II). Despite the relatively high pacing thresholds, nophrenic nerve stimulation was observed. Until now,single-lead DDD pacing is limited by these high atrialpacing thresholds, causing an unacceptably high cur-rent drain of the device. These preliminary data in asmall number of patients may justify further studies todefine more precisely the efficacy and limitations ofthe new single-pass lead in a larger patient population.

In summary, this study confirms the possibilityof short- and long-term DDD pacing with atrialcapture through an atrial dipole using a single-passDDD lead, thereby eliminating the necessity anddisadvantages of a second (atrial) lead. Since atrialpacing thresholds are still relatively high, furthermodifications of the lead body configuration andthe atrial electrodes are desirable, allowing lowerstimulation thresholds and optimizing energy re-quirements as well as minimizing the possibility ofdiaphragmatic stimulation.

Acknowledgment: We gratefully acknowledge thetechnical assistance of Daniela Amstutz.

1. Curzio G. A multicenter evaluation of a single-pass lead VDD pacing system.PACE1991;14:434–442.2. Antonioli GE, Ansani L, Barbieri D. Italian multicenter study on a single leadVDD pacing system using a narrow atrial dipole spacing.PACE 1992;15(II):1890–1893.3. Antonioli GE, Ansani L, Barbieri D. Single lead VDD pacing. In: Barold SS,Mugica J eds. New Perspectives in Cardiac Pacing. Mount Kisco, NY: FuturaPublishing 1993:359–381.4. Crick JCP. European multicenter prospective follow-up study of 1002 im-plants of a single lead VDD pacing system.PACE1991;14(II):1742–1744.5. Naegeli B, Osswald S, Pfisterer M, Burkart F. VDD(R) pacing: short- andlong-term stability of atrial sensing with a single lead system.PACE 1996;19:455–464.6. Bongiorni MG, Bedendi N. Atrial stimulation by means of floating electrodes:a multicenter experience.PACE1992;15:1977–1981.7. Wainwright R, Crick J, Sowton E. Clinical evaluation of a single-pass im-plantable electrode for all modes of pacing. The ‘‘Crown of Thorns’’ lead.PACE1983;6:210–220.8. Linde C, Kruse IM, Heynen H, Norlander R, Ryde´n L. Acute and long-termexperience with a new single lead for VDD pacing, ‘‘SPAAR.’’Eur J CardiacPac Electrophysiol1992;4:274–282.

Direct-Current Cardioversion of AtrialTachyarrhythmias Under Oral Flecainide Therapy

Jean Francois Leclercq, MD, Jeanine Bizot, MD, Patrick Attuel, MD, andPhilippe Coumel, MD

Transthoracic direct-current (DC) cardioversion ofchronic atrial fibrillation (AF) was described 30

years ago. However, the success rate of this procedureremains relatively stable and does not exceed 70% to80%, despite the changes in biomedical technologythroughout this period. That is why some investigatorsrecently proposed performing an internal defibrillationderived from DC shock ablative techniques in such re-sistant patients. This procedure increases the success ratein both short- and long-term follow-up.1 Antiarrhythmicdrugs are another effective therapy to convert AF intosinus rhythm. They were classically contraindicated be-fore DC cardioversion, because of an increased inci-

dence of conduction disturbances or ventricular arrhyth-mias when it was performed with a high dosage ofdigitalis or quinidine.2,3Antiarrhythmic therapy has beenimproved during the last 30 years, and before performinginternal cardioversion, we usually try to use transthoracicDC cardioversion after a short period of antiarrhythmicdrug therapy. This report presents our results observedwith flecainide.

• • •This series included 48 procedures of DC cardio-

version of chronic atrial tachyarrhythmia in 43 pa-tients while they were taking flecainide acetate orally(1916 53 mg/day) from 146 26 days (range 3 to 89).The results of the procedure were compared withthose of a control series of 96 matched patients inwhom a cardioversion was performed without antiar-rhythmic therapy. Each case of the treated group wasmatched to 2 control patients in terms of age, sex, andunderlying heart disease. These patients were consec-

From the Departments of Cardiology, Lariboisiere University Hospital,Paris; and Centre Chirurgical Val d’Or, Saint Cloud, France. Dr.Leclercq’s address is: Centre Chirurgical Val d’Or, 16 rue Pasteur,92210 Saint Cloud, France. Manuscript received January 30, 1997;revised manuscript received and accepted May 8, 1997.

TABLE II Bipolar Atrial Stimulation Thresholds During Follow-Up (V/ms)

Day 1 Day 7 Day 30 Day 90 Day 180

su 5.8 6 1.4/0.4 6 0.2 5.8 6 1.4/0.8 6 0.1 5.0 6 0.0/0.8 6 0.3 5.8 6 1.4/0.7 6 0.7 5.8 6 1.4/1.1 6 0.8ri 6.7 6 1.4/0.7 6 0.2 5.8 6 1.4/0.8 6 0.3 5.0 6 0.0/0.8 6 0.1 5.8 6 1.4/0.3 6 0.1 5.0 6 0.0/0.7 6 0.7le 5.8 6 1.4/0.4 6 0.3 6.7 6 1.4/1.0 6 0.5 5.0 6 0.0/0.7 6 0.4 5.8 6 1.4/1.0 6 0.5 6.7 6 1.4/1.0 6 0.8si 6.7 6 1.4/0.6 6 0.3 7.5 6 0.0/1.1 6 0.3 5.8 6 1.4/0.9 6 0.1 6.7 6 1.4/0.8 6 0.6 5.0 6 0.0/0.8 6 0.7st 5.8 6 1.4/0.8 6 0.2 6.7 6 1.4/0.9 6 0.6 5.8 6 1.4/0.7 6 0.1 6.7 6 1.4/0.9 6 0.7 6.7 6 1.4/0.6 6 0.4br 6.7 6 1.4/0.8 6 0.3 6.7 6 1.4/1.1 6 0.3 5.8 6 1.4/1.0 6 0.5 5.8 6 1.4/0.8 6 0.7 5.8 6 1.4/0.7 6 0.7

Values are mean 6 SD.br 5 deep breathing; le 5 lying on the left side; ri 5 lying on the right side; si 5 sitting; st 5 standing; su 5 supine.

©1997 by Excerpta Medica, Inc. 0002-9149/97/$17.00 645All rights reserved. PII S0002-9149(97)00442-6

utively taken from a cohort of 350 procedures per-formed with the same protocol without drugs between1985 and 1992. The 2 series included all types ofchronic atrial disorders, e.g., AF and typical or atyp-ical atrial flutter.

DC cardioversion with R-wave synchronizationwas performed under short general anesthesia usingpenthotal or propofol, with a General Electric 667 Bor Hewlett-Packard 43120 A device (Palo Alto, Cali-fornia). Gel-covered electrodes were placed on thechest: the anode anteriorly and the cathode on the leftlateral chest wall. The programmed energy was 200 to250 J for the first shock in the patient with atrialflutter, and 300 to 360 J in the patient with AF. If thisshock failed to convert the arrhythmia, at least 2additional shocks at maximal energy (360 J) weredelivered. Results were judged on the electrocardio-gram recorded 10 minutes after DC shock: only stablesinus rhythm at this time was called a success, and animmediate defibrillation with prompt recurrence ofatrial arrhythmia was called a failure.

The statistical interpretation of the results used thecorrected chi-square test for comparison of the 2groups of patients.

• • •Table I lists the clinical characteristics of the 2

groups of patients: group I received shocks with fle-cainide therapy and group II received shocks withoutprevious antiarrhythmic drug treatment. A larger pro-portion of patients had atrial flutter, and QRS durationin AF was higher in group I; no other difference inclinical characteristics could be seen. Table II lists theefficacy rate of cardioversion in the 2 groups. It issuperior in patients pretreated with flecainide: 85% forthe first shock and 98% for the third shock comparedwith 51% and 78%, respectively, for the controlgroup. No clinical predictor of DC shock efficacy

could be found in our series: sex, age, and underlyingheart disease were not statistically different in thesuccess and failure groups. In some instances, wedocumented the organization of fibrillation into regu-lar atrial flutter by administering flecainide therapy.Figures 1 and 2 show an example of this finding, aswell as its efficacy in preventing immediate relapsesoccurring systematically in the absence of antiarrhyth-mic therapy. However, in patients with AF persistingeven with flecainide therapy, the efficacy of cardio-version is higher than that in the control group: 81%versus 49% after the first shock (p,0.01) and 96%versus 68% after 3 shocks (p,0.05) (see Table II).

Some complications were observed immediatelyafter cardioversion. The most frequent was a sinoatrialblock with long pauses. Its incidence was low (4% ofpatients) and similar in the 2 groups. A transientpacemaker dysfunction was seen in a few complexesin 2 of the 4 patients with previous implants (Figure2). No atrioventricular block, no sustained ventriculartachyarrhythmias, and no deaths were observed. No1/1 atrioventricular conduction during atrial flutterwas observed in this series.

• • •The classic interdiction of antiarrhythmic drugs

before cardioversion was justified by a high incidenceof immediate complications: long pauses or ventricu-lar tachyarrhythmias when high doses of digitalis orquinidine were given.2,3 However, antiarrhythmicdrugs administered before cardioversion is logical. Ithas been proven that relapses of AF occur frequentlyin the hours or days after DC shock, with a medianvalue after some weeks.4,5 Moreover, it has been dem-onstrated by randomized controlled studies that noantiarrhythmic therapy is a factor in relapse comparedwith quinidine6 or flecainide.7

According to classic guidelines, antiarrhythmic drugscould be initiated only some hours after cardioversion,and a high percentage of early relapses should be ex-pected. Antiarrhythmic therapy administered before car-dioversion may reduce these relapses. However, thesedrugs may increase the defibrillation threshold; it hasbeen demonstrated at the ventricular level in patientswith implanted defibrillators.8,9 Available data at theatrial level are controversial; clinical studies have showna decrease in threshold,10 no change,11 or an increase,especially with class IC drugs.12 With flecainide, anincrease in defibrillation threshold has been demon-strated only when a low voltage is used.13 It thereforeseemed logical to determine whether this potential dele-terious effect has a significant influence on the clinicalresults of the cardioversion procedure.

Our experience is in favor of antiarrhythmic usebefore cardioversion, with an increased efficacy withflecainide therapy. This benefit is probably due to adecreased incidence of immediate relapses, and at thedosage and voltage used, the clinical impact of theexperimentally demonstrated increase in defibrillationthreshold is negligible. Similar results have recentlybeen reported with propafenone,14 without significantchange in defibrillation threshold. In our routine pro-tocol, high voltage is always used in order to avoid

TABLE I Clinical Characteristics of the Two Groups

Control Group(n 5 96)

Flecainide Group(n 5 48)

Age (yr) 68 6 10 68 6 11Men/women 64/32 32/16Valvular disease 24 (25%) 13 (27%)Other heart disease 4 (4%) 1 (2%)Lone or hypertension 68 (71%) 34 (71%)Atrial flutter 10 (10%) 22 (46%)Atrial fibrillation 86 (90%) 26 (54%)QRS duration (ms) 98 6 5 109 6 8

TABLE II Efficacy of Direct-Current Shock

Control Group(n 5 96)

Flecainide Group(n 5 48)

Success at first shock 49 (51%) 41 (85%)*Atrial fibrillation 42/86 (49%) 21/26 (81%)*Atrial flutter 7/10 (70%) 20/22 (91%)

Success at third shock 75 (78%) 47 (98%)*Atrial fibrillation 65/86 (68%) 25/26 (96%)†Atrial flutter 10/10 (100%) 22/22 (100%)

*p ,0.01; †p ,0.05 by chi-square test.

646 THE AMERICAN JOURNAL OF CARDIOLOGYT VOL. 80 SEPTEMBER 1, 1997

FIGURE 1. Cardioversion of chronic atrial fibrillation in a patient with mitral valve disease, having a DDD pacemaker for sinus nodedisease, performed without previous antiarrhythmic therapy. Sinus rhythm resumes after each shock, but after a few beats, atrial fi-brillation recurred (3 attempts). DC 5 direct current.

FIGURE 2. Same patient as in Figure 1, after 4 days of flecainide therapy (100 mg twice daily). Sinus rhythm resumes after the first shockwithout recurrence of fibrillation. Note the transient pacemaker dysfunction due to atrial threshold elevation.

BRIEF REPORTS 647

severe complications—namely the induction of ven-tricular fibrillation—in applying the principle of ‘‘syn-chronous response threshold’’15: At high voltages, allventricular fibers will be depolarized and the risk ofventricular fibrillation minimized. In our experience,such events are rare and are not changed by flecainide.This is probably explained by parallel changes be-tween the defibrillation and vulnerability thresholds.16

Antiarrhythmic drugs could increase the defibrillationthreshold, but also automatically the threshold of in-duced fibrillation. In our initial experience of cardio-version, a higher percentage of arrhythmic complica-tions was reported—up to 4% with quinidine.17 Morerecent studies have not shown any proarrhythmic ef-fect of quinidine given 3 days before cardioversion.18

An increase in the incidence of long pauses has beenreported with class IC drugs13: this phenomenon is notsignificantly present in our series.

Another favorable effect of antiarrhythmic drugs istheir role in regularizing and organizing the atrialrhythm. That is probably why the incidence of flutter ishigher with flecainide. This effect is favorable beforecardioversion, because the defibrillation threshold islower in such arrhythmias.11 This regulizing effect of thedrugs is correlated with an increase in wavelength of theimpulse. This is usual with flecainide, which increasesmore refractoriness than it slows impulse velocity.19,20Itcould then be responsible for decreasing the number offunctional reentry circuits in the atria and inducing aslower and a more organized arrhythmia.

The percentage of patients successfully con-verted to sinus rhythm increased when flecainidewas used before DC shock, despite an increase inthe defibrillative threshold with this drug.

1. Levy S, Lauribe P, Dolla E, Kou W, Kadish A, Calkins H, Pagannelli F,Moyal C, Bremondy M, Schork A, Shyr Y, Das S, Shea M, Gupta N, Morady F.A randomized comparison of external and internal cardioversion of chronic atrialfibrillation. Circulation 1992;86:1415–1420.2. Lown B, Krieger R, Williams J. Cardioversion and digitalis drugs: changedthreshold to electric shock in digitalized animals.Circ Res1965;17:519–528.

3. Latour H, Puech P, Hertault J, Grolleau-Raoux R. Syncopes apre`s reduction defibrillation auriculaire par choc e´lectrique et hydroquinidine.Arch Mal Coeur1966;59:533–548.4. Van Gelder IC, Crijns HJ, Van Gilst WH, Verwer R, Lie KI. Prediction ofuneventful cardioversion and maintenance of sinus rhythm from direct-currentelectrical cardioversion of chronic atrial fibrillation and flutter.Am J Cardiol1991;68:41–46.5. Suttorp MJ, Kingma JH, Koomen EM, Van’t Hof A, Tijssen JGP, Lie KI.Recurrence of paroxysmal atrial fibrillation or flutter after successful cardiover-sion in patients with normal left ventricular function.Am J Cardiol 1993;71:710–713.6. Coplen SE, Antman EM, Berlin JA, Hewitt P, Chalmers TC. Efficacy andsafety of quinidine therapy for maintenance of sinus rhythm after cardioversion.A meta-analysis of randomized control trials.Circulation 1990;82:1106–1116.7. Van Gelder IC, Crijns HJGM, Van Gilst WH, Van Wijk LM, Harner HPM,Lie KI. Efficacy and safety of flecainide acetate in the maintenance of sinusrhythm after electrical cardioversion of chronic atrial fibrillation or atrial flutter.Am J Cardiol1989;64:1317–1321.8. Guarnieri T, Levine JH, Veltri EP, Griffith LSC, Watkins L, Juanteguy J,Mower MM, Mirowski M. Success of chronic defibrillation and the role ofantiarrhythmic drugs with the automatic implantable cardioverter/defibrillator.Am J Cardiol1987;60:1061–1064.9. Ruffy R. Pharmacological modulation of ventricular defibrillation. In: ZipesDP, Jalife J, ed. Cardiac Electrophysiology. From Cell to Bedside. Philadelphia:WB Saunders, 1990:959–962.10. Rossi M, Lown B. The use of quinidine in cardioversion.Am J Cardiol1967;19:234–238.11. Sodermark T, Edhag O, Sjo¨gren A, Jonsson B, Olsson A, Oro¨ L, DanielssonM, Rosenhamer G, Wallin H. Effect of quinidine on maintening sinus rhythmafter conversion of atrial fibrillation or flutter. A multicenter study from Stock-holm. Br Heart J 1975;37:486–492.12. Van Gelder IC, Crijns HJGM, Van Gilst WH, De Langen CDJ, Van WijkLM, Lie KI. Effects of flecainide on the atrial defibrillation threshold.Am JCardiol 1989;63:112–114.13. Guarnieri T, Tomaselli G, Griffith LS, Brinker J. The interaction of antiar-rhythmic drugs and the energy for cardioversion of chronic atrial fibrillation.PACE1991;14:1007–1012.14. Bianconi L, Mennuni M, Lukic V, Castro A, Chieffi M, Santini M. Effects oforal propafenone administration before electrical cardioversion of chronic atrialfibrillation: a placebo-controlled study.J Am Coll Cardiol1996;28:700–706.15. Fabiato A, Coumel P, Gourgon R, Saumont R. Le seuil de re´ponse synchronedes fibres myocardiques: application a` la comparaison expe´rimentale del’efficacite des differentes formes de chocs e´lectriques de de´fibrillation. Arch MalCoeur1967;60:527–544.16. Chen PS, Feld GK, Kriett JM, Mower MM, Tarazi RY, Fleck P, SwerdlowCD, Gang ES, Kass RM. Relation between upper limit of vulnerability anddefibrillation threshold in humans.Circulation 1993;88:186–192.17. Faivre G, Cherrier F, Gilgenkrantz JM. Traitement de la fibrillation auricu-laire par choc e´lectrique externe. I. Re´sultats en fonction de l’e´tat du malade.Coeur Med Int1969;6:5–19.18. Hillestad L, Dale J, Storstein O. Quinidine before direct current counter-shock. A controlled study.Br Heart J 1972;34:139–142.19. Frame LH, Rhee EK, Fei H, Luchetti W. Proarrhythmic and antiarrhythmiceffects of flecainide on nonsustained reentry around the canine atrial tricuspidring in vitro. PACE1991;14:1728–1734.20. Wang Z, Page P, Nattel S. Mechanism of flecainide’s antiarrhythmic actionin experimental atrial fibrillation.Circ Res1992;71:271–287.

Comparison of Left Ventricular Mass and GeometricRemodeling in Treated and Untreated Men and

Women >50 Years of Age With Systemic HypertensionMiguel Zabalgoitia, MD, S. Noor Ur Rahman, MD, William E. Haley, MD,

John Amerena, MD, Lisa Krause, RDCS, Lori Oneschuk, RDCS, Steven Yarows, MD,Carla Yunis, MD, and Charles Lucas, MD

S ince cardiac hypertrophy is more prevalent inpostmenopausal women than in age-matched men,

we hypothesized that persistence of left ventricular

(LV) hypertrophy, despite antihypertensive treatment,may contribute to increasing their higher cardiovascu-lar risk compared with their premenopausal counter-parts.1,2 Echocardiography has been extensively usedin determining quantitatively (LV mass index) andqualitatively (cardiac remodeling) the cardiac adapta-tion to pressure overload imposed by high blood pres-sure (BP). This study assesses by echocardiographythe impact of prior treatment and efficacy upon LV

From the Department of Medicine, Division of Cardiology, The Uni-versity of Texas Health Science Center in San Antonio, Texas. Dr.Zabalgoitia’s address is: Department of Medicine/Cardiology, TheUniversity of Texas Health Science Center at San Antonio, 7703 FloydCurl Drive, San Antonio, Texas 78284-7872. Manuscript receivedFebruary 17, 1997; revised manuscript received and accepted May2, 1997.

648 ©1997 by Excerpta Medica, Inc. 0002-9149/97/$17.00All rights reserved. PII S0002-9149(97)00443-8