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Effects of Atropine on Induction and Maintenance of Atrioventricular Nodal Reentrant Tachycardia DELON WU, M.D., PABLO DENES, M.D., ROBERT BAUERNFEIND, M.D., RAMESH C. DHINGRA, M.D., CHRISTOPHER WYNDHAM, M.D., AND KENNETH M. ROSEN, M.D. SUMMARY The electrophysiologic effects of atropine were studied in 14 patients with dual atrioventricular (AV) nodal pathways and recurrent paroxysmal supraventricular tachycardia (PSVT). During PSVT, all patients used a slow pathway (SP) for antegrade and fast pathway (FP) for retrograde conduction. Atropine enhanced both SP antegrade and FP retrograde conduction, shown by a decrease in paced cycle lengths (atrial and ventricular) producing AV and ventriculoatrial block. Five patients had induction of sustained PSVT before and after atropine. Seven patients failed to induce or sustain PSVT before atropine, because of retrograde FP refractoriness. All seven had induction of sustained PSVT after atropine due to facilitation of FP retrograde conduction. Two patients had only single atrial echoes before atropine, reflecting SP antegrade refractoriness. After atropine, sustained PSVT was inducible in one, and nonsustained in the other. PSVT cycle length could be compared in seven patients before and after atropine and decreased from 383 + 25 to 336 ± 17 (p < 0.05). Thus, in patients with dual AV nodal pathways, atropine facilitated SP antegrade and FP retrograde conduction, shortened cycle length of PSVT and potentiated ability to sustain PSVT. Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017 Methods DUAL ATRIOVENTRICULAR (AV) nodal pathways can be demonstrated in most patients with AV nodal reentrant paroxysmal supraventricular tachycardia (PSVT).' 6 In these patients, the most common type of sustained AV nodal reentrance involves using a slow pathway for antegrade conduction and a fast pathway for retrograde conduction.' 6 Recent pharmacologic studies have demonstrated that digitalis, propranolol and verapamil may prevent induction of sustained AV nodal reentrant PSVT by increasing antegrade slow pathway refractoriness.34'4 7- Procainamide may prevent PSVT induction in patients with dual AV nodal pathways, by increasing retrograde fast pathway refractoriness.10 Limited data are available describing the effect of agents that facilitate conduction on AV nodal reentry. Akhtar and co-workers reported induction of AV nodal reentrant PSVT only after atropine in five patients with no previous history of PSVT, suggesting that vagolysis facilitated the development of AV nodal reentrant circus movements." In this study, we report the effects of atropine in patients with previously documented PSVT and electrophysiologically demonstrable dual AV nodal pathways. The effects of atropine on fast and slow pathways are quantitated, and the effects of this agent on PSVT induction noted. Patient Selection Criteria for inclusion in this study included: 1) a history of electrocardiographically documented recurrent PSVT; 2) absence of preexcitation on all available ECGs; 3) electrophysiological demonstration of dual AV nodal pathways with demonstration of discontinuous A1-A2, H,-H2 curves during atrial extrastimulus testing (10 patients) or demonstration of two sets of A-H intervals at identical atrial paced cycle lengths (four patients)." 12-16 The latter demonstrations were during the same trial of incremental atrial pacing, the two sets of A-H reflecting fatigue (block) in the fast pathway with resultant slow pathway conduction, and 4) demonstration of AV nodal reentrant PSVT (see Results).", 2, 17-19 Fourteen patients, nine females and five males, ages 24-81 years (mean ± SD 59 ± 16 years) were studied. Electrophysiological Studies Electrophysiological study was performed with the patient in the nonsedated supine state. Cardiac drugs were discontinued at least 72 hours before study. Informed written consent was obtained in each patient. A #7 quadripolar electrode catheter was placed across the tricuspid valve percutaneously via the right femoral vein. The proximal two electrodes were used for His bundle recording, while the distal two electrodes were used for ventricular pacing.20 A second #6 hexapolar electrode catheter was positioned in the distal coronary sinus via an antecubital vein. The distal two electrodes were used for recording of left atrial electrograms, the middle two electrodes for recording of high right atrial electrogram, and the proximal two electrodes for high right atrial pacing. Multiple surface and intracardiac electrograms were recorded simultaneously via a multichannel oscilloscopic recorder (Electronics for Medicine DR-16, White From the Cardiology Section, Department of Medicine, Abraham Lincoln School of Medicine, University of Illinois College of Medicine, and West Side Veterans Administration Hospital, Chicago, Illinois. Supported in part by NIH training grant HL 07387-OlAl and NIH grant HL 18794-04, and Basic Institutional Support, MRIS 1828, West Side Veterans Administration Hospital, Chicago, Illinois. Address for reprints: Kenneth M. Rosen, M.D., Cardiology Section, University of Illinois Hospital, P.O. Box 6998, Chicago, Illinois 60680. Received June 21, 1978; revision accepted November 8, 1978. Circulation 59, No. 4, 1979. 779 780 CIRCULATION Plains, New York) at a paper speed of 100 and 200 mm/sec. Stimuli were provided via a programmable digital stimulator (manufactured by M. Bloom, Narbeth, Pennsylvania) with a strength of approximately twice diastolic threshold and 2 msec long. Antegrade and retrograde conduction properties, refractory periods and echo zones were studied with atrial and ventricular incremental pacing and extrastimulus technique.1' 10, 14 Retrograde His bundle potentials could not be reliably recorded at all coupling intervals during ventricular extrastimulus testing in most of the patients. After control recording, studies were initiated 15 minutes after administration of 0.5-1 mg atropine intravenously. Electrophysiological Definitions Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017 HRA1, A1, H1, and V1 were the high right atrial, low septal right atrial, His bundle, and ventricular responses to driven stimuli (S1), respectively. HRA2, A2, H2, and V2 were the high right atrial, low septal right atrial, His bundle and ventricular responses to test stimuli (S2), respectively. Ae, He and Ve were the atrial, His bundle and ventricular responses of AV nodal reentrant echo beats, respectively. Conduction intervals, refractory periods, echo zones, and critical A-H and V-A intervals (for induction of AV nodal reentrant echoes and PSVT) were measured and defined as previously described." 10, 14 Antegrade dual AV nodal pathways were diagnosed when discontinuous A-A2, H,-H2 curves were demonstrated, or when two sets of A-H intervals were demonstrated at identical atrial paced cycle lengths." 12-16 Both antegrade and retrograde effective refractory periods of the fast and slow pathway were defined as previously described." 10, 14 The diagnosis of AV nodal reentrant PSVT was made with combinations of the following diagnostic criteria: 1) induction of PSVT related to achievement of a critical A-H delay, with both incremental atrial pacing and with atrial extrastimulus testing;" 2, 21-23 2) demonstration of discontinuous A1-A2, H,-H2 curves, suggesting dual AV nodal pathways, with induction of PSVT relating to antegrade block in the fast pathway;"' 2, 13-1' 3) demonstration of atrial activation before or simultaneous with onset of ventricular activation during PSVT, suggesting that the ventricles were not part of an AV reentrant circus movement;" 2, 17 4) normal retrograde atrial activation sequence during PSVT, with low septal right atrium being activated earlier than all other atrial recording sites;24' 25 5) increase of ventriculoatrial (VA) interval with incremental ventricular pacing with type I VA block at critical rate, suggesting retrograde AV nodal conduction;"' 17 6) demonstration of His bundle activation (H2) preceding the atrial activation (A2) with ventricular extrastimulus testing during ventricular pacing and/or PSVT, suggesting retrograde AV nodal conduction;"' 17 7) absence of previously described criteria for diagnosis of concealed extranodal pathways, or sinoatrial reentry.1 2, 26-3 All patients manifested criteria 4 and either 3 or 6. VOL 59, No 4, APRIL 1979 Sustained PSVT was defined as induced PSVT that lasted longer than 2 minutes. Sustained PSVT was always terminated with single, double or multiple atrial extrastimuli. Nonsustained PSVT was defined as induced PSVT terminated spontaneously (within 2 minutes). In almost all instances, nonsustained PSVT terminated spontaneously within 10-20 seconds of PSVT induction. In patients with nonsustained PSVT, the site of block (weak-link) in the circuit was determined by noting whether PSVT was terminated with an atrial response (block in antegrade limb) or with a QRS complex (block in retrograde limb).10 The determinants of reentrance (antegrade slow pathway and retrograde fast pathway) were evaluated as previously described.34 The evaluation of antegrade slow pathway primarily depended on noting the paced atrial cycle length producing AV nodal block. Since in the patient with dual pathways, the antegrade fast pathway has a longer refractory period than the antegrade slow pathway, this paced cycle length reflects slow pathway refractoriness. For the retrograde fast pathway, this evaluation primarily depended on noting the paced ventricular cycle length producing VA block. This procedure is based on the assumption that the shortest VA retrograde refractory period in these patients is that of the retrograde fast pathway, rather than the retrograde slow pathway. This assumption is based on the following observations: 1) Retrograde conduction curves (H1-H2, A,-A2) are smooth and suggest one retrograde pathway; 2) VA conduction times are short (there are not two populations of retrograde conduction times) and are consistent with observed antegrade fast pathway conduction times; 3) retrograde conduction is via AV node (normal retrograde activation sequence, and H2 and A2 are both driven out of the QRS with closely coupled ventricular extrastimuli). Retrograde fast pathway effective refractory period cannot be directly measured in most patients with dual AV nodal pathways because of either limiting ventricular refractoriness or limiting refractoriness between the ventricle and His bundle. Results PSVT Induction (table 1) In seven of the 14 patients, sustained AV nodal reentrant PSVT could not be induced before atropine administration, despite achievement of sole conduction in the antegrade slow pathway (antegrade failure of the fast pathway) with atrial extrastimulus testing and/or rapid incremental atrial pacing (cases 1-7). In three of these patients (cases 1-3), nonsustained AV nodal reentry was induced before atropine, with spontaneous termination of PSVT due to block in the retrograde fast pathway (inadequate retrograde fast pathway conduction) (fig. IA). In four of the patients (cases 4-7), no AV nodal reentrant atrial echoes were noted because of inadequate retrograde fast pathway conduction (fig. 2B). After atropine, all seven patients had induction of sustained AV-nodal PSVT due to enhanced retrograde fast pathway conduction (figs. ATROPINE AND AV NODAL REENTRY/Wu et al. 781 Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017 TABLE 1. Effects of Atropine on Induction and Maintenance of Atrioventricular Nodal Reentrant Tachycardia PSVT Ability to Weak CL Antegrade (msec) Retrograde (msec) Case Induction sustain link (msec) FP-ERP SP-ERP Echo zone CL-AVB FP-ERP SP-ERP Echo zone CL-VAB 1 C Echo 330 0 (-) No 340 Ret 320 0 300 280 400 A Yes 0 Yes No 300 300 0 300 260 250 316 (-) 2 C Yes 0 No Ret 300 <230 <353 270 370 300-230 375 (-) A Yes Yes No 315 270 0 <250 270-250 <300 <250 (-) <316 3 C Yes No Ret 320 <240 330-240 333 <355 435 0 (-) 500 A Yes Yes No 350 280 <230 0 261 <325 0 316 (-) 4 C No (-) Ret 0 (-) 0 550 (-) 650 375 <315 667 A Yes Yes No 350 < 320 0 316 <310 0 (-) 333 (-) 5 C No (-) 0 () Ret 320 > 500 0 400 370 429 (-) A Yes Yes No 340 300 <290 330-290 375 <230 0 (-) <353 6 C No (-) (-) 0 (-) Ret 410 353 430 <270 333 0 A Yes Yes No 305 <260 0 0 284 (-) 325 () 300 7 C No (-) 0 (-) Ret 462 420 350 0 390 <290 375 A Yes Yes No <260 365 0 0 261 <240 () (-) 284 8 C Echo No Ant (-) 370-340 375 390 () <340 360 400-365 500 A Yes Yes No <310 0 500 (-) 0 333 < 340 () <300 9 C Echo 0 300 No Ant (-) (-) <350 390 <260 370-260 429 A Echo No Ant (-) <310 0 353 <350 (-) 0 () <300 10 C Yes Yes 0 No <333 305 () 270 <210 270-210 <230 300 A Yes Yes No 300 <270 (-) 0 284 <230 0 () <300 11 C Yes Yes No 0 355 295 <300 <280 290-280 () < 175 333 A Yes 0 (-) Yes <300 No 300 () <200 < 175 0 <273 12 C Yes < 353 Yes No 0 480 () 410 280 380-280 462 <370 A Yes <353 0 Yes No () 390 <280 t-) 0 <273 <370 13 C Yes () Yes No 420 (-) <310 470-260 <316 0 <333 250 A Yes (-) Yes No 400-290 <375 400 () <290 <300 0 280 14 A Yes <316 Yes No 315 (-) 295 0 <255 295-255 333 <340 C Yes Yes No 300 260 <300 <255 260-250 <316 0 <316 () Abbreviations: PSVT = paroxysmal supraventricular tachyeardia; CL = cycle length; FP-ERP effective refractory period of the fast pathway; SP-ERP = effective refractory period of the slow pathway; CL-AVB iongest atrial paced cycle length producing atrioventricular block; CLVAB - longest ventricular paced cycle length producing ventriculoatrial (VA) block; C = control; A = atropine; Ant = antegrade; Ret = retrograde. IC and 2C). PSVT was induced with either rapid atrial pacing (all seven patients) or with double atrial extrastimuli (cases 1-3, 6, 7). In only two patients was PSVT inducible with single atrial extrastimulus testing after atropine (cases 2 and 5). In two of the 14 patients, sustained PSVT was not induced before atropine due to inadequate antegrade slow pathway conduction (cases 8 and 9). In both patients only single AV nodal reentrant atrial echoes were induced after achievement of sole antegrade slow pathway conduction (fig. 3A). After atropine, one of these patients had induction of sustained PSVT due to enhanced antegrade slow pathway conduction (case 8) (fig. 3B), while the other continued to have induction of only single AV nodal reentrant atrial echoes (case 9). Five of the 14 patients had induction of sustained PSVT before atropine (cases 10-14) (fig. 4A). In all five patients, PSVT was inducible with rapid atrial pacing and in four with single atrial extrastimulus testing (cases 10-12 and 14). After atropine administration, all five patients had induction of sustained PSVT with either rapid atrial pacing (at faster paced rates than those necessary for induction prior to atropine) or with double atrial extrastimuli (A1, A2, A3, testing) (figs. 4B and 4C). In only one patient was PSVT inducible with single atrial extrastimulus testing after atropine (case 14). Conduction Curves and Echo Zones (table 1) Discontinuous A1-A2, H,-H2 curves suggesting dual AV nodal pathways were demonstrated in 10 of the 14 patients before atropine (cases 1-3, 7-12 and 14) (figs. 2A, 2B and 5). In eight of these 10 patients, an echo zone could be defined which coincided with either the whole slow pathway curve or the leftward portion of the slow pathway curve. In two patients, an echo zone was not defined, despite demonstration of the discontinuous curve (cases 1 and 7) (fig. 5, left panel). After atropine, discontinuous A1-A2, H1-H2 curves were demonstrated in four of these 10 patients (cases 1-3 and 14). Three of these four had echo zones before atropine, and two of four had echo zones (and PSVT ; @;^*^|1l;^A|L~ ~ ~ CIRCULATION 782 A Control ,%. CL=353 , u Ae , k- RA HBE B Ri RA HBE CL =375 t---7- IIAe -ih Ae VOL 59, No 4, APRIL 1979 Ae Ae h i 1~ ~ ~ ~ ~ ~1 I A"-T- I A-V-1-7 F-- v A Ae .1 V- I A Ii Atropine C II Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017 RA HBE D RA HBE FIGURE 1. Recordings from case 2, showing induction of sustained atrioventricular (A V) nodal reentrant paroxysmal supraventricular tachycardia (PSVT) after atropine and the effects of atropine on antegrade and retrograde conduction. Shown are lead II, the right atrial electrogram (RA) and His bundle electrogramr (HBE). S, A, and H are stimulus artifact, atrial and His bundle responses, respectively, during atrial pacing. Ae and He are atrial and His bundle responses of the A V nodal reentrant beats. Time lines are at I second and paper speed is 100 mm/sec. Paced cycle length (CL) is listed on top of each panel, and the critical A-H interval is listed on bottom of the panel. Panel A demonstrates induction of nonsustained PSVT after cessation of rapid atrial pacing at a paced CL of 353 msec before atropine (antegrade slow-pathway conduction). CL of PS VT was 370 msec. The heavy vertical black line represents a 4-second discontinuity in recordings. PSVT was terminated when He was not followed by an atrial response, suggesting retrograde block in the fast pathway. Panel B demonstrates second degree ventriculoatrial (VA) block at a ventricular paced CL of375 msec before atropine. Panel C demonstrates induction ofsustained PSVT after atropine following cessation of rapid atrial pacing at a paced CL of 300 msec. CL of PSVT was 315 msec. Panel D demonstrates one-to-one V-A conduction after atropine at a shorter ventricular paced CL of 316 msec. induction) after atropine (cases 2 and 14). In six patients (cases 7-12), discontinuous A1-A2, H1-H2 curves became continuous after atropine due to facilitation of fast pathway conduction (see below) and echo zones were not defined (fig. 5, middle panel). Antegrade block in the fast pathway with antegrade slow pathway conduction (with echoes and PSVT) in these six patients was achieved with rapid atrial pacing and/or double atrial extrastimuli after atropine (figs. 2C, 3B, 4B, 4C and 5, right panel). Continuous A,-A2, H1-H2 curves were demonstrated in four of the 14 patients before atropine (cases 4-6 and 12). In three of these four patients, atrial functional refractory period was longer than the effective refractory period of the fast pathway (cases 4, 6 and 13), and in the other (case 5) only the slow pathway was used for antegrade conduction at the tested driven cycle length. Echo zones were not demonstrated in these four patients, although in one patient (case 13) sustained PSVT was inducible with rapid atrial pacing. After atropine, continuous curves without definition of an echo zone were demonstrated in three of the four patients (cases 4, 6 and 13). In all three patients, sustained PSVT could be induced after atropine with rapid atrial pacing and/or double atrial extrastimuli. In the remaining patient (case 5, the patient with only slow pathway conduction with extrastimulus testing), A1-A2, H1-H2 curve became discontinuous after atropine due to shortening of antegrade fast pathway refractory period. An echo zone was ~ ~ ~-N ;I7 ATROPINE AND AV NODAL REENTRY/Wu et al. Control A IL. RA " CSA a HBE w Al -A2 =350 B _u RA Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017 CSA % 0% A H BE --~~ A Si Si i. li ---T S2 .L op -- I.- i VI r- - -. Ik pg. .- --A -it I HILA _mA0 I Atropine 783 I -K _ i jA . _ IV K iIL hslw i H2 AWLA- -'---A1 I I IV I L1 lr I L- --- ------ -- - - A FIGURE 2. Recording from case 7, demonstrating induction of sustained paroxysmal supraventricular tachycardia (PS VT) after atropine. Left atrial electrogram recordedfrom coronary sinus (CSA) is also shown. S1, A1, and H1 are stimulus artifact, atrial and His bundle responses to the basis driven beat, respectively; S2, A2, and H2 are stimulus artifact, atrial and His bundle responses to the test beat, respectively; S3, A3, and H3 are stimulus artifact, atrial and His bundle responses to a second test beat. Paced cycle length (CL), A1-A2, and A2-A3 intervals are listed on top ofeach panel, and A2-A2 or A3-H3 are listed on bottom of each panel. The basic driven CL was 400 msec before and after atropine. RA = right atrial electrogram; HBE = His bundle electrogram. Panel A demonstrates antegrade fast-pathway conduction of A2 at A 1-A2 of 360 msec before atropine. Panel B demonstrates antegrade block of the fast pathway with conduction via the slow pathway at A1-A2 of 350 msec before atropine. Note lack of atrioventricular nodal reentrant atrial echo despite achieving a slow-pathway A2-H2 of400 msec. Panel C demonstrates induction of sustained PSVT after atropine with A1A2A testing. At A1-A 2 of270 msec, A2 was still conducted via the fast pathway. However, A3 was blocked in the fast pathway and conducted via the slow pathway at A2-A3 of 250 msec. Sustained PSVT was induced at A3-H3 of 425 msec. 3 defined, and coincided with the whole slow pathway Antegrade Slow Pathway Properties (table 1) curve. Refractoriness of the antegrade slow pathway could be evaluated in 12 patients before and after atropine by noting the longest atrial paced cycle length producing AV nodal block (cases 1, 3-12 and 14). The atrial paced cycle length producing AV block was 373 18 msec (range 300-500 msec) before atropine, and decreased to <301 ± 11 msec (range <273-375) after atropine (p < 0.01). Antegrade effective refractory period of the slow pathway could be compared with extrastimulus tech- Antegrade Fast Pathway Properties (table 1) Antegrade fast pathway effective refractory periods measured in 11 patients before and after atropine (cases 1-3, 5, 7-12 and 14) (fig. 5, left and right panels). Antegrade fast-pathway effective refractory period was <340 ± 21 msec (mean ± SEM, range 270 to <500) before atropine, and decreased to <276 ± 9 msec (range <200 to 300) after atropine (p < 0.01). were VOL 59, No 4, APRIL 1979 CIRCULATION 784 Control Atropine B CL =333 s em.A-' rww., r. RA= AW I i HBE no k. s S sIIa - H 11 1 9MMOR -VW Ae A_ 1|,r n_AI.l IlI-II~ I- - ~ #,Iipm6 I -itl , I I He -i., . 91, 1 40 tA i -1-lv- -_ A e ~~~~~- Ae &-I I He I --y- -1I if-- L Ae 11 k Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017 FIGURE 3. Recordings from case 8 demonstrating induction of sustained paroxysmal supraventricular tachycardia (PSVT) after atropine. RA = right atrial electrogram; HBE = His bundle electrogram. Panel A demonstrates induction of only a single atrioventricular nodal reentrant atrial echo after cessation ofrapid atrialpacing at a paced cycle length (CL) of 500 msec before atropine. The critical A-H (slow-pathway conduction) was 610 msec. The atrial echo (Ae) was not followed by His bundle and verltricular responses, suggesting antegrade block in the slow pathway. Panel B demonstrates induction of sustained PSVT after atropine following cessation ofrapid atrial pacing at a paced CL of333 msec, which achieved a slow-pathway A-H of 400 msec. CL of PS VT was 500 msec. nique before and after atropine in only two patients, and was decreased in both patients after atropine (cases 1 and 5). shorter than that of the slow pathway or shorter than the ventricular functional refractory period (continuous V1-V2, A,-A, curves). Retrograde Fast Pathway Properties (table 1) Cycle Lengths of PSVT (table 1) Retrograde fast pathway conduction could be evaluated in nine patients before and after atropine by noting the longest ventricular paced cycle length producing VA block34 (cases 1-9) (figs. lB and ID). VA conduction was via fast pathway at short paced cycle lengths in most patients before atropine, and in all patients after atropine (see below).34 The ventricular paced cycle length producing VA block was 429 ± 36 msec (range 375-667 msec) before atropine, and decreased to <313 ± 7 msec (range 284-333) after atropine (p < 0.01). The retrograde effective refractory period of the fast pathway could be compared before and after atropine in seven patients (cases 1, 2, 4-7 and 13) and decreased from 390 ± 51 msec (range 250-650 msec) to <271 ± 14 msec (range <230-325 msec) after atropine (p < 0.05). The retrograde effective refractory period decreased in six of these seven patients. In seven patients (3, 8-12 and 14), retrograde fast pathway effective refractory periods could not be measured because of limiting ventricular refractoriness. Cycle lengths of PSVT could be compared in seven patients before and after atropine (cases 2, 3, 10-14) (figs. 1 A and C and 4A and C). Cycle lengths of PSVT ranged from 305-480 msec (mean ± SEM 383 ± 25 msec) before atropine, and ranged from 300-400 msec (mean ± SEM 334 ± 17 msec) after atropine. The cycle lengths of PSVT shortened significantly after atropine (p < 0.05). This shortening reflected decrease in both antegrade slow pathway conduction time (mean ± SEM). The A-H interval during PSVT decreased from 294 ± 18 to 226 ± 12 msec after atropine (p < 0.05), and retrograde fast pathway conduction time H-A during PSVT decreased from 89 ± 16 to 71 ± 12 msec after atropine (p < 0.05). A-H and H-A are only approximate measures of antegrade slow and retrograde fast pathway conduction time (H is distal to the final common pathway). Retrograde Slow Pathway Properties (table 1) Although retrograde effective refractory period of the slow pathway was achieved in four patients before atropine (1, 4, 6 and 7), it was not achieved in any of the 14 patients after atropine because retrograde effective refractory period of the fast pathway was either Discussion AV Nodal Reentrant PSVT Dual AV nodal pathways are demonstrable in most patients with AV nodal reentrant PSVT. In these patients, critically timed atrial premature stimuli block in a fast AV nodal pathway resulting in sudden increase in A-H interval (sole antegrade slow pathway conduction). If the blocked fast pathway is available for retrograde conduction, PSVT induction may result. The usual circus movement in these patients ATROPINE AND AV NODAL REENTRY/Wu et al. Control A 785 C L =333 VI _ ttl r- i S v S S s s %OA RA Al .l II !t CSA .. .-i Ae 'Ae iAe Ae ) 1. 71 He H HBE He'W He ,_ _ - 450 CL=273 Atropine B VI II RA -WY Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017 g CS A 9- S I 14"MN l-- ;iwtov j u -" I" RA 1 IpY m IF K mvftl.. He He .ll-.. -N. At_A2=220 A2-A3 = 270 CL=400 - J1 , -4 .SP_ 130~~~~~~~~~~~~~~~~~~~~~ _'l,;t),+~~~~~~~~~~~~~~~ C L-- VA t ---E- Ie S I \\ HBEE VI v , s <__l S ~FT1V\ViB S2 !i li[ CSA , I 8 . HBEA,HI4, H BE tY --' o 6 r Ik1 -1s'- A; AlHI 14 A2 H2 3 H3 He ns He l L_~ He N He k,N 340 FIGURE 4. Recordings from case 1I demonstrating induction ofsustained paroxysmal supraventricular tachycardia (PSVT) before and after atropine. RA = right atrial electrogram; CSA = coronary sinus electrogram; HBE = His bundle electrogram. Panel A demonstrates induction of sustained PSVTbefore atropine after cessation of rapid atrialpacing at a atrial paced cycle length (CL) of 333 msec, which achieved a slow-pathway A-H of 450 msec. CL of PSVT was 355 msec. Panel B demonstrates no induction of PSVT after atropine at a shorter atrial paced CL of 273 msec with an A-H (fast-pathway conduction) of 130 msec. Panel C demonstrates induction ofsustained PSVT after atropine with atrial extrastimulus testing. The basic driven CL was 400 msec. A ,-A2 was 220 msec, and A2 was still conducted via the fast-pathway. PSVT was induced by a premature atrial beat (PA B) (A3) after A2. The A3 achieved slow-pathway conduction with an A3-H3 of 340 msec. CL of PS VT was 300 msec. consists of a slow AV nodal pathway (antegrade), a fast AV nodal pathway (retrograde), a proximal common pathway, and a distal common pathway.1- 8 10, 12-16, 33-39 The occurrence of sustained AV nodal reentry requires the capability of repetitive antegrade slow pathway conduction and the capability for repetitive retrograde fast pathway conduction.'0' 33, 34 The cycle length of PSVT must be longer than the effective refractory period of any component of the circus pathway. '0 34 In patients with dual AV nodal pathways, inability to sustain PSVT reflects either depressed antegrade slow pathway or depressed retrograde fast pathway conduction. In patients with depressed slow pathway conduction, only single AV nodal reentrant atrial echoes or nonsustained PSVT can be induced with atrial stimulation.34 Termination of PSVT in these patients occurs when atrial responses are not followed by His bundle or ventricular responses, suggesting block in the antegrade limb of the circuit. In patients with depressed retrograde fast pathway conduction, induction of AV nodal reentrant atrial echoes may not be possible, or only nonsustained PSVT may be induced with atrial stimulation.34 Termination of PSVT in these patients occurs when QRS complexes are not followed by atrial responses, suggesting block in the retrograde limb of the circuit.'0 CIRCULATION 786 Control msec. 700 Atropi ne msec CL-400 - 700r '0.* 600 600k - A, -A, 7400 A, -AII-270 0 0 0 CL 400 - msec. 500- 500 F H, -H2 H2-H3 0 400- 0 400 400 msec. 5OOr7 0 0 -01 300L msec. 0 500r Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017 A2- H2 200 200 00*. 300 A0-Hs 200 100' S 1001 0 , I 200 300 400 Al - Al 500 0 400k 300 300 A2- H2 . 0 00 200 msec. 400r 00.o0 400 0 300 300L 0 0 H,- H2 200 300 400 Al - A2 200 300 A,-A3 Antiarrhythmic Agent and AV Nodal Reentrance Previous electrophysiological studies have demonstrated that antegrade and retrograde properties of both fast and slow pathway can be modified by antiarrhythmic agents, and the ability to induce or sustain PSVT may be suppressed or enhanced after drug administration.3 4 7-10 Propranolol, digitalis and verapamil increase antegrade slow pathway refractoriness.3' 4 7-8 There is little information regarding the effects of propranolol and verapamil on retrograde fast pathway conduction. Digitalis appears to have little effect on retrograde fast pathway refractoriness.3 All of these drugs inhibit the ability to sustain PSVT in some patients with AV nodal reentrance, by increasing refractoriness in the antegrade limb of the circus movement. Procainamide depresses retrograde fast pathway conduction and inhibits the ability to induce or sustain PSVT in the majority of the patients with AV nodal reentrant PSVT.10 However, procainamide may enhance antegrade slow pathway conduction due to vagolytic effect and potentiates the ability to sustain PSVT in a minority of patients with AV nodal reentrance. Effects of Atropine In this study, we demonstrated that atropine enhanced retrograde fast pathway and antegrade slow pathway conduction, and thus potentiated the ability to induce sustained PSVT. In seven patients with either no induction of AV nodal reentrant atrial echoes or induction of nonsustained PSVT due to depressed retrograde fast pathway conduction, improvement of retrograde fast pathway conduction was sufficient to allow induction of sustained PSVT after |- VOL 59, No 4, APRIL 1979 FIGURE 5. Atrioventricular (AV) conduction curves before and after atropine in case 7. The basic driven cycle length {CL) was 400 msec. Solid circles represent responses without echoes, while open circles represent responses with echoes. Left panel demonstrates discontinuous A1-A2, A2-H2 and A1A2, H1-H2 curves, suggesting dual A V nodal pathways before atropine. The effective refractory periods of the fast and slow pathway were 420 msec and < 290 msec, respectively. An echo zone was not defined. Middle panel demonstrates continuous A1A2, A1-H1 and A,-A2, H1-H2 curves after atropine. The curves became continuous because of shortening in antegrade fastpathway effective refractory period (< 260 msec). Right panel demonstrates discontinuous A2-A3, A4-H3 and A2-A3, H2-H3 curves after atropine, suggesting dual A V nodal pathways. The driven CL (A1-A1) was 400 msec, and A1-A2 was 270 msec. The effective refractory periods of the fast and slow-pathway were 290 msec and < 255 msec. The echo zotie coincided with the whole slow-pathway curve. atropine. In one of the two patients with induction of only single AV nodal reentrant atrial echoes due to depressed antegrade slow pathway conduction, the improvement of antegrade slow pathway conduction after atropine was sufficient to allow induction of sustained PSVT. Although atropine facilitated the induction of sustained AV nodal reentrant PSVT in patients with dual pathways with either inadequate antegrade slow pathway, or inadequate retrograde fast pathway conduction, PSVT induction in the laboratory was frequently more difficult after atropine administration. This reflected the effects of atropine on fast and slow pathways. Facilitation of fast pathway conduction frequently changed discontinuous to continuous conduction curves (decrease of fast pathway effective refractory period so that it was less than atrial functional refractory period). This prevented achievement of antegrade slow pathway conduction with the atrial extrastimulus technique. Despite the continuous conduction curves in these patients, failure of the fast pathway (with resultant antegrade slow pathway conduction and PSVT induction) could be achieved after atropine using either rapid incremental atrial pacing (repetitive rapid conduction may produce block in the fast pathway) or S1S2S3 stimulation. Even when discontinuous conduction curves were present after atropine administration, echo zones might not be delineated because of facilitation of antegrade slow pathway conduction, making achievement of the slow critical pathway A-H necessary for reentry difficult. Critical slow-pathway A-H could be achieved after atropine using other forms of atrial stimulation (rapid incremental atrial pacing and/or S1S2SS technique). In patients who had PSVT before and after ATROPINE AND AV NODAL REENTRY/Wu et al. atropine, atropine shortened the cycle length of PSVT, primarily due to shortening antegrade slow pathway conduction time (A-H). Although retrograde fast pathway conduction time (H-A) was also shortened after atropine, the amount of shortening was relatively small compared with shortening of antegrade slow pathway conduction time. Since induction of sustained PSVT requires the cycle length of PSVT to be longer than the effective refractory periods of any component of the reentrant circuit, it is theoretically possible (although not noted in our study) that atropine could also abolish the ability to sustain PSVT if shortening of PSVT cycle length exceeded shortening of refractory period of a portion of the reentrant circuit. Electrophysiological Applications Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017 This study has increased our knowledge of the nature of the fast AV nodal pathway. In a recent study, we demonstrated that procainamide selectively depressed retrograde and not antegrade fast pathway conduction, an unexpected response.10 We could not distinguish whether the retrograde fast pathway was an intranodal, atrionodal or extranodal structure. We also did not know whether the retrograde fast pathway was anatomically identical to the antegrade fast pathway. The present demonstration of marked facilitation of both antegrade and retrograde fast pathway conduction with atropine strongly suggests that the fast pathway is partially or totally within the AV node. In conclusion, atropine enhances antegrade slow pathway conduction, antegrade and retrograde fast pathway conduction, and allows induction of sustained PSVT. Facilitation of both antegrade and retrograde fast pathway conduction by atropine is consistent with the hypothesis that the fast pathway is partially or totally within the AV node. Induction of PSVT after atropine usually requires faster atrial paced rates (than before atropine) and/or double atrial extrastimuli. Inability to induce sustained PSVT in the catheterization laboratory in some patients with known PSVT due to AV nodal reentry probably reflects inadequate antegrade slow pathway or retrograde fast pathway conduction on the day of study (autonomically mediated). Administration of atropine in these patients may be useful in potentiating PSVT induction, thus helping to delineate the mechanism of tachycardia. References 1. Wu D, Denes P, Amat-y-Leon F, Wyndham C, Dhingra R, Rosen KM: Clinical electrocardiographic and electrophysiological observations in patients with paroxysmal supraventricular tachycardia. Am J Cardiol 41: 1045, 1978 2. Josephson ME, Kastor JA: Supraventricular tachycardia: mechanisms and management. Ann Intern Med 87: 346, 1977 3. 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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 recording in the isolated rabbit heart. Circ Res 28: 403, 1971 Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017 Effects of atropine on induction and maintenance of atrioventricular nodal reentrant tachycardia. D Wu, P Denes, R Bauernfeind, R C Dhingra, C Wyndham and K M Rosen Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017 Circulation. 1979;59:779-788 doi: 10.1161/01.CIR.59.4.779 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1979 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. 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