of clinical
Serum myoglobin
in acute
infarction:
A clinical
study
literature
cardiology
myocardial
and review
of the
Pa.
680
November,
Chest pain
ECG changes
None
No
changes
Atypical
Non-specific
ST-T
changes
Enzyme
changes
None
Transient
slight
elevation
*Interpretation:
definite AMI.
Materials
5 to 6 points = Definite
2
Typical
pain
New Q waves
evolutionary
ST-T
changes
Sequential
rise and
fall of
levels
AMI;
< 5 points = No
and methods
0002~8703/78/110680
+ 09$00.90/O
0 1978 The
C. V. Mosby
Co.
-3
UPER NORMAL
---__.---lE_----_--I-
CHEST
PAIN
NO
Ml
Fig.
Serum
myoglobin
in acute
clinical
I
II
III
IV
II
\I
myocardial
subsets
infarction.
SUBSET)
ACUTE ?!I
@ = alive
in acute
+
+
IV/J
III
w
(CLINICAL
DEFINITE
at two weeks;
0 = dead at ho
lli. Profile
I
2
3
No
AMI definite
Definite
of patients
AM1
5
s
sveekm:
studied
see
-.--.
-.-.
38
637 c
22 I4
16 F
63.34 i14.27
22
37%
14 M
EF
63.41 i
12.71
--_1_-
*Lsee Table I.
low BP or tachycardia),
puhnoaary
congestion
(rales, tachypnea,
abnormal
chest x-ray), presence of musculoskeletal
trauma
01 ~~r~~~era~
vascular
disease. Clinical
and hemodynamic
subsets were assigned according to the classificaLion of Forrester
(Table II). AI1 patients were
evaluated and managed by a standa.rd coronary
care protocol, which included serial enzymes and
electrocardiograms,
and
conventhai
blood
chemistry.
Intramuscular
Demeroi imeperidine)
Varki
et al.
10
20
TIME AFTER
30
40
50
60
iig. 2. Relationship
of myoglobin
levels to onset symptoms
in acute myocardial
weeks; o = dead at two weeks; o-1 = died shortly
after sample collection.
682
70
infarction.
= alive
at two
The profile of the population studied for possible AM1 is indicated in Table III. Thirtythree per cent of patients (22 of 60) had definite
AM1 (Group l), and 63 per cent (38 of 60) (Group
2) had equivocal or negative criteria. The two
groups were comparable by age and sex distribution.
*From
Nuclear
Medicine
Systems,
Inc.,
Newport
November,
Beach,
Cal.
92663.
Fig. 3. Myoglobin
American
Ffeart cdournal
683
Varki
et al.
Table
Jutzy
Normal
values of
SMb. (ng./ml.)*
Assay
technique
Reference
Kagen
in myocardial infarction
Complement
Radio
fixation
immunoassay
assay
Not
(RIA)
Patient
selection
method
Admissions
detectable
20.9
CCU
to CCUi
admissions
k 23.3
Stone
RIA
CCU admissions
(consecutive
?)
Not specified
6-85
Stuart
Abstract
RIA
Klocke
Abstract
RIA
25 k 23
(5-75)
CCU
admissions
RIA
31 + 1.3
CCU
admissions
Stone
Not
detectable
(SE)
685
Kollman
RIA
NS
Consecutive
CCU admissions
Patients
with chest
Emergency
room
< 75
Gilkeson
RIA
6-85
Reichlin
RIA
25 2 23
RIA
< 85
Present
*Smb
tCCU
study
= Serum myoglobin
values
= coronary
care unit.
in ng./ml.
Admissions
Consecutive
admissions
pain
in
to CCU?
CCU
I 1 S.D.
= acute
myocardial
infarction.
684
November,
1978,
Vol.
96, No.
On admission
(5)~serial
QlH x 6brs
Q3H x 12hr-s
QZHH x Sdays
Variable serial in 9
patients
QlH x 12f;rs
24hrs-from 48hrs
onset
Not specified
(frequent)
Variable (some
serially)
Not specified
On admission
Discussed in relation to
onset of symptoms
NS
NS
NS
NS
Related to admission
NS
Related to admission
NS
300
-3700
216
-6800
11/21
(52%)
30/30
(100%)
380 t 53
195 2 47
46-200
1390
f 1350
528
k 76
> 100
6-Shrs.
NS
Not specified
NS
1368
+ 1357
172
t 124
On admission Day
2 & Day 3 (A.M.)
Discussed in relation to
onset of symptoms
Not
3ezectabie
9.12brs. from
onset
2-88
18/2O
(90%)
5/5
(100%)
8-f2hrs. from
admission
7-lOhrt-3. from onset
41 I 6
31131
(100%)
62/64
(96.8%)
Early
162 c 5%
4 hrs. from
admission
44 f 6.0
> ;5
8/9
(88%)
5/13
(38%)
9/12
(75%)
32/32
(100%)
19/22
(86%)
Not detectab:e
162
.52(8)
38 5 ?6(!1:
63.6
27 62.38
O/12
(0%)
o/20
(0%)
i/21
(4.8%1)
O/2
(0%)
S/18
(44%)
2/44
(4.5%)
o/13
(0%)
;/53
,uEG;
s/:9
(42%)
d/38
(21%)
Varki
et al.
Table
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
19.
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
Table
*Present
IV)
study.
686
November, 1978,
ome. In the ot,her three, no apparent explanan was found. It is possible that some of these
patients may have had a small infarction
which
could not be detected by conventional
methods.
However, there was no trend towards increasing
myoglobin levels with increasing suspicion (highons are very sensitive for
AMI, they are certainly not specific. Table V lists
the conditions in which elevated myoglobin levels
were found by various workers.
In the present
study, 58 per cent of postoperative
(noncardiac)
patients, 50 per cent of patients receiving frequent
IM injections, and 27 per cent of patients admitted to an intensive care unit for critical noncardisc illnesses showed significant
elevations
of
SMb (Fig. 3). Open heart surgery resulted in very
high levels of SMb,. I2 Other conditions in which
myoglobinemia
has been reported include extensive trauma,
rhabdomyolysis,
acute vascular
occlusion of an extremity,
grand ma1 seizures,
metastatic
cancer
and following
ventricular
tachycardia
without
definite evidence of myocardial infarction
(Table V). Because myoglobin
is
normally
cleared rapidly by the kidney,
SMb
cult to interpret in the presence of
acute or chronic renal failure. There is no data
available at the present time which allows correlation of the severity of the renal failure with the
degree of elevation of the SMb. While myoglobinuria by itself is well known to be associated with
renal failure, the quantities released in AM1 are
not significant in this regard.
While rigorous exercise is well known to cause
significant rhabdomyo~ysis, bicycle stress testing
and moderate exercise did not appear to raise the
XMb., 3
While Stuart and associateP found that five
subjects given 10 C.C. saline injections did not
show elevated SMb, other studies, including the
indicate that patients receiving frequent
injections can have significant myogloStone and colleagues found that
cardiac catheterization did not alter myoglobin
levels,
It is evident that many factors, some of them
rather non-specific, can alter myoglobin levels.
The SMb in. myocardial infarction should, therefore, be interpreted only in light of other assoThe transient and dramatic nature of the
myoglobin peak suggests that a distinct second
Varki
et al.
of early
tion.
recurrent
AMI
or extension
The authors
wish to acknowledge
assistance
of Elizabeth
Smith, B.S.
the excellent
of infarctechnical
REFERENCES
1.
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3.
4.
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17.
18.
19.
20.
Donald,
T. C., Cloonan,
M. J., et al.: Excretion
of
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Heart J. 39:29;1977.
Stone, M. J., Willerson,
J. T., et al.: Radioimmunoassay
of myoglobin
in human
serum-results
in patients
with
acute myocardial
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56:1334,
1975..
Klocke, F. J., Visco, J. P., and Reichlin,
M.: Myoglobinemia as an index of myocardial
infarction
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Kollmann,
G., Shapiro,
B., et al.: Serum myoglobin
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in
the
early
diagnosis
of myocardial
infarction
(Abstract),
Chicago,
June, 1977, The Clinical
Radioimmunassay
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Stuart,
B. C., Palmer,
J., et al.: Serum myoglobin
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Am. J. Cardiol.
55:171,1975.
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in man an intermittent
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Lwebuga-Mukasa,
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Jutzv.
R. V.. Nelson.
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Circulation
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Gilkeson,
B. S., Stone, M. J., et al.: Detection
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in human
sera: its usefulness
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AM. HEART J: 95:70, 1978.
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I
.,
information
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688
November,