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4

10 Brief Communications

alized by this method, 3, 4 and the presence f an abnormal

coronary flow into the pulmonary artery can be demon-

strated with pulsed Doppler echocardiography.15,6 Color

Doppler flow mapping has added the capability of analyz-

ing the spatial distribution of flow, which has potentially

increased he sensitivity of the noninvasive diagnosis,not

only for the anomalousorigin of the left coronary artery,

but also for the anomalousorigin of the right coronary

artery.17-21 hus color Doppler flow mapping has supple-

mented the two-dimensional and pulsed Doppler echocar-

diographic assessment f these uncommondisorders. Our

observationssuggest hat color Doppler flow mapping can

alsobe quite useful during the postoperative follow-up to

verify the patency of the connection and to detect poten-

tial complications elated to this surgical procedure. Since

similar methodsare sometimes sed or anastomosing or-

onary arteries to the neo-aortic root during arterial switch

procedures or transposition of the great vessels,he capa-

bilities of flow mapping to study these communications

may assume ncreased mportance in this population of

growing infants as we11.22n view of the small size of the

fistula in our patient, her asymptomatic status, and the

continuous forward flow into the left coronary artery

despite the fistula, plus a normal exercise thallium study

subsequentlyobtained, our decisionhasbeen o follow this

patient medically, including serial color Doppler echocar-

diograms and repeated stress thallium studies in the

follow-up evaluations.

REFERENCES

1. Bland EF, White PD, Garland J. Congenital anomalies of cor-

onary ar tery: Report of unusual case associated with cardiac

hypertrophy.

AM HEART J 1933;8:787-801.

2. Askenazi J. Nadas AS. Anomalous left coronarv artery origi-

3.

4.

5.

6.

7

8

9.

10.

nating from the pulmonary artery. Circulation 1575;51:576-87.

Perry LW, Scott LP. Anomalous left coronary artery from

pulmonary artery. Report of 11 cases: review o f indications for

and results of surgery. Circulation 1970;41:1043-52.

Neches WH, Mathews RA, Park SC, Lenox CC, Zuberbulher

JR, Siewers RD, Benson HT. Anomalous origin of the left cor-

onary artery from the pulmonary artery. Circulation 1974;

50~582-7.

El Said GM, Ruzyllo W, Williams RL, et al. Early and late re-

sults of saphenous vein graft s for anomalous origin of lef t cor-

onary artery from pulmonary artery. Circulation 1973;48

(Suipl

111):2-6.

Grace RR, Angelini P, Cooley DA. Aortic implantation of

anomalous le ft coronary artery arising from pulmonary artery.

Am J Cardiol 1977;39:608-131

Pinsky WW, Fagan LR, Mudd JFG, Willman VL. Subclavian-

coronary artery anastomosis in infancy for the Bland White-

Garland syndrome. A three-year and five -yea r follow-up. J

Thorac Cardiovasc Surg 1976;72:15-20.

Takeuchi S, Imamura H, Katsumoto K, Hayashi I , Katohgi T,

Yozu R, Ohkura M, Inoue T. New surgical method for repair

of anamolous left coronary artery from pulmonary artery. J

Thorac Cardiovasc Surg 1979;78:7-11.

Bunton R, Jonas RA, Lang P, Azaria JJT, Rein AJ, Castaneda

AR. Anomalous origin of lef t coronary artery from pulmonary

artery. Ligation versus establishment of a two coronary artery

svstem. J Thorac Cardiovasc Surp. 1987;93:103-8.

%i&ley FM, Watson DC, Scott LP, Kuehl KS, Perry LW,

Galioto FM, Ruckman RN, Shapiro SR. Repair of anomalous

origin of the left coronary artery in the infant and small child.

J Am

Co11 Cardiol 1984;4:1231-4.

Il.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

August 1999

American Heart Journal

Rein AJ, Colan SD, Parnes IA, Sanders SP. Regional and glo-

bal LV function in infants with anomalous origin of the left

coronary artery from the pulmonary trunk: preoperative and

postoperative assessment . Circulation 1987;75:115-23.

Robinson PJ, Sullivan ID, Kumpeng V, Anderson RH, Mac-

artney FJ. Anomalous origin of left coronary artery from pul-

monary trunk. Potential for false negative diagnosis with

cross-sectional echocardiography. Br Heart J 1984;52:272-7.

Fisher EA, Sepehri B, Lendrum B, Luken J, Levitski S. Two-

dimensional echocardiographic visualization of the lef t coro-

nary artery in anomalous origin of the left coronary artery

from the pulmonary artery. Circulation 1981;63:698-704.

Terai M, Nagai Y , Toba T. Cross-sectional echocardiographic

findings of anomalous origin of lef t coronary ar t,ery from pul-

monary artery. Br Heart J 1983;50:104-5.

Diamant S, Luber JM Jr, Brunson SC, Gootman N. Two-di-

mensional and pulsed Doppler echocardiography in anoma-

lous origin of the lef t coronary artery from the pulmonary ar-

tery: pre- and postoperative studies.

AM HEART J 1987:

113:195-8.

King DH, Danford DA, Huhta JC, Gutgesell HP. Noninvasive

detection of anomalous origin of the lef t main coronary artery

from the pulmonary trunk by pulsed Doppler echocardio-

graphy. Am J Cardiol 1985;55:608-9.

Vaksmann G, Mauran P, Rey C, Francart C, Dupius C. Visu-

alization of anomalous origin of the lef t coronary artery from

the pulmonary trunk by pulsed and color Doppler echocar-

diography.

AM HEA RT J 1988;116:181-2.

Swensson RE, Murillo-Olivas A, Elias W, Bender R, Daily PO.

Sahn DJ. Noninvasive Doppler color flow mapping for detec-

tion of anomalous origin of the lef t coronary artery from pul-

monary artery and for evaluation of surgical repair. J Am Co11

Cardiol 1988;11:659-61.

Baldwin HS, Mahoney LT, Ardinger R, Knoedel D, Marvin

WJ. Color flow mapping of anomalous origin of the left coro-

nary artery from the pulmonary artery. Echocardiography

1988;5:179-82.

Schmidt KG, Cooper MJ, Silverman NH, Stanger P. Pulmo-

nary artery origin of the left coronary artery: diagnosis by

two-dimensional echocardiography, pulsed Doppler ultra-

sound and color flow mapping. J Am Co11Cardiol1988;11:396-

402.

Shah RM, Nanda NC, Hsiung MC, Moos S, Roitman D. Iden-

tification of anomalous origin of the left coronarv arterv from

pulmonary artery trunk by Doppler color flow &apping. Am

J Cardiol 1986:57:366-7.

Yacoub MH, Radley-Smith R. Anatomy of the coronary

arteries in transposition of the great arteries and methods fo r

their transfer in anatomical correction. Thorax 1978;33:418-

24.

Post-exercise asystolic arrest in a young

man without organic heart disease: Utility

of head-up tilt testing in guiding therapy

Wes R Pedersen,MD, Denise L. Janosik, MD,

Irvin F. Goldenberg, MD, Linda L. Stevens, RN, and

Robert M. Redd, MD. St. Louis, MO.,

and

Minneapolis, Minn.

From the Department of Internal Medicine Division of Cardiology

St. Louis University Medical Center; and The Minneapolis Heart Insti-

tute.

Reprint requests: Denise L. Janosik MD Division of Cardiology St. Louis

University Medical Center Vista at Grand Blvd. Box 15250 St. Louis MO

63110.

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Volume118

Number 2

Brief Communications

4 11

Vasovagal and/or vasodepressor eactions are relatively

commoncausesof syncope n otherwise healthy patients.

Post-exerciseasystole s an unusual causeof syncope hat

hasbeen at least partially attributed to an exaggeratedva-

sovagal eflex.le4We report a caseof markedly prolonged

asystole and hemodynamic collapse ollowing exhaustive

exercise n a young man without organic heart disease nd

the usefulness f head-up tilt testing in reproducing symp-

toms and in guiding medical therapy.

A 29-year-old man was eferred for a maximal symptom-

limited exercise readmill test, as equired by his new em-

ployer. He exercised or 13 minutes and 23 seconds ccord-

ing to the Bruce protocol, achieving a peak heart rate of 187

beats/min and a peakblood pressureof 130/70mm Hg. The

test was erminated due to exhaustion. He experiencedno

chestpain and there were no ischemicST segment hanges.

Three minutes following exercise, he patient complained

of dizzinessand nauseaassociatedwith a decreasen blood

pressure o 90/70 mm Hg. At 8 minutes and 55 seconds f-

ter exercise, he blood pressuredropped suddenly to 50/30

mm Hg followed by sinus bradycardia, sinus arrest, and

hemodynamiccollapse Fig. 1). Sinus arrest and ventricu-

lar asystolepersisted or 17seconds nd were accompanied

by respiratory arrest and a brief episodeof myoclonus.Be-

fore resuscitative efforts could be initiated, the episode

spontaneously resolved with a gradual increase n blood

pressure nd heart rate. The patient was mmediately alert

and oriented with no neurologic sequelae.His past medi-

cal history was remarkable for cigarette smoking and a

spontaneouspneumothorax requiring chest tube decom-

pression4 months previously. During chest tube insertion,

he had a g-secondsinusarrest with near syncope. He had

experienced no other episodes f syncopeor near syncope.

The patient had no history of organic heart disease r neu-

rologic symptoms. He was aking no medication. Physical

examination was unremarkable. Routine blood chemis-

tries, blood count, and chest x-ray films werewithin normal

limits. A 12-lead electrocardiogram (ECG) demonstrated

sinus bradycardia and was otherwise normal. A 24-hour

ambulatory electrocardiographic monitor revealed a min-

imum heart rate of 52 beats/min and no evidence of atri-

oventricular (AV) conduction disease.A two-dimensional

echocardiogram demonstrated no structural cardiac ab-

normalities.

Due to the life-threatening nature of the vasovagal eac-

tion, a limited electrophysiologic study was performed in

the unmedicated state to rule out significant sinoatrial or

AV nodal diseaseprior to the administration of beta-

adrenergic blockade. Basic cycle lengths and AH and HV

intervals werewithin normal limits. Bilateral carotid sinus

massage

was performed without evidence of carotid sinus

hypersensitivity. Sinus node recovery times and sinoatrial

conduction times were within normal limits. With incre-

mental atria1 pacing, there was 1:l AV conduction up to a

cycle length of 500 msec,when AV nodal Wenckebach de-

veloped. The AV nodal effective refractory period deter-

mined during atria1 pacingat a cycle ength of 500msecwas

prolonged at 490 msec.The prolonged AV nodal refractory

period was elt to reflect enhancedvagal tone, which was

Recovery

8~55

9:33

Fig. 1. Interrupted sequential lead II ECG strips re-

corded following treadmill exerciseat a paper speedof 25

mm/set. Eight minutes and 55 secondsnto recovery, sud-

den slowing of the sinus rate occurred, followed by a

17-second inusarrest associatedwith ventricular asysto-

le. Nine minutes and 33 seconds post-exercise, sinus

rhythm spontaneously esumed.

suggestedby significant slowing of the sinus rate during

this part of the study. Programmedventricular stimulation

was not performed.

The patient was then tilted using an electrically con-

trolled tilt table to an 80-degreeupright position with con-

tinuous electrocardiographic and intra-arterial hemody-

namic monitoring. At baseline n the supine position, the

heart rate was 71 beatslmin and the blood pressurewas

138/60 mm Hg (Fig. 2,

A).

After being maintained in an

upright tilt position for 3 minutes, the patient complained

of lightheadednessand nauseaassociatedwith a gradual

decrement n blood pressure.After 3 minutes and 45 sec-

onds n the upright position, the patient lost consciousness

when the blood pressure decreased to 42/24 mm Hg

accompanied y a decreasen the sinus ate to 48beats/min

(Fig. 2,

B).

He was returned to a supine position and

abruptly regained consciousness ith a return to baseline

hemodynamics.Ten milligrams of intravenous metoprolol

was hen administered without significant change n base-

line heart rate or blood pressure.He wasagain tilted to an

80-degreeupright position and after 3 minutes developed

profound hypotension, followed by bradycardia with near

syncope. On this occasion, t was documented that there

was no hemodynamic or symptomatic benefit from ven-

tricular pacing. Prior to frank syncope,he was eturned to

a supine position with resolution of symptoms. An addi-

tional 9 mg of metoprolol wasadministered ntravenously,

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412

Brief Communications

August 1989

American Heart Journal

150 mmHg

100 mmHg

50 mmHg L

A

Arterial BP

lllllllllll~lllli lllliilllllllllli,~~~I~l llllllllllli llllllllillll:l~lllllllllllllliilllllll~i~~IIl~l

Head-up Tilt

100

mmHg -

50

mmHg -

Arterial BP

Fig. 2. Simultaneousarterial blood pressureand lead II ECG monitoring at 50 mm/set paper speed.

Baseline supineheart rate 71 beats/min and blood pressureof 138/60 mm Hg. 6, After 3 minutes and 45

secondsof tilt, blood pressure ell to 42/24 mm Hg and heart rate decreased o 48 beats/min.

establishinga new baselineheart rate of 48 beatslmin and

a blood pressureof 97136mm Hg. The patient was again

tilted to an 80-degree pright position. He remained otally

asymptomatic for 6 minutes and then complained of mild

lightheadednessover the remainder of the lo-minute

monitoring period. The minimum heart rate recorded was

52 beats/min and the blood pressurewas 60/26 mm Hg.

Following electrophysiologic and head-up tilt testing,

the patient wasstarted on oral metoprolol and wasgradu-

ally increased o a doseof 100 mg twice daily. A 24-hour

ambulatory ECG demonstrateda minimum heart rate of 38

beatslmin during sleep. There were no significant sinus

pausesor evidence of AV conduction abnormalities. He

underwent repeat maximal exercisestress esting while on

a steady-state regimenof metoprolol. He exerciseda total

of 13minutes according to the Bruce protocol, achieving a

peak heart rate of 131beats/min and a peak blood pressure

of 150/75mm Hg. The test was terminated becauseof ex-

haustion. The patient remained asymptomatic, and pro-

longed observation during the recovery period failed to

demonstrate any post-exercise hypotension or bradycar-

dia. Becauseof the profound nature of the initial post-ex-

ercisearrest and his reluctance to avoid strenousexertion,

we elected to maintain this patient on metoprolol for an

indefinite period. On long-term follow-up, he has emained

active and symptom-free.

Mild nonlife-threatening vagal reactions following ex-

haustive exercisehave been previously described n up to

0.2 of stress tests.2 There have been several prior

reports1m4f post-exercise asystolic arrest in young and

middle-agedmen without organicheart disease.t hasbeen

postulated that an exaggerated vagal response o marked

beta-adrenergic stimulation is the mechanism esponsible

for this unusual phenomenon.4There are recent data5

demonstrating the utility of head-up tilt testing in evalu-

ating syncope and abnormal hemodynamic responses.We

report the first case n which head-up tilt testing was uti-

lized to reproduce the symptoms and guide the therapy of

post-exerciseasystole.

Head-up tilt testing is useful in defining the pathophys-

iology of vasovagaland vasodepressor yncope. t is postu-

lated that venous pooling and decreased entricular filling

result in reflex adrenergic discharge and stimulation of

baroreceptors.5Vigorous ventricular contraction around a

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Volume 118

Number 2

relatively empty cavity then may cause an inappropriate

stimula tion of cardiac sensory receptors with nonmyeli-

nated (C-fiber) vagal afferents.5T6 This results in arterial

vasodilation and bradycardia, which is at least part ially

due to parasympathetic discharge. In most patients with

neurally mediated syncope studied by head-up tilt testing,

hypotension precedes bradycardia.5 Once bradycardia oc-

curs, hypotension is exacerbated and the process tends to

be self-perpetuating. In our patient, a decrease in blood

pressure correlated with the onset of symptoms and pre-

ceded bradycardia by approximately 45 seconds. The fail-

ure of ventricular pacing to alleviate symptoms or hypoten-

sion further supports arterial vasodilation as the primary

cause of syncope.

Beta-adrenergic blockers may blunt the profound brady-

cardia and hypotension reflex to upright tilt in patients

with neurally mediated syncope by preventing overstimu-

lation of left ventricular C-fiber receptors. Since an exces-

sive vagal reflex in response to marked beta-adrenergic

stimulation is also the most likely mechanism for post-ex-

ercise vasodepressor and vasovagal reactions, beta-blocking

agents may be effective by preventing the initiating exces-

sive beta stimulation. As demonstrated by this case and by

one previously reported case,4 severe life-threatening post-

exercise vagal reactions can be abolished by the adminis-

tration of oral beta blockers. This case demonstrates the

utility of head-up tilt testing in predicting which patients

with post-exercise vasovagal reactions will respond to

long-term beta-adrenergic therapy.

REFERENCES

1.

2.

3.

4.

5.

6.

Eichna LW, Horvath SM, Bean WB. Cardiac asystole in a

normal young man following physical effort. AM HEART J

1947;33:i54-62.

Schlesinger Z. Life-threatening vagal reaction to physical

fitness test. JAMA 1973:226:1119.

Fleg JL, Asante AVK. Asystole following treadmil l exercise in

a man without organic heart disease. Arch Intern Med 1983;

143:1821-2.

Huycke EC, Card HG, Sobol SM, Nguyen NX, Sung RJ. Post-

exertional cardiac asystole in a young man without organic

heart disease. Ann Intern Med 1987;106:844-5.

Abi-Samra F, Maloney JD, Fouad-Tarazi FM, Castle LW. The

usefulness of head-up til t testing and hemodynamic investi-

gations in the work-up of syncope of unknown origin. PACE

1988;11:1202-14.

Mark AL. The Bezold-Jarisch reflex revisited: clinical impli-

cations of inhibitory reflexes originating in the heart. J Am

Co11Cardiol 1983;1:90-102.

Progressive prolongation of the second

conduction interval throughout successive

3:2 Wenckebach sequences: The double

Wenckebach phenomenon

Giuseppe Oreto, MD, Francesco Luzza, MD, and

Gaetano Satullo, MD. Messina, Italy

Fromhe Istituto luridisciplinare di Clnica Medica Cattedra di Malattie

Cardiovasco lari Universita di Messina .

Reprint requests: Professor Giuseppe Oreto Via Terranova 9 98122

Messina Italy.

Brief Communications

4 13

A second-degree lock with Wenckebachphenomenonmay

complicate the conduction of an impulse at any cardiac

site.1A single mpulsemay at times traverse two successive

zonesof block, both of the Wenckebach type: a situation

where more than one Wenckebach mechanism s mani-

fested by the samebeat. This occurs, for example, in the

presenceof a double-level atrioventricular (AV) block with

Wenckebachphenomenonboth in the AV node and in the

bundle of His. This presentation reflects a new manifesta-

tion of the Wenckebach phenomenon,where two distinct

Wenckebach mechanisms ccur

simultaneously.

Namely,

the delayed conduction of an impulse acrossa singlezone

of block can beviewed as he expressionof two independent

but simultaneousWenckebachmechanisms. his situation

may be termed

the double Wenckebach phenomenon.

The tracing (Fig. 1, a continuous recording of lead Vi)

reflects the following: (1) There is an atria1 tachycardia at

a rate of 200per minute. (2) The tachycardia iscomplicated

by second-degree V block, more often of the Wenckebach

type, with a 3:2 ratio of conduction. Moreover, some

episodes f 2:l block occur, resulting in relatively long R-R

intervals, suchas0.59second

middle strip)

or 0.58second

(bottom strip).

(3) The long pauses ue to 2:l block are re-

sponsible or aberrant conduction of the ensuingatria1 m-

pulse,as evealed by an rsRs complex. This is because

short cycle is precededby a relatively long cycle (a mani-

festation of the Ashman phenomenon2). 4) Each episode

of 2:l AV block is followed by several 3:2 Wenckebach se-

quencesof conduction, ending in a further episodeof 2:l

block, and so on. This phenomenon s analyzed in the

two

bottom strips.

After the pauseof 0.59 second,provoked by

an by episode of 2:l AV block, eight consecutive 3:2

Wenckebach periods occur. These are labeled with letters

(a to

h).

Concerning a definition of terms: Pl = the first con-

ducted atria1 impulse of a 3:2 Wenckebach sequence;

P2 = the second onsecutive conducted atria1 impulseof a

3:2 Wenckebach sequence;Rl = the ventricular complex

resulting from conduction of Pl; R2 = The ventricular

complex resulting from conduction of P2; and R2-Rl = the

pauseoccasioned y the nonconducted atria1 mpulse of a

3:2 Wenckebach sequence.This pausecontains a blocked

atria1 mpulse.The Pl-Rl, P2-R2, and R2-Rl intervals are

listed in Table I. Numbers above the tracing of Fig. 1 re-

flect the Pl-Rl and P2-R2 intervals, whereasnumbersbe-

low the tracing correspond o the R2-Rl intervals. Analy-

sisof Fig. 1 and Table I reveals that: (1) the Pl-Rl inter-

vals are constant, and reflect a duration of 0.14 second n

all the sequencesexcept the last one, where a slight

prolongation up to 0.16 secondoccurs. (2) The P2-R2 in-

tervals reflect a progressiveprolongation from 0.19 second

(sequence ) to 0.36 second (sequence

).

(3) The pauses

(the R2-Rl intervals) gradually decrease hroughout the

eight Wenckebach sequences.

The second mpulse n any 3:2 Wenckebach sequence s

associatedwith a conduction interval that is necessarily

longer than that of the first conducted impulse. Neverthe-

less, he progressiveprolongation of the secondconduction

interval throughout a seriesof successive :2 Wenckebach

sequencess an uncommon phenomenon.This represents

a Wenckebach mechanismaffecting the secondconducted