July I, 1967 THE AMERICAN JOURNAL OF CARDIOLOGY Volume 60

pacemaker-dependent and, particularly in young pa- tients, replaces the native disease with an iatrogenic one. Thus, maintenance of normal AV conduction in these patients remains a desirable objective. Signifi- cant hemorrhage is often encountered during dissec- tion within the AV groove. Thus, techniques permit- ting lesser degrees of bleeding could be desirable. Lastly, safe and effective ablative techniques that could be suitable for transcatheter application could be valuable in reducing the risks associated with ac- cessory pathway ablation by avoiding the need for cardiac surgery and increasing patient acceptance for ablative therapy.

With these objectives in mind, we evaluated the use of argon laser energy for ablation in the atrium and AV groove. Lower energies were required for vaporization in the atrium and AV sulcus than in normal or diseased human ventricle.6 Energies lower than 25 J at 1 site often resulted in atria1 perforation. High-power con- tinuous-wave argon laser discharges were difficult to control and frequently resulted in this complication. Thus,’ we developed the use of low-power pulsed ar- gon laser discharges that delivered equivalent energy but permitted controlled, bloodless incision, visualiza- tion of extent of tissue damage, and limited penetra- tion. The tissue lesion-energy dose relation developed suggested that energy densities of 25 to 50 J/cm2 were adequate for performance of atriotomy or atria1 abla- tion in normal atria. This early clinical report used these guidelines and confirmed their validity. Pulsed argon laser energy can be used successfully for atria1 incision and, in conjunction with blunt dissection, ac- cessory pathway ablation. It is now recognized that accessory pathway location can be intramural or epi- cardial in the AV groove. Thus, both regions need to be ablated. Permanent damage to vascular structures or the specialized AV conduction is avoided. The experi- mental electrophysiologic effects of laser ablation are focal and precise.7 With greater experience, laser dis- section in the AV groove can be considered. Accessory pathway conduction was interrupted in 2 patients and modified in the third patient, with preservation of the AV nodal-His bundle conduction. This has been not-

ed for intranodal reentry and we ave recently per- formed laser ablation of the AV node with similar results in 2 patients.* This has permitted control of SVT in these 3 patients without need for permanent pace- maker implantation. During follow-up, orthodromic SVT or atria1 flutter/fibrillation has not recurred in any patient. Adverse effects such as thrombosis at the atria1 incision site, embolic events, new atria1 arrhyth- mias or mitral regurgitation have not been observed. There has been no disruption of the laser incision site, suggesting good healing characteristics. Our initial ex- perience suggests that intraoperative laser ablation in patients with SVT with WPW syndrome merits further evaluation. Future development of the transcatheter method will require suitable guiding catheter systems, permitting controlled laser energy delivery.g Com- parison with alternative ablation energies is also warranted.lO

1. Scaly WC, Hatler BG Jr, Blumenschein SD, Cobb FR. Surgical treatment of Wolff-Parkinson-White syndrome. Ann Thorac Surg 1969;8:1-8. 2. Gallagher JJ, Sealy WC, Cox JL, German LD, Kasell JH, Bardy GH, Packer DL. Results of surgery for preexcitation caused by accessory atrioventricular pathways in 267 consecutive cases. In: losephson ME, Wellens HJJ, eds. Tachycardias. Mechanisms, Diagnosis, Treatment. Philadelphia: Lea b Fe- biger, 1984;259-269. 3. Saksena S, Gadhoke A. Laser therapy for tachyarrhythmias: a new fron- tier. Pacing Cfin Electrophysiol 1986;9:533-550. 4. Saksena S, Ciccone J, Chandran P, Rothbart ST, Pantopoulos D, Lee B. Laser ablation of normal and diseased human ventricle. Am Heart J 1986;112:52-60. 5. Saksena S, Hussain SM, Gielchinsky I, Gadhoke A, Pantopoulos D. Intra- operative mapping-guided argon laser ablation of malignant ventricular tachycardia. Am J Cardiol 1987;59:78-83. 6. Saksena S, Hussain SM, Gielchinsky I. Gadhoke A, Pantopoulos II. Laser abiation of human atrium and accessory pathways: experimental observations and early clinical experience (abstr). Pacing CJin Electrophysiol 1987;10:427. 7. Merillat JE, Levine JH, Weisman HF, Stern MD, Spear JF, Moore EN, Kadish AA, Fonger J, Guzman R, Guarnieri T. Laser ablation leads to more focal electrophysiologic effects compared to catheter delivered high energy ablation labstrl. lACC 1968:7:237A. 8. Pritchett EL&Anderson kW, Benditt DG, Kasell J, Harrison L, Wallace AG, Scaly WC, Gallagher JJ. Reentry within the atrioventriculal node: surgical cure with preservation of atrio;entricuJar conduction. Circulation l&&o: 440-446. 9. Saksena S, Tarjan P, Bharati S, Boveja B, Cohen D, Joubert T. A new technique for successful low energy His bundle ablation using a suction elec- trode catheter (abstr). Circulation 1986;74:suppl II:Ii-387. 10. Saksena S, Furman R, Gadhoke A, Osypka P. Feasibility of radiofrequen- cy ablation ofsupraventricular and ventricular tachyarrhythmias (abstr). Pac- ing CJin Electrophysiol 1987;10:414.

“Pseudo-Malfunction” of a DDD Pacemaker

SATISH KOHLI, MD KEVIN I. ERKKILA, BS JANG B. SINGH, MD

P acemaker hardware and software systems have be- come extremely complex. A little-known eccentricity of the Intermedics Cosmos (28341) DDD system that

From the Department of Cardiology, St. Vincent Hospital, 25 Winthorp Street, Worcester, Massachusetts 01604. Manuscript received February 2, 1987; revised manuscript received and accepted March 13,1987.

has raised concerns about lead dislodgement and de- vice malfunction is cross stimulation, which is defined as the ability to stimulate 1 chamber through a lead or output circuit to the opposite cardiac chamber. Elec- trocardiographic manifestations and clinical rele- vance of this phenomenon are discussed.

An 85-year-old woman was admitted with repeat- ed episodes of syncope and a known history of system- ic hypertension. Her pulse was 68 beats/min and blood pressure was 140/90 mm Hg without any ortho- static changes. Examination of the chest revealed bi- basilar crepitations. Auscultation revealed an S3 with a grade Z/6 ejection systolic murmur at the apex. An electrocardiogram showed sinus rhythm with incom- plete left bundle branch block. An x-ray of the chest showed borderline cardiomegaly with vascular redis- tribution. A Holter monitor revealed episodes of Mo-

200 BRIEF REPORTS

< MAGNET

FIGURE 1. A = atrial stimulus; V = ventricular stimulus. See text for explanation.

FIGURE 2. See text for explana- tion.

Magnet On Maghet Off

bitz type II second-degree heart block with periods of 2:l atrioventricular (AVJ block with a ventricular rate of about 30 beats/min associated with symptoms of lightheadedness.

Because of symptomatic bradyarrhythmia with preserved sinus mechanism and the presence of hy- pertensive heart disease and congestive heart failure, she underwent placement of a DDD pacemaker (In- termedics Cosmos model 28341). Capture threshold measured 0.5 V on the ventricular channel and 1.05 V on the atria1 channel at a pulse width of 0.45 ms. The pacemaker was programmed in DDD mode with nominal parameters and a lower rate limit of 60 beats/ min. The pacemaker was checked later on in the day, and in magnet mode revealed that during the first cycle, both A and V spikes fell in the refractory period of preceding sinus beat (Fig. I]. In the next 3 cycles, the first stimulus resulted in a ventricular stimulation with second stimulus falling within the QRS complex. Nor- mal atria1 and ventricular capture is noted in the fifth complex followed by DO0 pacing. Removal of the magnet results in atria1 synchronous ventricular pac- ing. Since the atria1 spike resulted in a QRS complex, a diagnosis of atria1 lead dislodgment was considered and the patient underwent fluoroscopic examination which demonstrated that the leads were normally positioned,

a rate of 90 beats/min and a short AV delay of 100 ms upon application of a magnet. This is followed by DO0 pacing at programmed rate and AV delay. In this case, the morphologic characteristics of the ventricular com- plex generated by the atria1 stimulus were similar to those of the complex generated by the ventricular stimulus. This would be unlikely if the complex were originating from a displaced atria1 lead. This phenom- enon has been reported in the literature1 and relates to failure of the ventricular discharge switch to open dur- ing the 4 asynchronous cycles in the magnet mode. This provides a relatively low-impedance pathway through the pacemaker, allowing a small amount of current to travel through the ventricular electrode dur- ing atria1 output. This can result in a paced QRS com- plex if the initial stimulation threshold is low. The same phenomenon occurs.for 1 cycle when the magnet is taken off (Fig. 2). This is likely to occur less with time once the stimulation threshold of the ventricular lead increases. It is unlikely to result in a ventricular spike being delivered on the T wave because the AV delay is automatically shortened during the first 5 cycles in the magnet mode. Although of little clinical consequence, this phenomenon should be recognized because it may raise the possibility of dislodgment of the atria1 lead and malfunction of the DDD device.

This pacemaker device is designed to pace asyn- chronously for 4 pacing cycles (5 pacing complexes) at

1. Levine PA, Rihanek BD, Sanders R, Sholder J. Cross-stimulation: the unex- pected stimulation of the unpaced chamber. PACE 1985;8:600-606.