Self-Initiated Conversion of Paroxysmal Atrial Flutter Utilizing a Radio-Frequency Pacemaker
CHRISTOPHER R. WYNDHAM, MB, FRACP DELON WU, MD, FACC PABLO DENES, MD, FACC DANIEL SUGARMAN, MD SIDNEY LEVITSKY, MD KENNETH M. ROSEN, MD, FACC
A patient is described with drug-resistant recurrent paroxysmal atrial flutter. Electrophysiologic studies demonstrated that flutter was inducible with rapid atrial stimulation (stimulation rates of 375 to 4OO/min) and convertible with rapid atrial stimulation (rates of 400 to 460/min). Because of the latter response, a radio-frequency atrial pacemaker was implanted, which allowed self-initiated conversion of flutter episodes with rapid stimulation.
Chicago, Illinois
Rapid atria1 pacing has been utilized for successful conversion of atria1 flutter. In previous reports, rapid atria1 stimulation was performed utilizing temporary electrodes either in the catheterization laboratory or in the intensive or coronary care unit. l-l4 There is no previous study using rapid atria1 pacing with a permanently implanted system for conversion of chronic recurrent paroxysmal atria1 flutter. In this report, we describe a patient with incapacitating recurrent paroxysmal atrial flutter in whom control of the arrhythmia was achieved with self-initiated rapid atria1 pacing utilizing a radio-frequency pacemaker. Report of Case
From the Department of Medicine, Cardiology Section, University of Illinois Hospital, Chicago, Illinois. This study was funded in part by Training Grant HL 05879-07 and PHS Grant HL 18794-02, from the U. S. Public Health Service, Bethesda, Maryland. Manuscript received November 8,1977; revised manuscript received January 25. 1978, accepted January 25, 1978 Address for reprints: Kenneth M. Rosen, MD, Cardiology Section, Unrverstty of Illinois Hospital, P.O. Box 6998, Chicago, lllrnors 60680.
The patient, a 55 year old man with diabetes, was referred to the Umversity of Illinois Hospital in October 1975 with a history of recurrent paroxysmal atria1 flutter since 1964. Episodes of atria1 flutter were accompanied by chest discomfort, dizziness, fatigue and sweating. Attacks had increased in frequency to approximately one to three per day since 1973, with most individual attacks lasting from 30 minutes up to 12 hours. The patient required 20 direct current cardioversions in 1975 for episodes lasting 12 to 48 hours and was forced to retire prematurely from work. Previous medications had included digoxin (up to 0.75 mg/day) and propranolol (up to 160 mg/day), without slowing of ventricular response or prevention of attacks. Quinidine (600 mg/day) produced intolerable diarrhea without preventing arrhythmia. Physical examination was within normal limits. Electrocardiograms were within normal limits, except for sustained paroxysms of atria1 flutter with 2:1 block (Fig. 1). Chest X-ray film, echocardiogram, treadmill exercise test, left ventriculogram and coronary angiograms were within normal limits. Electrophysiologic studies were performed in November 1975, using a quadripolar electrode catheter placed in the high right atrium for right atria1 recording and stimulation, and a tripolar catheter for recording of His bundle electrograms. A-H and H-V intervals were within normal limits (82 and 30 msec, respectively) during sinus rhythm at a cycle length of 660 msec. Rapid incremental atria1 pacing resulted in atrioventricular (A-V) nodal Wenckebach periodicity at paced rates of 200lmin and greater, and reproducible induction of sustained atria1 flutter at paced rates of 375 to 400/min (Fig. 2A). Atria1 flutter cycle length was 200 msec with 21 A-V conduction. Termination of atria1 flutter, either directly to sinus rhythm or by way of brief nonsustained atria1 fibrillation, occurred reliably after short bursts of atria1 pacing at 400 to 460/min (Fig. 2B). May 22, 1978
The American Journal of CARDIOLOGY
Volume 41
1119
&____
A,trial_ Pacing
CL* I,60 y--7i
1
aVL
aVF
__.
_.
_-
--
- ---
FIGURE 3 (bottom). Postoperative lead II rhythm strip showing atrral flutter, mductron of radio-frequency-triggered to normal sinus rhythm after nonsustarned atrral frbrillatron.
atrtal pacing at 470/mm wrth atria1 capture and conversion
FIGURE 2 (center). Electrode catheter induction (A) and termrnation (6) of atrrai flutter Shown tn each panel are lead II and a high right atrial electrogram (HRA). CL = paced cycle length (msec); NSR = normal sinus rhythm
FIGURE 1 (top). Electracardrogram showing typrcal atrial flutter wrth 21 atrioventricular response.
1
aVR
PACEMAKER
Implantation of radio-frequency pacing system: After initial study, the quadripolar catheter was left indwelling for high right atria1 stimulation during subsequent daily intravenous drug trial. Atria1 flutter was reliably induced both before and after intravenous administration of ouabain (0.75 mg), propranolol (7.5 mg) and procainamide (750 mg) on subsequent days. All induced episodes (as well as spontaneous episodes) of atria1 flutter were readily converted to sinus rhythm with rapid atria1 stimulation. Because of inability to define drug therapy that prevented induction of atria1 flutter, a transthoracic bipolar radio-frequency pacing system (Medtronics model 1258) using pediatric plaque electrodes (Medtronics model 5815) attached to the anterolateral right atrium was implanted in December 1975. Bipolar stimulus threshold was 0.7 v at 1.3 milliamperes as measured with a Medtronics model 5300 pacing systems analyzer delivering a rectangular impulse of 1 msec duration. In the postoperative period, multiple episodes of atria1 flutter were converted with radio-frequency atrial stimulation at a rate of 450/min to atria1 fibrillation and then to sinus rhythm (Fig. 3). The patient was instructed in the use of the system and discharged 10 days later. Subsequent course: The patient did well for 3 weeks, using the radio-frequency pacemaker for self-initiated conversion of atria1 flutter approximately one to four times daily, activating the transmitter for 5 to 10 seconds at a rate of 450/min. However, within 2 weeks of discharge, sustained episodes of atria1 fibrillation were induced, rather than immediate conversion of atria1 fibrillation to sinus rhythm. The patient was again readmitted to the University of Illinois in January 1976. With use of the radio-frequency pacemaker to induce flutter, it was easily demonstrated that both procainamide alone (3 g/day) and propranolol (160 mg/day) potentiated conversion of flutter to sinus rhythm by preventing induction of sustained atrial fibrillation. Oral propranolol, 160 mg/day, was given. The patient was discharged in February 1976 and returned to full employment, using the radio-frequency pacemaker to convert atria1 flutter to sinus rhythm approximately one to three times daily. In March 1977, the frequency of attacks increased, the patient having to use the pacemaker up to five to six times at night, and repeatedly during the day. Procainamide (2 g/day) decreased the frequency of attacks to two to four daily. The patient now uses his pacemaker two to four times daily and has had a beneficial effect from combined therapy designed to limit the frequency of attacks of atria1 flutter (procainamide) and to limit the duration of pacinginduced atria1 fibrillation (propranolol). He has now been followed up a total of 21 months since pacemaker implantation.
Discussion This is the first reported case of reproducible induction of atria1 flutter by rapid atria1 stimulation (rates of 375 to 400/min) in a patient with known recurrent paroxysmal atria1 flutter. The reproducible conversion (either directly to sinus rhythm or by way of atria1 fibrillation) with rapid stimulation at rates of 400 to 460/min are consistent with previous reports using temporary electrode catheters. These electrophysiologic findings are most consistent with an atria1 reentrant mechanism as a basis for flutter in this patient.15 Advantages of radiofrequency pacemaker system: The prior history of intractability to drug therapy,
CONVERSION
OF ATRIAL FLUTTER-WYNDHAM
ET AL
as well as the inability to define a drug that inhibited induction of flutter, suggested that an invasive mode of therapy would be indicated. In light of previous reportsl6-22 of successful use of a radio-frequency pacemaker for self-conversion of paroxysmal supraventricular tachycardia, a radio-frequency pacemaker system was implanted with epicardial leads sutured on the right atrium. This system had the following advantages: (1) An external power source that was easily replaceable; (2) external control of atria1 rate within a wide range; and (3) ability to initiate rapid stimulation by external control (by either physician or patient). The implanted system was then demonstrated to allow physician- and patient-initiated conversion of atria1 flutter with rapid atria1 stimulation. It is probable that other pacemaker systems allowing self-initiation of rapid atria1 stimulation would have achieved identical results. Although the system functioned adequately from the time of implantation, additional pharmacologic therapy was needed to achieve clinically satisfactory control of arrhythmia. Propranolol was demonstrated to prevent induction of sustained atria1 fibrillation by the radiofrequency pacemaker. Procainamide was successfully used to decrease the frequency of attacks, necessitating less frequent use of the system.
Requirements for successful tem: Use of the radio-frequency
application
of sys-
pacemaker requires that the patient be sufficiently well motivated to tolerate investigation involving repetitive arrhythmia induction and termination and also be sufficiently clinically disabled by the arrhythmia to justify this approach. Similarly, providing such a pacemaker to a patient is only practicable when the patient fully understands the working of the unit and when it should be used; that is, he should have some definite means of identifying the presence of the arrhythmia and be able to ascertain the presence or absence of sinus rhythm after use of the pacemaker. Successful use of the radio-frequency pacing system also requires extensive prior electrophysiologic studies and a full understanding of the nature and mechanism of the patient’s arrhythmia. Furthermore, permanent pacing therapy is appropriate only when previous extensive trial has shown that the arrhythmia is resistant to several appropriate drugs, singly or in combination, or that drug toxicity has prevented pharmacologic control. The general principle to be derived from our findings is that, in the management of a patient with a paroxysmal tachyarrhythmia that can be reliably and reproducibly induced and terminated by pacing techniques and for which extensive pharmacologic trial has proved unsuccessful, an external patient- or physician-controlled radio-frequency pacing system may provide a practical alternative mode of therapy. Acknowledgment Dr. Elaine Rosin, Cincinnati, Ohio kindly referred the patient. Medtronics, Inc. generously donated the radio-frequency pacemaker. The expert assistance of Loretta Kasparas, RN, Charles Christensen and Therese Molyneux is appreciated.
May 22, 1978
The American Journal of CARDIOLOGY
Volume 41
1121
PACEMAKER
CONVERSION
OF ATRIAL FLUTTER-WYNDHAM
ET AL
References 1 Zeft HG, Cobb FR, Waxman MB, et al: Right atrial stimulation In the treatment of atrial flutter. Ann Intern Med 70:447-456, 1969 2 Hafl JI, Kosowsky BD, Lau SH, et al: Termination of atrial flutter by raprd electrical pacing of the right atrium Am J Cardiol 20. 239-244, 1967 3 Gulotta SJ, Aronson AL: Cardioversron of atrial tachycardra and flutter by atrial stimulation. Am J Cardrol 26.262-269, 1970 4. Chamberlain DA, Coltarl DJ, Ead HA: Conversion of atrial flutter or tachycardia to atrial fibrillation by rapid atrial stimulation (abstr). Br Heart J 33.613, 1971 5. Zipes DP: The contribution of artificial pacemaking to understanding the pathogenesis of arrhythmias Am J Cardiol 28:211-222, 1971 6. Cheng TO: Rapid atrial pacing in treatment of atrial flutter and atrial tachycardia (abstr). Clin Res 19:307, 1971 7. Plttman DE, Makar JS, Kooros KS, et al: Right atria1 stimulation. successful method of conversion of atrral flutter and atrial tachycardra Am J Cardiol: 32:700-706, 1973 a. Preston TA: Atrial pacing to convert atrial flutter (abstr) Am J Cardiol 32:737, 1973 9 Puech P, Grolleau R, Latour H, et al: Trartement du flutter auricularre par la stimulation auriculaire endocavitaire Arch Mal Coeur 66.159-167, 1973 10 Rosen KM, Slnno MZ, Gunnar RM, et al: Failure of rapid atrial pacing in the conversion of atrial flutter Am J Cardiol 29524-528, 1972 11 Vergara GS, Hildner FJ, Schoenfeld CB: Conversion of supraventricular tachycardias with rapid atrial stimulation. Circulation 461788-793, 1972 12. Plttman DE, Gay TC, Pate1 II: Termination of atria1 flutter and atrial tachycardias with rapid atrial stimulation Angiology 26:784-802, 1975
1122
May 22, 1976
The American
Journal of CARDIOLDGY
13. Orlando J, Cassldy J, Aronow WS: High reversion of atrial flutter to sinus rhythm after atrial pacing in patients with pulmonary disease. Chest 71:580-582, 1977 14. MacLean WAH, Karp RB, Kouchoukos NT, et al: Uniformly successful interruption of atrial flutter with rapid atrial pacing in 100 patients (abstr). Circulation 54. Suppl 11~11-167, 1976 15. Wu D, Denes P: Mechanisms of paroxysmal supraventncular tachycardia. Arch Int Med 135.437-442. 1975. 16 Glenn WWL, Mauro A, Longo E, et al: Remote stimulatron of the heart by radio-frequency transmission N Engl J Med 261:948-951, 1959 17. Glenn WWL, Furman S, Gordon AJ, et al: Radio-frequency controlled catheter pacemaker Clrnical applrcatron N Engl J Med 275:137-140, 1966 la. Davidson RM, Wallace AG, Sealy WC, et al: Electrically induced atrial tachycardra with block. A therapeutrc applicahon of permanent radio-frequency atrial pacing. Circulation 44:1014-1021, 1971 19 Williams DO, Davison PH: Long-term treatment of refractory supraventricular tachycardia by patient-controlled inductive atrial pacing. Br Heart J 36:336-340, 1974 20. Goyal SL, Lichsfein E, Gupta PK, et al: Refractory reentrant atrial tachycardia. Successful treatment with a permanent radio-frequency triggered atrial pacemaker Am J Med 58 586-590, 1975 21. Dreifus LS, Arriaga J, Watanabe Y, et al: Recurrent Wolff-Parkinson-white tachycardia in an infant. Successful treatment by a radio-frequency pacemaker. Am J Cardiol 28586-591, 1971 22. Fruehan CT, Meyer JA, Klie JH, et al: Refractory paroxysmal supraventricular tachycardia. Treatment with patient-controlled permanent radio-frequency atrial pacemaker Am Heart J 87. 229-237,1974
Volume 41
CHRISTOPHER R. WYNDHAM, MB, FRACP DELON WU, MD, FACC PABLO DENES, MD, FACC DANIEL SUGARMAN, MD SIDNEY LEVITSKY, MD KENNETH M. ROSEN, MD, FACC
A patient is described with drug-resistant recurrent paroxysmal atrial flutter. Electrophysiologic studies demonstrated that flutter was inducible with rapid atrial stimulation (stimulation rates of 375 to 4OO/min) and convertible with rapid atrial stimulation (rates of 400 to 460/min). Because of the latter response, a radio-frequency atrial pacemaker was implanted, which allowed self-initiated conversion of flutter episodes with rapid stimulation.
Chicago, Illinois
Rapid atria1 pacing has been utilized for successful conversion of atria1 flutter. In previous reports, rapid atria1 stimulation was performed utilizing temporary electrodes either in the catheterization laboratory or in the intensive or coronary care unit. l-l4 There is no previous study using rapid atria1 pacing with a permanently implanted system for conversion of chronic recurrent paroxysmal atria1 flutter. In this report, we describe a patient with incapacitating recurrent paroxysmal atrial flutter in whom control of the arrhythmia was achieved with self-initiated rapid atria1 pacing utilizing a radio-frequency pacemaker. Report of Case
From the Department of Medicine, Cardiology Section, University of Illinois Hospital, Chicago, Illinois. This study was funded in part by Training Grant HL 05879-07 and PHS Grant HL 18794-02, from the U. S. Public Health Service, Bethesda, Maryland. Manuscript received November 8,1977; revised manuscript received January 25. 1978, accepted January 25, 1978 Address for reprints: Kenneth M. Rosen, MD, Cardiology Section, Unrverstty of Illinois Hospital, P.O. Box 6998, Chicago, lllrnors 60680.
The patient, a 55 year old man with diabetes, was referred to the Umversity of Illinois Hospital in October 1975 with a history of recurrent paroxysmal atria1 flutter since 1964. Episodes of atria1 flutter were accompanied by chest discomfort, dizziness, fatigue and sweating. Attacks had increased in frequency to approximately one to three per day since 1973, with most individual attacks lasting from 30 minutes up to 12 hours. The patient required 20 direct current cardioversions in 1975 for episodes lasting 12 to 48 hours and was forced to retire prematurely from work. Previous medications had included digoxin (up to 0.75 mg/day) and propranolol (up to 160 mg/day), without slowing of ventricular response or prevention of attacks. Quinidine (600 mg/day) produced intolerable diarrhea without preventing arrhythmia. Physical examination was within normal limits. Electrocardiograms were within normal limits, except for sustained paroxysms of atria1 flutter with 2:1 block (Fig. 1). Chest X-ray film, echocardiogram, treadmill exercise test, left ventriculogram and coronary angiograms were within normal limits. Electrophysiologic studies were performed in November 1975, using a quadripolar electrode catheter placed in the high right atrium for right atria1 recording and stimulation, and a tripolar catheter for recording of His bundle electrograms. A-H and H-V intervals were within normal limits (82 and 30 msec, respectively) during sinus rhythm at a cycle length of 660 msec. Rapid incremental atria1 pacing resulted in atrioventricular (A-V) nodal Wenckebach periodicity at paced rates of 200lmin and greater, and reproducible induction of sustained atria1 flutter at paced rates of 375 to 400/min (Fig. 2A). Atria1 flutter cycle length was 200 msec with 21 A-V conduction. Termination of atria1 flutter, either directly to sinus rhythm or by way of brief nonsustained atria1 fibrillation, occurred reliably after short bursts of atria1 pacing at 400 to 460/min (Fig. 2B). May 22, 1978
The American Journal of CARDIOLOGY
Volume 41
1119
&____
A,trial_ Pacing
CL* I,60 y--7i
1
aVL
aVF
__.
_.
_-
--
- ---
FIGURE 3 (bottom). Postoperative lead II rhythm strip showing atrral flutter, mductron of radio-frequency-triggered to normal sinus rhythm after nonsustarned atrral frbrillatron.
atrtal pacing at 470/mm wrth atria1 capture and conversion
FIGURE 2 (center). Electrode catheter induction (A) and termrnation (6) of atrrai flutter Shown tn each panel are lead II and a high right atrial electrogram (HRA). CL = paced cycle length (msec); NSR = normal sinus rhythm
FIGURE 1 (top). Electracardrogram showing typrcal atrial flutter wrth 21 atrioventricular response.
1
aVR
PACEMAKER
Implantation of radio-frequency pacing system: After initial study, the quadripolar catheter was left indwelling for high right atria1 stimulation during subsequent daily intravenous drug trial. Atria1 flutter was reliably induced both before and after intravenous administration of ouabain (0.75 mg), propranolol (7.5 mg) and procainamide (750 mg) on subsequent days. All induced episodes (as well as spontaneous episodes) of atria1 flutter were readily converted to sinus rhythm with rapid atria1 stimulation. Because of inability to define drug therapy that prevented induction of atria1 flutter, a transthoracic bipolar radio-frequency pacing system (Medtronics model 1258) using pediatric plaque electrodes (Medtronics model 5815) attached to the anterolateral right atrium was implanted in December 1975. Bipolar stimulus threshold was 0.7 v at 1.3 milliamperes as measured with a Medtronics model 5300 pacing systems analyzer delivering a rectangular impulse of 1 msec duration. In the postoperative period, multiple episodes of atria1 flutter were converted with radio-frequency atrial stimulation at a rate of 450/min to atria1 fibrillation and then to sinus rhythm (Fig. 3). The patient was instructed in the use of the system and discharged 10 days later. Subsequent course: The patient did well for 3 weeks, using the radio-frequency pacemaker for self-initiated conversion of atria1 flutter approximately one to four times daily, activating the transmitter for 5 to 10 seconds at a rate of 450/min. However, within 2 weeks of discharge, sustained episodes of atria1 fibrillation were induced, rather than immediate conversion of atria1 fibrillation to sinus rhythm. The patient was again readmitted to the University of Illinois in January 1976. With use of the radio-frequency pacemaker to induce flutter, it was easily demonstrated that both procainamide alone (3 g/day) and propranolol (160 mg/day) potentiated conversion of flutter to sinus rhythm by preventing induction of sustained atrial fibrillation. Oral propranolol, 160 mg/day, was given. The patient was discharged in February 1976 and returned to full employment, using the radio-frequency pacemaker to convert atria1 flutter to sinus rhythm approximately one to three times daily. In March 1977, the frequency of attacks increased, the patient having to use the pacemaker up to five to six times at night, and repeatedly during the day. Procainamide (2 g/day) decreased the frequency of attacks to two to four daily. The patient now uses his pacemaker two to four times daily and has had a beneficial effect from combined therapy designed to limit the frequency of attacks of atria1 flutter (procainamide) and to limit the duration of pacinginduced atria1 fibrillation (propranolol). He has now been followed up a total of 21 months since pacemaker implantation.
Discussion This is the first reported case of reproducible induction of atria1 flutter by rapid atria1 stimulation (rates of 375 to 400/min) in a patient with known recurrent paroxysmal atria1 flutter. The reproducible conversion (either directly to sinus rhythm or by way of atria1 fibrillation) with rapid stimulation at rates of 400 to 460/min are consistent with previous reports using temporary electrode catheters. These electrophysiologic findings are most consistent with an atria1 reentrant mechanism as a basis for flutter in this patient.15 Advantages of radiofrequency pacemaker system: The prior history of intractability to drug therapy,
CONVERSION
OF ATRIAL FLUTTER-WYNDHAM
ET AL
as well as the inability to define a drug that inhibited induction of flutter, suggested that an invasive mode of therapy would be indicated. In light of previous reportsl6-22 of successful use of a radio-frequency pacemaker for self-conversion of paroxysmal supraventricular tachycardia, a radio-frequency pacemaker system was implanted with epicardial leads sutured on the right atrium. This system had the following advantages: (1) An external power source that was easily replaceable; (2) external control of atria1 rate within a wide range; and (3) ability to initiate rapid stimulation by external control (by either physician or patient). The implanted system was then demonstrated to allow physician- and patient-initiated conversion of atria1 flutter with rapid atria1 stimulation. It is probable that other pacemaker systems allowing self-initiation of rapid atria1 stimulation would have achieved identical results. Although the system functioned adequately from the time of implantation, additional pharmacologic therapy was needed to achieve clinically satisfactory control of arrhythmia. Propranolol was demonstrated to prevent induction of sustained atria1 fibrillation by the radiofrequency pacemaker. Procainamide was successfully used to decrease the frequency of attacks, necessitating less frequent use of the system.
Requirements for successful tem: Use of the radio-frequency
application
of sys-
pacemaker requires that the patient be sufficiently well motivated to tolerate investigation involving repetitive arrhythmia induction and termination and also be sufficiently clinically disabled by the arrhythmia to justify this approach. Similarly, providing such a pacemaker to a patient is only practicable when the patient fully understands the working of the unit and when it should be used; that is, he should have some definite means of identifying the presence of the arrhythmia and be able to ascertain the presence or absence of sinus rhythm after use of the pacemaker. Successful use of the radio-frequency pacing system also requires extensive prior electrophysiologic studies and a full understanding of the nature and mechanism of the patient’s arrhythmia. Furthermore, permanent pacing therapy is appropriate only when previous extensive trial has shown that the arrhythmia is resistant to several appropriate drugs, singly or in combination, or that drug toxicity has prevented pharmacologic control. The general principle to be derived from our findings is that, in the management of a patient with a paroxysmal tachyarrhythmia that can be reliably and reproducibly induced and terminated by pacing techniques and for which extensive pharmacologic trial has proved unsuccessful, an external patient- or physician-controlled radio-frequency pacing system may provide a practical alternative mode of therapy. Acknowledgment Dr. Elaine Rosin, Cincinnati, Ohio kindly referred the patient. Medtronics, Inc. generously donated the radio-frequency pacemaker. The expert assistance of Loretta Kasparas, RN, Charles Christensen and Therese Molyneux is appreciated.
May 22, 1978
The American Journal of CARDIOLOGY
Volume 41
1121
PACEMAKER
CONVERSION
OF ATRIAL FLUTTER-WYNDHAM
ET AL
References 1 Zeft HG, Cobb FR, Waxman MB, et al: Right atrial stimulation In the treatment of atrial flutter. Ann Intern Med 70:447-456, 1969 2 Hafl JI, Kosowsky BD, Lau SH, et al: Termination of atrial flutter by raprd electrical pacing of the right atrium Am J Cardiol 20. 239-244, 1967 3 Gulotta SJ, Aronson AL: Cardioversron of atrial tachycardra and flutter by atrial stimulation. Am J Cardrol 26.262-269, 1970 4. Chamberlain DA, Coltarl DJ, Ead HA: Conversion of atrial flutter or tachycardia to atrial fibrillation by rapid atrial stimulation (abstr). Br Heart J 33.613, 1971 5. Zipes DP: The contribution of artificial pacemaking to understanding the pathogenesis of arrhythmias Am J Cardiol 28:211-222, 1971 6. Cheng TO: Rapid atrial pacing in treatment of atrial flutter and atrial tachycardia (abstr). Clin Res 19:307, 1971 7. Plttman DE, Makar JS, Kooros KS, et al: Right atria1 stimulation. successful method of conversion of atrral flutter and atrial tachycardra Am J Cardiol: 32:700-706, 1973 a. Preston TA: Atrial pacing to convert atrial flutter (abstr) Am J Cardiol 32:737, 1973 9 Puech P, Grolleau R, Latour H, et al: Trartement du flutter auricularre par la stimulation auriculaire endocavitaire Arch Mal Coeur 66.159-167, 1973 10 Rosen KM, Slnno MZ, Gunnar RM, et al: Failure of rapid atrial pacing in the conversion of atrial flutter Am J Cardiol 29524-528, 1972 11 Vergara GS, Hildner FJ, Schoenfeld CB: Conversion of supraventricular tachycardias with rapid atrial stimulation. Circulation 461788-793, 1972 12. Plttman DE, Gay TC, Pate1 II: Termination of atria1 flutter and atrial tachycardias with rapid atrial stimulation Angiology 26:784-802, 1975
1122
May 22, 1976
The American
Journal of CARDIOLDGY
13. Orlando J, Cassldy J, Aronow WS: High reversion of atrial flutter to sinus rhythm after atrial pacing in patients with pulmonary disease. Chest 71:580-582, 1977 14. MacLean WAH, Karp RB, Kouchoukos NT, et al: Uniformly successful interruption of atrial flutter with rapid atrial pacing in 100 patients (abstr). Circulation 54. Suppl 11~11-167, 1976 15. Wu D, Denes P: Mechanisms of paroxysmal supraventncular tachycardia. Arch Int Med 135.437-442. 1975. 16 Glenn WWL, Mauro A, Longo E, et al: Remote stimulatron of the heart by radio-frequency transmission N Engl J Med 261:948-951, 1959 17. Glenn WWL, Furman S, Gordon AJ, et al: Radio-frequency controlled catheter pacemaker Clrnical applrcatron N Engl J Med 275:137-140, 1966 la. Davidson RM, Wallace AG, Sealy WC, et al: Electrically induced atrial tachycardra with block. A therapeutrc applicahon of permanent radio-frequency atrial pacing. Circulation 44:1014-1021, 1971 19 Williams DO, Davison PH: Long-term treatment of refractory supraventricular tachycardia by patient-controlled inductive atrial pacing. Br Heart J 36:336-340, 1974 20. Goyal SL, Lichsfein E, Gupta PK, et al: Refractory reentrant atrial tachycardia. Successful treatment with a permanent radio-frequency triggered atrial pacemaker Am J Med 58 586-590, 1975 21. Dreifus LS, Arriaga J, Watanabe Y, et al: Recurrent Wolff-Parkinson-white tachycardia in an infant. Successful treatment by a radio-frequency pacemaker. Am J Cardiol 28586-591, 1971 22. Fruehan CT, Meyer JA, Klie JH, et al: Refractory paroxysmal supraventricular tachycardia. Treatment with patient-controlled permanent radio-frequency atrial pacemaker Am Heart J 87. 229-237,1974
Volume 41
