 160 135 ASHD 155 None 148 ASHD 160
65 82 86 88 90 90
90 78 50 85 80 92
40 45 50 48 45 45
145 140 295 195 250 290
Pt/Age/Sex
Dx
K.M./27/F H.H./66/M
MVP ASHD IMI MVP ASHD MVP
M.B./17/F W.P./56/M E.H./37/F
M.U./55/M L.R./18/F C.N./72/F
*All values are given in msec. Abbreviations: ASHD = atherosclerotic heart disease; MVP = mitral valve prolapse; IMI = inferior myocardial infarction.
figures 1-3. Note in particular that the low right atrium is depolarized: a) 30 and 20 msec early in beats 2 and 4 of figure 1; b) 25 msec early in beat 3 of figure 2; c) 70 msec early in beat 3 of figure 3A and 100 msec early in beat 3 of figure 3B. Furthermore, the coronary sinus is depolarized 120 msec early in figure 3A and 55 msec early in figure 3B. The configuration of the high and low atrial electrograms were different in the atrial premature depolarizations (Ap) when compared to the atrial echoes (Ae). In addition, the atrial electrograms of the premature depolarizations introduced from the right or left atrium were recorded before the onset of the His bundle deflection in the patient illustrated in figure 3. Thus in each of these three cases, that part of the atria giving rise to the high right atrial electrogram, low right atrial electrogram (in the His bundle recording), and in one case the coronary sinus electrogram, could be prematurely depolarized without interrupting the tachycardia. Since the atrial refractory periods of our patients were 210-300 msec, the atria would have been refractory for at least 200 msec after Ap, during which time Ae would have appeared (10 to 130 msec after the atrium was prematurely
depolarized). In patient K.M., two premature atrial depolarizations (Ap) could be introduced which depolarized both the high and low right atrium without terminating the tachycardia (fig. 4). In addition, after the two stimulated atrial FIGURE 1. A trial stimulation during supraventricular tachycardia in patient K.M. This figure and all subsequent intracardiac recordings are similarly organized. From top to bottom are ECG leads I, II, III, V1; high right atrial electrogram (HRA), His bundle electrogram (HBE), and timelines (T) generated at 10 and 100 msec. During supraventricular tachycardia (SVT), which has a stable cycle length of 340 msec, each QRS is associated with atrial echoes (Ae) reflecting retrograde depolarization of the atria. Note that the atrial electrogram of the A e in the HBE precedes that in the HRA. A trial premature beats (Ap) are introduced at a coupling interval of 22S msec after thefirst and third QRS complexes. In the Ap, the HRA precedes the atrial electrogram in the HBE and both occur earlier than they would during the tachycardia. Despite the fact that the atrium is depolarized prior to the time the Ae would normally occur. the tachycardia continues its cycle length unaffected by the stimulated atrial beats. S represents the stimulus artifact.
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FIGURE 2. A trial stimulation during supraventricular tachycardia in patient M.B. The panel is organized as in figure 1. Supraventricular tachycardia is present at a cycle length of 470 msec. After the third QRS an atrial premature beat (Ap) is introduced at a coupling interval of 400 msec. In the Ap, the HRA precedes the atrial depolarization in the His bundle electrogram (JIBE), a reversal of the sequence of the atrial echo (A e). Despite this, the tachycardia is unaffected. Also note the change in the atrial electrograms produced by Ap.
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tiated in the absence of an atrial echo (Ae) (fig. 5). On other occasions, an atrial echo was seen following the stimulated atrial premature depolarization (A2) if the resulting A2H interval exceeded 200 msec. This was the only patient we observed in whom no atrial echo followed the atrial premature depolarizations initiating the tachycardia. In two of the eight patients, A-V nodal refractory curves were consistent with "dual pathways."5
premature depolarizations, there is a pause in atrial activity followed by what appears to be a sinus P wave (A.). A8 does not conduct because the A.H interval of 40 msec is too short (AH during sinus rhythm was 70 msec). Thus a period of A-V dissociation resulted without termirnating the tachycardia. That A8 arises in the area of the sinus is supported by: a) the sequence of atrial activation (high right atrium activated prior to low right atrium), and b) the normal appearance of the P wave seen in the surface ECG (heavy arrow, fig. 4). The pause and transient change in ventricular cycle length developed because the first Ap penetrated the A-V node and depolarized the ventricles while the second Ap did not penetrate the A-V node. The tachycardia continued even though no atrial echoes (Ae) were seen following the fifth and sixth QRS complexes. In patient W.P., supraventricular tachycardia was ini-
A
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Discussion The purpose of these studies was to determine whether the atria form part of the re-entrant circuit in patients with A-V nodal re-entrant tachycardia.1 3 In an attempt to answer this question, premature atrial depolarizations were introduced during the tachycardia prior to the time the atria would have been retrogradely activated during the tachycardia. Per-
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FIGURE 3. A trial stimulation during supraventricular tachycardia in patient E.H. Panels A and B are organized from top to bottom leads I, aVF, V1, high right atrial electrogram (HRA), coronary sinus electrogram (CS), His bundle electrogram (HBE) and timelines (T). Supraventricular tachycardia (SVT) is present at a cycle length of 370 msec in each panel. Note that during supraventricular tachycardia, the atrial electrograms in the JBE, HRA and CS follow the onset of the His deflection. In panel A, an atrial premature beat (Ap) is stimulated from a catheter in the distal coronary sinus 250 msec after the prior CS electrogram. This results in depolarization of both the high and low atrium, as well as that part of the left atrium recorded by the CS electrogram prior to the inscription of the His bundle, without altering the H-H interval or cycle length of the supraventricular tachycardia. Thus both atria were depolarized 70-120 msec prior to the time Ae would have occurred without altering the SVT. In panel B, an Ap from the high right atrium is introduced 240 msec after the prior high right atrial electrogram. The high and low right atrial and coronary sinus electrograms appear 130, 100, and 55 msec premature respectively without altering the SVT.
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FIGURE 4. A trial premature beats causing A- Vdissociation during supraventricular tachycardia in patient K.M. During SVT, two Ap's are introduced depolarizing both the high and low atrium prematurely without terminating the tachycardia. The next spontaneous atrial depolarization (As) has the appearance of a sinus beat both by its surface ECG appearance (heavy arrow) and the sequence of atrial activation. Clearly the HRA precedes the atrial electrogram in the HBE as it does in sinus beats. A period of A-V dissociation is present since As occurs almost simultaneously with the His deflection and could therefore not be responsible for it. Thus, no Ae is seen after the fifth and sixth QRS complexes, and in spite of transient A-V dissociation, the SVT continues.
sistence of the tachycardia without change of cycle length in the face of atrial capture was considered presumptive evidence that the recorded atrium did not form part of the re-entrant circuit. This technique of atrial "pre-excitation" has been previously utilized in an effort to determine the role of the atrium in the production of ventricular echoes.6' The role of the atrium in the initiation and maintenance of A-V nodal re-entrant tachycardia has not yet been evaluated in
arrhythmia. If any atrial tissue is necessary, it may be a very small rim immediately adjacent to the A-V node that was not recorded by our catheters. Resolution of this question must come from appropriate intra-atrial mapping and stimulation during open heart surgery in patients with A-V nodal re-entrant tachycardia.
man.
One could postulate that each premature atrial depolarization was conducted down the antegrade limb of the re-entrant circuit and fortuitously failed to alter the cycle length of the tachycardia due to an exact "compensatory" delay of conduction down that limb. However, premature atrial depolarizations could be delivered over a range of 20-50 msec without changing the tachycardia. Some irregularity of cycle length should have been noted during the scanning interval. Furthermore, in the presence of premature capture of the low right atrium by as much as 100 msec (fig. 3B), it seems very unlikely that the impulse would not have altered the cycle length of the tachycardia. Fortuitous atrial participation certainly could not explain the findings noted in figure 4 in which two successive premature depolarizations capture the atrium without interrupting the tachycardia. Although the first Ap could have and probably did capture the ventricle, the second could not possibly have penetrated the re-entrant circuit since it had just been depolarized by the first Ap and would have been refractory. The persistence of the tachycardia after two Ap's, despite the altered cycle length, the absence of echoes, and subsequent period of A-V dissociation, argues strongly against fortuitous atrial participation. In one patient, W.P., the tachycardia was initiated in the absence of an atrial echo following the premature beat (fig. 5). This phenomenon, not previously described, strongly implies that the atrium was not necessary to initiate the tachycardia. Superficial examination of the record might lead one to suggest that retrograde atrial depolarization did
The Route of A-V Nodal Re-entry
The physiologic basis of A-V nodal re-entry depends on the presence of longitudinal dissociation of the A-V node into two pathways: one with fast conduction and a long refractory period (beta pathway), and the other with slower conduction but shorter refractoriness (alpha pathway). Sustained tachycardias develop when atrial premature depolarizations are blocked in the beta pathway but conduct sufficiently slowly down the alpha pathway so that the impulse can retrogradely activate the previously refractory beta pathway returning through atrial tissue back to the alpha pathway to complete the circuit. This concept proposed by Moe and Mendez8 I included the atrium as a necessary link in the re-entrant circuit. The data obtained in this study suggest that most, if not all, of the atria are uninvolved in the re-entrant circuit. In each case, both the high and low right atrium could be depolarized without altering the tachycardia. In addition, the left atrium could be "captured" without influencing the tachycardia in three cases, suggesting that the demonstration of atrial "capture" without altering the tachycardia was unrelated to the direction of the wavefront of the premature atrial depolarization. Furthermore, A-V dissociation during the tachycardia was produced in one patient (fig. 4), and an atrial echo was not required to initiate the tachycardia in another (fig. 5). These findings suggest that none of the recorded atrial tissue was required to sustain the
Alternative Explanations
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occur but that the atrial electrogram was "buried" in the ventricular electrogram. This conclusion is unlikely for three reasons. First, during the tachycardia the atrial electrogram clearly appears before each QRS, and would therefore certainly be present in that position for the initiation. Second, if atrial depolarization did occur and was buried within the ventricular electrogram, one would have to assume simultaneous intra-atrial block preventing it from propagating to the high right atrium since there is no evidence of activity at that site. No intra-atrial block or latency was seen at similar coupling intervals during premature stimulation and these phenomena are less likely to occur in this situation since the introduction of A2 would shorten atrial refractoriness for the subsequent beat. Third, with a greater increase in the A2H interval, the atria had time to recover and an Ae was demonstrated at the onset of the tachycardia. Thus evidence for "hidden" atrial depolarization after A2 is lacking.
V
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FIGURE 5. Initiation of supraventricular tachycardia without a critical atrial echo. The panels are organized as in figure 1, but in addition, the top panel has a ladder diagram underneath depicting the mechanism of the arrhythmia. In the ladder diagram and top panel, A, is eighth of a series ofpaced atrial beats at a cycle length of 700 msec. A, represents the premature beat. In the ladder diagram, A is atrium, A VN is A - V node, HPS is His-Purkinje, and V is ventricle. A, is introduced at a coupling interval of 300 msec and SVT is initiated. However, no atrial echo is seen during or after the stimulated beat, but is present in subsequent beats of the SVT. As depicted in the ladder diagram, re-entry occurs within the A - V node; the atrium is not depolarized initially because it is still refractory. The lack of an initial Ae strongly suggests that the Ae is not necessary to initiate SVT. In panel opposite, A2 is delivered at a coupling interval of 300 msec after the eighth paced beat at a cycle length of 600 msec. The resulting A2H of 220 msec is long enough to allow atrial refractoriness to recover and atrial echo to resume.
Therapeutic Implications
Clinical practice has established that drugs and maneuvers which prolong A-V nodal conduction can interrupt and prevent episodes of supraventricular tachycardia. Electrophysiologic studies have demonstrated that digitalis,10 propranolol,'1 Valsalva maneuver,'2 and carotid sinus pressure2' 13 prolong A-V nodal conduction and refractoriness, thereby altering the temporal relationships within the A-V node that must be established to initiate and sustain supraventricular tachycardia. Quinidine and procainamide, which are less useful in the treatment of supraventricular tachycardia, have minimal effects on A-V nodal conduction and tend to shorten A-V nodal refractoriness by their vagolytic properties.'4' '5 Similarly, because of its lack of effect on the A-V node, lidocaine is of little value in the management of supraventricular tachycardia. However, quinidine and procainamide are useful in preventing supraventricular tachycardia by suppressing the atrial or ventric-
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SUPRAVENTRICULAR TACHYCARDIA/Josephson, Kastor
ular premature beats that initiate the arrhythmia. It has been recently demonstrated that extra-nodal bypass tracts exist and can function as part of the retrograde limb of the re-entrant circuit, even in the absence of their utilization in an antegrade fashion.'6"'i Demonstration that the atrium is not required to sustain supraventricular tachycardia argues against the presence of functional bypass tracts during the tachycardia. From a pharmacologic standpoint, if such retrograde bypass tracts and atrial tissue formed part of the re-entrant pathway, drugs affecting atrial and bypass conduction and refractoriness, i.e., quinidine and procainamide, would be useful.", "I Occasionally, permanent atrial or ventricular pacing is employed to treat patients whose supraventricular tachycardia is refractory to drug therapy.2" 22 The success of pacemaker therapy in supraventricular tachycardia depends on the ability of the induced atrial or ventricular beat to penetrate the re-entrant circuit and interrupt the arrhythmia. Infrequently, the use of single atrial beats is ineffective; the atrium may be depolarized without terminating the arrhythmia. In such cases, lack of atrial requirement during supraventricular tachycardia may explain the lack of success. Evidence from Animal Experiments
Whether or not the atrium forms a requisite link in sustaining atrial echoes, supraventricular tachycardia, or ventricular echoes has not been resolved in the animal laboratory. The original mechanism of supraventricular tachycardia described by Moe and Mendez", I included the atrium and a longitudinally dissociated A-V node to form the re-entrant circuit. More recently, Wit et al.23 showed that in the isolated rabbit heart, a small but significant portion of the right atrium was required to sustain supraventricular tachycardia. However, Janse and co-workers,2' using a similar preparation with a plaque electrode over the A-V node, came to the opposite conclusion, i.e., that reentry was entirely subatrial, located entirely in the A-V node. Both these latter studies demonstrated that infranodal structures were unnecessary to sustain supraventricular tachycardia. Findings in studies attempting to evaluate the role of the atrium in the production of ventricular echoes have contributed to the controversy. Using the technique of "atrial pre-excitation," Mignone and Wallace25 found that ventricular echoes resulted from re-entry within the A-V node and did not require the atrium. Mendez and Moe' came to the opposite conclusion in the isolated rabbit heart. Thus, several carefully designed animal studies have failed to resolve the question of atrial requirement in these reentrant arrhythmias. Conclusion Our data strongly suggest that in certain patients with A-V nodal re-entrant supraventricular tachycardia, no part of the recorded atrium is required to sustain or initiate A-V nodal re-entrant tachycardia. The demonstration of lack of the atrial requirement could be shown in the absence of A-V nodal refractory curves demonstrating "sdual pathways."5 It therefore seems likely that, in these cases, the basic re-entrant circuit is limited to the A-V node and that the atrial and ventricular responses during supraventricular
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tachycardia are "secondary" phenomena. The finding of lack of atrial requirement in a patient with paroxysmal supraventricular tachycardia suggests the absence of a functional extranodal bypass tract and directs pharmacologic therapy toward those drugs which have a major action on A-V nodal conduction and/or refractoriness. Since the atria can be captured without terminating the tachycardia, an explanation is now available for the occasional inability to terminate supraventricular tachycardia with induced atrial premature beats. References 1. Bigger JT, Goldreyer BN: The mechanism of supraventricular tachycardia. Circulation 42: 673, 1970 2. Goldreyer BN, Bigger JT Jr: Site of re-entry in paroxysmal supraventricular tachycardia. Circulation 43: 15, 1971 3. Goldreyer BN, Damato AN: The essential role of atrioventricular conduction delay in the initiation of paroxysmal supraventricular tachycardia. Circulation 43: 679, 1971 4. Scherlag BJ, Lau SH, Helfant RH, Berkowitz WD, Stein E, Damato AN: Catheter technique for recording His bundle activity in man. Circulation 39: 13, 1969 5. Denes P, Wu D, Dhingra R, Chuguimia R, Rosen KM: Demonstration of dual A-V nodal pathways in patients with paroxysmal supraventricular tachycardia. Circulation 48: 549, 1973 6. Schuilenburg RM, Durrer D: Further observations on the ventricular echo phenomenon elicited in the human heart. Circulation 45: 629, 1972 7. Narula OS: Ventricular echoes without atrial participation. (abstr) Am J Cardiol 35: 160, 1975 8. Moe GK, Mendez C: The physiologic basis of reciprocal rhythms. Prog Cardiovasc Dis 8: 461, 1966 9. Mendez C, Moe GK: Demonstration of a dual A-V nodal conduction system in the isolated rabbit heart. Circ Res 19: 378, 1966 10. Przybyla AC, Paulay KL, Stein E, Damato AN: Effects of digoxin on atrioventricular conduction patterns in man. Am J Cardiol 33: 344, 1974 11. Seides SF, Josephson ME, Batsford WP, Weisfogel GM, Lau SH, Damato AN: The electrophysiology of propranolol in man. Am Heart J 88: 733, 1974 12. Josephson ME, Seides SF, Batsford WP, Caracta AR, Damato AN, Kastor JA: The effects of carotid sinus pressure in re-entrant paroxysmal supraventricular tachycardia. Am Heart J 88: 694, 1974 13. Goldreyer BN: Mechanisms of supraventricular tachycardia. Ann Rev Med 26: 219, 1975 14. Josephson ME, Seides SF, Batsford WP, Weisfogel GM, Akhtar M, Caracta AR, Lau SH, Damato AN: The electrophysiological effects of intramuscular quinidine on the atrioventricular conduction system in man. Am Heart J 87: 55, 1974 15. Josephson ME, Caracta AR, Ricciutti MA, Lau SH, Damato AN: Electrophysiologic properties of procainamide in man. Am J Cardiol 33: 596, 1974 16. Spurrel RAK, Krickler DM, Sowton E: Concealed bypass of the atrioventricular node in patients with paroxysmal supraventricular tachycardia revealed by intracardiac electrical stimulation and verapamil. Am J Cardiol 33: 590, 1974 17. Coumel P, Barold SS: Mechanisms of supraventricular tachycardia. In Clinical His Bundle Electrocardiography and Clinical Electrophysiology, edited by Narula OS. Philadelphia, F. A. Davis, 1975, pp 205-241 18. Coumel P, Attuel P: Localization of the circus movement of reciprocating tachycardia in Wolff-Parkinson-White syndrome. In Clinical His Bundle Electrography and Clinical Electrophysiology, edited by Narula OS. Philadelphia, F. A. Davis, 1975, pp 343-366 19. Zipes DP, DeJoseph RL, Rothbaum DA: Unusual properties of accessory pathways. Circulation 49: 1200, 1974 20. Wellens HJJ, Durrer D: Effect of procainamide, quinidine, and ajmaline in the Wolff-Parkinson-White syndrome. Circulation 50: 114, 1974 21. Schnitzler RN, Goldreyer BN, Westura EE, Damato AN: Demand coronary vein pacemakers for drug-resistant supraventricular tachycardia. (abstr) Circulation 44: 97, 1971 22. Kitchen JG III, Goldreyer BN: Demand pacemaker for refractory supraventricular tachycardia. N Engl J Med 287: 596, 1972 23. Wit AL, Goldreyer BN, Damato AN: An in vitro model of paroxysmal supraventricular tachycardia. Circulation 43: 862, 1971 24. Janse MJ, van Capelle FJL, Freud GE, Durrer D: Circus movement within the A-V node as a basis for supraventricular tachycardia as shown by multiple microelectrode recordings in the isolated rabbit heart. Circ Res 28: 403, 1971 25. Mignone RJ, Wallace AG: Ventricular echoes. Evidence for dissociation of conduction and reentry within the A-V node. Circ Res 19: 638, 1966
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Paroxysmal supraventricular tachycardia: is the atrium a necessary link? M E Josephson and J A Kastor Circulation. 1976;54:430-435 doi: 10.1161/01.CIR.54.3.430 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1976 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539
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