Cycle length in atrioventricular nodal reentrant paroxysmal tachycardia with observations on the lown-ganong-levine syndrome

Cycle Length in Atrioventricular Nodal Reentrant Paroxysmal Tachycardia With Observations on the Lown-Ganong-Levine Syndrome

ROBERT A. BAUERNFEIND, MD, FACC BRONTE F. AYRES, MD CHRISTOPHER C. WYNDHAM, MD, FACC RAMESH C. DHINGRA, MD, FACC STEVEN P. SWIRYN, MD, FACC BORIS STRASBERG, MD KENNETH M. ROSEN, MD, FACC Chicago,

Illinois

From the Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine, University of Illinois College of Medicine, Chicago, Illinois. This study was supported in part by Institutional Training Grant HL 07387 and Research Grants HL 18794 and HL 23566irom ths National Heart, Lung, and Blood Institute, Bethesda, Maryland. Manuscript received November 5, 1979; revised manuscript received January 8, 1980, accepted January 9,198O. Address for reprints: Robert A. Bauernfeind, MD, Assistant Professor of Medicine, Cardiology Section, University of Illinois, P.O. Box 6998, Chicago, Illinois 60680.

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Sixty-five patients with dual pathway atrioventricuiar (A-V) nodal reentrant paroxysmal tachycardia were studied. Gf these 65 patients, 11 (17 percent) had a short P-R interval (0.12 second or less) and 3 (5 percent) had a short A-H interval (53 ms or less) during sinus rhythm, suggesting the Lown-Ganong-Levine syndrome. Frequency distribution analyses of P-R and A-H intervals in the 65 patients demonstrated continuous unimodai functions, suggesting a continuum of A-V nodal properties. Regression analyses of P-R and A-H (fast pathway) intervals versus cycle length of paroxysmal tachycardia revealed an r value of 0.11 and 0.10, respectively (not stgnifkant). The cycle iength of paroxysmal tachycardia did not differ between the 11 patients with a short P-R interval (370 f 20 ms) and the 54 patients without a short P-R interval (382 f 11 ms). Regression analysis of the slow pathway A-H interval versus cycle length of paroxysmal tachycardia revealed an r value of 0.68 (p
Atrioventricular (A-V) nodal reentrance is the most common mechanism of paroxysmal supraventricular tachycardia in human beings.1-3 In patients with A-V nodal reentrant paroxysmal tachycardia, atria1 extrastimulus testing usually demonstrates discontinuous Al-As, Hi-Hz conduction curves, suggesting the presence of dual pathways (fast and s~ow).~~~~~ Some patients with discontinuous curves and recurrent paroxysmal tachycardia have a short P-R interval during sinus rhythm,6s suggesting the possibility of partial or complete bypass of the A-V node by way of atrionodal or atriofascicular tracts.s-ll These patients may be designated as having the Lown-Ganong-Levine syndrome.12 Benditt et a1.8 compared the cycle length of A-V nodal reentrant paroxysmal tachycardia in 4 patients with a short P-R interval and in 11patients with a normal P-R interval, and noted that the patients with a short P-R interval had a faster rate of tachycardia. These observations suggested that patients with a short P-R interval might constitute a distinct subgroup of patients with A-V nodal reentrance. In this study, we examined a large series of patients with dual pathway A-V nodal reentrant paroxysmal tachycardia. We address several questions: (1) In a large group of patients with A-V nodal reentrant paroxysmal tachycardia, are P-R (and A-H) intervals during sinus rhythm unimodally or bimodally distributed? (2) Is the cycle length of

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A-V nodal reentrant p.aroxysmal tachycardia a function of the P-R (or A-H) interval during sinus rhythm? (3) Is, the cycle length of A-V nodal reentrant paroxysmal tachycardia a function of slow pathway conduction time? (4) Is there a relation between fast and slow pathway conduction t.imes in patients with A-V nodal reentrant paroxysmal tachycardia? Our results are germane to use of the eponym “Lown-Ganong-Levine syndrome.”

Methods Patient selection: The criteria for inclusion in the present study were (1) a histor,y of electrocardiographically documented recurrent parox:ysmal supraventricular tachycardia; (2:) availability of multiple electrocardiograms during normal sinus rhythm; (3) abse:nce of delta waves and wide QRS complexes in all available electrocardiograms; and (4) demonstration of dual pathway A-V nodal reentrance as the mechanism of the recurrent tachycardia (see later). Sixty-five patients studied between September 1972 and May 1979 fulfilled these criteria. The group consisted of 33 men and 32 women, between the ages of 20 and 81 years (mean f standard deviation 53, f 16). Thirty (46 percent) of these patients had clinically diagnosed organic heart disease, whereas 35 (54 percent) did not. Electrophysiologic studies: These studies were performed with patients in the postabsorptive, nonsedated state, after cardioactive drugs had been discontinued for at least 48 hours. Informed written consent was obtained from all patients. A quadripolar electrode catheter was percutaneously passed into a femoral vein and advanced across the tricuspid valve for a Hlis bundle recording.13 A second quadripolar catheter was advanced from an antecubital vein into the coronary sinus for recording left atria1 activation during induced tachycardia. A hexapolar catheter was advanced to the right ventricular apex from an antecubital vein. The distal two electrodes were utilized for ventricular pacing, the middle two electrodes for recording right atria1 electrograms, and the proximal two electrodes for right atria1 pacing. Surface electrocardiographic leads I, II, III and Vi as well as intracardiac electrograms were recorded simultaneously on a multichannel oscilloscopic recorder (Electronics for Medicine DR-16) at paper speeds of 100 and 200 mm/s. Pacing stimuli were provided by a prognammable digital stimulator (manufactured by M. Bloom, Narberth, Pennsylvania) with a strength of approximately twice diastolic threshold and a duration of 2 ms. Electrophysiologic

studies included at least the following:

(1) recording of conduction intervals (during regular sinus rhythm) at a paper speed of 200 mm/s; (2) incremental atria1 pacing; (3) atria1 extrastimulus testing during sinus rhythm, and at one or more shorter (paced) atria1 cycle lengths; and (4) mapping of the ret.rograde atria1 activation sequence during induced paroxysmal supraventricular tachycardia from multiple sites including at least low septal right atrium, coronary sinus (proximal, lmiddle and distal) and lateral right atrium. In addition, the following were usually, but not invariably, performed: (5) incremental ventricular pacing; (6) ventricular extrastimulus testing at a ventricular paced cycle length; and (7) atria1 and ventricular extrastimulus testing during induced tachycardia. Definitions: The P-R interval was measured from a standard electrocardiogram (paper speed 25 mm/s) taken during regular sinus rhythm after cardioactive drugs had been discontinued for at least 48 hours. This interval was defined as the longest P-R interval in leads I, II and III, measured to the nearest 0.02 second. The value for the A-H interval (fast

ET AL.

pathway) was the mean of 10 consecutive A-H intervals during sinus rhythm, recorded at a paper speed of 200 mm/s and measured to the nearest 5 ms.‘4 Anterograde

dual A-V nodal pathways

were diagnosed

when discontinuous AI-AZ, Hi-Hz conduction curves were demonstrated by atria1 extrastimulus testing at one or more atrial cycle lengths.4J5-1s The slow pathway A-H interval was arbitrarily defined for purposes of analysis as the Az-Hz interval just to the left of the discontinuity in Al-As, Hi-Hz conduction curves (fast pathway effective refractory period). When discontinuous curves were observed at more than one basic cycle length, this measurement was made at the cycle length closest to 600 ms. All patients included in this study met each of the following criteria for diagnosis of dual pathway A-V nodal reentrant paroxysmal tachycardia2: (1) induction of tachy-

cardia related to achievement of a critical A-H delay with both incremental atria1 pacing and atria1 extrastimulus testing’s; (2) demonstration of anterograde dual A-V nodal pathways with induction of tachycardia relating to anterograde block in the fast pathway49 ls-18; (3) atrial activation occurring before or simultaneously with the onset of ventricular activation during tachycardiazO; and (4) normal retrograde atria1 activation sequences during tachycardia.21 The cycle length of paroxysmal supraventricular tachycardia was defined as the stable cycle length of induced A-V nodal reentrant tachycardia measured to the nearest 5 ms. Statistical analyses: Frequency distribution histograms of P-R and A-H intervals were constructed and analyzed. Regression analyses and t tests for unpaired data were performed by computer, utilizing standard statistical methods.

Results P-R and A-H intervals: The P-R intervals of the 65 patients studied ranged from 0.10 to 0.24 second (mean f standard deviation 0.158 f 0.032). Eleven (17 percent) of the 65 patients had a short P-R interval measuring 0.12 second or less. l2 A-H intervals during sinus rhythm (fast pathway A-H intervals) ranged from 50 to 197 ms (87 f 29). Three (5 percent) of the 65 patients had a short A-H interval measuring 53 ms or less.14 Slow pathway A-H intervals (see Methods) for the 65 patients ranged from 170 to 710 ms (299 f 111). The cycle lengths of induced A-V nodal reentrant paroxysmal tachycardia ranged from 260 to 630 ms (380 f 79). The frequency distribution of P-R intervals was a continuous, unimodal function with a rightward skew (Fig. 1). Similarly, the frequency distribution of A-H intervals during sinus rhythm (fast pathway A-H intervals) was a continuous, unimodal function with a rightward skew (Fig. 2). As expected, regression analysis of the P-R interval versus the A-H interval yielded an r value of 0.76, which was statistically highly significant (p
tachycardia yielded an r value of 0.11, which was not statistically significant (Fig. 3A). Similarly, regression analysis of the A-H interval versus the cycle length of tachycardia yielded an r value of 0.10, which was not statistically significant (Fig. 3B). Cycle length of tachycardia: The cycle length of A-V nodal reentrant paroxysmal tachycardia in the 11

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RGURE 1. Frequency distributionhistogram of P-R intervals (in seconds) during sinus rhythm in 65 patients. P-R intervals are on the horizontal axis and the number of patients with each P-R interval is on the vertical axis. The frequency distribution of P-R intervals was a continuous unimodal function with a rightward skew.

FIGURE 2. Frequency distribution histogram of (fast pathway) A-H intervals (in milliseconds) during sinus rhythm in 65 patients. Classes of A-H intervals are on the horlrontal axis, and the number of patients in each class of A-H intervals is on the vertical axls. The frequency distribution of A-H intervals was a continuous unimodal function with a rightward skew.

patients with a short P-R interval ranged from 330 to 545 ms (mean f standard error of the mean 370 f 20). In the 54 patients with a normal or long P-R interval this cycle length ranged from 260 to 630 ms (mean 382 f 11) (not significant). In the three patients with a short A-H interval it ranged from 290 to 330 ms (mean 310 f 12); and in the 62 patients with a normal or long A-H interval it ranged from 260 to 630 ms (mean 383 f 10) (NS = not significant).

terval, wide QRS complex with delta waves and recurrent paroxysmal supraventricular arrhythmia) and the Lown-Ganong-Levine syndrome (short P-R interval, narrow QRS complex and recurrent paroxysmal supraventricular arrhythmia).12J2 The diagnosis of Wolff-Parkinson-White syndrome has specific pathophysiologic and clinical significance. The short P-R interval and delta wave reflect conduction over an anomalous A-V pathway. 23 Paroxysmal supraventricular tachycardia in these patients usually reflects the occurrence_of A-V reentrance, utilizing the A-V node and His bundle for anterograde conduction and the anomalous pathway for retrograde conduction.2ep2s Furthermore, the occurrence of paroxysmal atria1 fibrillation in these patients may result in very rapid ventricular rates, if anomalous pathway refractoriness is short.24

Regression analysiyof the slow pathway A-H interval versus the cycle length of A-V nodal reentrant

paroxysmal tachycardia yielded an r value of 0.68, which was statistically highly significant (p
In contrast, what is the significance of a diagnosis of Lown-Ganong-Levine syndrome? It has been sug-

Wolff-Parkinson-White versus Lown-GanongLevine syndrome: There is some similarity between the Wolff-Parkinson-White syndrome (short P-R in-

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FIGURE 3. A, relation between the P-R interval during sinus rhythm (horizontal axis)1 and the cycle length of A-V nodal reentrant paroxysmal tachycardia (PSVT CL) (vertical axis). Regression analysis yielded an r value of 0.11, which is not statistically significant. B, rela-

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CYCLE LENGTH IN PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA-BAUERNFEIND

physiologic studies, demonstrating abbreviated A-H intervals in patients with the Lown-Ganong-Levine syndrome, have supported this hypothesis.26-2gThe anatomic substrate of the A-V nodal bypass could be atpionodal or atriofascicular tracts, described morphologically by James9 and Brechenmacher and his colleagues.10,11These bypass tracts might serve as anterograde or retrograde limbs of a reentrant pathway.23 Alternatively, a short P-R (or A-H) interval in a patient with paroxysmal supraventricular arrhythmia could reflect one end of a continuous spectrum of A-V nodal properties.

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Slow Pathway A-H (ms) FIGURE 4. Relation between the slow pathway A-H interval (horizontal axis) and the cycle length of A-V nodal reentrant paroxysmal tachycardia (PSVT CL) (vertical axls). Regression analysis yielded an r value of 0.68, which is statistically highly significant (p
atrial paced cycle lengths7T17p3t; (3) increase in refractoriness after administration of propranolol or ouabain4p5p7; and (4) decrease in refractoriness after administration of atropine.31132 Benditt et a1.s reported that A-V nodal reentrant paroxysmal tachycardia is faster in patients with a short P-R interval than in patients with a normal P-R interval. This observation was surprising in that the reentrant pathway in this variety of tachycardia is believed to consist primarily of the anterograde slow A-V nodal

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The’continuum of fast pathway conduction times, suggested by this study, is most consistent with either of two hypotheses: All fast pathways (including those

with conduction times inconsistent with the LownGanong-Levine syndrome) reflect conduction over A-V nodal bypass tracts, or intranodal conduction.3e This study does not allow discrimination between these alternative hypotheses. YHowever, several previous reports have demonstrated that the anterograde fast pathway has A-V nodal properties. These include: (1) prolongation of conduction time with increasing rates of atrial pacing7; (2) increase in refractoriness with decreasing

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Paroxysmal supraventricular tachycardia is the most common tachycardia seen in the Lown-GanongLevine syndrome.12 Denes et a1.6demonstrated dis-

continuous conduction curves and A-V nodal reentrant paroxys-al tachycardia in a patient with LownGanong-Levine syndr’ome. More recently, Josephson and Kastor7 studied six patients with a short P-R interval and paroxysmalsupraventriculartachycardiaand found A-V nodal reentrance to be the mechanism of tachycardia in all patients. Benditt et al.8subsequently reported that 4 patients with a short P-R interval and A-V nodal reentrance had a faster rate of tachycardia than 11 patients with a normal P-R interval and A-V nadal reentrance. This suggested that patients with a short P-R interval and A-V nodal reentrantparoxysmal tachycardia might constitute a special group, giving significance to the eponym “Lown-Ganong-Levine syndrome.” Continuum of fast-pathway conduction times in A-V nodal reentrant tachycardia: To determine whether patients with short P-R intervaland A-V nodal reentrant paroxysmal tachycardia constitute a group with a unique pathophysiology, we examined a large series of patients with this mechanism of paroxysmal tachycardia. If frequency distribution analyses of P-R (and A-H) intervals h.ad demonstrated discontinuous or bimodal functions, it would have suggested the presence of two groups of patients with A-V nodal reentrance, that is, one with short P-R (and A-H) intervals possibly reflecting A-V nodal bypass, and another with longer P-R (and A-H) intervals reflecting normal intranodal conduction. However, the continuous unimodal distributions demonstrated in this study suggest that there is a continuum of fast pathway conduction times and imply that there is only one group of ;;atktts with A-V noldalreentrant paroxysmal tachy-

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FlGURE 5. Relation between the (fast pathway) A-H interval during sinus rhythm (horizontal axis) and the (slow pathway) A-H interval (vertical axis). Regression analysis yielded an r value of 0.21, which is not statistically significant (N.S.).

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pathway and the retrograde fast A-V nodal pathway.2,41sJ73s3 Th e cycle length of tachycardia is therefore the sum of conduction times in these two limbs. Because A-V nodal reentrant paroxysmal tachycardia is characterized by a relatively long A-H interval and a relatively short H-A interval,34 we would hypothesize that the cycle length of A-V nodal reentrant paroxysmal tachycardia should reflect primarily the slow and not the fast pathway A-H interval. However, the fast pathway A-H interval could correlate with the cycle length of tachycardia, if the former correlated with the slow pathway A-H interval. These hypotheses were tested in this study. Regression analysis showed no significant correlation between the P-R (or A-H) interval during sinus rhythm and the cycle length of A-V nodal reentrant paroxysmal tachycardia. When the results were looked at in a different way, patients with a short P-R interval (LownGanong-Levine syndrome) did not have a faster tachycardia rate than patients with a normal or long P-R interval. Similarly, a small subgroup of patients (three) with a short A-H interval did not have a significantly faster rate of tachycardia than patients with a normal or long A-H interval. In contrast to the lack of correlation between P-R (or A-H) interval and tachycardia cycle length, regression analysis demonstrated a strong correlation between slow pathway A-H interval and cycle length of A-V nodal reentrant paroxysmal tachycardia. Additional regression analyses suggested that the P-R (and A-H) interval during sinus rhythm did not correlate with the cycle length of tachycardia because they did not correlate with the slow pathway A-H interval. Clinical implications: Our study is relevant to the “Lown-Ganong-Levine syndrome.” Lown et a1.i2 found that patients with a short P-R interval (and a normal QRS complex) had a greater incidence of paroxysmal supraventricular arrhythmia than patients with a normal P-R interval.12 The most common mechanism of paroxysmal supraventricular tachycardia in patients with a short P-R interval, as in the general population, is A-V nodal reentrance.7*8 Our study suggests that patients with A-V nodal reentrance have a continuum of P-R (and A-H) intervals during sinus rhythm, implying that a diagnosis of Lown-Ganong-Levine syndrome in these patients may be arbitrary and arti-

ET AL

ficial. Furthermore, the cycle length of A-V nodal reentrant paroxysmal tachycardia does not correlate with the P-R interval during sinus rhythm. However, a short P-R interval may have some significance in patients with a paroxysmal supraventricular arrhythmia other than A-V nodal reentrance. Benditt et a1.8 reported that atrioventricular reentrant tachycardia, utilizing a concealed anomalous pathway for retrograde conduction, was faster in patients with a short P-R interval than in patients with a normal P-R interval. This finding is expected because most patients with this type of reentrance do not have discontinuous A-V nodal conduction curves.2,3 Therefore, in these patients, the P-R interval during sinus rhythm reflects conduction time over the same pathway (A-V node) that is the anterograde limb of the reentrant pathway during paroxysmal tachycardia. Benditt et a1.8 also reported that ventricular rates during atria1 fibrillation were faster in patients with a short than in patients with a normal P-R interval. This finding could also be expected because A-V nodal refractoriness tends to be a function of A-V nodal conduction time.35 In both of these situations (atrioventricular reentrance in patients with concealed anomalous pathways, and atria1 fibrillation), one would expect the correlation between the P-R interval and the heart rate during tachycardia to hold over the entire spectrum of P-R intervals. Therefore, even in these situations, the short P-R interval probably does not designate the presence of a distinct subgroup of patients, but rather one end of a continuous spectrum of A-V nodal conduction times. One final question is of interest: Do patients with a short P-R interval (and narrow QRS complex) have an increased incidence of paroxysmal supraventricular arrhythmia? Our study, limited to patients with A-V nodal reentrant paroxysmal tachycardia, does not allow us to address this question directly. However, the 17 percent incidence rate of a short P-R interval found in the present series of patients is probably higher than that expected in the general population.36 This might imply that patients with a short P-R interval have a larger incidence of A-V nodal reentrant paroxysmal tachycardia than patients with a normal P-R interval. If this is true, the pathophysiologic mechanism for this association is not clear.

References 1. Goidreyer BN, Bigger JT. Site of reentry in paroxysmal supraventricular tachycardia in man. Circulation 1971;43: 15-26. 2. Wu D, Denes P, Amat-y-Leon F, Dhingra R, et al. Clinical, electrocardiographic and eiectrophysiologic observations in patients wfth paroxysmal supraventricuiar tachycardia. Am J Cardiol 1978; 41:1045-51. 3. Farshidi A, Josephson ME, Horowitz LN. Electrophysiologic characteristcs of concealed bypass tracts: clinical and electrocardicgraphic correlates. Am J Cardiol 1978;41:1052-60. 4. Wu D, Denes P. Dhingra R, Khan A, Rosen KM. The effects of propranoioi on induction of A-V, nodal reentrant paroxysmal tachycardia. Circulation 1974;50:665-77. 5. Wu D, Wyndham CR, Amat-y-Leon F, Denes P, Dhingra RC,

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Rosen KM. The effects of ouabain on induction of atrioventricular nodal reentrant paroxysmal supraventricular tachycardia. Circuiation 1975;52:201-7. 6. Denes P, Wu D, Rosen KM. Demonstration of dual A-V pathways in a patient with Lown-Ganong-Levine syndrome. Chest 1974; 65~343-6. 7. Josephson ME, Kaetor JA. Supraventricuiar tachycardia in Lown-GanongLevine syndrome: atrioncdai versus intranodal reentry. Am J Cardioi 1977;40:521-7. 8. Benditl DG, PrHcheK ELC, Smith WM, Wallace AG, Gallagher JJ. Characteristics of atrioventricular conduction and the spectrum of arrhythmias in Lown-Ganonglevine syndrome. Circulation 1978;57:454-65.

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9. James TN. Morphology of the human atrioventricular node, with remarks pertinent to its electrophysiology. Am Heart J 1961; 62:756-71. 10. Brechenmacher C. Atrio-His bundle tracts. Br Heart J 1975;37: 653-5. 11. Anderson RH, Becker AB, Brechenmacher C, Davies MJ, Ross1 L. Ventricular preexcitai:ion. A proposed nomenclature for its substrates. Eur J Cardiol 1975;3:27-36. 12. Lown 8, Ganong WF, Levine SA. The syndrome of short P-R interval, normal QRS complex and paroxysmal rapid heart action. Circulation 1952;5:693-706. 13. Bcherlag BJ, Lau BN, Helfant RH, Berkowttz WD, Stein E, Damato AN. Catheter technique for recording His bundle activity in man. Circulation 1969;39:13-8. 14. Dhlngra RC, Rosen KM, Rahlmtoola SH. Normal conduction intervals and responses in sixty-one patients using His bundle recording and atrial pacing. Chest 1973;64:55-9. 15. Rosen KM, Mehta A, Miller RA. Demonstration of dual atrioventricular nodal pathways in man. Am J Cardiol 1974;33:291-4. 16. Denes P, Wu D, Dhlngra RC, Chuqulmla R, Rosen KM. Demonstration of dual A-V nodal pathways in patients with paroxysmal supraventricular tachycardia. Circulation 1973;46:549-55. 17. Denes P, Wu D, Dhingra R, Arnat-y-Leon F,.Wyndham CR, Rosen KM. Dual atrioventricular nodal pathways. A common electrophysiological response. l3r Heart J 1975;37:1069-76. 18. Bauernfelnd RA, Wu D, Denes P, Rosen KM. Retrograde block during dual pathway atrioventricular nodal reentrant paroxysmal tachycardia. Am J Cardiol 1978;42:499-505, 19. Goldreyer BN, Damato AN. The essential role of atrioventricular conduction delay in the ilnitiation of paroxysmal supraventricular tachycardia. Circulation 1971;43:679-87. 20. Wellens HJJ, Durrer D. The role of an accessory atrioventricular pathway in reciprocal tachycardia. Observations in patients with and without the Wolff-Parkinson-White syndrome. Circulation 1975; 52:58-72. 21. Amat-y-Leon F, Dhingra RC, Wu D, ,Denes P, Wyndham CR, Rosen KM. Catheter mapping of retrograde atrial activation. Observations during ventriclular pacing and A-V nodal reentrant paroxysmal tachycardia. Br Heart J 1976;38:355-62. 22. Wolff L, Parkinson J, White PD. Bundle-branch block with short P-R interval in healthy young people prone to paroxysmal tachycardia. Am Heart J 1930;5:685-704. 23. Durrer D, Schuilenburg FlY, Wellens HJJ. Preexcitation revisited.

Am J Cardiol 1970;25:690-7. 24. Wellens HJ, Durrer D. Wolff-Parkinson-White syndrome and atrial fibrillation. Relation between refractory period of accessory pathway and ventricular rate. Am J Cardiol 1974;34:777-82. 25. Ferrer Ml. New concepts relating to the preexcitation syndrome. JAMA 1967;201:162-3. 26. Castellanos A, Castillo CA, Agha AS, Tessler M. His bundle electrograms in patients with short P-R intervals, narrow QRS complexes, and paroxysmal tachycardias. Circulation 1971;43: 667-78. 27. Bissett JK, Thompson AJ, deBoyza N, Murphy ML. Atrio-ventricular conduction in patients with short P-R intervals and normal QRS complexes. Br Heart J 1973;35:123-7. 28. Caracta AR, Damato AN, Gallagher JJ, et al. Electrophysiologic studies in the synckome of short P-R interval, normal QRS complex. Am J Cardiol 1973;31:245-53. 29. Iannone LA. Electrophysiokrgyof atriil pacing in patients with short P-R interval, normal QRS complex. Am Heart J 1975;89:74-8. 30. Rosen KM, Bauernfelnd RA, Wyndham CR, Dhlngra RC. Retrograde properties of the fast pathway in patients with paroxysmal atrioventricular nodal reentrant tachycardia. Am J Cardiol 1979; 431863-5. 31. Neusa H, Schlepper Y, Spies HF. Effects of heart rate and atropine on “dual A-V conduction.” Br Heart J 1975; 37:1216-27. 32. Wu D, Denes P, Bauemfeind R, Dhingra RC, Wyndham CR, Rosen KM. Effects of atropine on induction and maintenance of atrioventricular nodal reentrant tachycardia. Circulation 1979;59: 779-88. 33. Denes P, Wu D, Amat-y-Leon F, Dhingra R, Wyndham CR, Rosen KM. The determinants of atrio-ventricular nodal reentrance with premature atrial stimulation in patients with dual A-V nodal pathways. Circulation 1977;56:253-9. 34. Akhtar M, Damato AN, Ruskln JN, et al. Antegrade and retrograde conduction characteristics in three patterns of paroxysmal atrioventricular junctional reentrant tachycardia. Am Heart J 1978; 95:22-42. 35. Bisaett JK, deSoyza M, Kane JJ, Murphy ML. Altered refractory periods in patients with short P-R intervals and normal QRS complex. Am J Cardiol 1975;35:487-91. 36. Hiss RG, Lamb LE, Allen MF. Electrocardiographic findings in 67,375 asymptomatic subjects. X. Normal values. Am J Cardiol 1960;6:200-31.

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