Letters

to the Editor
Cardioversion after valve
replacement
To the Editor:
I read with interest the annotation by Drs.
Jenzer and Lown dealing with cardioversion after
valve replacement (AM. HEART J. 84:840, 1972).
In reading it, it became obvious that the authors
have omitted reference to two critical issues. Unless
such information is provided, their comments and
recommendations lose most of their relevance. These
issues are :
1. How many of the 102 patients with valve re-
placement and the 58 patients with mitral val-
votomy developed atria1 fibrillation after the opera-
tion?
2. How many patients who were successfully car-
dioverted remained in sinus rhythm for more than
two months?
We have demonstrated,rs2 and others have amply
confirmed our observations, that postoperative atria1
fibrillation, and atrial fibrillation present prior to
mitral valve surgery, are two entirely different con-
ditions. The former is an acute reaction to surgical
trauma that bears no relation to the underlying
disease (it occurs not only after cardiac, but also
after pulmonary operations) and is virtually 100 per
cent convertible to sinus rhythm. The latter is a
specific complication of mitral valve disease, one that
eventually leads to anatomic damage of atria1 mus-
culature.3 Our series showed a success rate in post-
operative conversion of patients in the second cate-
gory of 77 per cent, but more than half of these
lapsed back into atria1 fibrillation after varying
periods of time.
If an article describes the value of cardioversion
and we recognize that cardioversion is good for
oranges but only fair for apples, shouldnt we know
how many apples and oranges were mixed in the
basket?
Arthur Seizer, M.D.
Cardiology Division
Presbyterian Hospital
San Francisco, Calif. 94120
REFERENCES
1. Seizer et al.: Treatment of atria1 fibrillation after
surgical repair of the mitral valve, Annals Intern.
Med. 62:1213, 1965.
2. Popper, R. W., Knott, J. M. S., Seizer, A., and
Gerbode, F.: Arrhythmias after cardiac surgery
I. Uncomplicated atria1 septal defect, AM.
HEART J. 64:455, 1962.
3. Bailey et al.: Relation of left atrial pathology to
atria1 fibrillation in mitral valvular disease,
Annals Intern. Med. 69:13, 1968.
282
Reply
To the Editor:
Dr. Selzer raises questions not germane to the
intent of our brief communication. The objective
was simply to provide evidence that valve replace-
ment does not diminish the efficacy of cardioversion
in restoring atria1 fibrillation to sinus rhythm;
furthermore, it was to demonstrate that in these
patients the procedure is not fraught with an in-
creased incidence of immediate or late complications.
If the physician, therefore, believes that sinus
rhythm needs to be re-established, cardioversion
affords a simple, safe, and effective method.
Of course, Dr. Selzers questions can be factually
answered. Of the 102 patients with valve replace-
ment, 19 developed atria1 fibrillation for the first
time after the operation. The success rate of cardio-
version and the required energy were the same
irrespective of when the arrhythmia first occurred.
Our experience to date indicates that if atria1 fibril-
lation has been present for less than one year prior
to valvular surgery, the likelihood for sustained
sinus rhythm for the ensuing year approximates
50 per cent.
We are, of course, well aware that sinus rhythm
has a greater chance of being maintained in patients
in whom atria1 fibrillation follows rather than pre-
cedes valvular operation. The crucial question,
therefore, is which patient following valve correction
will maintain sinus rhythm after cardioversion when
the arrhythmia has been established for some
months. We are not aware of any clinical shibboleth
to permit sush distinction. In the absence of guide-
lines, we believe that all such patients should be
subjected to the relatively innocuous procedure of
cardioversion. Whether the arrhythmia merely pre-
cedes or follows valvular operation is far too simple
and inadequate a discriminant. Dr. Selzer hails from
a state well known for the abundance and variety
of its fruit; he should, therefore, have no difficulty in
distinguishing apples from oranges.
Hans Jenzer, M.D.
Bernard Lcwn, M.D.
Cardiovascular Laboratories
Harvard School cf Public Health
Cardiology Division
Peter Bent Brigham Hospital
Boston. Mass. 02115
The Yogic claim of voluntary control
over the heart beat:
an unusual demonstration*
To the Editor:
Yogis in India have long been reputed to develop
a remarkable control over bodily functions. Theo-
*A detailed report on the Yogi is appearing in The Indian
Journal of Medical Research. November, 1973.
Vokme 86
Number 2 Letters to the Editor 283
retically, it is believed that all visceral functions can
be brought under voluntary control by prolonged
yogic training, but perhaps their most fascinating
claim has been the ability to stop the heart at will.
However, in most instances where this has been
investigated so far, it has turned out to be an exag-
gerated Valsalva maneuver in some form, which
makes the pulse and heart sounds imperceptible
while the heart continues to beat at a slow rate.,
Recently we had the rare opportunity of investi-
gating an altogether different and very interesting
demonstration of this supposed yogic control over
the heart. Yogi Satyamurti, a sparsely built man
of about 60 years of age, remained confined in a
small underground pit for 8 days in what according
to him was a state of Samadhi, or deep medita-
tion, with all bodily activity cut down to the barest
minimum. The pit was a 1.5 meter cube, dug out in
an open lawn surrounded by the Medical Institute
buildings, and was completely sealed from the top
by bricks and cement mortar. The Yogi squatted
on the floor of the pit with nothing on except a light
cotton garment. About 5 liters of water was placed
in one corner, presumably for drinking but accord-
ing to the Yogi only for keeping the air fully humid.
An ECG (Lead II) was continuously monitored
during these 8 days and various other laboratory
investigations were carried out before and after.
The ECG leads were kept short enough not to allow
any free movement inside the pit.
The 12-lead ECG recorded before closing the pit
was within normal limits (Fig. 1, strip A), but a
significant sinus tachycardia developed soon after.
It increased progressively, reaching a heart rate of
250 per minute on the second day (Fig. 1, drifi B).
At 535 P.M. on the second day, when the Yogi had
been inside for about 29 hours, to our great surprise
a straight line replaced the ECG tracing (Fig. 1,
strip C). There was no electrical disturbance of any
sort even at higher amplification and with different
leads. There had been no slowing of the heart or
signs of ischemia preceding this.
The straight line on the ECG persisted till the
eighth morning. Then, to our astonishment, electrical
activity returned about half an hour before the pit
was scheduled to be opened. After some initial dis-
turbance, a normal configuration appeared. Al-
though some sinus tachycardia was still there, there
was no other significant abnormality (Fig. 1, strip D).
The Yogi had informed us beforehand that he would
begin to come out of his deep trance or suspended
animation after nearly 7 days, much in the same
way that a normal person wakes up after a few
hours sleep.
When the pit was opened on the eighth day, the
Yogi was found sitting in the same posture. One of us
immediately went in to examine him. He was in a
stuporous condition and was very cold (oral tem-
perature was 34.8O C). On being taken out of the
pit he developed severe shivering and this persisted
for nearly 2 hours. A 12-lead ECG repeated in the
laboratory subsequently was again within normal
limits (Fig. 1, strip E).
The Yogi and his admirers felt more than satisfied
at this scientifically documented proof of a remark-
able Yogic feat, while we were left rather perplexed
and confused. We were expecting some bradycardia
A
b
e
32
E
Fig. 1. ECG tracing of the Yogi, Lead II. (Panel A),
first day at 11 :OO A.M., one hour before closing the
pit. Normal sinus rhythm. Heart rate was 106 per
minute, PR interval was 0.16 second, QRS interval
was 0.08 second, and there was an upright T wave.
(Panel B), second day at 5:OO P.M. Severe sinus
tachycardia with a heart rate of 250 per minute, a
PR interval of 0.12 second, a QRS interval of 0.06
second, and a high uptake of the ST segment.
(Panel C), second day at 6:00 P.M. There is a straight
line with no electrical disturbance. This continued
for the next 5 days. (Panel D), eighth day at 7:30
A.M., half an hour before opening the pit. Sinus
tachycardia is in evidence with a heart rate of 142
per minute, slightly prolonged PR interval of 0.20
second, a QRS interval of 0.06 second, and an up-
right T wave. (Panel E), eighth day at 10:00 A.M.,
two hours after coming out of the pit. The tracing
is normal, with a heart rate of 98 per minute, PR
interval of 0.16 second, a QRS interval of 0.08 second,
and an upright T wave.
and possible signs of myocardial ischemia, but con-
trary to this there was severe tachycardia followed
by a complete disappearance of all complexes. Any
instrumental failure was ruled out by thoroughly
checking the machine and also by the spontaneous
reappearance of the ECG on the last day. A dis-
connection of the leads by the Yogi, quite a likely
explanation, ought to have given rise to considerable
electrical disturbance, but there was hardly any.
Later on, we tried all sorts of manipulations with
the leads to simulate what the Yogi could have done
284 Letters to the Editor
Am. Heart I.
August. 1973
inside the pit (notwithstanding the total darkness
and his ignorance of ECG technique), but in every
case there was marked disturbance. Therefore, al-
though it is obviously difficult to believe that the
Yogi could have completely stopped his heart or
decreased its electrical activity below a recordable
level, we still had no satisfactory explanation for
the ECG tracings before us.
Apart from this, the Yogi had of course endured
total starvation, sensory deprivation, as well as the
discomfort of a very humid, closed atmosphere for
8 days. We did not pay much attention to anoxia,
thinking that sufficient ventilation could occur
through the bare earth on the sides of the pit. The
loss of weight (4.5 kilograms) and other biochemical
changes were essentially the same as can be ex-
pected in starvation under similar conditions. They
certainly discount any remarkable depression of the
metabolic rate.
The more optimistic amongst us considered this
feat to be a marvelous extension of the hypometa-
bolic wakeful state of yogic meditation as described
by Wallace and co-workers,3 and the conditioned
learning of autonomic responses in rats reported by
DiCara. The skeptics, however, were inclined to
take the whole thing as some cleverly disguised
trick. But, for the present, we only want to put this
interesting experiment on record just as an in-
triguing and inconclusive attempt of a Yogi to
demonstrate a voluntary control over his heart beat.
L. K. Kothari, M.Sc., M.A.M.S.
Reader in Physiclogy
Arm Bordia, M.D.
Reader in Cardiology
0. P. Gufita, M.D.
Professor of Pathology
Ravindra Nath Tagore Medical College
and Hospital, Udaipur, India
Reprint requests to L. K. Kothari. M.Sc., M.A.M.S.
REFERENCES
Anand, B. K., and Chhina, G. S.: Investigations
on yogis claiming to stop their heart beats, Indian
J. Med. Res. 49:90, 1961.
Wenger, M. A., Bagchi, B. K., and Anand, B. K.:
Experiments in India on voluntary control of
the heart and pulse, Circulation 24:1319, 1961.
Wallace, R. K., Benson, H., and Wilson, A. F.:
Wakeful hypometabolic physiologic state, Am.
J. Physiol. 221:795, 1971.
DiCara, L. V.: Learning in the autonomic ner-
vous system, Sci. Am. 222:31, 1970.
Atropine in acute myocardial
infarction
To the Editor:
The discussion of the value of atropine in acute
myocardial infarction at the last meeting of the
American College of Cardiology in San Francisco
(Medical World News, March 9, 1973) is the reason
for the following comments.
The risk of giving atropine in patients with coro-
nary disease has been demonstrated many years ago
by Wayne and Laplace. They found in patients
with angina pectoris, that after administration of
atropine a lesser physical exertion elicited angina1
pain. Scherf and Schnabels demonstrated that fol-
lowing an intravenous injection of 2 mg. of atropine
in patients with syphilitic aortitis and angina pec-
toris due to stenosis of the orifice of a coronary
artery, angina1 pain with marked depression of the
RS-T segments appeared. The increased rate in-
duced by atropine in many (not all) patients with
coronary disease is responsible for these results. This
is illustrated by another observation reported by
the same authors. A diabetic patient died several
minutes after the intravenous injection of K mg.
of atropine. The autopsy revealed severe arterio-
sclerosis of both coronary arteries.
Because the appearance of a marked increase of
rate following an injection of atropine cannot be
predicted, I consider this medication risky in pa-
tients with coronary disease.
David Sckerf, M.D.
Dept. of Medicine
New York Medical Ccllege
1249 Fifth Ave.
New York, N. Y. 10029
REFERENCES
1. Wayne, E. J., and Laplace, L. B.: Observations
on angina of effort, Clin. Sci. 1:103, 1933.
2. Scherf, D., and Schnabel, P.: Atropin bei Angina
pectoris, Klin. Wochenschr. 13:1397, 1934.
Practolol in treating
tachyarrhythmias
To the Editor:
We read with great interest the article of Dr. H.
Formgren entitled Practolol in the treatment of
tachyarrhythmias in patients with bronchial
asthma (AM. HEART J. 84:710, 1972). We would,
however, like to take issue with his statement that
Practolol has not been previously given to asth-
matics for treatment of concomitant cardiovascular
disorder.
Since 1969 we have indeed been using practolol
for the treatment of acute tachyarrhythmias and
have reported our results previously.r-* We would
therefore like to report briefly our experience in
patients with bronchospasm due to asthma bronch-
iale or chronic obstructive lung disease.
When assessing the antiarrhythmic effectiveness
of a drug we feel that it always should be given intra-
venously and under continuous electrocardiographic
recording. Practolol was given as follows: 5 mg.
every minute until a therapeutic result was obtained
or a total dose of 25 mg. was reached; if necessary,
a maintenance dose of 100 to 200 mg. twice daily
was given.
The results obtained in 29 patients hospitalized
with acute respiratory failure can be summarized
as follows:
1. Lowering of the heart rate (H.R.) below 100
beats per minute (average reduction = 31.7 per cent)
in 10 patients with sinus tachycardia.