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Case Report

GuillaineBarr�e syndrome after acute myocardialinfarction: 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, Indiab Consultant Physician, Apollo Hospitals, Near Old MLA Quarters, Hyderabad, AP, 500095, Indiac Consultant Neurologist, Apollo Hospitals, Near Old MLA Quarters, Hyderabad, AP, 500095, Indiad Consultant Nephrologist, Apollo Hospitals, Near Old MLA Quarters, Hyderabad, AP, 500095, Indiae Medical Registrar, Apollo Hospitals, Near Old MLA Quarters, Hyderabad, AP, 500095, Indiaf 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:

GuillaineBarr�e syndrome

Acute myocardial infarction

Primary percutaneous angioplasty

* Corresponding author. Tel.: þ91 939317873E-mail address: pankaj_jariwala@hotmai

Please cite this article in press as: Jariwsentation, Apollo Medicine (2014), http://

http://dx.doi.org/10.1016/j.apme.2014.05.0090976-0016/Copyright © 2014, Indraprastha M

a b s t r a c t

The association of acute coronary syndrome with any immunological mediated poly-

radiculopathy like GuillaineBarr�e syndrome is very rare. We report such a rare association

of acute myocardial infarction and GuillaineBarr�e 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 GuillaineBarr�e 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

GuillaineBarr�e 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.

8.l.com (P. Jariwala).

ala P, et al., GuillaineBadx.doi.org/10.1016/j.apm

edical Corporation Ltd. A

There are few case reports in the literature of rare as-

sociation of development of GuillaineBarr�e 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 GuillaineBarr�e

syndrome, which despite management could not

rr�e syndrome after acute myocardial infarction: A rare pre-e.2014.05.009

ll rights reserved.

a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1e52

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 extremitywas 80/60mmHg 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

Fig. 1 e Electrocardiogram pre and post primary percutaneous

leads II, III, AVF with reciprocal ST depression with complete h

resolution of ST elevation and reciprocal ST depression with no

Please cite this article in press as: Jariwala P, et al., GuillaineBasentation, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apm

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

angioplasty. 1a: Electrocardiogram shows ST elevation of

eart block. 1b: Post primary angioplasty ECG shows >75%rmal Sinus rhythm.

rr�e syndrome after acute myocardial infarction: A rare pre-e.2014.05.009

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.

a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1e5 3

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

Fig. 3 e Nerve conduction study shows the grossly reduced CM

velocities suggestive of axonal motor neuropathy.

Please cite this article in press as: Jariwala P, et al., GuillaineBasentation, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apm

continued through a tracheotomy. Supportive measures

in the form of total parental nutrition, antibiotics, respira-

tory physiotherapy initiated to improve his respiratory

efforts.

AP amplitudes with normal with normal conduction

rr�e syndrome after acute myocardial infarction: A rare pre-e.2014.05.009

Fig. 4 e Shows normal sensory conduction studies.

a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1e54

The detailed neurological examinationwas 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,

Table 1 e Summery of case reports of development of Guillainliterature.

Sr. No. Author & Year ofpublication

Age/sex Windowperiod

C

Acutesynd

1 McDonough &

Dawson4 1987

46 years/male 17 days Acute infe

wall myoc

infarction

65 years/Female 1 week Acute ant

myocardia

2 M. Sharma

et al7 2002

46 years/Male 6 days Acute evo

Antero-lat

myocardia

Please cite this article in press as: Jariwala P, et al., GuillaineBasentation, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apm

but despite these efforts, patient conditions deteriorated and

the patient expired after 2 weeks secondary to sepsis and

respiratory failure.

3. Discussion

The GuillaineBarr�e 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 GuillaineBarr�e 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

eBarr�e syndrome after Acute myocardial infarction in

linical presentation Diagnosis Recovery

coronaryrome

Neurologicalsymptoms

rior

ardial

Generalized

weakness of

arms and legs.

LP & NCV After 2 months with

physiotherapy.

erior

l infarction.

Lethargy and

paresthesia in

the distal arms

and legs

LP & NCV After 3 months with

physiotherapy.

lved

eral

l infarction.

Paresthesias and

weakness of both

legs and arms

LP & NCV After 30 days with

plasmapheresis.

rr�e syndrome after acute myocardial infarction: A rare pre-e.2014.05.009

a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1e5 5

infectious spinal arachnoiditis can be considered but sym-

metric and diffuse absence of deep tendon reflexes negates

the diagnosis of spinal arachnoiditis.7

GuillaineBarr�e 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.

Please cite this article in press as: Jariwala P, et al., GuillaineBasentation, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apm

r e f e r e n c e s

1. Guglin M, Novotorova I. Neurogenic stunned myocardiumand takotsubo cardiomyopathy are the same syndrome: apooled analysis. Congest Heart Failure (Greenwich, Conn).2011;17(3):127e132.

2. Yoshii F, Kozuma R, Haida M, et al. Giant negative T waves inGuillaineBarr�e syndrome. Acta Neurol Scand. 2000Mar;101(3):212e215.

3. Dagres N, Haude M, Baumgart D, Sack S, Erbel R. Assessmentof coronary morphology and flow in a patient withGuillaineBarr�e syndrome and ST-segment elevation. ClinCardiol. 2001 Mar;24(3):260e263.

4. McDonagh AJ, Dawson J. GuillaineBarr�e syndrome aftermyocardial infarction. Br Med J (Clin Res Ed). 1987 Mar7;294(6572):613e614.

5. Ng E, Stafford PJ. GuillaineBarr�e syndrome after myocardialinfarction. Int J Cardiol. 2003 Jul;90(1):129e130.

6. Hartung H, Willison HJ, K B. Acute immuno-inflammatoryneuropathy: update on GuillaineBarre syndrome. Curr OpinNeurol. 2002;15:571e577.

7. Huynh W, Kiernan MC. Nerve conduction studies. Aust FamPhysician. 2011 Sep;40(9):693e697.

8. Sharma M, Kes P, Ba�si-Kes V, et al. GuillaineBarre syndromein a patient suffering acute myocardial infarction. Acta ClinicaCroatica. 2002;41(3):255e257.

9. Okuyan E, Cakar MA, Dinckal MH. GuillaineBarr�e syndromeafter thrombolysis with streptokinase. Cardiology Res Pract.2010 Jan;2010:315856.

10. Eshraghian A, Eshraghian H, Aghasadeghi K. GuillaineBarr�esyndrome after streptokinase therapy for acute myocardialinfarction. Intern Med. 2010;49(22):2445e2446.

11. Patras NK. GuillaineBarre syndrome after treatment withstreptokinase. BMJ. 1992;304(May):1992.

12. Kaiser R, Kaufmann R, Czygan M, et al. GuillaineBarr�esyndrome following streptokinase therapy. Clin Investig. 1993Oct;71(10):795e801.

rr�e syndrome after acute myocardial infarction: A rare pre-e.2014.05.009

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