exercise response before and after termination of atrial tachycardia after congenital heart disease...

HU Wessel, DW Benson, Jr, EA Braunlin, A Dunnigan and MH Paulcongenital heart disease surgery

Exercise response before and after termination of atrial tachycardia after

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106

Exercise Response Before and AfterTermination of Atrial Tachycardia After

Congenital Heart Disease SurgeryHans U. Wessel, MD, D. Woodrow Benson Jr., MD, PhD, Elizabeth A. Braunlin, MD,

Ann Dunnigan, MD, and Milton H. Paul, MD

We studied exercise performance before and after conversion of atrial tachycardia to sinusrhythm, atrial bradycardia, or junctional rhythm in 10 patients 9-25 years of age 8-20 yearsafter congenital heart disease surgery (complete transposition of the great arteries, seven of 10patients). The same maximal cycle (five of 10 patients) or treadmill (five of 10 patients) exerciseprotocol was performed in atrial tachycardia and sinus rhythm 1-232 days after atrialtachycardia (mean, 34 days). Electrocardiogram, heart rate, and pulmonary gas exchange wererecorded. Sinus rhythm exercise increased peak Vo2 (mean, 28.7 [sinus rhythm] vs. 24.7 [atrialtachycardia], p<0.01), exercise time (p<0.01), and 02 pulse at rest (p<0.01) and at peakexercise (NS). Mean resting heart rate decreased from 109 to 70 beats/min (p<0.01). In atrialtachycardia, peak exercise heart rate was low (80-163 beats/mmn) because of fixed conduction(six of 10 patients) or high as conduction approached 1:1 (176-252 beats/min) (four of 10patients). In sinus rhythm, rest to peak exercise heart rate increased in six of 10 patients(p<0.05). The data show improved exercise performance in sinus rhythm primarily because ofimproved heart rate adaptation to exercise, by either permitting increased heart rate responseor eliminating excessively high heart rate with inadequate diastolic filling. (Circulation 1989;80:106-111)

A trial tachycardia, thought to be due to intra-atrial reentry, is one of the more commonand clinically more troublesome late com-

plications after surgical treatment of congenital car-diac defects that involve extensive intra-atrial sur-gery. In a multicenter 15-year follow-up study of372 patients after Mustard operation, active arrhyth-mias, including supraventricular tachycardia, junc-tional tachycardia, atrial flutter, and atrial fibrilla-tion, varied from 2% to 7% during the first 10 yearsand subsequently increased.1 Electrical or pharma-cologic termination of atrial tachycardia is anaccepted mode of therapy even in patients withoutovert untoward symptoms.The purpose of this study was to examine the

effect of atrial tachycardia on exercise performance

From the Children's Memorial Hospital, Division of Cardiol-ogy, Willis J. Potts Children's Heart Center, McGaw MedicalCenter, Northwestern University, Chicago, Illinois; and TheDepartment of Pediatrics, University of Minnesota Hospital andClinic (E.A.B., A.D.), Minneapolis, Minnesota.Supported in part by the Helping Hearts Research Fund, The

Children's Memorial Hospital, Chicago, Illinois.Address for correspondence: Hans U. Wessel, MD, The

Children's Memorial Hospital, 2300 Children's Plaza, Chicago,IL 60614.Received July 28, 1988; revision accepted March 7, 1989.

by comparing the response to graded maximal tread-mill or cycle ergometer exercise before and aftertermination of atrial tachycardia. We hypothesizedthat differences in exercise response between atrialtachycardia and the basic underlying rhythm stateswould vary between patients depending on a numberof factors, including the ventricular rate during atrialtachycardia at rest and during exercise, the ventric-ular rate response of the basic underlying rhythmduring exercise, and global myocardial function. Wespeculated that conversion of atrial tachycardia wouldresult primarily in longer exercise times and greaterpeak 02 uptakes (Vo2) but not in significant Vo2increases at low-to-moderate work rates.

MethodsPatientsWe studied 10 patients characterized in Table 1.

Seven had complete transposition of the great arter-ies. One had complete atrioventricular canal, onehad a double outlet right ventricle, and one had aventricular septal defect associated with valvar andinfundibular pulmonic stenosis. Including atrial sep-tostomy (patients 2, 6-8, and 10) and pacemakerinsertion (patients 4-6 and 10), the 10 patients



Wessel et al Exercise Response 107

TABLE 1. Clinical, Anthropometric, and Age Data

Intracardiac Onset of AT 1st exercise Height (cm) Weight (kg)Patient Gender Diagnosis repair (yr) (min) (percentile) (percentile) Days*

1 M TGA, IVS, PDA 3.57 15.02 15.02 165.8 (25-50) 54.9 (25-50) 2322 F TGA, IVS, PDA 2.33 9.50 12.07 142.0 (10) 30.6 (5) 193 F TGA, IVS 3.59 9.55 17.91 157.4 (10-25) 41.2 (<5) 14 F Complete AV 8.53 22.20 25.49 156.2 (10) 63.8 (75) 14

canal, PS5 F TGA, IVS, PDA 1.91 6.10 14.48 146.2 (<5) 44.8 (10-25) 86 M DORV, PDA 1.39 4.74 9.48 125.7 (5) 22.4 (<5) 77 M TGA, VSD, SUB 6.81 16.27 17.95 165.1 (5) 47.7 (<5) 9

pulmonarystenosis

8 M TGA, IVS 2.15 16.32 20.83 166 (5) 68.2 (50) 89 M VSD, PS 6.30 24.97 25.02 171 (10-25) 71.9 (50) 7

10 M TGA, VSD 2.45 8.13 22.53 177 (25-50) 74.0 (75) 4Mean 3.90 13.28 18.08 157.2 52.0 30.9±1 SD ±2.44 ±6.80 ±5.40 ±15.42 ±17.67 ±70.8

AT, atrial tachycardia; TGA, transposition of the great arteries; IVS, intact ventricular septum; PDA, patent ductus arteriosus; PS,pulmonary valve stenosis; DORV, double outlet right ventricle; VSD, ventricular septal defect.

*Time between studies in days.

underwent a total of 27 palliative and correctivecardiac surgical procedures. Each patient had hadone or more episodes of atrial tachycardia. Using apreviously described technique,2 we established adiagnosis of atrial tachycardia during transesoph-ageal pacing study based on the following charac-teristics: a regular atrial tachycardia cycle length(mean, 229.5+±37 msec; range, 170-280 msec) andtermination of atrial tachycardia with pacing. Inthese cases, atrial tachycardia is probably due tointra-atrial reentry, and such tachycardias are oftenreferred to as atrial flutter.The time between intracardiac repair and initial

onset of atrial tachycardia ranged from 3.4 to 18.7years (mean, 9.39+5.0 years). The time betweenonset of atrial tachycardia and the first exerciseevaluation was 0-14.4 years (mean, 4.8+4.5 years).The time between exercise before and after conver-sion of atrial tachycardia was <19 days in ninepatients and 232 days in patient 1. Antiarrhythmicmedications at the time of the study included digoxin(six patients), propranolol (one patient), and pro-cainamide (one patient), either alone or in combi-nation. In each patient, drug regimens were identi-cal during exercise before and after atrial tachycardiaconversion.Anthropometric data at the time of the first exer-

cise study indicate that height was less than the 25thpercentile in all but two patients. In patients 5-8,height was 5th percentile or less. The percentile forweight was less then that for height in four (patients2, 3, 6, and 7), the same in patient 1, and greater infive (patients 4, 5, and 8-10).

Exercise StudiesAll patients were exercised to the end of their

tolerance, which was defined as an inability tocontinue. Patients 1-5 were studied at the Univer-

sity of Minnesota Variety Club Children's Hospitalwith either the Bruce or a modified Balke protocolfor treadmill exercise. Patients 6-10, evaluated atthe Children's Memorial Hospital, Chicago, workedon the cycle ergometer (Model 840, Quinton, Seat-tle, Washington) with stepwise increasing work rateincrements of 1- or 4-minute duration. However,each patient performed the same exercise protocolbefore and after conversion of atrial tachycardia.ECG and heart rate were monitored continu-

ously. Systemic blood pressure was recorded inter-mittently. Ventilation and pulmonary gas exchangewere measured breath by breath. The Minnesotapatients were studied with the System 2000 (Med-ical Graphics, St. Paul, Minnesota); the Chicagopatients were studied with the method previouslydescribed in detail.3,4

Data AnalysisData analysis is based on means of breath-

by-breath data averaged during the last 15 seconds ofeach minute (Minnesota patients) or during eachexercise minute (Chicago patients). The ventilatoryresponse to exercise was evaluated by linear regres-sion of minute ventilation (VE 1/min BTPS) on CO2elimination (Vco2 ml/min STPD) and expressed asVE at a Vco2 of 1 1/min from the regression (VE1000).Peak 02 uptake (Vo2) was expressed in milliliters perminute STPD and milliliters per minute per kilogrambody weight. Percentages of predicted 02 uptake arebased on the standards for maximal Vo2 by Mocellinand Bastanier.5 Significance of differences betweenpreconversion and postconversion data were evalu-ated by paired comparison (Student's two-tailed ttest) and linear regression analysis.

Control GroupsSeventy-eight patients who were exercised twice

with the same exercise protocol between 1976 and



108 Circulation Vol 80, No 1, July 1989

1987 (group 2A) and one patient with thalassemiamajor and normal exercise performance who wasstudied 12 times between 9 and 17 years of age atthe Children's Memorial Hospital (group 2B) servedas controls to compare test-retest reproducibility ofminute-by-minute Vo2 measurements of the studypatients. All controls were studied on the cycleergometer with stepwise increments of work rate(16.4 W) of 1-minute duration to the end of tolerance.

In each of the three groups (the 10 tachycardiapatients in this study [group 1], the 78 patients[group 2A], and the multiple studies of the singlepatient [group 2B]), we computed the mean Vo2difference (second minus first study) of rest and allexercise minutes and for the last exercise minute atthe same power alone by paired comparison. Dif-ferences between group means were evaluated byunpaired comparison. Significance was evaluatedby Student's t test.

ResultsIn group 1, conversion of atrial tachycardia

resulted in sinus rhythm, atrial bradycardia, orjunctional rhythm, collectively labeled as sinusrhythm. Sinus rhythm (Table 2) was associated withlonger average exercise times (p<0.01), higher aver-age peak Vo2 (p<0.01), and greater average resting(p<0.01) and peak exercise (p=NS) oxygen pulse.Average resting heart rate was lower during sinusrhythm (p<0.001). Average peak exercise heartrates were also lower during sinus rhythm, but thedifference was not significant. Paired comparisonrevealed no significant differences for peak exercise

TABLE 2. Exercise Studies in Atrial Tachycardia and After Con-version to Sinus Rhythm

Atrial SinusVariable tachycardia rhythm p

Exercise time (min) 8.6+2.8 9.8+3.3 <0.01Peak Vo2ml/min STPD 1,245±531 1,452±584 <0.01ml/min/kg 24.7±6.4 28.7±8.1 <0.01

02 pulse (ml/beat)Rest 2.39+1.04 3.98±1.94 <0.01Peak exercise 8.04+4.20 10.02+4.15 NS

Heart rateRest 109±26.7 70.2±17.8 <0.01Peak exercise 168±44 152±31 NS

Vo2, 4th minute exercise(ml/min STPD) 876±3.07 898±287 NS

VEIOOO (1/min BTPS) 39.31+7.69 36.64±6.84 NS

p value based on paired comparison.

respiratory exchange ratio (r: atrial tachycardia,1.036±0.095; sinus rhythm, 1.084±0.089) and peakrespiratory rate (atrial tachycardia, 49.0+1 1.2 beats/min; sinus rhythm, 47.8±9.0 breaths/min). Thesefindings suggest that the patients were workedapproximately to the same level of their capacityduring the two tests. There was also no significantchange of the ventilatory response to exercise asexpressed by the linear regression ofVE (1/min BTPS)on Vco2 (1/min STPD) in terms of slope (atrialtachycardia, 36.8±8.3 beats/min; sinus rhythm,34.7±7.5 1 VE/1 Vco2), intercepts (atrial tachycardia,2.09±2.3 beats/min; sinus rhythm, 2.42+2.41 BTPS),VE1000 (atrial tachycardia, 38.9±7.8 beats/min; sinus

TABLE 3. Exercise Studies Before and After Conversion of Atrial Tachycardia to Sinus Rhythm

AVo2 restand

Exercise Rhythm Peak exercise hr Peak exercise Vo2 Peak exercise Vo2 exercisetime (min) after (hr span) (ml/min STPD) (ml/min/kg) (mean± SD)

Patient AT SR conversion AT SR AT SR IAVo2 AT SR % SR-AT1 11 13 S 252 (125) 177 (91) 1,570 1,940 370 29.3 34.1 (76) 58+1352 13 15 J 176 (71) 180 (120) 853 912 59 27.4 29.5 (78) 20+753 8 9 S 152 (46) 187 (97) 676 853 177 16.4 20.7 (59) 55+984 8 8 S 157 (25) 143 (46) 1,200 1,288 88 18.9 19.9 (57) 53+1395 11 13 J 200 (72) 117 (59) 967 1,310 343 25.0 29.1 (81) 66±1736 4 5 P 163 (78) 146 (76) 758 968 210 33.8 43.0 (96) 11±847 6 7 S 156 (61) 157 (86) 902 1,205 303 18.9 25.5 (57) 95±67*8 9 9 S 189 (115) 135 (79) 2,162 2,390 228 31.7 35.0 (78) 77±71*9 10 12 S 152 (68) 182 (109) 2,070 2,410 340 28.8 33.5 (74) 36±48t10 6 6.5 J 80 (-21) 94 (58) 1,294 1,249 -45 17.2 16.9 (38) -80+56*AllMean 8.6 9.8 168 (64) 152 (82) 1,245 1,452 207 24.7 28.7 (69.4)±SD ±2.8 +3.3 +44 (±42) ±31 (±23) +531 ±584 ±139 ±6.4 +8.1 (±16.5)

p<0.01 NS (NS) p>0.01 p<0.01 p<0.01HR span, difference between peak exercise and resting heart rate just before exercise (sitting). %, percentage of predicted (Reference

4). AVo2 rest and exercise mean±SD of difference between Vo2 in sinus rhythm and Vo2 in atrial tachycardia based on paired comparisonof rest and all exercise minutes in each patient. S, sinus; J, junctional; P, pacemaker and occasional junctional premature beats. AT,atrial tachycardia; SR, sinus rhythm.

*p<0.0l; tp<0.05.




rhythm, 37.2±6.8 1/min BTPS), or the correlationcoefficients (atrial tachycardia, 0.988+0.01; sinusrhythm, 0.975±0.05).

Heart Rate ResponseDuring atrial tachycardia, patient 2 had 2: 1 atrio-

ventricular conduction at rest with a ventricularrate of 159 beats/min. All others showed variableconduction (2:1-4:1). After conversion to sinusrhythm, resting heart rate decreased in all (mean,34.0±21.1 beats/min;p<0.001). During atrial tachy-cardia exercise, two patterns of atrioventricularconduction were observed. Six patients did notachieve greater than 2:1 atrioventricular conduc-tion during exercise when in atrial tachycardia. Infive of these, peak exercise heart rates ranged from152 to 163 beats/min, whereas in patient 10, heartrate increased from 101 beats/min at rest to 105beats/min during the 4th minute of exercise (400kg. m/min) but decreased to 80 beats/min during thefinal 2 minutes of work. In these six patients, peakexercise heart rate during sinus rhythm wasunchanged in one, decreased in two, and increasedin three patients when compared with peak exerciseheart rate during atrial tachycardia. The remainingfour patients showed a gradual increase toward 1:1atrioventricular conduction during exercise in atrialtachycardia, with peak heart rates ranging from 176to 252 beats/min. Exercise during sinus rhythm inthese four patients resulted in markedly lower peakheart rates in three (patients 1, 5, and 8) and nochange in the fourth patient (see Figure 1).

Vo2 ResponsePatients 1-9 increased peak exercise Vo2 after

conversion to sinus rhythm regardless of whether ornot they increased exercise time (range, 79-370 ml/min STPD, p<0.001) (Table 2, Figures 2 and 3).Minute-by-minute paired comparison of Vo2 in eachpatient between sinus rhythm and atrial tachycardia(i.e., excluding the minutes of increased exercisetime after conversion to sinus rhythm) also showeda small increase of average Vo2 after conversion.However, these mean differences (1AVo2=Vo2 sinusrhythm-Vo2 atrial tachycardia) were significant onlyin three patients (7-9). In patient 10, peak exerciseVo2 decreased slightly (-45 ml/min STPD) afterconversion of atrial tachycardia to sinus rhythm, andminute-by-minute LVo2 was significantly lower insinus rhythm (p<0.01).

Minute-by-minute group means of Vo2 indicatedno significant differences at rest and during the 1st 4minutes of exercise (Figure 3). During subsequentminutes, AVo2 tended to become progressivelygreater (significant for the 5th, 7th, and 9th minutesof work) after conversion to sinus rhythm. Compar-ison of the last minute of work achieved duringatrial tachycardia with the corresponding minute insinus rhythm, irrespective of work rate, also yieldeda significant mean AVo2 (p<0.01). By contrast,AVo2 between 2nd and 1st study of either control

250

200

150

100

50

250

200

150

100

AT

SR

50HeartRatel .. min. Ex.min. R 2 4 6 8 10 12 14 16

FIGURE 1. Plots ofheart rate response to exercise in 10patients before (top panel) and after (bottom panel)conversion of atrial tachycardia (AT) to sinus rhythm(SR).

group was not significant for the last minute of workat the same work rate (Table 4), but AVo2 of thepatients in group 1 was greater than that of patientsin both control groups (p<0.02).

DiscussionIn this study, we showed a significant increase of

exercise performance (peak work rate, peak Vo2)after conversion of atrial tachycardia to sinus rhythmin a group of late survivors of surgery for complexcongenital cardiac defects. The majority had under-

2500 I

2000 P

1500 I

1000 h

500V02

milmin.

1245 1452 904±531 ±584± 307

K f

ATPeak Ex.

SR

920 mean±259 ±1 SD

AT SR4th min. Ex.

FIGURE 2. Plots ofoxygen uptake (Vo2) atpeak exercise(left) and during 4th minute ofexercise (right) before andafter conversion ofatrial tachycardia (AT) to sinus rhythm(SR). Yxs p<0.01.



110 Circulation Vol 80, No 1, July 1989

200

100

0

-100

-200

\AV02mil/min.

mean AV02±1SD x ,

R 2 4 6 8 10 12 L PEx. Time, min

FIGURE 3. Plot of mean+±SD of Vo2 difference (sinusrhythm study-atrial tachycardia study) at rest and dur-ing exercise. L, last minute of work at the same workrate; P, peak exercise. x, p<0. 05; xx, p<O. 01. Numbersrefer to number of comparisons at each minute.

gone an atrial baffle procedure (Mustard procedure)for transposition of the great arteries. Rhythm dis-turbances are common in such patients and includejunctional rhythm or sinus bradycardia at rest,1inability to increase sinus rate appropriately duringexercise, and atrial tachycardia.6'7 In one study of60 patients with transposition of the great arteriesafter Mustard procedure operation, spontaneousclinical episodes of atrial flutter and tachycardias(17%) and electrophysiologically inducible sus-tained atrial flutter (55%) were noted.8 The progres-sive nature of atrial tachycardia development' isalso suggested in our patients by the long timeinterval (mean, 9.4+5.0 years; range, 3.4-18.7 years)

TABLE 4. Oxygen Uptake Difference Between Second and FirstExercise Study

Comparisonsat samework rate Patients

Mean+SD p (n) (n)Rest and all exercise minutes at the same work rate*Group 1 33.8±105.6 <0.01 94 10

p<O.001Group 2A 19.7+145.2 <0.01 493 78

p=NSGroup 2B 15.8±88.7 NS 88 12

Last exercise minute at the same work ratetGroup 1 160.9+131.8 <0.01 10

p<0.02Group 2A 16.0±+161.8 NS 78

p<0.02Group 2B 46.6+119 NS 11

Group 1 comprised 10 patients; Group 2A comprised 78patients with various diagnoses exercised twice, months or yearsapart with the same work protocol and one patient withthalassemia major and normal exercise tolerance studied 12times 6-12 months apart from age 9-17 years.

*Includes rest (sitting) and all exercise minutes.tComparisons of last minute of exercise at the same work rate.

See text.

between operation and onset of atrial tachycardia.It has previously been noted that atrial tachycardiamay be tolerated quite well,2 probably because ofself-restriction of physical activity. Patients we stud-ied reported few symptoms due to atrial tachycar-dia, and the time from initial onset of atrial tachy-cardia to the time of study was long (mean, 4.8+4.5years; maximum, 14.4 years). Further, even thoughthe average peak Vo2 of 27.4 ml/min/kg in this groupis below normal when in atrial tachycardia, thislevel of peak Vo2 is sufficient so that a patient canadapt to an asymptomatic lifestyle in the UnitedStates.

Atrial tachycardia may affect cardiac perfor-mance at rest and in response to exercise in anumber of ways: 1) by altering ventricular fillingdue to the absence of an effective atrial systole, 2)by improving an irregular variation in cycle length(most pronounced at rest), 3) by limiting the heartrate response to exercise (ventricular response >2 1atrioventricular conduction), and 4) by impairingventricular function due to increased ventricularrate when atrioventricular conduction approaches1:1 with increasing exercise, which results in exces-sive shortening of diastolic filling time. Finally, thehemodynamic status or inotropic state of a givenpatient will determine to what extent and at whatlevel of work rate during exercise these factors willbegin to limit exercise performance. In most ofthese postoperative patients, exercise performanceis impaired significantly, independently of abnormalheart rate.6,7,9Given the adaptability of the cardiovascular oxy-

gen delivery system, one would expect that theprimary effect of atrial tachycardia would be to limitpeak performance and peak exercise Vo2. At lowerwork rates, the ability to deliver 02 to the workingmuscle per se is unlikely to be impaired, and thesame 02 uptake will be delivered but with a differentcombination of heart rate, stroke volume, and arterio-venous 02 difference. This was found to be true inthis study and has been demonstrated in an exercisestudy of "lone atrial fibrillation" before and afterconversion to sinus mechanism.10 During steady-state work (6 minutes), for work rates of up to 600kg - m/min, the Vo2 during atrial fibrillation andsinus rhythm was the same even though sinusrhythm resulted in significantly increased cardiacoutput and stroke volume and a significantlydecreased heart rate and arteriovenous 02 differ-ence. These findings are in keeping with our ownobservation" that the linear relation between steady-state Vo2 and work rate is independent of age, sex,and cardiovascular status and does not differ fromnormal in postoperative patients with tetralogy ofFallot, aortic stenosis, coarctation of the aorta,transposition of the great vessels, and tricuspidatresia. However, during non-steady state work(i.e., for progressive work rate increments of only1-minute duration), the linear slope of Vo2 on workrate was significantly less in all patient groups and




significantly less in patients with transposition ofthe great vessels after Mustard correction com-

pared with that in normal subjects."In our study, the increases of exercise time and

peak Vo0 were rather small after conversion fromatrial tachycardia to sinus rhythm, and all but one

patient experienced the first exercise testing beforeconversion. Therefore, the possibility cannot beexcluded that the improvement after conversionmay have been related wholly or in part to otherfactors, including greater familiarity with test pro-

cedure, greater motivation to do well, and greaterencouragement to continue exercise. However, com-

parison with the control groups (Table 4) suggeststhat this was not the case. This is also suggested bythe insignificant differences of peak respiratoryexchange ratio and respiratory rate between the twotests.

Clinical experience to date has shown the diffi-culty in preventing recurrent atrial tachycardia inthe postoperative patient. When preventing atrialtachycardia is not possible, therapeutic strategy isdirected to impairing atrioventricular conduction toprevent an excessive ventricular rate response.However, results of our study suggest that evenwhen ventricular response during atrial tachycardiais not excessive, conversion of atrial tachycardia tosinus rhythm leads to improved exercise toleranceand peak Vo2 primarily by improving heart rateresponse to exercise. This seems particularly impor-tant in the type of postoperative patients repre-sented by our study group who have as a ruleless-than-normal exercise performance even in theabsence of atrial tachycardia.6,7,9 Thus, treatment toprevent or promptly convert recurrent atrial tachy-cardia is important because of the demonstratedslight improvement of exercise capability andbecause of a possible association of atrial tachycar-dia with sudden death in the postoperative patient.12However, it must be recognized that recurrence ofatrial tachycardia is common. In this group, onlyfour patients (patients 1 and 7-9) have remained insinus rhythm after conversion before the sinusrhythm exercise study. The others have had multi-ple recurrences and subsequently have undergonereconversion 2-8 times. Patient 2 has required 27reconversions since sinus rhythm exercise in 1983but is currently well without pacemaker or anti-

arrhythmic medication. Patients 3, 4, and 5 under-went insertion of an antitachycardia pacemakersince the exercise studies. Patient 6 required tworeconversions, 1 and 4 months after the sinus rhythmexercise. Three months later he had a cardiac arrestwhile on Encainide therapy, suffered severe hypoxicbrain damage, and died several months later.

References1. Flinn CJ, Wolff GS, MacDonald D II, Campbell RM, Borcat

G, Casta A, Hordof A, Hougen TJ, Kavey RE, Kugler J,Liebman J, Greenhouse J, Hess P: Cardiac rhythm after theMustard operation for complete transposition of the greatarteries. N Engl JMed 1984;310:1635-1638

2. Butto F, Dunnigan A, Overholt ED, Benditt DG, BensonDW Jr: Transesophageal study of recurrent atrial tachycar-dia after atrial baffle procedures for complete transpositionof the great arteries. Am J Cardiol 1986;57:1356J-1363J

3. Wessel HU, Stout RL, Pauli MH: Minicomputer basedsystem for breath-by-breath analysis of ventilation and pul-monary gas exchange. Proc 5th Annu Conf Computers inCardiology. New York, IEEE Computer Society, pp 97-104, 1979

4. Wessel HU, Stout RL, Bastanier CK, Paul MH: Breath-by-breath variation of FRC: Effect on Vo2 and Vco2 mea-sured at the mouth. JAppl Physiol: Respir Environ ExercisePhysiol 1979;46:1122-1126

5. Mocellin R, Bastanier CK: Zur Frage der Zuverlassigkeit derW170 als Mass der korperlichen Leistungsfahigkeit bei derBeurteilung von Kindern mit Herzkrankheiten. Eur J Pedi-atr 1976;122:223-239

6. Hesslein PS, Gutgesell HP, Gilette PC, McNamara DG:Exercise assessment of sinoatrial node function followingthe Mustard operation. Am Heart J 1982;103:351-357

7. Mathews RA, Fricker FJ, Beerman LB, Stephenson RJ,Fischer DR, Neches WH, Park SC, Lenox CC, ZuberbuhlerJR: Exercise studies after the Mustard operation in transpo-sition of the great arteries. Am J Cardiol 1983;51:1526-1529

8. Vetter VL, Tanner CS, Horowitz LN: Inducible atrial flutterafter the Mustard repair of complete transposition of thegreat arteries. Am J Cardiol 1988;61:428-435

9. Paul MH, Wessel HU, Muster AJ, Idriss FS: Exercise andventricular function in transposition of the great arteriespatients 10 years after atrial (Mustard) repair. Am J Cardiol1987;60:637

10. Resnekov L, McDonald L: Electroversion of long atrialfibrillation and flutter including haemodynamic studies atrest and on exercise. Br Heart J 1971;33:339-350

11. Wessel HU: Integrated cardiopulmonary approach to exer-cise testing in pediatrics. Pediatrcian 1986;13:26

12. Garson A Jr, Bink-Boelkens M, Hesslein PS, Hordof AJ,Keane JF, Neches WH, Porter CJ: Atrial flutter in theyoung: A collaborative study of 380 cases.JAm Coll Cardiol1985;6:871-878

KEY WORDS * cardiac defects, congenital * transposition ofthe great arteries * tachycardia * exercise



exercise response before and after termination of atrial tachycardia after congenital heart disease...

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