Self-conversion of drug-resistant paroxysmal atrial

tachycardia

Menashe B. Waxman, md; Clarence H. Felderhof, md; Eugene

John E. Morch,

md

Summary: A 56-year-old woman had paroxysmal atrial tachycardia (PAT) that was recurrent, drug-resistant and required frequent electroversion. The mode of onset and termination of initiated episodes of PAT suggested an AV junctional reentrant mechanism. The problem was successfully managed by a permanent electrode implanted transvenously in the coronary sinus and connected to a subcutaneous radio frequency receiver. For the past 24 months the patient has successfully terminated all episodes of PAT (at least 60) by activating an external radio frequency transmitter that transmits impulses to the implanted receiver and electrode catheter. Conversion to sinus rhythm requires 5 seconds or less of pacing.

Resume: Un cas de tachycardie paroxystique auriculaire pharmacoresistante traite par autoconversion Une femme de 56 ans souffrait d'une tachycardie paroxystique auri¬ culaire (TPA) qui etait recidivante, pharmacoresistante et exigeait de frequentes electroversions. La maniere dont I'episode de TPA debutait et se terminait permettait de croire a la presence d'un mecanisme reentrant a la jonction atrioventriculaire. Pour regler le probleme de cette malade de facon satisfaisante, on a implante une electrode permanente dans le sinus coronaire par voie intraveineuse et on I'a connectee a un recepteur de frequence radiophonique implante dans le tissu souscutane. Au cours des derniers 20 mois la malade a pu mettre fin, elle-meme, a tous les episodes de TPA (au moins 50) en activant une transmetteur externe de frequence radiophonique qui envoyait I'onde au recepteur implante et a I'electrode. De retour au rythme sinusal demandait au maximum 5 secondes de stimulation

Downar, md; Bernard S. Goldman, md;

recur infrequently, are confined to spe¬ cial circumstances, are of short dura¬ tion and terminate spontaneously.1 Moreover, many of these individuals are young and are free of any form of heart disease and therefore do not have hemodynamically adverse symp¬ toms. Some individuals, however, suffer considerable disability from this

in combination over the years but they had failed to prevent, modify or effect spontaneous conversion of the tachycar¬ dias. These drugs included digoxin, 0.25 to 0.5 mg/d; quinidine sulfate, 200 to 600 mg q6h; propranolol, 20 to 80 mg q6h; and procainamide, 250 to 500 mg q4-6h. Because of moderate obesity she had been unable to use the Valsalva maneuver or carotid sinus massage to effect self-conversion to sinus rhythm. Physical examination disclosed no ab¬ normalities apart from moderate obesity. The chest radiograph was normal. The resting electrocardiogram (ECG) after ad¬ mission was normal and without signs of ventricular pre-excitation in the form of a short PR segment or delta waves (Fig.

Case report

proximal portions of the ST segments. The attacks of PAT began and ended suddenly and Fig. 2 shows they could be abruptly ended by carotid sinus massage. The last RR interval of the tachycardia

tachyarrhythmia. We recently saw a 56-year-old fe¬ male patient who, although free of overt heart disease, had severe disability from recurrent PAT. Her repeated need for electroversion and her dependence on medical facilities made her life miserable. We success¬ 1). Fig. 2 illustrates a typical PAT episode fully used an external radio frequency tachycardia at about 150 pacemaker coupled to a permanent with a regular beats/min. The QRS complexes are narcoronary sinus electrode to terminate row. The P waves, which cannot be seen, her episodes of PAT. are buried within the QRS complexes and History and clinical findings A 56-year-old woman was admitted to the Toronto General Hospital in March was slightly prolonged. 1973 for evaluation of PAT. She had an 8-year history of PAT which recurred Selection of self-conversion method with varying frequency up to several times a week. Most of the attacks lasted many Induction of PAT: In order to assess hours and electroversion had often been the possibility of self-conversion we needed required. Drugs had been used singly or a reliable method of initiating attacks of

I

FIG. delta

1.Resting ECG recorded

at 25

mm/s. PR interval is normal. There

are no

waves.

CSM

cardiaque. The great majority of individuals who have paroxysmal atrial

(PAT)

are

because the

tachycardia significantly disabled, episodes of tachycardia

not

From the department of medicine of the University of Toronto and the cardiovascular unit of the Toronto General Hospital This work was supported in part by the Ontario Heart Foundation and the Medical Research Council of Canada. Reprint requests to: Dr. Menashe B. Waxman, Cardiovascular unit, Toronto General Hospital, 101

College St., Toronto, Ont. M5G 1L7

FIG. 2.Lead II recorded at 25 mm/s. Typical episode of PAT, with conversion to sinus rhythm after carotid sinus massage (CSM). The first beat after conversion is fusion between a sinus impulse and a ventricular escape beat.

600 CMA JOURNAL/MARCH 8, 1975/VOL. 112

a

Single well-timed premature atrial well as rapid atrial pacing, were effective in evoking PAT. Against the background of a constant spontaneous sinus rhythm, single premature atrial beats were introduced after every 10th basic beat. The entire cycle was scanned at 10-ms intervals until PAT was initiated. Fig. 3 illustrates the consequences of introduction of a very early premature atrial beat with a coupling interval of 330 ms. AV node conduction time slowed greatly, as reflected by a very prolonged A2H2 interval (compared with control interval A,H,). Typical PAT at 180 beats/min PAT.

beats,

as

HBE

f ift

%)

i

then occurred, during which atrial activity coincided with the QRS complexes so that P waves could not be seen on the surface ECG tracing. The effects of premature atrial beats on AV conduction are summarized in Fig. 4, which depicts a plot of the coupling in¬ terval of the premature atrial beat AiA.. against the interval between the basic His deflection and the His deflection of the premature beat HiH2. Late coupled pre¬ mature beats did not introduce any addi¬ tional AV delay and therefore the AiAo intervals equal the HxH2 intervals. These points fail along a 45° slope. As the

Hy*"Tfr

f-Hfl

fmmTi', r*"iVr*

coupling interval was shortened, the re¬ fractory period of the AV node was encroached on and the HiH2 response deviated from the line of identity as an

expression of the increase in AV node conduction time. PAT was initiated when the encroachment was sufficient to prolong AV node conduction time to a critical degree. A coupling interval of about 330 ms was highly consistent in

evoking PAT. Atrial pacing, when sufficiently rapid to produce a delay in AV node conduc¬ tion time similar to that seen in Fig. 4, induced PAT (Fig. 5). The atria were paced at increasing rates through the coronary sinus. AV node conduction time, most easily seen as stimulus artefact (de¬ noted by arrows) to QRS complex time, increased as the pacing rate increased. The PR interval lengthened so much that the stimulus artefacts were increasingly closer to the preceding QRS complex. The stimulator was turned off at the last ar¬ row and the last seven beats are part of an initiated episode of PAT.

BAE-H

800

600

H1H2 ms FIG. 3.Induction of PAT by premature atrial beat. Upper panel shows simultaneous recording of lead Vu His bundle electrogram (HBE) and bipolar atrial electrogram (BAE), with induction of PAT by premature atrial beat (introduced at arrow); vertical lines at 1-s intervals. Lower panel represents ladder diagram, indicating probable AV junctional reentrant circuit.

400

PAT4

200

^

Lll

00

400

600

800

ms

FIG. 4.Plot of coupling interval of atrial premature beat (AxA2) against in¬ terval between basic His deflection and His deflection of premature beat (HiH?;. Arrow indicates coupling interval at which PAT was induced.

FIG.

5.Rapid atrial pacing through coronary sinus (lead II, 50 mm/s). Increasing pacing slowed AV conduction interval (arrows represent stimulus artefacts).

rate of

Pacemaker was turned off at last arrow and the last part of an initiated attack of PAT at 165 beats/min.

seven

beats

are

Termination of PAT: Termination of the tachycardia could be achieved easily by single premature atrial depolarizations or by rapid right atrial pacing so that the atria were "captured" just before they were due to be depolarized by the PAT process. Fig. 6 illustrates how a single well-timed premature atrial stimulus ter¬ minated an episode of PAT. Because of the complexities involved in

permanent pacing using single specifically timed pulses,

in

V" BAE-

J*m*J*mmJ*mmJfi*mAV WAl

m.X

FIG. 6.Simultaneous recording of leads I, III, Vt and BAE during episode of PAT. Premature atrial depolarization (arrow) terminated tachycardia. Vertical lines at l-s

intervals.

we determined whether rapid asynchronous right atrial pacing, which is much simpler to use, might be equally effective in converting episodes of PAT. Accordingly, an episode of PAT was ini¬ tiated and the right atrium paced at 270 beats/min (Fig. 7); within 1 second of pacing, the PAT was converted back to normal sinus rhythm. Electrode implantation Having established the ease with which asynchronous right atrial pacing could stop the PAT, we turned our attention to possible electrode sites. Because of the potential difficulties in maintaining a stable and secure atrial endocardial site, and because we did not wish to subject

CMA JOURNAL/MARCH 8, 1975/VOL. 112 601

this woman to a thoracotomy, we implanted an electrode in the coronary sinus (Fig. 8). This position proved to be as effective as any intra-atrial site, and a rate of 300 beats/mm terminated 100% of attacks within 5 seconds. We also assessed whether coronary sinus pacing would directly stimulate the ventricles; despite high current pulses, coronary sinus pacing always produced supraventricular capture and did not directly stimulate the ventricles. Because of the asynchronous nature of the pacing, the inadvertent induction of atrial fibrillation and its effect on the ventricular response appeared possible problems. Attempts to purposely induce atrial fibrillation failed. Accordingly, the coronary sinus was paced at 300 beats! mm; the ventricular response never exceeded 2:1 under resting or exercise conditions. The electrode was connected to a small subcutaneous radio frequency receiver. Whenever the patient wishes to convert an episode of PAT she simply transmits impulses from a pocket-sized transmitter across the skin to the coronary sinus. Over the 24 months since the implantation the electrode position has remained stable and the patient has terminated all episodes of PAT (more than 60) with the pacemaker. Fig. 9 shows conversion of PAT as a result of coronary sinus pacing for 3 seconds initiated by the patient. Discussion Much clinical24 and animal5'6 experimentation suggests that PAT most frequently is a reentrant arrhythmia involving the AV junction. Premature depolarization of the reentrant circuit by single or multiple atrial or ventricular premature beats can terminate such tachycardias.7 A critical increase in AV node conduction time induced by premature atrial beats or by rapid right atrial pacing was essential in initiating the PAT of our patient. This strongly suggests that in her, PAT was a reentrant arrhythmia involving the AX1 node. Termination of the tachycardia by carotid sinus massage further supports the concept of a reentrant circuit involving a vagally innervated structure such as the AV node or sinus node. The

!

V

!

RR interval prolongation before PAT termination by :carotid sinus massage (Fig. 2) is consistent with slowing of conduction within an AV junctional reentrant circuit.4 Temporary right atrial and right ventricular pacing have been used to terminate episodes of PAT or atrial flutter.8'. But currently we know of only four reports describing the use of permanent pacemakers to convert or slow the ventricular response in recurrent attacks of PAT.'3-'6 Three of the patients whose cases were reported had the Wolff-Parkinson-White syndrome.'3-'5 In two of the four patients asynchronoUs right ventricular pacing was used to terminate episodes of PAT.13"5 Conceivably competitive ventricular pacing could induce an episode of ventricular tachycardia or fibrillation.'7 In the other two patients the electrodes were implanted directly on the right or left atrial appendage by thoracotomy.'4"6 We used the transvenous route to implant the electrode into the coronary sinus. From our experience with this patient and the experience of others,'8 we believe that the coronary sinus is a suitable, safe and stable site for right atrial pacing. One must ensure, however, that direct ventricular capture does not result. The advantages in transvenous implantation over thoracotomy are obvious in an obese patient such as ours, or in selected patients who are seriously ill, very young or very old. We selected a radio frequency type of external pacemaker for several reasons: first, the patient controls it; second, the rapid rate required for selftermination could drain a battery rapidly and therefore external replacement of power cells seemed desirable; and third, the pacing rate required for conversion could easily be adjusted when necessary. The authors thank Miss Darla Dawes for her secretarial work, Mr. Paul Citron of the Medtronic Company for supplying the radio frequency pacemaker, and Dr. James J. Morris, Jr. of Duke University for his helpful advice.

References 1. FRIEDBERO CK: Diseases of the Heart, third edition. Philadelphia, Saunders, 1966 2. HUNT NC, COBB FR, WAXMAN MB, et al: Conversion of supraventricular tachycardias with atrial stimulation: evidence for reentry mechanisms. Circulation 38: 1060, 1968 3. BIGGER JT JR, GOLDREYER BN: The mechanism of supraventricular tachycardia. Circulation 42: 673, 1970 4. GOLDREYER BN, BIGGER JT .i.: Site of reentry in paroxysmal supraventricular tachycardia in man. Circulation 43: 15, 1971 5. WIT AL, GOLDREYER BN, DAMATO AN: An in vitro model of paroxysmal supraventricular tachycardia. ibid, p 862 6. MoE GK, COHEN W. VICE RL: Experimentally induced paroxysmal A-V nodal tachycardia in the dog. .4m Heart J 65: 87, 1963 7. WELLENS JHH: Electrical Stimulation of the Heart in the Study and Treatment of Tachycardias. Baltimore, Univ Park, 1971 8. MAssuMI RA, KIsTIN AD, TAWAKEOL AA: Termination of reciprocating tachycardia by atrial stimulation. Circulation 36: 637, 1967 9. ZEFT HJ, Coes FR, WAXMAN MB, et al: Right atrial stimulation in the treatment of atrial flutter. Ann Intern Med 70: 447, 1969 10. LISTER JW, COHEN LS, BERNSTEIN WH, et al: Treatment of supraventricular tachycardias by rapid atrial stimulation. Circulation 38: 1044, 1968 11. VERGARA GS, HILDNER FJ, SCHOENFELD CB. et al: Conversion of supraventricular tachycardias with rapid atrial stimulation. Circulation 46: 788, 1972 12. ZEFT JH, MCGOWAN RL: Termination of paroxysmal junctional tachycardia by right ventricular stimulation. Circulation 40: 919, 1969 13. RYAN GF, EASLEY RM JR, ZAROFF LI, et al: Paradoxical use of a demand pacemaker in treatment of supraventricular tachycardia due to Wolff-Parkinson-White syndrome: observations on termination of reciprocal rhythm. Circulution 38: 1037, 1968 14. PRESTON TA, KIRsH MM: Permanent pacing of the left atrium for treatment of WPW Iachycardia. Circulation 42: 1073, 1970 15. DREIFUS LS, ARRIAGA J, WATANABE Y, et al: Recurrent Wolff-Parkinson-White tachycardia in an infant: successful treatment by a radio frequency pacemaker. Am I Cardiol 28: 586, 1971 16. DAvIDsoN RM, WALLACE AG, SEALEY WC, et

al: Electrically induced atrial tachycardia with block: a therapeutic application of permanent radio frequency atrial pacing. Circulation 44: 1014, 1971 17. SURAWICZ B: Ventricular fibrillation. Am I Cardiol 28: 268. 1971 18. KRAMER DH, Moss AJ: Permanent pervenout atrial pacing from the coronary vein. Circulation

4"

427

1970

'

BAE-'.m--' .

FYI

IlF'I

Ij

'II,' ii I:

HG. 8-Anteroposterior chest radiograph after implantation of electrode in coronary sinus. Receiver is beneath left shoulder.

L II

H H

H

H11

H

LII J\JJy. A A

A

A

A

A

A

t.P.-

FIG. 7-Simultaneous recording of BAE, HBE and lead 11 during episode of PAT: His bundle potentials indicated by H. Asynchronous right atrial pacing (arrows) at 270 beats/mm terminated the tachycardia. Vertical lines at I-s intervals.

i-

FIG. 9-Lead 11 during episode of spontaneous PAT 5 months after implantation of electrode. Patient selfconverts tachycardia by coronary sinus pacing (dots) lasting 2.5 s at a rate of 300 beats/mm.

CMA JOURNAL/MARCH 8, 1975/VOL. 112

603

Self-conversion of drug-resistant paroxysmal atrial tachycardia.

A 56-year-old woman had paroxysmal atrial tachycardia (PAT) that was recurrent, drug-resistant and required frequent electroversion. The mode of onset...
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