Download Acute myocardial infarction in a child with myocardial bridge

70 Liu et al
World J Emerg Med, Vol 2, No 1, 2011
Case Report
Acute myocardial infarction in a child with
myocardial bridge
Xiao-dong Liu, Chun-lei Sun, Su-ping Mu, Xiao-mei Qiu, Hai-ying Yu
Department of Pediatrics, Weifang People’s Hospital Affiliated to Weifang Medical College, Weifang 261041, China
Corresponding Author: Xiao-dong Liu, Email: [email protected]
BACKGROUND: Myocardial infarction (MI) is rare in children, and Kawasaki disease is now
recognized as the main cause for MI. In this report, we present a child with MI caused by myocardial
bridge (MB).
METHODS: A 7.5-year-old boy was admitted to Weifang People’s Hospital on September
16, 2008 for heart disease. By electrocardiogram, coronary CT angiography, emission computed
tomography, and other examinations, he was initially diagnosed as having (1) acute inferior
myocardial infarction and extensive anterior myocardial infarction; (2) fulminant myocarditis; or (3)
coronary myocardial bridge. He was treated with oxygen, thrombolysis, myocardial nutrition, vitamin
C (4.0 g per time), dexamethasone (7.5 mg per time), a large dose of gamma globulin, and interferon.
RESULTS: Myocardial enzymes, liver function, C-reactive protein, and troponin-I returned to
normal at 21 days after treatment. At 29 days, electrocardiogram indicated that II, III, aVF, V4 - V6
leads had abnormal Q wave, and ST-T changed. The patient was discharged.
CONCLUSION: Myocardial bridge may be one of the causes of MI in children.
KEY WORDS: Myocardial bridge; Electrocardiogram; Acute myocardial infarction
World J Emerg Med 2011;2(1):70-72
DOI: 10.5847/wjem.j.1920-8642.2011.01.013
INTRODUCTION
Myocardial infarction (MI) is rare in children, and
Kawasaki disease is now recognized as the main cause
for MI. [1] In this report we present a child with MI
caused by myocardial bridge (MB).
CASE REPORT
A boy of 7.5 years old was admitted to the hospital
on September 16, 2008 because of paroxysmal chest pain
for 16 hours plus pale and sweat for 2 hours. Two days
ago, the boy had a high fever of unknown reason, and the
fever diminished after administration of one package of
nimesuli prescribed by his parents. Next afternoon, the
boy had chest pain for 10-20 minutes with an interval
of 1-2 hours, and he didn't receive any treatment. On
the third day, the chest pain aggravated with dyspnea,
vomiting, sweat, and pale. The boy was transferred to
Weifang People’s Hospital Affiliated to Weifang Medical
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© 2011 World Journal of Emergency Medicine
College. He had no history of Kawasaki disease nor
familial history of lipid metabolism disorders. Physical
examination showed T 37.4 °C, P 118 beats/min, RR 32
beats/min, weight 40 kg, BP 110/90 mmHg, and HR 100
beats/min. He was pale, sound minded, slightly irritable,
and had poor spirit and shortness of breath. The breath
sound in the right lung was lower than that in the left
lung, and there was no rale. The abdomen was soft, the
liver was soft at 2.5 cm from the rib and 1.0 cm from the
xiphoid. There was no edema in the lower extremities
nor positive sign in the nervous system.
Laboratory examinations showed that WBC
9.50×10 9/L, RBC 4.87×10 12/L, Hb 140 g/L, platelet
count 472×10 9 /L, the relative value of neutrophils
0.75, relative value of lymphocytes 0.17, the relative
value of monocytes 0.03; urine, stool (-); erythrocyte
sedimentation rate 27 mm/h; C-reactive protein 84.40
mg/L; anti-O 20 IU/mL; blood electrolytes (mmol/L):
sodium 134 (130-147), K 3.92 (3.2-5.3) , Cl 93.0 (98-
World J Emerg Med, Vol 2, No 1, 2011
71
110), calcium 2.0 (2.1-2.7); liver function (IU/L): alanine
aminotransferase 184 (5-40), aspartate aminotransferase
(AST) 422 (8-47). Renal function was normal;
anticardiolipin antibody IgM (+); routine coagulation
tests: prothrombin time 12.8 seconds (8.8-18.8), activity
74% (80%-130%), international normalized ratio 1.09
(0.8-1.2), part of the prothrombin time 33.80 seconds
(26-42), thrombin time 17.4 seconds (10.3-17.6),
fibrinogen 326 mg/dL; D-dimer183 ng/mL (0-500); and
myocardial enzymes and troponin-I increased obviously
(Table 1).
At 2 days after admission, echocardiography showed
(1) large heart, a small amount of mitral regurgitation
and tricuspid regurgitation; (2) cardiac function 25%,
fractional shortening 11%; (3) pericardial effusion. X-ray
showed a median amount of pleural effusion in the right
thorax cavity and an increased heart shadow. At 6 days
after admission, coronary CT angiography showed the
patent coronary artery without stenosis; myocardial
bridge in the left anterior descending coronary artery
(Figure 1); and a small amount of pericardial effusion.
Radionuclide myocardial perfusion imaging revealed
myocardial ischemia and myocardial infarction signs in
the left ventricular apex, a partition near the apex of the
heart and the inferior wall.
The boy was initially diagnosed as having (1) acute
inferior myocardial infarction and extensive anterior
Table 1. Change of myocardial enzymes and troponin-I (CTnI)
Cardiac markers
1st day
2nd day
3rd day
AST (IU/L)
422
490
596
LDH (IU/L)
1211
1250
1552
α-HBDH (U/L)
1165
1218
1234
CK (U/L)
2248
761
336
CK-MB (IU/L)
147
72
35
CTnI (ng/ml)
43.43
26.45
19.43
A
5th day
246
960
994
98
22
5.41
myocardial infarction; (2) fulminant myocarditis; or (3)
coronary myocardial bridge.
After admission, the boy was monitored with
cardiogram. He was treated with oxygen, thrombolysis,
myocardial nutrition, vitamin C (4.0 g per time),
dexamethasone (7.5 mg per time), a large dose of gamma
globulin, and interferon. At 3 days after treatment,
edema occurs in the face and lower limbs. The liver was
tenacious and tenderness at 3.5 cm from the rib and 4.0
cm from the xiphoid. Then the boy was administered
with cedilanid and diuretics. At the 4 days after
treatment, BP decreased to 80-90/50-60 mmHg, and HR
decreased to 40 beats/min. He was then administered
with 20 mg dobutamine, and at 5 days, BP and HR
returned to normal. At 15 days, the results of chest X-ray
examination showed that pleural effusion was absorbed,
and the heart shadow became normal.
Echocardiography showed normal cardiac function,
cardiac function 64%, fractional shortening 35% as
well as a little amount of mitral regurgitation, tricuspid
regurgitation and pericardial effusion. Myocardial
enzymes, liver function, C-reactive protein, and troponin-I
returned to normal at 21 days after treatment; at 29 days,
ECG indicated that II, III, aVF, V4 - V6 leads had abnormal
Q wave, and ST-T changed. The patient was discharged. At
21 days after discharge, ECG indicated that II, III, aVF, V4
- V6 leads had more obvious abnormal Q wave.
11th day
52
573
556
37
18
1.59
21th day
37
286
259
28
14
0.05
B
29th day
42
231
204
33
7.0
0.03
Reference number
8-47
103-198
95-165
26-140
0-15
0-0.04
C
Figure 1. Coronary CT angiography (CTA) of the heart. The arrow in the A and B indicated the location of MB; the arrow in the C indicated
cross-sectional coronary artery under cardiac muscle fibers.
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72 Liu et al
DISCUSSION
The major coronary arteries, which are normally
distributed over the epicardial surface of the heart,
occasionally have a segmental intramyocardial course.
During systole, this segment of the vessel is compressed,
a condition referred to as milking or systolic "myocardial
bridging". [2,3] This phenomenon was first recognized
more than 200 years ago,[4] was first reported in depth in
1951, and was recognized angiographically in 1960.
The diagnosis of myocardial bridging is largely
dependent on angiography. On angiography, bridging is
recognized as compression of a segment of the coronary
artery during systole, resulting in narrowing that reverses
during diastole. It has been thought that most instances
of bridging are of less clinical significance. However,
reports suggest that severe bridging of the left anterior
descending coronary artery can produce myocardial
ischemia or sudden death.[5-7]
The reported prevalence of bridging varies in
pathologic and angiographic studies. Necropsy studis
have found a mean frequency of myocardial bridging
of 25% (range 5%-86%).[8-12] In one autopsy study, the
incidence was 50%. [13] Although all major epicardial
coronary arteries can be affected, involvement of the left
anterior descending coronary artery is the most common.
The initial ECG of the boy indicated that ST
segment elevated 0.3-0.6 mV in the II, III, aVF, V2V6 leads. Combined with upright T, ST segment wave
formed a single curve, and Q wave appeared after the
disappearance of the curve. This was in accordance with
the Towbin diagnosis.[14]
Cardiac troponin-I, which appears in the blood at 4-6
hours after MI and continues to increase at 7 to 10 days, is
a sensitive and specific marker of MI. In this boy, the initial
cardiac troponin-I and CK-MB increased by 400 times
and 100 times, respectively; at 3 weeks after discharge,
ECG indicated abnormal Q wave; the MI area showed by
ECT was similar to the change of ECG, and pericardial
effusion and pleural effusion transiently appeared. These
findings all supported the diagnosis of MI.
Severe myocarditis may have the same manifestations
of ECG as MI, but does not show the typical change of
ST-T as MI, and abnormal Q wave disappears at 3-5 days.
Cardiac troponin-I and CK-MB are slightly or moderately
increased. Hence it is not difficult to distinguish severe
myocarditis from MI. Kawasaki disease, systemic lupus
erythematosus, and coronary artery dysplasia can also
cause MI, but the boy we present here did not show the
above diseases, and he had no family history of high
cholesterol. This suggested that the occurrence of MB was
associated with MI.
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World J Emerg Med, Vol 2, No 1, 2011
Funding: None.
Ethical approval: Not needed.
Conflicts of interest: No benefits in any form have been received
or will be received from a commercial party related directly or
indirectly to the subject of this article.
Contributors: Liu XD wrote the main body of the report. All
authors approved the final version.
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Received October 9 , 2010
Accepted after revision January 27, 2011