The association of acute coronary syndrome with any immunological mediated polyradiculopathy like Guillain–Barré syndrome is very rare. We report such a rare association of acute myocardial infarction and Guillain–Barré syndrome. Our patient underwent primary angioplasty successfully, but developed respiratory failure while in hospital. While the difficulty in weaning off from ventilator a suspicion of neuromuscular disease was made. The further investigations, including nerve conduction study confirmed a diagnosis of Guillain–Barré syndrome. Despite treatment, the patient died secondary to multi-organ dysfunction. Our case is 4th reported in the literature without use of any thrombolytic agent for such association.

1.
Guilla
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2. Case Report
GuillaineBarre syndrome after acute myocardial
infarction: A rare presentation
Pankaj Jariwala a,*
, Harikishan Boorugu b
, Gopal Chevuru c
,
Arshad Punjani b
, Shaeq Mirza b
, Dilip Babu Madhawar d
,
Nikhilkumar Kotla e
, Srinivasrao Bopparaju f
a
Consultant Cardiologist, Apollo Hospitals, Near Old MLA Quarters, Hyderabad, AP, 500095, India
b
Consultant Physician, Apollo Hospitals, Near Old MLA Quarters, Hyderabad, AP, 500095, India
c
Consultant Neurologist, Apollo Hospitals, Near Old MLA Quarters, Hyderabad, AP, 500095, India
d
Consultant Nephrologist, Apollo Hospitals, Near Old MLA Quarters, Hyderabad, AP, 500095, India
e
Medical Registrar, Apollo Hospitals, Near Old MLA Quarters, Hyderabad, AP, 500095, India
f
Consultant Nephrologist, Matrix Hospital, Ramanthapur, Hyderabad, AP, 500013, India
a r t i c l e i n f o
Article history:
Received 11 February 2014
Accepted 1 May 2014
Available online xxx
Keywords:
GuillaineBarre syndrome
Acute myocardial infarction
Primary percutaneous angioplasty
a b s t r a c t
The association of acute coronary syndrome with any immunological mediated poly-
radiculopathy like GuillaineBarre syndrome is very rare. We report such a rare association
of acute myocardial infarction and GuillaineBarre syndrome. Our patient underwent pri-
mary angioplasty successfully, but developed respiratory failure while in hospital. While
the difficulty in weaning off from ventilator a suspicion of neuromuscular disease was
made. The further investigations, including nerve conduction study confirmed a diagnosis
of GuillaineBarre syndrome. Despite treatment, the patient died secondary to multi-organ
dysfunction. Our case is 4th reported in the literature without use of any thrombolytic
agent for such association.
Copyright © 2014, Indraprastha Medical Corporation Ltd. All rights reserved.
1. Introduction
GuillaineBarre syndrome and its association with cardiovas-
cular diseases are rare. There are a few case reports of auto-
nomic dysfunction leading to the manifestation of cardiac
dysfunction in the form of transient variant of Tako-Tsubo
cardiomyopathy,1
STeT changes in the form of giant T wave
inversions2
and ST elevations with normal coronaries3
in the
literature.
There are few case reports in the literature of rare as-
sociation of development of GuillaineBarre syndrome
following acute myocardial infarction.4,5
Whether this
is mere (part of the association) coincidence or neurological
manifestation secondary to myocardial infarction needs
to be established. We report such a case of acute myocardial
infarction with cardiogenic shock with acute left ventricular
failure who could not be weaned off ventilator and
subsequently diagnosed to have the GuillaineBarre
syndrome, which despite management could not
* Corresponding author. Tel.: þ91 9393178738.
E-mail address: pankaj_jariwala@hotmail.com (P. Jariwala).
Available online at www.sciencedirect.com
ScienceDirect
journal homepage: www.elsevier.com/locate/apme
a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1 e5
Please cite this article in press as: Jariwala P, et al., GuillaineBarre syndrome after acute myocardial infarction: A rare pre-
sentation, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apme.2014.05.009
http://dx.doi.org/10.1016/j.apme.2014.05.009
0976-0016/Copyright © 2014, Indraprastha Medical Corporation Ltd. All rights reserved.

3. survive secondary to respiratory and kidney failure leading
to death.
2. Case report
A 56 years old male arrived at an emergency room of a pe-
ripheral non-PCI hospital with complaints of retrosternal
chest pain for 6 h associated with diaphoresis and breath-
lessness at rest.
On examination, he had tachypnea and he was restless
with heart rate of 40 per min and blood pressure recorded in
the left upper extremity was 80/60 mm Hg and respiratory rate
was 42 per minute. His right upper limb had post-polio re-
sidual paralysis with wasting and atrophic changes. There
were no cyanosis and edema.
On Cardio-respiratory examination, though he had normal
heart sounds without any murmurs, but there were bilateral
basal crackles in less than 50% of the lungs. Nervous system
examination revealed normal higher functions and patient
was moving all limbs well, except the polio affected right
upper limb (which had power of 3/5).
The ECG showed an acute ST elevation in the inferior
leads and V1 with reciprocal ST depression in Antero-lateral
leads [Fig. 1a]. Cardiac rhythm showed AV dissociation.
Hence, clinical diagnosis of inferior wall myocardial
infarction [STEMI] with complete heart block with Cardio-
genic Shock was made. Bedside 2 D echocardiography
showed hypokinesia of inferior wall and posterior wall with
hyper contractile other segments with ejection fraction of
35%. There was no mitral regurgitation or ventricular septal
defect [Mechanical complication]. The patient was shifted to
PCI hospital where on arrival patient was in normal sinus
rhythm and shifted to the Cath lab after initial stabilization.
Coronary angiography revealed osteal chronic total occlusion
of left anterior descending artery with normal left circumflex
and OM arteries. RCA injection showed thrombotic total oc-
clusion of the mid segment [TIMI 0]. Primary PCI of RCA done
after thrombo-aspiration with implantation of BMS, which
restored TIMI 3 flow [Door to needle time e 94 min].
[Fig. 2aef] Post angioplasty ECG showed 75% resolution of
ST elevations in the inferior leads and reciprocal ST de-
pressions in Antero-lateral leads with normal sinus rhythm
[Fig. 1b].
Immediately after primary PCI patient developed in-
crease in breathlessness with a further drop in oxygen
saturation hence he was ventilated by inserting an
endotracheal tube and shifted to cardiac ICU intensive care
unit. The Patient required high doses of inotropes, blood
pressure which did not improve hence IABP was inserted
through the right femoral artery for hemodynamic stability.
On a ventilator, he had spikes of fever, hence blood culture
Fig. 1 e Electrocardiogram pre and post primary percutaneous angioplasty. 1a: Electrocardiogram shows ST elevation of
leads II, III, AVF with reciprocal ST depression with complete heart block. 1b: Post primary angioplasty ECG shows 75%
resolution of ST elevation and reciprocal ST depression with normal Sinus rhythm.
a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1 e52
Please cite this article in press as: Jariwala P, et al., GuillaineBarre syndrome after acute myocardial infarction: A rare pre-
sentation, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apme.2014.05.009

4. and endotracheal tube cultures were sent and initiated on
Meropenem. Despite these efforts his respiratory failure did
not improve hence on the 7th day percutaneous tracheos-
tomy was done under local anesthesia and ventilation
continued through a tracheotomy. Supportive measures
in the form of total parental nutrition, antibiotics, respira-
tory physiotherapy initiated to improve his respiratory
efforts.
Fig. 2 e Stepwise procedure of primary percutaneous coronary intervention of the RCA. a, b: Angiography of the left
coronary system showing chronic total occlusion of the LAD in LAO cranial and caudal views (arrows). c: angiography of the
RCA showing acute thrombotic occlusion (thick arrow) in its mid segment. d: establishment of flow in the RCA with the
passage of guide wire across the occlusion with translucency (thick arrow) suggestive of acute thrombus. e: thrombo-
aspiration using Export catheter. f: Final angiography after placement of stent showing TIMI 3 flow.
Fig. 3 e Nerve conduction study shows the grossly reduced CMAP amplitudes with normal with normal conduction
velocities suggestive of axonal motor neuropathy.
a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1 e5 3
Please cite this article in press as: Jariwala P, et al., GuillaineBarre syndrome after acute myocardial infarction: A rare pre-
sentation, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apme.2014.05.009

5. The detailed neurological examination was repeated at this
point in view of persisting poor respiratory effort. The patient
was found to have areflexic quadriparesis with a power of 1/5
in all limbs (including polio affected limb) along with poor
chest expansion suggesting a diffuse neuromuscular illness.
His plantars were flexors. Nerve conduction studies of all four
limbs revealed grossly reduced CMAP (compound muscle ac-
tion potential) amplitudes with normal SNAPs (sensory nerve
action potentials). F waves were completely absent. In view of
acute onset off quadriparesis, and areflexia with respiratory
involvement, nerve conduction suggestive of axonal motor
polyradiculoneuropathy, diagnosis of AMAN (acute motor
axonal polyradiculoneuropathy) variant of GuillianeBarre
syndrome was made [Figs. 3 and 4]. Lumbar puncture could
not be done as the patient was on anti-platelet and antico-
agulant therapy. A computed tomogram of the brain was
normal.
Intravenous immunoglobulin could not be given due to
cost constraints. Methyl Prednisolone therapy was started,
but despite these efforts, patient conditions deteriorated and
the patient expired after 2 weeks secondary to sepsis and
respiratory failure.
3. Discussion
The GuillaineBarre syndrome is an immune mediated acute
inflammatory polyneuropathy (predominantly demyelinating
type) and it has been reported to be associated with viral in-
fections, lupus erythematous, lymphoma, Hodgkin's disease
and other situations.6
Differential diagnoses for acute onset quadriparesis in our
patient include GuillaineBarre syndrome, hypokalemia, acute
transverse myelopathy and acute polyneuropathy secondary
to critical illness, etc. His serum potassium was normal, his
plantars were down going and absence of F waves and the
absence of proximal deep tendon reflexes differentiates it
from critical illness neuropathy. A possibility of acute
Fig. 4 e Shows normal sensory conduction studies.
Table 1 e Summery of case reports of development of GuillaineBarre syndrome after Acute myocardial infarction in
literature.
Sr. No. Author Year of
publication
Age/sex Window
period
Clinical presentation Diagnosis Recovery
Acute coronary
syndrome
Neurological
symptoms
1 McDonough
Dawson4
1987
46 years/male 17 days Acute inferior
wall myocardial
infarction
Generalized
weakness of
arms and legs.
LP NCV After 2 months with
physiotherapy.
65 years/Female 1 week Acute anterior
myocardial infarction.
Lethargy and
paresthesia in
the distal arms
and legs
LP NCV After 3 months with
physiotherapy.
2 M. Sharma
et al7
2002
46 years/Male 6 days Acute evolved
Antero-lateral
myocardial infarction.
Paresthesias and
weakness of both
legs and arms
LP NCV After 30 days with
plasmapheresis.
a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1 e54
Please cite this article in press as: Jariwala P, et al., GuillaineBarre syndrome after acute myocardial infarction: A rare pre-
sentation, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apme.2014.05.009

6. infectious spinal arachnoiditis can be considered but sym-
metric and diffuse absence of deep tendon reflexes negates
the diagnosis of spinal arachnoiditis.7
GuillaineBarre syndrome complicating acute myocardial
infarction is a very rare occurrence and till now in literature
we could find only two case reports with three cases reported
so far as summarized in Table 1.4,5,8
There are case reports of development of GB syndrome
following administration of thrombolytic therapy like strep-
tokinase, anisostraplase.9e12
But in our case, the patient underwent Primary PCI hence
there was no drug attributable to this neurological disease
particularly drugs causing peripheral neuropathy. There are
certain causative factors in these patients like secondary to
respiratory tract infection or certain cardiac drugs like carni-
tor which was used in this case.
4. Conclusion
We suggest that any patient who complains of generalized
weakness or difficulties in weaning off ventilator in cardiac
patients should undergo thorough neurological examination
and possibility of GB syndrome complicating myocardial
infarction should be considered as one the differential di-
agnoses. Occurrence of GBS after myocardial infarction is rare
and if more cases are reported, will need to look into associ-
ation of both.
Conflicts of interest
All authors have none to declare.
r e f e r e n c e s
1. Guglin M, Novotorova I. Neurogenic stunned myocardium
and takotsubo cardiomyopathy are the same syndrome: a
pooled analysis. Congest Heart Failure (Greenwich, Conn).
2011;17(3):127e132.
2. Yoshii F, Kozuma R, Haida M, et al. Giant negative T waves in
GuillaineBarre syndrome. Acta Neurol Scand. 2000
Mar;101(3):212e215.
3. Dagres N, Haude M, Baumgart D, Sack S, Erbel R. Assessment
of coronary morphology and flow in a patient with
GuillaineBarre syndrome and ST-segment elevation. Clin
Cardiol. 2001 Mar;24(3):260e263.
4. McDonagh AJ, Dawson J. GuillaineBarre syndrome after
myocardial infarction. Br Med J (Clin Res Ed). 1987 Mar
7;294(6572):613e614.
5. Ng E, Stafford PJ. GuillaineBarre syndrome after myocardial
infarction. Int J Cardiol. 2003 Jul;90(1):129e130.
6. Hartung H, Willison HJ, K B. Acute immuno-inflammatory
neuropathy: update on GuillaineBarre syndrome. Curr Opin
Neurol. 2002;15:571e577.
7. Huynh W, Kiernan MC. Nerve conduction studies. Aust Fam
Physician. 2011 Sep;40(9):693e697.
8. Sharma M, Kes P, Basi-Kes V, et al. GuillaineBarre syndrome
in a patient suffering acute myocardial infarction. Acta Clinica
Croatica. 2002;41(3):255e257.
9. Okuyan E, Cakar MA, Dinckal MH. GuillaineBarre syndrome
after thrombolysis with streptokinase. Cardiology Res Pract.
2010 Jan;2010:315856.
10. Eshraghian A, Eshraghian H, Aghasadeghi K. GuillaineBarre
syndrome after streptokinase therapy for acute myocardial
infarction. Intern Med. 2010;49(22):2445e2446.
11. Patras NK. GuillaineBarre syndrome after treatment with
streptokinase. BMJ. 1992;304(May):1992.
12. Kaiser R, Kaufmann R, Czygan M, et al. GuillaineBarre
syndrome following streptokinase therapy. Clin Investig. 1993
Oct;71(10):795e801.
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Please cite this article in press as: Jariwala P, et al., GuillaineBarre syndrome after acute myocardial infarction: A rare pre-
sentation, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apme.2014.05.009

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