Case

reports

Cerebrovascular
electrocardiographic

accident with
changes

unusual

Gary J. Anderson, M.D.
Robert Woodburn, M.D.*
Charles F&h, M.D., F.A. C. C.
Indianapolis,
Ind.

R

ecent reportslm4 and reviews5-7 have
drawn attention
to the electrocardiographic (ECG) changes in cerebrovascular disease. The purpose of this case report
is to describe interesting and relatively unusual electrocardiographic
changes in a
ten-year-old girl with pathologically
proven
intracerebral
hemorrhage.
Case report
The patient,
a ten-year-old
girl, was admitted
on June 19, 1971, because
of a left hemiparesis.
The child had previously
been in excellent
health
until
the morning
of admission,
when upon rising,
she complained
of abdominal
pain, pain over her
right
eye, and shortly
thereafter
developed
left
hemiparesis.
No seizure activity
was noted, nor was
a history
of trauma
elicited.
Physical
examination
revealed
a well-developed,
poorly-responsive
female child. The apical heart rate
was 60 and irregular,
and the blood
pressure
was
110/70 mm. Hg. Respirations
were 20 per minute.
Cardiac
auscultation
was unremarkable
except
for
the irregular
rhythm.
Neurological
examination
revealed
anisocoria,
R > L, and both pupils showed
a sluggish
light
response.
Dysconjugate
gaze was
noted.
Ophthalmoscopic
examination
was
un-

remarkable.
Left hemiplegia
was apparent,
and was
associated
with a positive
Babinski
sign on the left.
Complete
blood count,
serum sodium,
chloride,
CO* content
blood
urea
nitrogen,
calcium,
and
urinalysis
were all normal.
Serum potassium
was 2.8
mEq./L.
Arterial
oxygen
saturation
was 96.6 per
cent and PCO~ was 40.0 mm. Hg. Arterial
pH was
7.308. Sickle cell preparation
was negative.
Chest
x-ray
and skull films were unremarkable.
Cerebral
angiograms
were
within
normal
limits.
Lumbar
puncture
revealed
grossly bloody cerebrospinal
fluid.
A rhythm
strip obtained
in the emergency
room
(Fig. 1, top) demonstrated
Mobitz
Type
I second
degree AV block with junctional
escape beats and
periods
of AV dissociation.
The patient
was given
0.3 mg. of atropine
intravenously,
and 1 : 1 conduction resumed
with sinus tachycardia
and wandering
atrial pacemaker
(Fig. 1, bottom). The child’s clinical
course deteriorated
with deepening
coma and hypothermia
(rectal temperature
94” F.). A 12-lead ECG
at that time
(Fig. 2) revealed
sinus bradycardia
with a rate of 50 per minute
and a P-R interval
of
0.18 second. The ST segment
was elevated.
Maximal
ST segment elevation
occurred
in Leads VZ, V’s, and
Va with an elevation
exceeding
5 mm. The QT interval was 0.64 second and QT, was 0.58 second. The
patient
died 29 hours after admission.
Necropsy
examination
was unremarkable
except
for the findings
in the central
nervous
system.

From

The Krannert
Institute
of Cardiology,
Marion
County
General
Hospital,
and the Department
of Medicine.
Indiana
University
School of Medicine,
Indianapolis,
Ind.
Supported
in part by the Herman C. Krannert
Fund, United States Public Health Service Grants HL-0630%
HL-05363.
and HL-05749.
the Indiana
Heart Association,
and the American
Medical
Association
Committee
for Research
on Tobacco
and Health.
Received
for publication
Oct. 12, 1972.
Reprint
requests to: Gary J. Anderson.
M.D., 1100 West Michigan
St.. Indianapolis,
Ind. 46202.
*Dr. Woodburn
is a Resident
in Medicine,
Department
of Medicine,
Indiana
University
School of Medicine.
Indianapolis, Ind.

vol.

86,

No. 3, PP. 39.5-398

ScPte4er,

1973

Anlerican

Heart Journal

395

396

Anderson,

Wvodbum,

and Fisch

439873-1
SUBARAC~~N~ID
;

:

i

HEMORRHAGE
,

Kg. 1. Top panel,
Rhythm strip of the patient on admission demonstrating Mobitz Type 1 AV block with
periods of AV dissociation. Botto?rz panel, Restoration of 1 : 1 conduction with wandering
atrial
Imccmaker
after 0.3 mg. atropine intravenously.
A vascular malformation was found to involve the
cingulate gyrus at the right frontal-parietal junction.
This vascular malformation had ruptured resulting
in intraventricular
and subarachnoid hemorrhage.
Transtentorial
and transforaminal herniation had
occurred.
Discussion
The case reported
is characterized
by two
interesting
electrocardiographic
changes.
Fig. 1 demonstrates
second degree AV
block and periods of AV dissociation
with
return of AV conduction
to normal
following administration
of atropine.
To our
knowledge
the Wenckebach
block seen in
this patient,
clearly
related
to a cerebrovascular
accident,
has not been previously
described,
although
2 : 1 block
has been
observed.4
Recent papers*-”
have drawn
attention
to the fact that increased
vagal tone contributes to the development
of the observed
arrhythmias
in cerebrovascular
accident.
Experimental
studies’? llave shown that the
production
of Wolff-Parkinson-White
preexcitation
and
AV
dissociation*,‘?
may
occur
with
electrical
stimulation
of the
mesencephalic
reticular
formation
or the
dorsomedial
hypothalamic
nucleus.
These
experimental
studies suggest that enhanced
vagal tone significantly
contributes
to the
development
of various
cardiac
arrbytbmias. Such enhanced
vagal tone may be a
result of stimulation
of vagal fibers innervating the circle of Willis,*3 enhanced
vagal

tone secondary
to the 1)aroreceptor
reflex,”
or stimulation
of Area 13, the chief cortical
representation
of the vagas nerve.s In our
patient
the lesion involved
tile cingulate
gyrus,
containing
Areas
23, 24, and 32.
These areas are thought
to control
autonomic functions
of the lleart.g,‘4
Thus, involvement
of the cingulate
gyrus may have
accounted
for the observed
cardiac
arrhythmia.
A second interesting
feature of this case
is the ST and T \vave changes.
Cerebrovascular
accidents
are, as a rule, associated
with ST segment prolongation
and depression’ and T wave inversion,‘r3
occasionally
simulating
myocardial
infarction.‘“,‘6
On
the other band, ST segment elevation
is less
frequently
observed .I6 It has I)een proposed’ that such changes may I)e secondary
to electrolyte
imbalance,
pH, and I)lood gas
almornialities,
the latter
supported
111
experimental
studies.*7,‘8
Almormalities
of
serum K+ and pH n-ere observed
in the
reported
case and may have contrilnlted
to the ECG pattern
of elevated
ST segnient.18 Hypoknlemia
has also lIeen implicated in the development
of second degree
heart l)lock.‘g
The second positive
deflection at the J junction
(Fig. 2, Leads II, III,
aVF, and VI through
V,), as \vell as the
prolonged
QT,
may have been due, in
part,
to hypotl~ermia,~n~~~
in addition
to
enhanced
vagal tone.
Experimental
studies have demonstrated

ECG changes in CVA

Fig. 2. Twelve

lead

397

electrocardiogram approximately 24 hours after admission (see text).

that intracerebral
disease may induce subendocardial
hemorrhage6
and ultrastructural myocardial clranges.22~23 Such changes
may be of sufficient magnitude to induce
Q waves6 While the association
between
cerebrovascular
accidents and myocardial
infarction has been made in patients prone
to both conditions,16 the question may be
raised as to whether ST segment elevation
may be due to myocytolysis
alone. The
case reported demonstrated
normal microscopic examination of the heart, suggesting
that the ST segment changes were rnediated either by alteration of autonomic tone,
pH, electrolyte disturbances,
or a combination of all of these factors.
Summary

This case report describes a lo-year-old
girl sustaining a cerebrovascular accident
secondary to a vascular malformation involving the cingulate gyrus. The patient
developed a ;\Iobitz Type I block with
periods of A\J dissociation. A 12-lead electrocardiogram revealed the frequently observed prolongation of the QT interval.
Her ECG also demonstrated diffuse ST
segment elevation.
Neurophysiological
mechanisms are discussed.
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