Interference with pacemaker function by cardiokymographic testing

362

BRIEF

REPORTS

References 1. Deckelbaum LI, Isner JM, Konstam MA, Salem DN. C&her-induced versus spontaneous spasm. Do these coronary bedfellows deserve to be estranged? Am f Med 1985;79:1-4. 2. MacAlpin RN. Relation of coronary arterial spasm to sites of organic stenosis. Am J Cardiol 1980;46:143-153. 3. Raizner AE, Ishimori T, Chahine RA. Recurrent catheter-induced coro-

nary artery spasm.Cothet Cordiovosc Diogn 1977;3:187-194. 4. Matsuda Y, Takashiba K, Hamada V. Hyakuna E, Ebihara H. Cotheterinduced spasm during l985;8:314-317.

spontaneous

attack of variant

angina. Clin Cardiol

5. Mautner RK, Cooper MD. Phillips JH. Catheter-induced

coronary artery spasm: an angiographic manifestation of vasospastic angina? Am Heart J 1983;106:659-665. 6. Waters DD, Miller DD. Bouchard A, Bosch X, Theroux P. Ciradian variation in variant angina. Am J Cardiol 1984;54:61-64.

Interference with Pacemaker Function by Cardiokymographic Testing

with inhibition of the atrial output. Pacemaker function reverted to normal (DDD) immediately upon removal of the transducer. The patient was asymptomatic during ECG monitoring.

PEILIANGKUAN, MD, MA JAY H. KOZLOWSKI, MD MARK J. CASTELLANET, MD MYRVIN H. ELLESTAD, MD

The cardiokymograph is an electromagnetic instrument that incorporates a planar, spiral coil of a very high frequency (15.6 MHz], low power oscillator. The electromagnetic field around the coil may interfere with pacemaker function and cause the pacemaker to track at its upper rate limit in the DDD mode. In atria1 or ventricular inhibited pacing, a stimulus is delivered if the intrinsic rate [in the sensed chamber) falls below the pacemaker rate. With intrinsic rates higher than the pacemaker rate, the pacer is inhibited. Triggered mode pacemakers may interpret certain signals as internal and respond by pacing at an accelerated rate or a maximal tracking rate. Pacemakers, which have an inhibited mode, will interpret signals with peak energies of about 30 Hz and repetition frequencies of 60 to 120 per minute as coming from the heart. Ventricular asystole and Stokes-Adams attacks may result from inappropriate inhibitions. The electromagnetic field created by the CKG transducer is apparently not great enough to cause these inhibited phenomena, however. Some programmable pacemakers may have their settings changed by external signals6 In our small series, we encountered no such distortion of settings. The physicians involved with the care of patients with pacemakers must recognize the potential for such problems. We have reported herein several patients with pacemakers who underwent CKG evaluation. In 1 patient a Pacesetter DDD pacemaker converted to the upper rate limit tracking mode for the period of CKG transducer contact. This is presumably related to the electromagnetic field that the apparatus creates. Why it affected this pacemaker and not others, including those with similar functions and sensitivities, is not understood. Filter characteristics vary from 1 make to another; thus, response to interference may vary as well. The physicians involved with the care of patients with pacemakers must be aware of the potential interference with pacer function by CKG testing, and may seek alternative diagnostic investigations to prevent this newly described consequence.

E

nvironmental hazards for patients with pacemakers have long been recognized.lJ Interference with pacemaker function by diagnostic and therapeutic modalities is of particular concern to physicians. Sources of disturbance include surgical diathermy, electrical defibrillation, radiation therapy, electrical muscle stimulation, low-frequency acupuncture and dental ultrasonic cleaning. Cardiokymography is being used clinically at some institutions to detect segmental wall motion abnormalities sf the heart.3-5 Observation of a case of pacemaker interference by the cardiokymographic (CKG) transducer prompted us to examine other patients with pacemakers in a similar manner. We tested patients

with pacemakers who were clinic. During electrocardiographic (ECG] monitoring at rest, the CKG transducer was placed at 3 positions on each patient: ECG V3 position, ECG V4 position and over the patient’s pulse generator. The ECG was recorded for 10 seconds in each CKG transducer position. Pacemakers with varied functions from 4 major manufacturers were tested for possible CKG interference with pacing. The AA1 mode was tested in 5 units, the VVI in 5, the DVI in 3 and the DDD in 6. There was only 2 incident of CKG transducer-induced pacemaker dysfunction. This occurred with a Pacesetter 283 pacemaker set in the DDD mode. Atrial and ventricular sensitivities of this patient’s unit were 0.8 mV and 2.0 mV, respectively. The patient initially showed normal DDD function with pacing of the atrium and ventricle at a rate of 80 beats/min. The sinus rate occasionally exceeded the pacing rate and was sensed normally with inhibition of the atria1 output and normal tracking in an atrioventricular synchronous manner. Upon placement of the CKG transducer in the V3 position, the pacemaker converted to its fixed tracking rate of 110 beats/min seen in the pacer follow-up

From the Division of Cardiology, Memorial Medical Center of Long Beach, University of California-Irvine, Irvine, California. Manuscript received October 18, 1985; revised manuscript received and accepted February l&1986.

Acknowledgment: sistance in preparing

We thank Lila Ellerholz this manuscript.

for as-

References 1. Sowton E. Environmental [London] 1982;16:159-164.

hazards for pacemaker

patients. J R Co11 Phys

August

2. O’Brien E. Environmental dangers for the patient with (I pacemaker. Br Med J 1982;285:1677-1678. 3. Silverberg RA, Diamond GA, Vas R, Tzivoni D, Swan HJC, Forrester JS. Non-invasive diagnosis of coronary artery disease: the cardiokymographic stress test. Circulation 1980;61:579-589. 4. Weiner DA, McCabe CH, Dagostino G. C&ler SS, Ryan TJ. Cardiokymo-

PercutaneousBalloon Valvuloplasty for Stenosis of a Porcine Bioprosthesis in the Tricuspid Valve Position FREDERICK FEIT, MD PETER J. STECY, MD MARK S. NACHAMIE, MD

1, 1986

THE

AMERICAN

JOURNAL

OF CARDIOLOGY

Volume

58

363

graph during exercise testing; a new device for the detection of coronary artery disease and left ventricular wolf motion abnormalities. Am r Cordial 1983;51:13O7-1311. 5. Kuan P, Ellestad MH. The cardiokymography in the diagnosis of coronary artery disease (abstr]. VIII Asian-Pacific Congress of Cardiology, 1983;A-335. 6. Furman S. Spurious pacemaker programming. PACE 1980;3:517-518.

TABLE

I

Hemodynamic

Data Before

Heart rate (beatslmin) Pressures (mm Hg) Pulmonary artery Right ventricle (RV) Mean right atrium (RA) RA-RV mean diastolic gradient Cardiac output (literslmin) Cardiac index (literslmin/m*) Calculated tricuspid valve area (Gorlin formula, cm*)

and After

Valvuloplasty

Pre

Post

100

108

42121

40/20 4018 24 15 8.69 3.55 1.22

42112

38 22 5.71 2.33 0.69

R

ecently, percutaneous balloon dilatation has been successfully used for treatment of congenital aortic and pulmonary valvular sten0ses.l We report the first case of percutaneous valvuloplasty of a severely stenosed porcine bioprosthetic valve. A 46-year-old man with a long history of intravenous opiate abuse presented with severe fatigue, marked peripheral edema and syncope. Ten years earlier, after 3 episodes of endocarditis, severe tricuspid regurgitation developed and the patient underwent valve replacement with a No. 31 Hancock porcine prosthetic valve. For the past 3 years he has had progressive fatigue, dyspnea and peripheral edema despite therapy with furosemide and digoxin. The jugular veins were distended. A left parasternal diastolic thrill during inspiration was palpated and a grade 4/6 diastolic rumble that increased with inspiration was heard at the left sternal border. There was a grade I/6 early systolic murmur at the lower left sternal border. An electrocardiogram showed atria1 fibrillation and nonspecific ST- and T-wave changes. Doppler study was consistent with severe tricuspid stenosis. Diagnostic catheterization and angiography showed severe tricuspid stenosis and mild tricuspid regurgitation. The patient underwent percutaneous valvuloplasty of the porcine tricuspid valve. He was premeditated with oral diphenhydramine hydrochloride and pentoFrom the Department of Medicine, New York University School of Medicine, 550 First Avenue, New York, New York 10016. Manuscript received October 21, 1985; revised manuscript received December X,1985, accepted December 27,1985.

barbital. Right-sided cardiac catheterization using a No. 7Fr flow-directed pulmonary artery catheter inserted percutaneously through the right femoral vein revealed a mean right atria1 pressure of 38 mm Hg and a right ventricular pressure of 42/12 mm Hg. The mean diastolic gradient between right atrium and right ventricle was 22 mm Hg. Cardiac outputs were measured by the thermodilution technique. The catheter was then positioned in the right atrium and a No. 7Fr Cournand catheter was inserted through a second percutaneous right femoral vein puncture and positioned in the pulmonary artery. A 0.035-inch Teflon@coated exchange wire was passed through this catheter, which was then removed. A No. 9Fr 20-mm-diameter balloon catheter (Meditech) was passed over this wire through a No. 12Fr introducer. There was minimal resistance to the passage of this catheter at the tricuspid valve. The balloon was then centered in the prosthesis and inflated a total of IO times, with a 50:50 mixture of contrast and saline solution, to a peak pressure of 45 psi for durations of 10 to 30 seconds. After the final 2 inflations there was no further decrease in right atria1 pressure. Each inflation was accompanied by mild tachycardia and hypotension. Initially there was a defect in the balloon, but this resolved with serial inflations [Fig. I) The hemodynamic findings immediately before and after valvuloplasty are shown in Table I. After the postvalvuloplasty hemodynamic values were measured a right ventricular angiogram was done; it revealed mild tri-