Atropine-resistant atrioventricular block in non-Q-wave myocardial infarction: The role of low dose aminophylline (case report)

(1)

Vol 3, No 4, October-Deceuber 1994 _{Aminoplryllins}_on_AV

Block

23I

Atropine-Resistant

Atrioventricular

Block

in

Non-Q-wave

Myocardial

Infarction:

The Role of

Low

Dose

Aminophylline

(case

report)

Peter

Kabo,

Asikin

Hanafiah

ABSTRAK

ton-Q-wave mioknrd infark akut yang kecil tanpa ilt sanping.

lttporan

ini nenyaranka,'t penggunaan dosis kecil aninofilin pada blok AV yang

atopiniresistanî

yang niokard infurk akut.

ABSTRACT

Besides Bez.old-Jarisch refle.r, activatiott of adenositle receptors by adenosine released

fronr

ischetrtic ,1)tocsrd'aI tissue is the second tnechanism respottsiblefor

epto

atrioventricular (AV) block during acute inferior ,ryo"oràiol ittfarctio,l (MCI). Atttittophylline, a as

beet

everse this _4'peofatropine-resistanî AV btock.

In

this article, ati episode

lock

and

by

120

ophylline, a conpetilive adenosine receptor antagonist, itt a patient with

dverse

rePort suggests a use of low dose atttittiphylline

iit

atropine-resistant AV

Keywords: Atttittophl,!!!ns, Atopine-resistant AV block

INTRODUCTION

It

is

well

documented

that

atrioventricular (AV) block

occurs more

commonly in

patients

with inferior

than

anterior myocardial

infarction (MCI).

According

to Berger

and

Ryan

review,l

high-de-gree

AV block

complicating

acute

inferior

myocardial

infarction may be

caused

by

Bezold-Jarisch reflex

which is

atropine-sensitive

and

occurs

usually within

24

hours

after the infarction,

and activation

of

adenosine receptors

by

adenosine released

from

is-chemic myocardium which is

atropine-resistant,

but may be

aminophylline-sensitive. It

_occurs

usually after

24

hours

of

infarction

and

is

associated

with a

large

infarct

area.2

In

this

article,

we report

an

atropine-resistant

but

aminophylline-sensitive

of

complete heart block,

which

occurs

within

24 hours

in

a

small non-e-wave

myocardial

infarction.

CASE REPORT

A

60-year-old woman

was

referred

from

the

Air-force

Hospital after being given

Dopamine

drip,

pethidine

50

mg, Cedocard

10

mg,

and

Nitrodisc who

was diag_

nosed

with

acute

non-Q-wave myocardial infarction

complicated

by

severe

hypotension

and

bradycardia.

She

had

an

angina

attack at

9.OO

AM,

and

had been

given anti-anginal therapy. However,

_at

night

_she

suffered

from

a

typical infarction

chest

pain

and

drow-siness,

which

drived

her

to

the

hospital.

The

risk

factors

from

having coronary artery

dis_ ease

were

diabetes

mellitus

and

hypertension,

Physical examination on

arrival

She looked pale and somnolence. Blood

pressure

(BP)=66/40

mmHg,

heart

rate

(HR)=40 x/min,

respiratory

rate

(RR)=24 x/min,

normal

jugular

venous

NttÎionol Cardiac Centre'

Runnh

Sakit Janlung Harapan

Kita,

Departtttent

of

Cartliology,

Facultl,

of

Medicine, lJttiversity

of

(2)

232

Kabo and Hanafiah

pressure, weak heart sound,

normal respiratory

sound, and

cold extremities.

ECG

showed

a

second degree

(Mobitz type

II)

AV-block, atrial rate: 96 x/min, ventricular

rate:

44

x/miq, normal QRS axis, ST-

depression

and

T-in-verted on

lead

I, aVL, V3-V6.

Laboratory findings:

Hemoglobin:

8.7 g/l;

Leukocytes : 8

700/pl

_{; Hematocrite}: 27 v ol%o

; Creatine

kinase

(CK):242

prll; Creatine kinase

myocardial

band

(CKMB):11.8

pr/l; others

were

within normal limit.

Management

The

patient

was

first

given

oxygen and atropine

sul-phate

0.5 mg

(I.V).

Soon

after this

her

blood

pressure

rose

to

I2O|7O

mmHg.

The

ECG showed

a

sinus

after at

I

, Ten minutes after airopine I

,

. r i I i ; i i I

,i

SEp

94

0l

:23:

15

HR 105 LEAD

II

Soon after atropine

III

(0.5 mg)

Ten minutes after atropine

III

'; l:l

iii::ilrl

After aminophylline 120 mg (I.V.)

i,ililirii,;i

Med

J

Univ Indon

tachycardia

with ventricular

rate

of

110

x/min

(Figure

l),

and the

patient

resumed

consciousness. However,

aftet.10 minutes, the blood

pressure dropped again

accompanied

with

severe

bradycardia.

These

events

occurred repeatedly

three

times

in

a

row.

While

the

temporary pace-maker was

being

prepared,

she was given

aminophylline I2O

mg

(2

mg/kgbw)

followed by

O.2

mg/kgbw/hr

drip.

At

this

time,

her

blood

pressure

and

heart rate

could

be

res-tored to normal

and

stabilized,

and

her

general

condi-tion

improved.

She

was then given medication

for

the

non-Q-wave myocardial infarction

and packed

red cells for

the anemia.

On

the

4th day,

the

patient

left

the

coronary

care

unit without

any complication.

;C2

SEP

AUTOGAiN_.:;ri

lrii

irrlll

ropine

I

(0.5 nrg)

(3)

Vol 3, No 4, October-Deceuber 1994

DISCUSSION

In

the

majority of

cases, second

or third

degree heart

block complicating

inferior

MCI

are response

to

atropine.'

However,

heart

block

occurred

after

the

first

24

hours

in a

large

inferior

MCI

is usually

atropine-resistant;

because

it

is

the

release

of

adenosine

by

the

ischemic myocardium, which

stimu-lates a

specific

adenosine receptors and

in turn

depres-ses

AV

conduction.4

Aminophylline which

possesses

positive

inotro-pic

and recepto release, terase,6

dial

cells.

It

was

therefore

able

to

reverse the

atropine-resistant complete

AV

block in

acute

inferior

MCI,2,8 and has been

reported

success

in

treating parcxysmal

sinus bradycardia,e

sick

sinus

syndrome-,lb

and

atrial

fibrillation with

a

slow ventricular

response.ll

The conventional

dose

of aminophylline wed

to

reverse

atropine-resistant heart

_block2'8

was 300-400

,

gi

ously

as a

single

dose).

nta

levelof aminophylline

0 - as has been

shown

that

in

this

therapeutic dose, aminophylline

shortened

.TîïIiÏiT:

aminophytline

as

tow

as 3,7

mg/liter

tî;:;j:it:il$

nodal

function

in

patients

with

sinus

bradycardia,

whic.ll

is

antagonism

of

adenosine

recep-tors.12

Indeed, as

in

present report,

low

dose-.of

aminophylline, thar

is

120

mg

(2

mg/kgbw)

could

control the

atropine-resistant

complete heart

block.

Other

than

this, we

have

the same

experience

in two

other

cases

where l2O

mg

of

aminophylline

could

reverse

atropine-resistant

AV

block complicating

in_

ferior MCI.

Complete

AV

block in

acute

MCI

should

be tem_

porar

College

of

Ca

idelinés

for

th

_te

MCI,

especiallly

if

theie

are

symptoms

of

low

cardiac

out-put and

atropine-resistant.

However,

temporary

car_

diac pacemaker may have many

complications include

ventricular arrhythmias, ventricular

perforation,

bleeding, infections, pneumothorax etc. More

over,

some

hospital

lity.

Therefore,

looking

for

an

pharmacologi-cal

treatments

_stant

AV block

are needed.

Anrinophylline

has

long

been proven to be able

to

treat

bradyarrhythmias

associated

with

ischemic

heart

Anûnophl,lline on AV

Block

233

disease.t3

The arrhythmogenic and vasodilatation

ef-fects

of

this agent have

limited

its use

in

this

condition.

However,

these

effects was

found to

occur

mostly in

the

therapeutic

serum

concentrations

ranged

from

lO-l5

mg/l.e or

mor..

14

In low concentrationlon

the

other

hand,

aminophylline

induced pulmonary

and

systemic

vasoc_onstriction''

and was

without

adrenergic

ef-fect. lo

ht

view

of

the

fact

that

increased sympathetic

tr

mYocardial

ly,

aminophyl-arr

The

present

data,

in

conjunction

with

inferior

wall

myocardial infarction.

Am

Heart J,

1984;108: 19-24.

4. Belardinelli L, Fenton R, West A, Linden J, Althaus J, Beme r action of adenosine and the antagonism on the atrioventricular conduction in iso_

lated perfused guinea pig and rat hearts. Circ. Res., l9g2;5 1:

569-79.

5. Vestal RE, Eviksson CE, Musser B, Ozaki LK, Halter JB. Effect

of

intravenous atninophylline on plasma levels

of

catecholamines and related candiovascular and metabolic responses _{in man. Circulation, 1983;67:}_{162_7L.}

6. Marcus ML, Skelton CL, Grauer LE, Epstein SE. Effects

of

theophylline on myocardial mechanics. Am J physiol, 1972; 222: l3L6-65.

7. Blinks JR, Olson CB, Jewell BR, Braveny

p.

Influence

of

caffeine and other methylxanthines

on

mechanical properties of isolated mammalian heart muscle: evidence

of

dual action. Circ Res, 1972;30:367-92.

8. Wesley RC, I-erman

BB,

DiMarco Jp, Berne RM, Belar_ dinelli

L.

Mechanism of atropine-resistant atrioventricular block _{during inferior myocardial infarction:}_{possible role}

of

adenosine.

I

Am Coll Cardiol, 1986; 8: L232-4.

9. Benditt DG, Benson DW, _{Kreitt I, Dunnigan A, pritzker MR,} Crouse

L,

Scheinman

MM.

_{Electrophysiologic effects}

of

theophylline in young patients with recurrent symptomatic bradyarrhythmias. Am

I

Cardiol, l9g3; 52: 1223-9. 10. Alboni P, Ratto B, Cappato R, Rossi p, Garto

E,

Antonioli

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Kobo and Hanafiah

tt.

dlboni P, Paparella N, Cappato R, Pirani R, Yiannacopulu

P, Antonioli GE. Long term effects of theophylline in atrial hbrillation with a slow ventricular response. Am J Cardiol,

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12. Alboni P, Rossi P, Ratto B, Pedroni P, Gatto E, Antonioli

GE. Electrophysiologic effect of oral theophylline in sinus bradycardia. Am

I

Cardiol, 1990;65: 1037-9.

13. Berne RM, DiMarco IP, Belardinelli

L.

Dromotropic

ef-fects

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Circulation, 1984; 69: l195-7.

Med

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Ed:

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Atropine-resistant atrioventricular block in non-Q-wave myocardial infarction: The role of low dose aminophylline (case report)

Block

ABSTRACT

with inferior

adenosine released

myocardial

angina

heart

x/miq, normal QRS axis, ST-

iii::ilrl

being

non-Q-wave myocardial infarction

atropine.'

atropine-resistant complete

shown

control the

especiallly

looking

concentrations

previous

inferior

ef-fects