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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