to
Letter
the Editor
Mutation
G20210A
Infarction Associated With the Prothrombin
Acute
Myocardial
To the
one
lesion
anterior
Editor:
showed
study
coronary artery)
cision made at that
(descending
coronary
The
G20210A mutation is associated
venous
with
circulation. The de-
goodcollateral
prothrombin
increased
with an
whether
risk of
thrombosis
but
was to
conservative
moment
(1),
apply
is also associated with
A
evaluation showedthat
the mutation
later
premature
(AMI)
therapy.
three
coronariographic
ar-
disease and acute
infarction
re-
vessels were
and a
affected,
in four locations.
artery
mains
coronary
myocardial
(2-5)
coronary
bypass
authors
do not find the
was
unclear. Some
tery
pro-
risk
performed
were
thrombin
mutation to constitute
a
Six months after the acute both
G20210A
patients
major
episode,
but
Unit for
a
that it is
with
im-
referred and Hemostasis
to our Thrombosis
others
associated
factor,
(6-9)
myocardial
substantially
suggest
an
infarction
and in both
the
ab-
increased risk of
more
and,
thrombophilia study,
normal was the
patients
of the
only
the risk
increases whenone ofthe
portantly,
finding
presence
prothrombin
A
G20210A mutation.
was
cardiovascular risk factors
diabetes
major
sion,
also
family
the first
of
(smoking, hyperten-
screening
performed
in In the
both cases.
the defect
or
is
mellitus,
hyperlipidemia,
obesity)
than 45
younger
family
patient,
son,
in
in AMIpatients
was also detected in her mother and her
whereas
present,
especially
of his sons were
them had had an
One of
the
of the second
two
(7,8).
Here we
patient,
anomaly.
family
also carriers of the
unrelated
with AMI
on two
report
patients
for the
2
of 18 after
whowere found to be
of
vein thrombosis at the
age
tuberculosis.
heterozygous
prothrombin
episode
deep
G20210A
first
was
a
weeks of bed rest because of
mutation. The
with no
pulmonary
patient
39-year-old
white
In
women
woman
of
heart
a
control
family history
coronary
population-based
study among
myocardial
prothrombin
disease or venous thrombotic events. The
was
had
18 to 44
the risk of
ofthe
infarction
G20210A
and 1.3%
patient
ages
years,
been
for
6
and
under
associated with
hypertensive
years
antihyper-
carriership
tensive treatment with Norvas
5
was
with 5.1 % of the
mutation
of
4.1 %,
the controls
(amlodipine)
mg twice/day.
(more
mg/day
patients
the
carriers of
and
20
In
addi-
Tenso-Stop
she was
(fosinopril)
being
prothrombin
a
smoker
than 20
G20210A mutation. The risk increased sixfold when as-
tion,
heavy
cigarettes/
nor obese
She was neither
with other
risk factors
cardiovascular
Ar-
sociated
ruda et al.
the
diabetic,
(7).
day).
hyperlipemic,
She
oral
was
in
a
and wasnot
admitted
obtained similar results
in which
(8)
prevalence
taking
contraceptives.
study
with acute chest
of
2
hours’ duration
to the
of the G20210A mutation
hospital
pain
prothrombin
that
out into the left arm and the
a
This
radiated
with
neck.
was found to be 3%
220patients with
among
myocardial
from the
creatine
level of
infarction and 0.7% in 295
1,431
U/L
phosphokinase
together
subjects
general
U/L
level of
2
and creatine
185
The mutation carriers
were
7;
male,
in the
in the
phosphokinase-MB
(n
population.
led
admitted into the Intensive Care
5 were
to the
included
3
of 63
being
female)
(4.7%)
(2.5%)
patient
electrocardiogram
patients
patients
showed
a
sinus
with
Unit. The
AMI
and
4
of 157
rhythm
conduction,
premature
nonpremature
group
and
intraventricular
normal atrioventricular
All seven carriers
in
had,
addition,
group.
of
the
depression
echocardiogram
without
R
wave between the VI and V3
one or
more
risk factors.
cardiovascular
poor expression
and
of
the ST
showed
et al.
also
(9)
increased
derivations,
segment through
normal left ven-
Recently,
prevalence
Doggen
reported
VI
V4. The
and
of the
G20210A allele in AMI
prothrombin
tricular function
thrombus in the left ventricular
infarction
male
than 70
Of
years.
men
the 560
patients younger
final
The
were found to be
was
myocardial
the anterior ventricular wall.
with
a
first
1.8%
MI,
diagnosis
located in
cavity.
heterozygous
whereas 1.2% ofthe
mutation. The risk
G20210A
without
carriers ofthe
646
wave,
mutation,
carried the
Q
healthy
The second
was
a
white man
male
ofMIin the
in-
patient
42-year-old
ischemic cardiac disease.
but
subjects
had
whose father
died of an
of the
presence
prothrombin
genotype
The
smoked more than 20
creased
50%. This risk rose
when
had
one of
substantially
risk factors was
patient
no other cardiovascular
cigarettes/day
factors and
by
risk
the
cardiovascular
also
practiced sports
admitted to the Intensive Care
major
present,
The
was
with odds ratios
The two
between 3 and 6.
patient
pain
varying
that wereport on
patients
regularly.
Unit with
of
ischemic characteristics last-
in
whomAMI
here,
precordial
hours. The
is
several
indicated an
associated with the
G20210A
electrocardiogram
infarction with no
mutation,
have one or more
ing
prothrombin
of
years
wave
anterior
and with
are less than 45
and
Q
myocardial
subepicardial
age
factors-smoking
The
anterior
ischemia.
cardiovascular risk
in
the case of the
coronariographic
111
Malyoth
