Download Demonstration of the Supernormal Period in the Intact Human Heart

SUPERNORMAL PERIOD IN INTACT HUMAN HEART
patient epicardial leads might have been used via thoracotomy if all other measures proved inadequate.
This case represents an uncommon pathologic and clinical circumstance; but if persons concerned with a case
of this nature are made aware of this possibility, proper
management may avoid preventable complications.
ACKNOWLEDGhIENTS: The author wishes to acknowledge
the invaluable help of the following colleagues for providing
data in this case report: Dr. Gerald Hancur, attending physician; Dr. Sheldon Steiner, cardiologist; Dr. Valerie Karvelis,
pathologist; Dr. hlyron Green, radiologist; and Dr. Jorge
Pollitt, sr~rgicalassociate.
I Sherman FE: Atlas of Congenital Heart Disease. Philadelphia, Lea and Febiger, 1963, p 73
2 Winter FS: Persistent left superior vena cava. Angiology
5:90-131, 1954
3 Karnegis JN, Wang Y, Winchell P, et al: Persistent left
superior vena cava, fibrous remnant of the right superior
vena cava and ventricular septa1 defect. Amer J Cardiol
14:573-577, 1964
Reprint requests: Dr. Kukral, Department of Surgery, 840
Sollth Wood Street, Chicago 60612.
Demonstration of the Supernormal
Period in the Intact Human Heart as
a Result of Pacemaker Failure*
David P. Parker, hI.D.,"
and Marvin A. Kaplan, M.D.t
A 47-year-old man with a 2Iyear history of complete
heart block and A-V junctional rhythm was treated with
a permanent pacemaker employing a demand type pulse
generator and a bipolar endocardial electrode in the right
ventricle. Fourteen months later the pulse generator
showed evidence of failure and it then became possible to
demonstrate that pacemaker stimuli could evoke a response only during a 50 millisecond period toward the
end of the T wave, this interval being the supernormal
period of the heart in this individual.
T
he supernormal recovery phase in cardiac muscle
follows the vulnerable portion of the refractory period and represents the time when the heart muscle will
respond to a subliminal stimulus which cannot evoke a
response a t any other time during the cardiac cycle. It
was first shown to exist in frog cardiac muscle by
Adrian' in 1920 and later by Nahum and Hoff2 in the
'From the Cardiology Section, Medical Service, Long Beach
Veterans Administration Hospital, and the University of
California College of Medicine, Irvine.
"Assistant Chief, Cardiolo y Section, Veterans Administration Hospital, Long ~ e a c f Assistant
;
Clinical Professor of
Medicine, University of California at Irvine, California
College of Medicine.
tchief, Cardiology Section, Veterans Administration Hospital, Long Beach; Assistant Professor of Medicine, University
of California at Irvine, California College of Medicine.
anesthetized cat. In 1960 Soloff and Fewell3 first demonstrated the supernormal period in the human heart
while pacing with subthreshold stimuli. O u r case demonstrates the same phenomenon during spontaneous
pacemaker generator failure. Relatively few such cases
have been reported because: ( 1 ) pacemaker generators
are routinely replaced before battery failure occurs, ( 2 )
the subliminal stimulus put out by the generator may b e
adequate to demonstrate the supernormal period for only
a brief period, a n d ( 3 ) of the variability of the myocardium in its response to the same weak stimulus, ie, the
same weak stimulus may or may not evoke a response
during this period. Furthermore, with the more ccmmon
use of the newer demand type cardiac pacemaker obviating the problem of competitive pacing, it is likely
that the supernormal period will only rarely b e demonstrated in the intact human heart and deserves re-emphasis.
The patient, a 47-year-old man, was admitted to the
Veterans Administration Hospital, Long Beach, California in
February, 1969, because his pulse rate was varying from 60
to 86 per minute. A demand type cardiac pacemaker had
been inserted in December, 1967, and set at a rate of 72
impulses per minute.
In 1945, at age 23, he lost consciousness and was found to
have a slow heart rate for the first time. Thereafter, the slow
rate continued and electrocardiograms through the years all
showed atrial flutter. com~lete heart block, and an AV
junctional rhythm with the ventricular rate ranging from the
30's to the 60's ( Fig 1 ). The patient was seen several times at
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PARKER AND KAPLAN
later, regardless of where the stimulus fell, no QRS complex
was elicited ( Fig 5 ) . The pacemaker generator was replaced
with a similar model and pacing at a rate of 75 beats per
minute was resumed ( Fig 6 ) .
the 1lo::pital in 1966 and 1967. No definite etiology for the
heart block could be determined. Inasmuch as the AV iunctional rhythm was stable, the heart rate increased with
exertion, and no evidence of congestive failure was present,
insertion of an artificial pacemaker was not felt to be indicated; however, in December, 1967, at another hospital, the
patient was felt to be in mild congestive heart failure and a
bipolar endocardial electrode0 was placed at the apex of the
right ventricle via the right external jugular vein and connected to a demand type pulse generatorov set at a rate of 72
impulses per minute. An electrocardiogram 26 days later
showed a pacemaker rhythm at a rate of 72 per minute (Fig
2).
One year later, selective right and left coronary arteriograms were normal.
In February, 1969, the patient found his pulse rate to be
varying from 60 to 86 beats per minute (the pulse generator
rate had been set at 72 per minute). He was hospitalized and
an electrocardiogram on February 24, 1969 showed a pacemaker rhythm with the pulse generator discharging at a rate
of 65 pulses per minute, each stimulus being followed by a
QRS complex ( Fig 3 ). Two days later ( February 26, 1969)
an electrocardiographic monitor lead showed complete heart
block with AV junctional rhythm at a rate of 43 per minute
(Fig 4 ) . Pacemaker stimuli at a rate of 103 per minute were
visible, but were not followed by a QRS response except
when the sti~nulusfell 370-420 milliseconds after the patient's own QRS complex, indicating that toward the end of
the T wave there was a period of 50 milliseconds during
which time the heart was capable of responding. One day
'Chardack bipolar endocardial electrode, Model 5816, manufactured by Medtronic, Inc.,
lis, Minnesota.
OChardack-Greatbrtch i m p l a n t a E " Z X k demand pulse
generator, hlodel 5841, manufactured by Medtronic, Inc.,
Minneapolis.
A supernormal period of myocardial excitability in the
human heart has been known to exist under varying
circumstances. Katz and Pick-' have suggested that the
supernormal period is not demonstrable in normal myocardial muscle, but can be shown in a depressed myocardium. FeldmanGtudied ten patients for the presence of
a supernormal period who were being paced by a right
ventricular catheter for slow heart rate. In addition to
regular pacing by one stimulator, another stimulator was
used to introduce single pulses of varying amplitude at
v a ~ y i n gintervals from the regular beat. In none of the
ten patients could a supernormal period b e elicited. Our
case differs in that the pacemaker stimulus was introduced in conjunction with the patient's own rhythm
been able to
rather than a paced rhythm. 0thers""ave
demonstrate the existence of a supernormal period when
the opportunity has arisen to introduce an electrical
stimulus to the myocardium and vary the stimulus in
amplitude and timing.
With the advent of fixed rate permanent ventricular
pacing as a method of treatment for heart block, numerous instances of competitive pacing have resulted and
occasionally allowed for the demonstration of a supernormal period in the intact human hearts7-lo Dressler,
Jonas and Schwartzn studied five patients with implanted pacemakers whose stimuli had dropped to subthreshold values. T h e stimuli evoked a response only
when they fell close to the beat of the basic ventricular
rhythm. T w o of these patients could b e studied in greater detail and it was found that in one the supernormal
FIGURE3. Electrocardiogram 14 months following insertion of
pacemaker. The pacemaker rate has slowed to 65 per minute.
CHEST, VOL. 59, NO. 4, APRIL 1971
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SUPERNORMAL PERIOD IN INTACT HUMAN HEART
I
I
I
FIGURE
4. Monitor ECG lead (continuous strip) obtained two days following that in Figure 3.
Atrial flutter continues. Complete heart block is present and the rhythm controlling the ventricles
is now AV junctional at a rate of 43 per minute. Pacemaker stimuli are present at a rate of 103
per minute and are followed by a QRS response only when the stimulus occurs 0.37-0.42 seconds
after the end of the junctional QRS complex. (The tracing has been retouched for purposes of
reproduction ) .
phase occurred at the end of the T wave and in the
second somewhat earlier, closer to the nadir. Burchell,
Connolly and Ellis9 noted that in one of their cases in
whom the electrical pacemaker was failing and sinus
rhythm was present, a propagated beat occurred only
when the stimulus fell a t the end of the T wave. Walker,
Elkins and Woodln reported a case of cardiac pacemaker failure in a patient whose cardiac rhythm had
FIGURE
5. Monitor ECG lead (continuous strip) one day following that obtained in Figure 4.
No QRS response to pacemaker stimuli occurs regardless of their location. (The tracing has been
retouched for purposes of reproduction ) .
CHEST, VOL. 59, NO. 4, APRIL 1971
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FIGURE
6. hlonitor ECG lead following replacement of faulty pacemaker generator.
reverted back to complete heart block with idioventricular rhythm. T h e ventricle responded to a stimulus only
when it fell in a period extending from the later half of
the terminal slope of the T wave to the initial portion of
the U wave. T h e supernormal period was approximately
150 milliseconds in duration.
In our case, the supernormal period was demonstrated
a t a time when the pacemaker generator was failing and
discharging subthreshold stimuli. At this time, the patient's own intrinsic rhythm was atrial flutter with
complete heart block and A-V junctional rhythm. Stirnuli, all of the same intensity, were visible at varying
intervals after the QRS complex ( F i g 4 ) . At no time did
they elicit a response except during a 50 millisecond
interval toward the end of the T wave. That this period
represents one of supernormality is evidenced by the fact
that during the period of complete recovery, ie, in the
interval following the T wave a n d prior to the next QRS
complex, when a stimulus should normally b e propagated, the same subthreshold stimulus failed to evoke a
QRS response. T h e following day the generator stimulus
failed to evoke a QRS response a t any time (Fig 5 ) , but
when a new pulse generator was implanted normal
pacing took place immediately and continued to d o so
( F i g 6 ) indicating that there was no defect in the
bipolar endocardia1 electrode.
This case represents a clear demonstration of the
supernormal period in the intact human heart.
1 Adrian ED: The recovery process of excitable tissues,
part I. J Physiol54:1, 1920
2 Nahum LH, Hoff HE: The interpretation of the U wave
of the electrocardiogram. Amer Heart J 17685, 1939
3 soloff LA, ~
~JW: ~h~
~
~
l phase
l
of ventricular excitation in man. lts bearinr on the of
ventricular premature systoles, and a note on atrioventricular conduction. Amer Heart J 59:869, 1960
4 Katz LK, Pick A: Clinical Electrocardiography. Part I,
The arrhythmias, Philadelphia, Lea and Febiger, 1956
5 Feldman DS: Excitability of the human heart on endocardial stimulation. Clin Research 11: 166, 1963
6 Dolara A, Camilli L: Supernormal excitation and conduction. Electrocardiographic observations during subthreshold stimt~lation in two patients with implanted pacemaker. Ainer J Cardiol21:746, 1968
7 Linenthal AJ, Zoll PJ: Quantitative studies of ventricular
refractory and supernormal period in man. Tr Assoc Amer
Physicians 75:285, 1962
8 Dressler W, Jonas S, Schwartz J: Supernormal phase of
myocardial excitability in man. Circulation 32 (Supp
II):79, 1965
9 Burchell HB, Connolly DC, Ellis FH Jr: Indication for
and results of implanting cardiac pacemakers. Amer J
Med 37:764, 1964
10 Walker WJ, Elkins JT, Wood LW: Effect of potassium in
restoring myocardial response to a subthreshold cardiac
pacemaker. New Eng. J. Med., 271:597, 1964
Reprint requests: Dr. Parker, VA Hospital, Long Beach 90801.
Endocarditis of the Pulmonic Valve
Simulating Cardiac ~ u m o r *
Shlorno Laniado, AI.D.; Robert W . M .Frater, M.D.;
Alphonzo lorclan, M.D.; Eugene C . Kafka, M.D.;
Anna S. Kadbh, M.D.; and Melvin Zelefsky, M.D.
A unique case of calcific bacterial endocarditis involving
the pulmonic valve, which simulated cardiac tumor, is
reported. The clinical, fluoroscopic and angiographic
findings are described and correlate well with the lesions
discovered at surgery. In this case, the diagnosis was
originally suspected because of the calcification noted
during fluoroscopy. However, the unusual auscultatory
findings may prove useful in detecting other cases of a
similar nature.
E
ndocarditis of the valves of the right side of the
heart is much less common than that involving the
left heart and frequently. presents
difficulties in diagnosis, as many clinical features typical of left-sided involvement are absent. Not infrequently the only signs of rightsided valvular endocarditis are persistent fever and recurrent episodes of pulmonary embolization and infect i ~ n . lT
- ~h e tricuspid valve is more commonly involved
in endocarditis of the right heart. Occasionally both the
tricuspid and the pulmonic valves are affected. Only
rarely does one encounter isolated involvement of the
pulmonic ~ a l v e . ~ . Q - l 3
In this case isolated pulmonic bacterial endocarditis
simulated a tumor of the right side of the heart.
The patient, a 47-year-old Negro woman with a long
history of alcoholisn~,had been treated for tuberculosis from
1959 to 1961 with isoniazid and cycloserine. There is no
history of rheumatic or congenital heart disease. On three
'From the Departments of Medicine (Division of Cardiology), Thoracic Surgery and Pathology, Albert Einstein
College of Medicine and Bronx Municipal Hospital Center,
Bronx, New York.
CHEST, VOL. 59, NO. 4, APRIL 1971
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