Familial occurrence of sinus bradycardia, short PR interval, intraventricular conduction defects, recurrent supraventricular tachycardia, and cardiomegaly.

Four members of a family presenting with sinus bradycardia, a short P-R interval, intraventricular conduction defects, recurrent supraventricular tachycardia (SVT), syncope, and cardiomegaly had His bundle studies and were found to have markedly shortened A-H intervals (30 to 55 msec.) with normal H-V times (35 to 50 msec.). Right atrial pacing at rates as high as 170 to 215 per minute failed to increase the A-H or H-V intervals significantly. The data are compatible with the presence of an A-V nodal bypass tract (James bundle) or even complete absence of an A-V node. Ventricular pacing and spontaneous ventricular premature beats resulted in a short ventriculoatrial conduction time (110 msec.) suggesting that if A-V nodal bypass tracts exist, they are utilized in an antegrade and retrograde fashion. None of the features of WPW syndrome was present. The mechanism of syncope in the mother and daughter was intermittent third-degree heart block. Both went on to develop permanent complete heart block despite electrophysiologic studies demonstrating 1:1 A-V conduction at extremely rapid atrial pacing rates and both required implantation of permanent pacemakers. The mechanism of syncope in the two brothers was possibly marked sinus bradycardia, but transient complete heart block has not been ruled out. Permanent pacemaker therapy was recommended for both. The nature of the cardiomegaly, which was mild in three patients, is not known. Although not well documented, several maternal relatives have had enlarged hearts, SVT, complete heart block, and syncope.     

Sinus node re-entrant tachycardia in man.

Sinus node re-entry (SNR) usually appears as a single beat. Tachycardias (SNRT) consistent with sustained SNR were seen in six patients and were initiated by premature stimulation of the high right atrium (six patients) and coronary sinus (four patients), and after continuous pacing from the high right atrium (four patients) or right ventricle (one patient) at rates of 130 to 200 per minute. During SNRT: (1) atrial beats exhibited a high-to-low atrial activation sequence, (2) the P-waves were similar in morphology to P-waves during sinus rhythm, and (3) re-entry in the A-V node or at the site of stimulation could be excluded. The cycle length of SNRT ranged from 625 to 320 msec. and SNRT either terminated spontaneously (six patients) or after premature atrial capture and/or vagal maneuvers (two patients). The electrophysiologic characteristics of SNRT and differentiation of SNRT from A-V nodal re-entry are discussed.     

Concealed bypasses of the atrioventricular mode in patients with paroxysmal supraventricular tachycardia revealed by intracardiac electrical stimulation and verapamil

Thirteen patients with paroxysmal Supraventricular tachycardia were studied with use of His bundle electrograms and programmed intracardiac stimulation. No patient had evidence of either the Wolff-Parkinson-White or Lown-Ganong-Levine syndrome. During ventricular pacing at a rate of 90 to 180 beats/min retrograde conduction time increased by an average of 80 msec in eight patients; in the remaining five patients the average increase was only 9 msec. The tachycardia was terminated in all 13 patients after intravenous administration of verapamil, 10 mg. This drug acts predominantly on the atrioventricular (A-V) node, and during termination of an A-V nodal reciprocal tachycardia both the antegrade and retrograde conduction times would be expected to be prolonged. During termination of the tachycardia antegrade conduction was prolonged by an average of 43 msec and retrograde conduction by an average of 79 msec in eight patients. However, in five patients antegrade conduction was prolonged by an average of 101 msec and retrograde conduction by an average of only 3 msec. The minimal effect of this drug on retrograde conduction and the minimal increase in retrograde conduction during ventricular pacing in these five patients is strong evidence for the presence of an A-V nodal bypass that was not apparent from the surface electrocardiogram. The potential hazards should atrlal fibrillation occur and allow rapid antegrade conduction in an A-V nodal bypass are discussed.     

One to one atrioventricular conduction during atrial pacing at rates of 300/minute in absence of wolff-parkinson-white syndrome

One to one atrioventricular (A-V) or atrio-His bundle (A-H) conduction occurred during right atrial pacing at rates of 300/min in two patients with short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias. Patient 1 had episodes of reciprocating A-V tachycardia and of atrial fibrillation with very fast rates (270 to 290/min) that were slowed to 100 to 135/min after administration of intravenous verapamil. Enhanced A-V (A-H) conduction was exposed only during stimulation from the high right atrium, but not from the low lateral right atrium or coronary sinus. Patient 2 had episodes of atrial flutter with 1:1 A-V conduction and rates of 290/min. The H-V interval was short (25 ms) during sinus rhythm and atrial pacing presumably because conduction occurred through an atrio-“distal” His bundle (atriofascicular) tract. In contrast, the H-V interval was normal (40 ms) in echo beats or when the “proximal” His bundle was stimulated.In these two patients, having as “common denominators” short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias, enhanced A-V (A-H) conduction was (1) possibly due to different electrogenetic mechanisms; (2) pacing-site dependent; (3) manifested, during atrial fibrillation and atrial flutter, by extremely fast ventricular rates; and (4) unrelated to the rate of reciprocating A-V tachycardias because the latter was predominantly a function of anterograde conduction through the “slow” nodal pathway.     

Intractable paroxysmal tachycardia caused by a concealed retrogradely conducting Kent bundle. Demonstration by epicardial mapping and cure of tachycardias by surgical interruption of the His bundle.

Electrophysiological and epicardial mapping studies are described in a patient without pre-excitation who had intractable recurrent paroxysmal supraventricular tachycardia. Electrophysiological studies revealed fixed VA conduction times during both rapid ventricular pacing and coupled ventricular stimulation. Catheter mapping of atrial activation during retrograde conduction and during induced paroxysmal supraventricular tachycardia revealed early distal coronary sinus activation (posterior left atrium) relative to the low septal, low lateral, and high lateral right atrium. These studies suggested the presence of a concealed left-sided bypass tract. The patient underwent surgical interruption of the His bundle for control of paroxysmal supraventricular tachycardia. Epicardial mapping of the atria (during ventricular pacing) confirmed the presence of a concealed left-sided bypass tract. Surgery produced antegrade av block (while retrograde conduction was maintained) and total cure of paroxysmal supraventricular tachycardia. This is the first reported case of a concealed retrograde extranodal pathway documented by epicardial mapping.     

Determinants of antegrade echo zone in the Wolff-Parkinson-White syndrome

Forty-five patients with the Wolff-Parkinson-White syndrome and reciprocating tachycardia which utilized the atrioventricular (A-V) node for antegrade conduction and an accessory pathway for ventriculo-atrial (retrograde) conduction were studied. The extrastimulus technique in the right atrium and coronary sinus at multiple pacing cycle lengths was used. Three types of "echo zones" were defined by the relationship of the antegrade effective refractory period (ERP) of the accessory pathway, the longest coupling interval accompanied by an atrial echo, the ERP of the A-V node, and the functional refractory period of the atrium. Eighteen of 45 patients (40%) had more than one type of echo zone demonstrated by changing either pacing site or pacing cycle length or both. Pacing site and intraventricular conduction delay were found to have important effects on the longest coupling interval accompanied by an atrial echo in those echo zones in which the longest coupling interval accompanied by an atrial echo was less than the antegrade ERP of the accessory pathway. The echo zone is a useful concept to explain the physiology of the common reciprocating tachycardia in patients with the Wolff-Parkinson-White syndrome. However, the echo zone is profoundly affected by pacing site and pacing cycle length. When these variables are changed, many patients can be shown to have more than one type of echo zone. Studies of the echo zone have limited value as therapeutic guides.     

Atrial response during ventricular fibrillation

Electrical activity of the bundle of His and atria were recorded during sinus rhythm and electrically induced ventricular fibrillation in 23 dogs. Multiple bipolar atrial electrograms obtained from several sites within the right and left atria permitted the determination of the frequency, regularity, and sequence of atrial activation (i.e., sinus or retrograde) during ventricular fibrillation. Prior to the induction of ventricular fibrillation, the capacity to retrogradely conduct across the A-V node was tested in each animal by pacing the right ventricle at various cycle lengths. Fourteen animals demonstrated consistent 1:1 retrograde conduction at various paced cycle lengths (Group A); in four animals (Group B) retrograde conduction was intermittent and in three animals (Group C) no retrograde conduction was observed at any paced cycle length. Ventriculo-atrial conduction was also absent in two animals (Group D) with antegrade A-V block within the His-Purkinje system.The most common conduction pattern noted at the onset of ventricular fibrillation was that of rapid, irregular, retrograde activation of both the bundle of His and atria. However, the frequency of retrograde activation of the atria was less than that of the bundle of His indicating that the A-V node was a site of retrograde concealment of impulses. This conduction pattern was noted in all animals of Groups A and B. In all animals of Groups C and D, the atria continued to be activated in a sinus sequence during ventricular fibrillation. In Group C animals, the A-V node was the site of both antegrade and retrograde concealment. In the two animals with A-V block (Group D), the site of retrograde concealment was distal to the site of block.In six studies, retrograde A-V nodal Wenckebach cycles with and without re-entry were observed for varying periods of time.Less often, the irregular atrial responses during ventricular fibrillation were accounted for by short periods of sinus capture interspersed with periods of retrograde capture.During ventricular fibrillation, retrograde conduction across the A-V node could be abolished by vagal stimulation.The results of this study indicate that retrograde concealed conduction within the A-V node is the major determinant of an irregular atrial response during ventricular fibrillation just as antegrade concealed conduction is the major determinant of an irregular ventricular response during atrial fibrillation.     

Incidence, determinants and significance of fixed retrograde conduction in the region of the atrioventricular node. Evidence for retrograde atrioventricular nodal bypass tracts.

Of 104 consecutive patients studied in our laboratory with His bundle electrograms, atrial and ventricular pacing and the atrial and ventricular extrastimulus techniques, 18 patients in whom the existence and utilization of ventriculoatrial (V-A) bypass tracts were excluded demonstrated evidence for fixed and rapid retrograde conduction in the region of the atrioventricular node (A-V) as suggested by the following: (1) short (36 +/- 2 msec [mean +/- standard error of mean]) and constant retrograde H2-A2 intervals during retrograde refractory period studies; (2) significantly (P less than 0.025) better V-A than A-V conduction; (3) significantly (P less than 0.025) shorter retrograde functional refractory period of the V-A conducting system than of the A-V conduction system; and (4) the retrograde effective refractory period of the A=V nodal region was not attainable in any of the 18 patients. Fourteen of the 18 patients (77 percent) had a history of palpitations and 10 (51 percent) had documented paroxysmal supraventricular tachycardia; in 13 (72 percent) single echoes or sustained reentrant supraventricular tachycardia, or both, could be induced during atrial pacing or atrial premature stimulation studies, or both. During tachycardia all these 13 patients had a short (37 +/- 2.4 msec) and constant conduction time in the retrograde limb (H-Ae interval) of the reentrant circuit that was identical to the H2-A2 interval. In conclusion, fixed and rapid retrograde conduction in the region of the A-V node (1) is seen in approximately 17 percent of patients, (2) is associated with a large incidence of reentrant paroxysmal supraventricular tachycardia, and (3) suggests the presence of A-V nodal bypass tracts (intranodal or extranodal functioning in retrograde manner).     

Inter- and intraatrial dissociation during spontaneous atrial flutter: Evidence for a focal origin of the arrhythmia

Programmed electrical stimulation of the heart was performed in 2 patients with spontaneous atrial flutter. Patient 1 was a young man with paroxysmal atrial flutter that had proved resistant to drug therapy and who was studied during an episode of sustained flutter. In this patient rapid atrial pacing from the coronary sinus at a critical rate faster than the intrinsic flutter rate provoked local atrial fibrillation in the mid and low right atrium which persisted after termination of pacing. In spite of persistent local fibrillation in these regions, atrial flutter continued in the left atrium and the high right atrium. A second burst of pacing resulted in restoration of sinus rhythm. Patient 2 was an elderly woman with probable sick sinus syndrome who developed spontaneous atrial flutter during the course of an electrophysiologic investigation. During flutter intracavitary recordings from multiple sites in the atria revealed a pattern of 3:2 Wenckebach conduction between the left atrium and the high right atrium, with block of every third atrial depolarization at the latter site. These results indicate that atrial flutter may exist at some sites in the atria which are functionally dissociated from the remainder of the atrial tissue, thus supporting the hypothesis that flutter in some patients may be focal in origin.     

Effects of atrial pacing site on atrial and atrioventricular nodal function.

The effects of the site used for atrial pacing on atrial and atrioventricular nodal conduction were assesed in 16 patients. In 13 patients, three atrial pacing sites were used: high right atrium, low lateral right atrium, and midcoronary sinus. Two recording sites were used: low septal right atrium, including His electrogram, and high right atrium. Stimulus (S) to high right atrium interval was longest with coronary sinus pacing (76 plus or minus 7 ms) (P less than 0.001), and shortes with high right atrial pacing (41 plus or minus 3 ms) (P less than 0.05). There was no significant difference in stimulus to low septal right atrium from all three pacing sites. Atrial functional and effective refractory periods were not significantly different. Mean low septal right atrium to His was significantly shorter from the coronary sinus (93 plus or minus 8 ms) (P less than 0.001), as compared to high right atrium (139 plus or minus 16 ms), and low lateral right atrium (129 plus or minus 13 ms) pacing. AV nodal functional and effective refractory periods, and the paced rate producing AV nodal Wenckebach were not significantly different when comparing the three sites. Left atrial appendage and high right atrium were similarly compared in three additional patients, and no significant differences were found in conduction times and refractory periods.     

Effects of atrial pacing site on atrial and atrioventricular nodal function.

The effects of the site used for atrial pacing on atrial and atrioventricular nodal conduction were assesed in 16 patients. In 13 patients, three atrial pacing sites were used: high right atrium, low lateral right atrium, and midcoronary sinus. Two recording sites were used: low septal right atrium, including His electrogram, and high right atrium. Stimulus (S) to high right atrium interval was longest with coronary sinus pacing (76 plus or minus 7 ms) (P less than 0.001), and shortes with high right atrial pacing (41 plus or minus 3 ms) (P less than 0.05). There was no significant difference in stimulus to low septal right atrium from all three pacing sites. Atrial functional and effective refractory periods were not significantly different. Mean low septal right atrium to His was significantly shorter from the coronary sinus (93 plus or minus 8 ms) (P less than 0.001), as compared to high right atrium (139 plus or minus 16 ms), and low lateral right atrium (129 plus or minus 13 ms) pacing. AV nodal functional and effective refractory periods, and the paced rate producing AV nodal Wenckebach were not significantly different when comparing the three sites. Left atrial appendage and high right atrium were similarly compared in three additional patients, and no significant differences were found in conduction times and refractory periods.     

A comparative analysis of antegrade and retrograde conduction patterns in man.

Patterns of antegrade and retrograde conduction and refractory periods were studied using His bundle electrogram recordings, incremental atrial and ventricular pacing and the extrastimulus technique. In 36/50 patients antegrade conduction was "better" than retrograde conduction (group I), as evidenced by a) onset of retrograde atrioventricular (A-V) nodal Wenckebach phenomenon at a slower rate compared to the antegrade counterpart (25 patients: group IA) or b) no ventriculo-atrial conduction at all ventricular paced rates (11 pts: group IB). The site of retrograde block in group IB patients was the A-V node. In eight patients (group II), antegrade and retrograde conduction appeared to be equal up to maximum paced rates of 160 beats/min. In six patients (group III) retrograde conduction was "better" than antegrade conduction, as indicated by onset of antegrade A-V nodal Wenckebach periods at slower rates than retrograde Wenckebach periods. During antegrade refractory period studies the area of maximum refractoriness was the A-V node in 19/40 patients, the His-Purkinje system (HPS) 6/40, and the atrial muscle in 15/40. During retrograde refractory period studies the A-V node was the area of maximum refractoriness in 12/36 pts (4/40 patients had A-V dissociation during ventricular pacing), the HPS in 12/36, and the ventricular muscle in 10/36. In 2/36 patients the site of maximum refractoriness retrogradely could not be determined: The area of maximum refractoriness during both antegrade and retrograde refractory period studies was the same in 11 patients (A-V node in seve and HPS in four), was different (i.e., A-V node or HPS) in 18 patients, and was the artrial or ventricular muscle in six patients. In five patients, including four patients in whom V-A conduction failed to occur, the above comparisons were not made. It is concluded that 1) antegrade conduction is better than retrograde conduction in most patients; 2) it is not always possible to predict area of maximum refractoriness during premature stimulation (both atrium and ventricle) from observations made during incremental pacing; 3) it is equally difficult to extrapolate patterns of retrograde conduction and refractory periods from results of antegrade conduction and refractory period studies.     

Limited benefit of septal pre-excitation in pace prevention of atrial fibrillation

BACKGROUND: Pre-excitation of the intra-atrial septum (IAS) by pacing at the ostium of the coronary sinus (CSO) can prevent atrial fibrillation (AF) in case of single atrial premature beats (APBs). We investigated whether pre-excitation of IAS, either by pacing at CSO or at the right ventricle in the presence of retrograde conduction (RV), can prevent atrial tachyarrhythmia triggered by single and multiple APBs. AF vulnerability was compared to pacing at the right atrium (RA) and sinus rhythm (SR). METHODS: Seventeen patients, age 52 +/- 21 years, who exhibited retrograde VA conduction and reproducible induction of atrial tachyarrhythmia during an electrophysiological procedure, were studied. Both during SR and pacing (S1-S1:600 ms) at RA, CSO, and right ventricle (RV), single (A1-S2:200 ms) and multiple premature stimuli (A1-S2-S3-S4:200-180-180 ms) were delivered at RA (4 x diastolic threshold). RESULTS: During pacing at RA, single and multiple APBs invariably induced runs of atrial tachyarrhythmia (mean duration 34 +/- 67 sec and 37 +/- 69 sec, range 1 sec to 20 min). During preventive pacing at CSO and RV, single APBs (A1-S2:200 ms) did not induce atrial arrhythmia (0 +/- 0 sec, 0 +/- 0 sec, P < 0.05 vs pacing at RA). In contrast, when multiple APBs were applied, pacing at CSO or RV failed to prevent initiation of AF (mean duration 36 +/- 63 sec, 38 +/- 65 sec, NS). Also during SR, single APBs did not induce AF (0 +/- 0 sec, P < 0.05 vs pacing at RA) whereas multiple APBs invariably induced AF (39 +/- 74 sec, NS). CONCLUSIONS: Compared to pacing at RA, pre-excitation of IAS either by pacing at CSO or at RV with retrograde conduction can prevent initiation of paroxysms of atrial tachyarrhythmia triggered by single but not by multiple right APBs. These findings imply that the potential benefit of choosing an optimal pacing site in patients requiring atrial-based pacing is limited. Moreover, in the absence of bradycardia, no specific pacing site offers incremental benefit over the natural "protective" effect of sinus rhythm.     

Paroxysmal tachycardia with atrioventricular dissociation in a patient with a variant of pre-excitation syndrome

We report a patient with a variant of the pre-excitation syndrome who has paroxysmal tachycardia with a pattern of left bundle branch block and ventriculo-atrial dissociation. The tachycardia is precipitated by exercise, reproduced by atrial pacing and terminated with lidocaine. Between attacks the electrocardiogram revealed prominent R waves in right precordial leads and the vectorcardiogram displayed anterior displacement of the mean QRS vector, but neither was diagnostic of pre-excitation. The resting P-R interval (140 msec) and A-H interval (60 msec) were within normal limits, but the H-V interval (30 msec) was at or slightly below normal limits. Increasing heart rate from 80 to 150/min with atrial pacing increased A-H from 70 to 160 msec, but did not change the H-V interval. With pacing at 160/min, A-H lengthened progressively from 160 to 190 msec, but A-V remained constant at the critical limit of 190 msec. Accordingly, the H-V interval decreased until the His spike disappeared into the QRS or did not occur because of A-V block. At this point, the QRS complex changed to that seen during spontaneous tachycardia. Pacing was stopped, but tachycardia continued at 160/min and ventriculoatrial dissociation appeared. Lidocaine promptly restored sinus rhythm. We speculate that the patient has anomalous conduction between the lower segment of the A-V node and the ventricular septum (Mahaim fibers) and a reciprocating tachycardia which results from antegrade conduction down the anomalous pathway and retrograde conduction up the His-Purkinje system and lower A-V node. Ventriculo-atrial Wenckebach during the tachycardia excludes participation of atria and upper part of the A-V node in the re-entrant tachycardia. This variant of pre-excitation syndrome could easily be mistaken for “true ventricular tachycardia” and serious heart disease.     

Antegrade conduction and AV node function in patients with unidirectional retrograde accessory pathways

In 26 patients with unidirectional retrograde accessory pathways (URAP), antegrade conduction properties were evaluated. During electrophysiologic study the interval from the low septal right atrial potential to the His bundle potential (LSRA-H) in sinus rhythm (SR) was found to be less than 60 msec in 7 out of the 18 patients with left-sided URAP and in one out of two patients with septal URAP. Each of the six patients with right-sided URAP had an LSRA-H equal to or greater than 70 msec. During atrial extrastimulus testing, LSRA-H failed to prolong more than 100 msec (LSRA-H increment equal to or less than 100 msec) in four of six patients with left-sided URAP and LSRA-H of less than 60 msec in SR as well as in the one of two patients with septal URAP in whom the LSRA-H in SR was less than 60 msec. During rapid atrial pacing, we found 1:1 AV node conduction at a pacing rate of more than 200 bpm in the one patient with septal URAP and in 7 out of 14 patients with left-sided URAP who could be assessed. Three of these patients had progression from 1:1 AV conduction to 2:1 AV block without intervening Wenckebach. In conclusion, accelerated AV node conduction in SR and reduced AV node function during rapid atrial pacing or extrastimulus testing was found in 44% of our patients with left-sided or septal URAP. Since these patients are at higher risk for faster ventricular response to atrial flutter and fibrillation and for high frequency during supraventricular tachycardia, these findings were of clinical relevance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Delineation of AV Conduction Pathways by Selective Surgical Transection: Effects on Antegrade and Retrograde Transmission

Introduction: The role for transitional cells as determinants of AH and HA conduction was examined in the superfused rabbit AV junction.Methods: Bipolar electrodes and microelectrodes were used to record antegrade A-H and retrograde H-A activation, before and after transection of the transitional cell input to the compact AV node.Results: During pacing from the high right atrium, inferior to the coronary sinus os, beneath the fossa ovalis, or on the anterior limbus, AV Wenckebach block (WB) was mediated by identical transitional cells grouped in close apposition to the compact AV node. Paced WB cycle lengths were shorter from the high right atrium (196 ± 12 msec) and inferior to the coronary sinus os (195 ± 8 msec) versus the fossa ovalis (217 ± 9 msec) or anterior limbus (206 ± 11 msec). With His bundle pacing, retrograde HA WB (211 ± 17 msec) was observed within the N cell region within the compact AV node. After transection of posterior and superior transitional cell input to the compact AV node, the antegrade AH WB cycle length was prolonged (245 ± 18 msec), with an increased WB incidence within the NH region (compact AV node)(5% to 41%; p = 0.014). The incidence of retrograde HA WB determined within the NH region was increased (30% to 88%), with a decrease in the stimulus-fast pathway conduction time (98 ± 7 to 49 ± 6 msec; p < 0.01).Conclusions: The data demonstrate (1) a common transitional cell population determining AH WB, independent of atrial stimulation site, and (2) a plasticity of transitional cell-compact AV node connections, with rapid AH and HA conduction favored by removal of posterior/superior AV nodal input.Supported by a grant from the American Heart Association, Oklahoma Affiliate.     

Atrial pacing during selective aortocoronary saphenous vein bypass angiography

Selective aortocoronary bypass graft angiography was performed in 30 postoperative subjects. Thirty-one of 39 patent graft injections resulted in cardiac arrhythmias including sinus bradycardia, premature ventricular depolarizations, sinoatrial arrest and atrioventricular (A-V) block. In contrast, only 2 of 39 graft angiograms performed during right atrial pacing produced arrhythmias. We conclude the following: (1) Routine prophylactic right atrial pacing is a valuable method for preventing certain cardiac arrhythmias during aortocoronary graft opacification; and (2) the potential for rapid institution of right ventricular pacing provides safety in the event that angiographically induced A-V block occurs.     

“Paradoxical” AH Shortening Caused By Proximal Coronary Sinus Stimulation During Orthodromic Reciprocating Tachycardia

AH Shortening During ORT. Introduction: During extrastimulation or entrainment of orthodromic atrioventricular (AV) reciprocating tachycardia (ORT), the atriuni-His (AH) interval as measured at the His-bundle recording site is expected to lengthen due to extrastimu-Lation-dependent or pacing rate-dependent slowing of AV nodal conduction by impulses that penetrate the tachycardia circuit. We report 6 patients in whom the AH interval “paradoxically” shortened during ORT in response to extrastimulation and rapid pacing from the proximal coronary sinus. Methods and Results: Accessory pathway location was right anterior (1 patient), right anteroseptal (1 patient), and left anterior (4 patients). Cycle length of ORT was stahle (variation ≤ 5 msec) and ranged from 325 to 410 msec. During ORT, extrastimulation and rapid pacing were performed from the proximal coronary sinus and the right atrium. Extrastimulation from the proximal coronary sinus late in diastole caused significant shortening of AH interval in all patients hy a mean of 18 ± 3 msec (range 15 to 20 msec). AH shortening was demonstrated without a change of either the timing or morphologic appearance of the low septal right atrium at the H is-bundle recording site. This phenomenon was not ohserved during right atrial extrastimulation. Rapid pacing from the proximal coronary sinus at cycle lengths of 305 to 390 msec (i.e., 15 to 20 msec shorter than the cycle length of each ORT) again demonstrated shortening of AH interval in all patients by a mean of 15 ± 3 msec (range 10 to 20 msec). By contrast, rapid pacing from the right atrium demonstrated classical AH prolongation at any paced cycle length. Conclusion: AH shortening without a change of either the timing or morphologic appearance of the low septal right atrium at the His-handle recording site confirms the existence of a distinct posterior atrial input to the AV node. In this setting low septal right atrial activation is not requisite for AV nodal conduction. Whether activation of the low septal right atrium is essential for. or contributes to, AV nodal conduction of atrial impulses from locations other than the proximal coronary sinus needs to he determined.     

Effect of mexiletine on human atrial vulnerability

The effect of mexiletine on human atrial vulnerability was investigated in 14 subjects (8 with paroxysmal atrial fibrillation, 2 with paroxysmal atrial tachycardia, 2 with ventricular tachycardia, 1 with sick sinus syndrome and 1 with Wolff-Parkinson-White syndrome). During the electrophysiologic study, after 8 consecutive stimuli (A1) were delivered through the electrode catheter positioned at high right atrium, premature stimulus (A2) was introduced, and following measurements were made; 1) Aw: atrial activity width of A1, 2) maximum atrial fragmentation (MAF): the longest atrial activity width of A2, which was expressed by the relative value against Aw, 3) fragmented atrial activity zone (FAZ): the zone of the coupling interval (A1A2) with the prolongation of the atrial activity width at A2 more than 150% against Aw, 4) conduction delay zone (CDZ): the zone of A1A2 with the prolongation more than 20 msec of the intraatrial conduction time at A2 from high right atrium to coronary sinus or low right atrium against the intraatrial conduction time at A1, and 5) right atrial effective refractory period (RAERP). These measurements were repeated after the intravenous administration of mexiletine (2 mg/kg/10 min). 3 cases (case 12, 13 and 14), whose FAZ and CDZ were 0 msec, were excluded from the following evaluation. Mexiletine showed little effect on Aw and RAERP, but significantly shortened MAF and FAZ (p less than 0.001 and p less than 0.05, respectively). CDZ were also reduced in 3 cases and remained unchanged in 6 cases, though no statistical difference of CDZ was recognized between before and after the administration of mexiletine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Double atrial responses to a single ventricular impulse due to simultaneous conduction via two retrograde pathways

Electrophysiologic studies were performed in two patients. In one patient (Case 1) with ventricular pre-excitation and paroxysmal supraventricular tachycardia, studies after diltiazem administration showed two QRS responses to a single atrial stimulus during atrial pacing at a cycle length of 300 ms. The first QRS response with full pre-excitation and short PR interval was consistent with accessory pathway conduction, while the second QRS response with a normal duration and an atrio-His bundle interval of 350 ms was consistent with normal pathway conduction. The second QRS response was followed by initiation of supraventricular tachycardia. Studies after verapamil administration on a separate day disclosed two atrial responses to a single QRS complex during ventricular pacing at cycle lengths between 330 and 280 ms, suggesting simultaneous retrograde accessory and normal pathway conduction. In Case 2 with a supraventricular tachycardia using a fast atrioventricular nodal pathway for anterograde and a slow ventriculoatrial pathway for retrograde conduction, two atrial responses to a single QRS complex were observed during ventricular pacing at cycle lengths between 500 and 400 ms. The first atrial response showed a stimulus to atrial interval of 120 ms and an atrial activation sequence with the low septal right atrium being earlier than other atrial sites, suggesting retrograde fast pathway conduction. The second atrial response showed a stimulus to atrial interval of 505 ms and an atrial activation sequence with low septal right atrium being simultaneous with the proximal coronary sinus, suggesting retrograde slow pathway conduction.(ABSTRACT TRUNCATED AT 250 WORDS)