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ACUTE ANTERIOR MYOCARDIAL
INFARCTION FOLLOWING ELECTROCUTION
*Omer A.A.,**Khalid M.K. and
*Gehani A.A.
Departments of *Cardiology & Cardiovascular Surgery
and**Accident & Emergency
Hamad Medical Corporation, Doha, Qatar
 Introduction:
Electrocution is a well known cause of cardiac
arrest, mostly secondary to ventricular fibrillation.
Acute myocardial infarction has been reported
in a few cases although the pathogenesis is not
clear. We report two cases of acute myocardial
infarction after electrocution, both confirmed
by electrocardiography and markedly elevated cardiac
enzymes. Echocardiography showed cardiac damage
evidenced by hypokinesia.
  Case
Report:
Case 1:
A twenty-five-year-old Nepali male was brought
to the Emergency Department of Hamad General Hospital
five minutes after electrocution and collapse
at work. He was unconscious and pulseless; a cardiac
monitor showed ventricular fibrillation. DC shocks
reverted the rhythm to sinus. Total CPR time was
two minutes. The patient was intubated and transferred
to CCU. His vital signs were temp 37ºC, pulse
120/min, B.P. 90/50 mmHg.
Initial laboratory investigations showed a normal
complete blood count, apart from a high WBC count
of 13.6 x 109 / L; blood urea 10.5mmol/L (normal
= 1.7- 8.3 mmol/L); serum creatinine 129 micromol/L
(normal = 53-124 micromol/L).
ECG showed sinus rhythm, significant ST elevation
in leads 1, avl, and V2-V4, (Figure 1). Echocardiography
revealed diffuse left ventricular hypokinesia
with akinetic left ventricular posterior wall
and apex, severe left ventricular dysfunction
with ejection fraction of 30%, no pericardial
effusion, no valvular abnormality. Urgent coronary
angiography revealed normal coronary arteries.
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Figure 1:
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Three days later the patient was successfully
extubated. Neurological examination showed evidence
of brain hypoxia while a CT scan was essentially
normal
His cardiac enzymes over 72 hours are shown in
Table 1.
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Time
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Initial
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24 hours
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32 hours
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40 hours
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50 hours
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72 hours
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CK
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725 U/L
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5342 U/L
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11754 U/L
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17610 U/L
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12710 U/L
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16100 U/L
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CK-MB
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23.3 ng/l
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94.2 ng/l
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104 ng/l
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80.2 ng/l
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36.9 ng/l
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31.1 ng/l
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Relative Index
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3.2 %
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1.8 %
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0.9 %
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0.5 %
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0.3 %
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0.2 %
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Troponin T level was 31.6
ng/ml (normal. = 0.00 - 0.1 ng/ml).
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Table 1
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There was a dramatic improvement during hospitalization
and he was discharged after seven days with good
neurological recovery. Two months later his neurological
examination was normal. His ECG showed slight
ST elevation in leads V2-V4 (Figure 2), Repeated
echocardiography showed normal Echo Doppler study
with an ejection fraction of 66%.
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Figure 2
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Case 2:
A twenty-nine-year-old Indian male was brought
to the emergency department unconscious 15 minutes
after sustaining electrocution while dealing with
a high voltage mainbox. He was unconscious, pulseless
with dilated pupils. There was an electrical burn
on the left hand. A cardiac monitor showed wide
complex tachycardia.
A series of 200, 200, 360 joule DC shocks were
delivered which reverted the rhythm to sinus.
He was intubated and a 100mg IV bolus injection
of lignocaine was given followed by infusion at
a rate of 4 mg/ min. His ECG after cardioversion
showed marked ST segment elevation in leads I,
aVL, V2-V6 with ST depression in leads II, III,
aVF consistent with extensive anterior myocardial
infarction .
Initial laboratory investigations including urea,
electrolytes, and creatinine were normal.
A series of cardiac enzymes is shown in Table
2.
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Time
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6 hours
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14 hours
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22 hours
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48 hours
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CPK
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407 U/L
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6890 U/L
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9040 U/L
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7150 U/L
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CPK-MB
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38.8 ng/L
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340 ng/L
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288 ng/L
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54.8 ng/L
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Relative index
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9.5 %
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4.9 %
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3.18 %
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0.7%
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Troponin test was positive;
serum cholesterol: 5.33 mmol/ L; triglyceride=1.43
mmol/ L.
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Table 2
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Echocardiography showed hypokinetic septum and
apex with an ejection fraction of 64%.
He remained unconscious over the next seven days.
His pupils were reactive to light with a positive
corneal reflex. He developed generalized convulsions,
which were controlled by intravenous diazepam
and phenytoin. His serial ECG’s over the next
seven days showed a gradual return of the ST segment
to base line. He was extubated after ten days
but his intellectual functions were impaired and
he could move only by using a wheel chair. His
family took him home to India and he was lost
to follow up.
  Discussion:
Acute myocardial infarction after electrocution
has been reported in few cases but the pathogenesis
is still debatable1 ,2. In all reported cases
there was structural damage or stunning of the
cardiac muscle, evidenced by hypokinesia on two-dimensional
echocardiography or radionuclide isotope scan
5 . In the acute onset there is usually significant
ST segment elevation in the ECG with marked enzyme
elevation reflecting the myocardial insult. There
is debate whether this enzyme elevation is due
to associated rhabdomyolysis but the elevated
troponin level and the normal blood urea, serum
creatinine and electrolytes make this possibility
unlikely.
The cases reported in this paper show evidence
of acute myocardial infarction manifested by marked
ST elevation in the ECG with significant rises
in CPK-MB enzyme and troponin. The two-dimensional
echocardiography shows hypokinesia in both cases
and a reduced ejection fraction in the first case.
The normal coronary angiography excludes the coincidence
of coronary artery disease.
One case has been reported of myocardial infarction
after electrical injury from diathermy equipment(1
). The electric shock caused an anteroseptal myocardial
infarction complicated by an apical aneurysm.
Coronary angiography showed proximal occlusion
of the left anterior descending artery and an
apical aneurysm on ventriculography. The most
probable mechanism is that electric current caused
damage to the walls of the coronary arteries with
direct thrombogenic effect. Myocardial infarction
and rhabdomyolysis after a high voltage shock
with successful resuscitation has been reported
in a 25 year old man, working as a varnisher near
power transmission lines, who sustained a 110,000
volt shock2 . Cardiac enzymes were markedly elevated;
the ECG showed significant ST segment elevation
in V2-V4. Coronary angiography was normal. Myocardial
infarction after an injury by lightning has been
reported also in one case3
Electric injury can affect many organ systems;
the damage may result from the conversion of electric
energy into heat4 . Radionuclide scintigraphy
has been used to demonstrate myocardial damage
after electrocution5 . A clear positive segment
image on 99m TC-pyrophosphate scintigraphy and
a defect on a 201- Thal SPECT scan at rest were
found in a young man who suffered severe antero-apical
myocardial necrosis caused by electrocution.
 References:
1. Myocardial infarction caused
by electric injury. Value of coronography, (in
French); Ann Med Interne (Paris) 1985; 136(8):
659-62.
2. Myocardial infarct and rhabdomyolysis
after a high-voltage accident with successful
resuscitation. Dtsch Med Wochenschr 1997 Mar 27;
122(13); 400-6.
3. Heat and electrocution. A case
of myocardial infarct after an electric injury
by lightning. Arch Mal Coeur Vaiss 1971 Oct; 64(10);
1516-31.
4. Differential diagnosis of acute
myocardial infarction caused by electrocution.
Rev Esp Cardiol 1996 June; 49(6): 470-3.
5. Myocardial necrosis by electrocution;
evaluation of noninvasive methods. J Nucl Med
1997 Feb; 38(2): 250-1.
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