Download IschemicaHy Mediated Sustained Monomorphic Ventricular

IschemicaHy
Mediated Sustained
Monomorphic
Ventricular
Tachycardia*
Resolution With Antiischemic Therapy
Robert
W Thters;
Gregory
M.D.;
A. Buser,
HyunJoseph
M.D.;
Kim,
and Michael
CASE
A 51-year-old
was
admission,
he
He began
receiving
developed
M.D.,
underwent
resistant
to sinus
Ph.D.
a patient with ischemically
mediated
sustained
ventricular
tachycardia
occurring
at rest and
to treatment
with intravenously
administered
procainamide.
plasty
was
transluminal
Percutaneous
successful,
initially
coronary
but rest angina
ular
tachycardia,
curred
2 weeks
resistant
later
and
isehemic
medication
ventricular
therapy.
We suggest
be of benefit
in patients
cardial
M
medical
may
arrhythmias
rhythm
tained
(Chest
is an important
of ventricular
death.
with
by
precipitated
ischemia
genesis
diac
responded
However,
ventricular
nonfatal
tachycardia
myo-
1993; 104:1613-14)
factor
in the
and
sudden
car-
ischemically
mediated
unusual.
susSeveral
studies
have examined
the effects of myocardial
revascularand anti-ischemic
pharmacologic
therapy
upon exercise-induced
ventricular
arrhythmias.’
Relatively
litfie is
known,
however,
about the effects of these interventions
upon ischemically
mediated
ventricular
arrhythmias
unassociated with exercise.
ization
*Fmm
the
Division
of Cardiology,
Department
of Medicine,
Administration
Medical Center,
School
of Medicine,
Baltimore.
Baltimore
Veterans
versity
ofMaryland
the
and the Uni-
.1’-
FIGURE
beats
and
a patent
anterior
descending
left
circumflex
marginal
was
left
internal
coronary
coronary
branches
coronary
artery
1. An ECC showing the six limb leads during
per minute.
The paper speed is 100 mm/s.
artery
graft
poor
distal
was occluded,
diseased.
The
occluded,
and
there
and then
intravenously.
Coronary
with
artery
had
to the
1). He converted
administered
mammary
diffusely
was
discomfort
to
surgery.
and
admission
(Fig
begun.
artery
were
dinitrate
After
disease
prior
bypass
artery
tachycardia
then
artery
months
isosorbide
procainamidewas
infusion
arteriography
to the left
runoff. The
and the obtuse
graft to the distal
was
a filling
defect,
presumably
thrombus,
occluding
the origin of the large posterior
descending
artery
Left ventriculography
revealed
overall
normal
left ventricular
function.
Subsequently,
the patient
experienced
intermittent
chest discomfort
followed by long runs of seif-terminating ventricular
tachycardia.
There
was no clear relationship
between
resting
of
flow.
The
rate
heart
and
artery
artery
coronary
arrhythmia
the
onset
gradually
of
the
at the
angioplasty
resulted
subsided,
arrhythmia.
origin
of the
in some resolution
and
procainamide
therapy
was discontinued.
Electrophysiologic
study,
in the drugfree state, revealed
no inducible
arrhythmias
during
programmed
stimulation
using
up to three
extrastimuli
at two right ventricular
sites
and two paced
cycle lengths.
Thallium
exercise
stress test
showed
small fixed defects
inferiorly
and apically, but no reversible
defects.
Ten days later, the patient’s
rest angina
recurred,
followed
by
sustained
ventricular
tachycardia
with morphologic
findings
iden-
to the original
tachycardia.
Therapy
with intravenously
adminprocainamide
was reinstituted,
and because he was a poor
interventional
candidate,
the dosage of metoprolol
was increased
to 150 mg twice a day and therapy with diltiazem
to 360 mg daily,
was added.
After
resolution
of the arrhythmia,
treatment
was
switched
to the oral form of procainamide,
and a repeat
electrotical
istered
I
.
Five
coronary
ventricular
Percutaneous
coronary
posterior
descending
trigger
arrhythmias
is relatively
malignant
spontaneous
2-vessel
when
revealed
right
ventric-
therapy,
reto aggressive
antithat anti-isehemic
to procainamide
isehemia.
yocardial
angio-
and
coronary
angina.
metoprolol
sustained
A maintenance
We describe
monomorphic
atherosclerotic
with
for crescendo
hospitalized
done well until 3 weeks prior to admission.
coronary
care unit, he experienced
chest
M.D.;
R. Gold,
man
REPORT
-t-1SS----
an episode
:
,14
ofventricular
tachycardia
CHEST
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21677/ on 05/12/2017
at a
rate
V
of 180
I 104 I 5 I NOVEMBER,
1993
1613
physiologic
study
exercise
from
stress
again
showed
no
test was unchanged,
inducible
arrhythmias.
and the patient
The
was discharged
the hospital.
The patient
was readmitted
6 weeks
later because
of presumed
procainamide-induced
lupus. Procainamide
therapy
was discontinued, but he developed
a life-threatening
lower gastrointestinal
hemorrhage,
necessitating
emergency
transverse
colectomy.
He
experienced
no anginal
symptoms
during
this period,
and no
ventricular
arrhythmias
were observed.
After uneventful
recovery,
he has remained
asymptomatic
with no further
ventricular
tachycardia
over
a 9-month
period
while
receiving
treatment
with
metoprolol,
diltiazem,
and
isosorbide
dinitrate.
DISCusSIoN
There
tachycardia
First,
are
several
factors
seen in our patient
it was
always
suggesting
that
was ischemically
preceded
by typical
ventricular
mediated.
anginal
symptoms.
Although
ischemic
symptoms
were not preceded
by obvious
tachycardia,
we cannot exclude
minor fluctuations
in heart
rate and blood pressure
as trigger
factors.
Alternatively,
spontaneous
alterations
have been
cardia
in patients
with
while
was
relatively
setting
of life-threatening
though
ischemically
curring
at rest
preserved
favorable
mic
not.
than
is unusual,
be
left ventricular
outcome.
While
re-
has
Al-
with
oc-
onstrate
are
common
that
patient’s
cardiac
the beneficial
role of beta
It has become
a common
this
death
has
has
practice
in
not
are
DA,
Levine
bypass
SR.
exercise
surgery
Klein
testing:
and
MD,
Ryan
TJ. Ventricular
mechanism,
prognostic
response
arrhyth-
Am
J Cardiol
RJ Jr. Gettes
LS.
Reproducibility
and treatment
JR.
Simpson
of exercise-induced
ventricular
5 The
and
CAST
Investigators
suppression
tachycardia.
Am
J
on
after
preliminary
mortality
report:
Effect
of encaimide
in a randomized
trial
of arrhythmia
myocardial
infarction.
N
Engl
J Med
its efficacy
present
Heart
of propranolol
results.
Attack
in patients
JAMA
Trial
Research
with
1982;
acute
247:1707-14
Group.
A randomized
myocardial
104:1614-16)
infarction.
refractory
ablation
effective
of accessory
in the
treatment
syndrome.
in eliminating
period
Recent
accessory
pathways
of patients
series
dem-
pathways
and
two
in
cases
which
intravenous
adenosine
‘concath-
REPORTS
1
energy
(55
disappearing
V)
was delivered
the first
for a total of
2 s. There
after
27
was
s
no
evidence
for accessory
pathway
conduction
during ventricular
or
atrial pacing
after
30 mlii. Adenosine
(12 mg) intravenously
demonstrated
transient
ventricular
preexcitation
(Fig 1, top). Further
radiofrequency
energy
was delivered
to the site and again preexcitation disappeared.
After 30 mm, adenosine
was repeated,
producbog transient
complete
atrioventricular
(AV) block.
The patient’s
ECG remains free ofpreexcitation
5 months after the procedure.
2
A 41-year.old
historyofatrial
6 B-Blocker
1993;
revealed
persistent
accessory
pathway
duction following presumed
successful
radiofrequency
eter ablation.
CASE
1989;
321:406-12
Mortality
highly
with preexcitation
1984;
flecainide
im-
ms
1984;
53:751-56
3 Lehrman
KL, lilkian
AG, Hultgren
HN, Fowles RE. Effect of
coronary
arterial bypass surgery on exercise-induced
ventricular
arrhythmias.
Am J Cardiol
1979; 44:1056-61
4 Josephson
ME, Horowitz
LN, Farhidi A, Kastor JA. Recurrent
sustained
ventricular
tachycardia.
Circulation
1978; 57:431-40
Cardiol
catheter
been
Radiofrequency
A, Foster
may
A 49-year.old
man had atrial fibrillation
and cardiac arrest.
An
ECG showed ventricular
preexcitation.
The pathway
was mapped
to the lateral mitral annulus.
The anterograde
effective
refractory
period (ERP) was 200 ms and the retrograde
ERP was less than 220
to coronary
significance.
ERPeffective
CASE
53:1553-57
2 Woolfel
Adenosine
administration
CASE
REFERENCES
during
M.D.
(Chest
WolflParlanson-White
We
to
inducible
in the electrophysiology
laboratory.
Our experience suggests
that aggressive
anti-ischemic
therapy
may be
ofbenefit
in some of these individuals.
mias
M.D.;
thereby
sparing patients
the need for life-long
drug therapy
or cardiac
surgery.’
Unfortunately,
accessory
pathway
conduction may recur days to months after apparently
successful
ablation.
Many of these failures may be due to modification
ofaccessory
pathway
conduction
that leaves the tissue viable
but transiently
unable to conduct.’
well-
blockers
automatic
implantable
cardioverter-defibrillators
with sustained
ventricular
arrhythmias
that
1 Weiner
Jack Krvn,
of radiofrequency
catheter
by manifesting
latent acces-
conduction.
adiofrequency
tachycardia
our
of sudden
therapy.
efficacy
pathways
I AVatrioventricular;
in the
function
played
a role in his
the experience
with antiarrhyth-
prevention
ablative
long-term
of accessory
pathway
hemorrhage.
suggesting
Perhaps
M.D.;
H. McAnulty,
and Blair D. Halperin,
of further
the
5017
of
but
even
symptoms
death,
fatal.
John
M.D.;
Silka,
ablation
may
M.D.;
Radiofrequency
catheter ablation
is very effective
in eliminating conduction
over accessory
pathways
in patients
with
Wolff-Parkinson-White
syndrome.
However,
accessory
pathway
conduction
recurs in approximately
5 to 9 percent
of patients
in the weeks to months following
ablation.
We
describe two cases in which intravenous
adenosine
revealed
persistent
accessory
pathway
conduction
after apparently
successful
ablation,
thus
providing
an indication
for the
prove
arrhythmia
drugs
ventricular
cardiac
may
in the
the
therapy,
ischemic
Michaelj
delivery
tachy-
90 percent
Third,
gastrointestinal
mediated
disappointing,’
well established.6
insert
patients
in greater
W Walker,
Kirk
is inducible
to anti-arrhythmic
to sudden
drugs
been
been
disease
to anti-ischemic
frequently
tone
ventricular
heart
it was
resistant
dramatically
entity
ischemic
patient
sponded
vasomotor
sustained
stimulation
in our
antecedents
coronary
Second,
with
programmed
cases,4
in
responsible.
Unmasking
Accessory
Pathway
Conduction
wfth Adenosineinduced Atrioventricular
Nodal
Block After Radlofrequency
Catheter Ablation*
man
fibrillation
had WolflParhinson-White
with rapid accessory
syndrome
and
pathway conduction.
a
trial
I.
*From
sity,
the Division
ofCar&ologc
Oregon
Health
Sciences
Univer-
Portland.
1614
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21677/ on 05/12/2017
Adenosine-Iriduced
AV Nodal Block (b%Wker et a!)