Evaluation of the effect of transthoracic cardioversion from ventricular tachycardia to sinus rhythm on left atrial mechanical function

to the loss of atria1 transport and to high ventricular rates. The results of this study suggest that a third mechanism for the reduction of cardiac output in patients with AF is irregularity of the ventricular rhythm. Catheter ablation of the AV junction and implantation of a rate-responsive pacemaker in patients with AF may offer hemodynamic benefit beyond rate control by eliminating the irregularity that is present with medical therapy or after radiofrequency modification of the AV node. 1. Linderer T, Chatterjee K, Parmley WW, Sievers RE, Glantz SA, Tyberg JV. Influence of atria1 systole on the Frank-Starling relation and the end-diastolic pressure-diameter relation of the left ventricle. Circulation 1983;67:10451053. 2. Shapiro W, Klein G. Alterations in cardiac function immediately following electrical conversion of atrial fibrillation to normal sinus rhythm. Circulation 1968;38:1074-1084. 3. Orlando JR, Van Herick R, Aronow WAS, Olson HG. Hemodynamics and echocardiograms before and after cardioversion of atria1 fibrillation to normal sinus rhythm. Chest 1979;76:521-526.

4. Naito M, David D, Michelson EL, Schaffenburg M, Dreifus LS. The hemodynamic consequences of cardiac arrhythmias: evaluation of the relative roles of abnormal atrioventricular sequencing, irregularity of ventricular rhythm and atrial fibrillation in a canine model. Am Heart J 1983;106:284-291. 5. Grossman W. Blood flow measurement: the cardiac output. In Grossman W, Bairn DS, eds. Cardiac Catheterization, Angiography and Intervention. Philadelphia: Lea & Febiger, 1991;105-123. 6. Gosselink ATM, Blanksma PK, Crijns HJG, Van Gelder IX, De Kam PJ, Hillege HL, Niemeijer MG, Lie KI, Meijler FL. Left ventricular beat-to-beat performance in atria1 fibrillation: contribution of Frank-Starling mechanism after short rather than long RR intervals. J Am CoU Cardiol 1995;26:15161521. 7. Edmands RE, Greenspan K, Fisch C. The role of inotropic variation in ventricular function during atria1 fibrillation J Clin Invest 1970;49:738746. 8. Karliner JS, Gault JH, Bovchard RJ, Holzer J. Factors influencing the ejection fraction and the mean rate of circumferential fiber shortening during atria1 fibrillation. Cardiovasc Res 1974;8:18-25. 9. No11 B, Goke B, Simon B, Maisch B. Cardiac natriuretic peptide hormones during artificial cardiac pacemaker stimulation and left heart catheterization. Clin Investig 1992;70:1057-1060. 10. Erlebacher JA, Danner RL, Stelzer PE. Hypotension with ventricular pacing: an atria vasodepressor reflex in human beings. JAm Coil Cardiol 1984;4:550555. 11. Ellenbogen KA, Thames MD, Mohanty PK. New insights into pacemaker syndrome gained from hemodynamic, humoral and vascular responses during ventriculo-atria1 pacing. Am J Cardiol 1990;65:53-59. 12. Herbert WH. Cardiac output and the varying RR interval of atria1 fibrillation. J Ekctrocardiol 1973;6:131-135.

Evaluation of the Effect of Transthoracic Cardioversion from Ventricular Tachycardia to Sinus Rhythm on Left Atrial Mechanical Function G. Alfred Dodds III, MD, William E. Wilkinson, PhD, Ruth Ann Greenfield, MD, Andrea Natale, MD, Joseph Kisslo, MD, and Edward L. C. Pritchett, MD

recent years there has been intense interest in the Iafternoccurrence and mechanism of atria1 dysfunction cardioversion from atria1 fibrillation.le5 Such mechanical dysfunction has been implicated in the pathophysiology of thromboembolic complications of cardioversion to sinus rhythm.2*6 The energy of electrical cardioversion has been postulated to cause stunning of the atria and therefore might contribute to transient atria1 dysfunction.2 To investigate this hypothesis, we measured left atria1 function during sinus rhythm before and after ventricular tachycardia (VT) was induced in an electrophysiology laboratory. Peak transmitral A-wave velocity from pulsedDoppler transthoracic echocardiography was used as a marker of left atria1 mechanical function. The difference between pre-VT and post-VT peak A-wave velocity in patients whose VT terminated spontaneously or by intracardiac pacing was compared with the difference in patients whose VT was terminated by a transthoracic shock. From the Divisions of Clinical Pharmacology and Cardiology, De partment of Medicine, and the Division of Biometry, Duke University Medical Center; and the Durham Veteran’s Administration Medical Center, Durham, North Carolina. This work was sup orted in part by Grant MO1 RR00030 from the National Center Por Research Resources, National Institutes of Health, Bethesda, Maryland. Dr. Pritchett’s address is: Room 2000, Duke South Hospital, Box 3477, Duke University Medical Center, Durham, North Carolina 27710. Manuscript received February 2 1, 1996; revised manuscript received and accepted June 14, 1996.

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. . .

We studied 29 adult patients undergoing electrophysiology study in whom monomorphic VT lasting 215 seconds was induced. Patients in sinus rhythm with adequate ultrasound image quality were eligible (1 patient in ventricular bigeminy who reverted to ventricular bigeminy after VT was included). Patients with mitral or aortic valvular prostheses, mitral or aortic valvular stenosis, or severe mitral or aortic valvular regurgitation were excluded, as were patients in whom isoproterenol infusion was required to induce sustained VT. Recruitment began January 1994, and ended January 1995. The study protocol was approved by the Institutional Review Board at Duke Medical Center (26 patients) and Human Studies Subcommittee at the Durham Veterans Affairs Medical Center (3 patients). Written informed consent was obtained from each patient before inclusion in the study. There were 28 men and 1 woman with a mean age of 60 + 14 years (range 16 to 79). Underlying cardiovascular disease included coronary artery disease (24 patients), idiopathic cardiomyopathy (2 patients), hypertension (2 patients, 1 of whom also had coronary artery disease), sarcoidosis (1 patient), and arrhythmogenic right ventricular dysplasia (1 patient). VT was induced using intracardiac programmed electrical stimulation. Monomorphic VT terminated DECEMBER

15,

1996

observer who was unaware of the clinical data. Peak E (early ventricSpont./Paced Group Shock Group ular filling) wave and peak A (atria1 (n = 13) (n = 16) contribution to ventricular filling) wave velocities, E/A wave velocity 60 + 11 (36-79) 59 k 17 (16-75) Age(yrbwl1 12 (92) 16 (100) Men (n [“‘%I) ratio, and heart rate were recorded 71 2 14 67+ 12 Heart rates (beats/min) for the pre-VT and post-VT studies. 25-35% 35-45% Qualitative ejection fraction The primary outcome variable (median category) was the difference in the peak A4.2 t 0.8 4.3 rt 0.7 Left atrial size (cm] 68.0 !I 23.8 80.0 i 24.1 wave velocity observed in each paPeak E-wave velocity (cm/s) 69.0 + 23.4 70.3 t 28.3 Peak A-wave velocity (cm/s) tient from immediately before the 1.2 (0.6) 0.8 (0.9) E/A wave velocity ratio* induction of VT to immediately af68.6 k 32.1 86.3 k 31.3 Time, preVl to post-VT study (min) ter return to sinus rhythm. Contin30.5 (24) 26 (22) Duration of induced VT* (s) uous distributions are characterized 3.6 k 1.6 4.2 + 2.0 Time of VT termination to post-VT study (min) by their mean +- SD and compared between the 2 groups using a 2-samValues are mean 2 SD, except median (interquartile range) (indicated by asterisk). See text for ejection ple t test with 2 exceptions. Distrifraction categories. Shock Group = terminated by tronsthorocic shock; Spont./Poced Group = terminated spontaneously or with intercardiac pocings; VT = ventricular tachycordia. butions related to the E/A velocity and the duration of induced VT are characterized by their median and spontaneously (n = 6) or with intracardiac pacing (n interquartile range and compared using the Wil= 10) in 16 patients (spot-n/paced group) and was coxon rank-sum test. Discrete distributions were terminated by transthoracic shock in 13 patients compared using Fischer’s exact test. A p value (shock group). Electrical cardioversion was accom- 10.05 was considered significant. The study was prospectively designed to provide plished using anteroposterior cutaneous patches. Intravenous benzodiazepines and narcotics were used adequate power to detect a 25 percentage point greater decrease in peak A-wave velocity in the for routine sedation during the electrophysiology procedure, but no additional agents were used spe- shock group than in the spent/paced group. Power calculations were based on the following assumpcifically before transthoracic shock. Two-dimensional (2D) imaging and 2D guided tions: (1) the peak A-wave velocity in patients before pulsed-Doppler transthoracic echocardiographic induction of VT would have a mean of approxistudies were performed (Sonos 1500, Hewlett-Pack- mately 57 cm/s with an SD of approximately 14 cm/ ard Co., Andover, Massachusetts) with 2.0- or 2.5 s; (2) the correlation between the 2 measurements of MHz phased-array transducers. Echocardiograms this velocity made on each patient (pre-VT and postwere performed in the electrophysiology laboratory VT) would be at least 0.5; (3) as many as two-thirds immediately before the start of the invasive proce- of the patients might be in 1 group. Under these asdure (pre-VT) and again immediately after the pa- sumptions, the SD of the difference of the 2 tient returned to sinus rhythm from the first induced measurements for each patient would be at most 14, episode of VT (post-VT). The times from pre-VT to so that a differential decrease in peak A-wave velocpost-VT study and from VT termination to post-VT ity of 25 percentage points would correspond to an study were measured. Because the patients had in- effect size of 1.0.8 Despite a higher than expected dwelling femoral catheters at the time of the post- SD of the peak A-wave velocity, the sample size VT study, echocardiographic studies were performed assumptions were met in part owing to a higher correlation between the 2 measurements. with the patients in the supine position. ... Left ventricular ejection fraction was measured The 2 groups were comparable with respect to the qualitatively and was categorized as < 15%, 15% to 25%, 25% to 35%, 35% to 45%, 45% to 55%, or baseline characteristics of age (59 vs 60 years), gen>55%. Left atria1 size was measured at end-systole der (100% vs 92% men), heart rate (67 vs 71 beats/ in the parasternal long-axis view.7 Pulsed-Doppler min), qualitative ejection fraction (median category transmitral inflow velocities were obtained from the 35% to 45% vs 25% to 35%) left atria1 size (4.3 vs apical 4-chamber view with the sample volume po- 4.2 cm), peak E wave (68 vs 80 cm/s) or A wave sitioned between the tips of the mitral leaflets. At- (70.3 vs 69 cm/s) velocity, and E/A wave velocity tention was paid to obtaining the same transducer ratio (median 0.8 vs 1.2) at pre-VT study (spent/ location on the chest, and also the same incident an- paced group vs shock group, respectively) (Table I). gle between Doppler sampling direction and mitral Time from pre-VT to post-VT study (68.6 vs 86.3 orifice from the pre-VT to post-VT studies. One in- minutes; p = 0.15), duration of induced VT (median 30.5 vs 26 seconds; p = 0.44), and time from tervestigator (G.A.D.) performed all studies. Doppler velocity profiles were saved on optical mination of VT to post-VT study (3.6 vs 4.2 minutes; disk (except 1 study, for which hard copy tracings p = 0.43) were also comparable (spent/paced group were used), allowing full digital reconstruction at the vs shock group, respectively) (Table I). time of measurement. Doppler data from 6 to 10 conIn the spent/paced group the peak A-wave velocsecutive beats were measured and averaged by an ity before VT was 70.3 ? 28.3 cm/s and after VT TABLE

I Baseline

Characteristics

BRIEF REPORTS 1437

was 68.1 2 22.0 cm/s. In the shock group the peak A-wave velocity before VT was 69.0 + 23.4 crnls and after VT was 62.7 -+ 21.4 cm/s. The difference between the before and after VT peak A-wave velocity in the shock group (6.3 + 12.9 cm/s) did not differ significantly (p >0.3) from that in the sponti paced group (2.2 ? 11.0) (Figure 1 and Table II). No difference was detected between the 2 groups in the change in peak E wave (p = 0.19), but there was a significant difference in the change in E/A velocity ratio between groups (p = 0.02) (Table II). The change in heart rate did not differ between the 2 groups (p = 0.61). The median number of shocks in the shock group was 1 (range 1 to 3) with a median total energy of 200 J (range 200 to 660). ... The results of this prospective study do not support the hypothesis that a transthoracic shock of mild to moderate energy diminishes atria1 mechanical function. We studied patients with inducible VT at electrophysiologic examination to isolate the effect on atria1 function of a transthoracic shock from the effect of a period of atria1 fibrillation. In addition, the underlying cardiovascular disease in this population is similar to the spectrum of underlying disease seen in patients with atria1 fibrillation who might be subjected to electrical cardioversion. The energy used on the majority of patients electrically cardioverted from VT in this study (1 shock, 200 J) is reported to be successful in most patients with atria1 fibrillation who will cardiovert electrically.9~‘0 Although our primary outcome variable, the change in peak A-wave velocity, did not show a significant decreaseafter a transthoracic shock, the E/A ratio in the shock group did change. The change in this ratio was 40 35 1

.

;

. .

-20

I -25 '

p=o.37

i

shock

FIGURE 1. Scatterplot of the difference in peak A-wave vekxi (before ventricular tachycardia [pre-WI - after ventricular tatTl ybars, mean value cardia (post-VT]) in the 2 grou 5. fforizond for group. shock = tennina tecr by transthoracic shock; spent/ paced = terminated spontaneously or with intracardiac pacing. 1438

THE AMERICAN JOURNAL OF CARDIOLOGY@

Post-VT) in Clinical

Spont./Paced Group [n = 16) Peak E-wave velocity (cm/s) Peak A-wave velocity (cm/s) E/A wave velocity ratio* Heart rate (beats/min) Values asterisk).

ore means

+ SD, except

0.6 2.2 0.0 -2.6 for median

k 9.3 k

11.0

(0.2) + 5.8 (interquartile

Shock Group (n = 13) -6.5 t 16.8 6.3 t 12.9 -0.1

-0.2 range)

(0.5)

t 15.6

(indicated

by

See text for p values.

Abbreviations

OS in Table I.

due to a small, nonsignificant decreasein the peak Awave velocity combined with a small, nonsignificant increase in the peak E-wave velocity after transthoracic shock. This change in E/A ratio may have no physiologic significance. Salerno et al” noted a very transient rise in serum norepinephrine level in patients cardioverted from VT, but no information was obtained concerning ventricular filling dynamics. An alternate explanation for impaired atrial function after cardioversion of atrial fibrillation is that the period of atrial fibrillation itself results in a localized atrial cardiomyopathy. There is evidence that pacing-induced tachycardia for 2 to 4 weeks causesa reversible ventricular cardiomyopathy”-‘3 which is accompanied by abnormal intracellular calcium regulation.14-‘6 Therefore, it is plausible that an atrial cardiomyopathy can be induced by a period of atrial tachyarrhythmia. Atrial dysfunction would then become evident upon return to sinus rhythm as the mechanical function is compared with normal patients in sinus rhythm or to the same patient’s anial function after several weeks of maintenance of sinus rhythm. Existing data showing a gradual return of atrial mechanical function after conversion of atrial fibrillation to sinus rhythm are consistent with this theory.3-5

Acknowledgment: We would like to acknowledge the technical assistance of Michael J. Strub, RDCS, and also thank Carl Nibley, MD, Keith Newby, MD, and the rest of the Duke University EP fellows for their help with patient recruitment, and the EP Laboratory nursing staffs of Duke University and the Durham VA Medical Center for their facilitation with the study. We would also like to thank Mark Willis for assistance with data management.

. sponffpaced

(Pre-VT Minus

Characteristics

We measured left atria1 function during sinus rhythm before and after VT was induced in an electrophysiology laboratory, using peak transmitral A-wave velocity from pulsed-Doppler transthoracic echocardiography as a marker of left atria1 mechanical function. The results of this prospective study do not support the hypothesis that a transthoracic shock of mild to moderate energy diminishes atria1 mechanical function.

.

.

TABLE II Change

VOL. 78

1. Conti CR. Atria1 fibrillation, tramesophageal echo, electrical cardioversion, and anticoagulation. Clin Cardiol 1994;17:639-640.

DECEMBER 15, 1996

2. Fatki” D, Kuchar DL, Thorbum CW, Fen&y MP. Transesophageal echocardiography before and during direct current cardioversio” of atria1 fibrillation: evidence for “atrial stunning” as a mechanism of thromboembolic complications. J Am Coil Cardiol 1994;23:307-316. 3. Manning WJ, Silverman DI, Katz SE, Riley MF, Come PC, Doherty RM, Munson JT, Douglas PS. Impaired left atria.1 mechanical function after cardioversion: relation to the duration of atria1 fibrillation. J Am Coil Curdiol 1994;23:1535-1540. A. Manning WJ, Leeman DE, Gotch PJ, Come PC. Pulsed Doppler evaluation of atria1 mechanical function after electrical cardioversion of atria1 fibrillation. JAm Call Cardiol 1989;13:617-623. 5. Shapiro EP, Effron MB, Lima S, Ouyang P, Siu CO, Bush D. Transient atria1 dysfunction after conversion of chronic atrial fibrillation to sinus rhythm. Am J Cardiol 1988;62:1202-1207. 6. Black IW, Fatkin D, Sagar KB, Khandheria BK, Leung DY, Galloway JM, Fen&y MP, Walsh WF, Grimm RA, Stollberger C, Verhorst PMJ, Klein AL. Exclusion of atria1 thrombus by transesophageal echocardiography does not preclude embolism after cardioversion of atria1 fibrillation: a multicenter study. Circulation 1994;89:2509-2513. 7. Sahn DJ, DeMaria A, Kiss10 J, Weyman A. Recommendations regarding quantification in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation 1978;58:1072- 1082. 8. Cohen J. Statistical Power Analysis for the Behavioral Sciences, 2nd ed. Hillsdale, NJ: Erlbaum, 1988. 9. Ewy GA. The optimal technique for electrical cardioversion of atrial fibrillation. Clin Curdiol 1994;17:79-84.

The Upper Turnover

10. Salerno DM, Katz A, Dunbar DN, Fjeldos-Sperbeck K. Serum electrolytes and catecholamines after cardioversion from ventricular tachycardia and atrial fibrillation. PACE 1993;16:1862-1871, 11. Cruz FES, Cheriex EC, Smeets JLRM, AtiC J, Peres AK, Penn OCKM, Brugada P, Wellens HJJ. Reversibility of tachycardia-induced cardiomyopathy after cure of incessant supraventricular tachycardia. J Am Co// Cardiol 1990;16:739-744. 12. Tomita M, Spinale FG. Crawford FA. Zile MR. Changes in left ventricular volume, mass, and function during the development and regression of supraventricular tachycardia-induced cardiomyopathy: disparity between recovery of systolic versus diastolic function. Circulation 1991;83:635-644. 13. Spinale FG, Zellner JL, Tomita M, Crawford FA, Zile MR. Relation between ventricular and myocyte remodeling with the development and regression supraventticular of tachycardia-induced cardiomyopathy. Circ Res 1991;69:1058-1067. 14. Spinale FG, Fullbright M, Mukherjee R, Tanaka R, Hu I, Crawford FA, Zile MR. Relation between ventricular and myocyte function with tachycardiainduced cardiomyopathy. Circ Res 1992;71: 174- 187. 15. Ishikawa Y, Sorota S, Kiuchi K, Shannon RP, Komamura K, Katsushika S, Vatner DE, Vatner SF. Homey CJ. Downregulation of adenylylcyclase types V and VI mRNA levels in pacing-induced heart failure in dogs. J Ch Invrst 1994;93:2224-2229. 16. Perreault CJ, Shannon RP, Komamura K, Vatner SF, Morgan JP. Abnormalities in intracellular calcium regulation and contractile function in myocardium from dogs with pacing-induced heart failure. J Clia hvrsr 1992:89:932938.

Site in the Reentry Common Atriai Flutter

Takeshi Tsuchiya,

Circuit

MD, Ken Okumura, MD, Toshifumi Tabuchi, MD, Atsushi Hirofumi Yasue, MD, and Hiroshige Yamabe, MD

is generally accepted that common atria1 flutter Iitst(AF) is due to reentry with an excitable gap and that circuit is located primarily in the right atrium.‘-‘” The activation sequence of AF is craniocaudal in the anterior free wall and caudocranial in the atria1 septum, and the lower turnover is in the narrow isthmus between inferior vena cava and tricuspid annulus.3-“’ The site of the upper turnover, however, is still unclear and it remains to be elucidated whether it is anterior or inferior to the orifice of the superior vena cava.’ Single extrastimulus testing is useful to determine the relative location of the pacing site to the reentry circuit.“* To reset the tachycardia with extrastimulus with a long coupling interval and the return cycle after the extrastimulus equal to or close to the tachycardia cycle length strongly suggests that the pacing site is on or close to the tachycardia reentry Circuita2S31 l,l* Using this diagnostic tool to identify the location of the reentry circuit, we examined the upper turnover site in the reentry circuit of AF, in particular to determine whether it is anterior or inferior to the superior vena cava. ... Eight patients (5 men and 3 women, aged 44 to 73 years [mean 601) with AF were included in this From the Division of Cardiology, Kumamoto University School of Medicine, Kumamoto; the Second Department of Internal Medicine, Hirosaki University School of Medicine, Hirosaki, and the Division of Cardiolo y Kumamoto City Hospital, Kumamoto, Japan. Dr. Okumurals o J,dress IS: Second Department of Internal Medicine, Hirosaki University School of Medicine, Zoifu-cho 5, Hirosaki, 036 Japan. Manuscrrpt received April 10, 1996, revised manuscript received and accepted July 10, 1996.

Iwasa,

of MD,

study. Three patients had underlying heart disease including open mitral commissurotomy (l), percutaneous transluminal coronary angioplasty (l), and complete atrioventricular block (1). The electrocardiogram taken during the tachycardia showed a negative saw-tooth pattern in the inferior leads typical for AF in all patients. All antiarrhythmic drugs were discontinued for >5 half-lives of each drug before the study. Written informed consent was obtained from all patients before the study. Using standard techniques, 2 6Fr quadripolar electrode catheters (Josephson, Bard Electrophysiology, Billerica, Massachusetts) were placed in the proximal portion of the coronary sinus and His bundle region and were used for recording bipolar electrograms. Two 7Fr deflectable quadripolar electrode catheters with a 2-mm interelectrode interval (Cordis Webster, Baldwin Park, California) were also placed at the anterior right atrium and at sequential sites for right atria1 mapping and pacing. All bipolar electrograms were filtered between a band pass of 50 and 600 Hz and recorded simultaneously with 3 electrocardiographic leads (I, II, and Vl) with the use of a polygraph (RMC-2000; Nihon Kohden, Tokyo, Japan). Atria1 pacing was performed at a stimulus strength of twice the diastolic threshold and a pulsewidth of 2 ms using a programmable stimulator (SEC-3102; Nihon Kohden). In 6 of the 8 patients, AF was present at the time of the study, whereas in the other 2 patients it was induced by atria1 pacing. All AF episodes studied showed a constant atria1 cycle length with a beat-to-beat variation zz10 ms in 5 patients and I 18 ms in 3 patients. BRIEF REPORTS

1439