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14 Clin Pathol 1995;48:124-128

124

Biochemical assessment of acute myocardial

ischaemia

M D Perez-Catrceles, E Osuna, D N Vieira, A Martinez, A Luna

Abstract remains macroscopically and microscopically

Departnent of
Forensic Medicine,
School of Medicine,
University of Murcia,
E-30100 Murcia, Spain
M D Perez-Carceles
E Osuna
A Luna
Institute of Legal
Medicine, P-3000
Coimbra, Portugal
D N Vieira
Department of
Biochemistry,
University Hospital,
E-30002 Murcia, Spain
A Martinez
Correspondence to:
Professor E Osuna.
Accepted for publication
19 July 1994
Aims-To evaluate the efficacy of bio-
chemical parameters in different fluids in
the diagnosis of myocardial infarction of
different causes, analysed after death.
Methods-The myoglobin concentration
and total creatine kinase (CK) and creatine
kinase MB isoenzyme (CK-MB) activities
were measured in serum, pericardial fluid,
and vitreous humour from seven diag-
nostic groups of cadavers classified ac-
cording to the severity of myocardial
ischaemia and cause of death. Lactate de-
hydrogenase (LDH) and myosin were
measured only in serum and pericardial
fluid, and cathepsin D only in pericardial
fluid. Routine haematoxylin and eosin and
acridine orange staining were used for
microscopy studies of heart tissue.
Results-In pericardial fluid there were
substantial differences between the
different groups with respect to CK, CK-
MB, and LDH activities and myosin con-
centrations. The highest values were found
in cases with morphological evidence of
myocardial ischaemia.
Conclusions-Biochemical parameters,
which reach the pericardial fluid via pass-
ive diffusion and ultrafiltration due to a
pressure gradient, were thus detectable in
this fluid earlier than in serum in cases
with myocardial ischaemia. These bio-
chemical parameters may be of use for
ruling out myocardial ischaemia in those
controversial cases in which reliable mor-
phological findings are lacking.
(J7 Clin Pathol 1995;48:124-128)
Keywords: Myocardial infarction, postmortem exam-
ination, pericardial fluid.
Cardiac disease is the most frequent cause
of sudden death. One of the most difficult
problems faced by the forensic scientist is to
diagnose sudden death in subjects with acute
cardiac processes that progress rapidly, with
non-specific symptoms in many cases,l1 and
lead to death without obvious morphological
alterations. Moreover, the beginning of myo-
cardial damage does not necessarily coincide
with the appearance of symptoms, and there-
fore an asymptomatic period may ensue.
From a practical point of view, myocardial
ischaemia may be extremely difficult to dem-
onstrate in routine forensic studies, as evident
structural alterations-which, as noted above,
do not always occur-are the only unequivocal
evidence for this process. Myocardial ischaemia
undiagnosed when it is the result of acute and
hyperacute processes in which tissue damage is
reflected by the release of biochemical markers
before structural lesions occur.5 This means
that when the period of evolution is brief, the
morphological findings may be normal, but
the values of biochemical markers will have
changed. Several studies have demonstrated
the efficacy of biochemical parameters in
the postmortem diagnosis of myocardial
necrosis.6-2
The use of biochemical parameters in post-
mortem diagnosis requires knowledge of
changes caused by autolysis, a factor closely
linked to the postmortem interval. Moreover,
the distribution of these biochemical elements
in different fluids of the cadaver depends on the
origin and location of tissue damage. Several
factors make pericardial fluid very useful for
postmortem diagnoses: production of this fluid
is a vital phenomenon; postmortem con-
tamination from immediately adjacent tissues
is limited; it lacks erythrocytes; pericardial and
myocardial irrigations are shared;9 1314 and it is
easily obtained from the cadaver. Thus, bio-
chemical markers released in response to car-
diac lesions may reach higher concentrations
in the pericardial fluid than in the serum. The
present study was designed to evaluate the
efficacy of biochemical parameters in different
postmortem fluids in the diagnosis of myo-
cardial infarction. We compared the results of
biochemical tests with morphological ob-
servations.
Methods
We studied 105 cases selected from routine
necropsies performed in the Institute of Legal
Medicine at the University of Coimbra. Mean
age of the subjects was 61-63 + 2-21 years (SD
21-71 years, range 13 to 97 years). Pathological
studies were carried out on heart tissue taken
from ischaemic or necrotic zones (when pres-
ent) and from eight zones of the heart, ac-
cording to the protocol established by Saukko.'
Routine staining with haematoxylin and eosin
was performed; some sections were also stained
with acridine orange for fluorescence micro-
scopy. Of the 105 cases, 71 had structural
evidence of myocardial or cardiac disease, while
34 had no structural heart lesions. Cases were
allocated to one of seven diagnostic categories
based on patient records, necropsy findings,
scene of death, and complementary histological
studies where appropriate. The seven cate-
gories were as follows: group 1, death from
definite myocardial infarction (n = 24); group
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Biochemical assessment of acute myocardial ischaemia 125

2, morphological signs of cardiac disease or
myocardial damage-chest trauma involved in
the cause of death (n = 8); group 3, mor-
phological signs of cardiac disease or myo-
cardial damage-death due to violent causes
excluding chest trauma (n = 27); group 4, mor-
phological signs of cardiac disease or myo-
cardial damage-death due to natural causes
(n =12); group 5, no morphological signs of
cardiac disease or myocardial damage-death
due to extensive multiple injuries (n = 21);
group 6, no morphological signs of cardiac
disease or myocardial damage-death due to
violent causes excluding trauma (n = 7); group
7, no morphological signs of cardiac disease
or myocardial damage-death due to natural
causes (n=6).
Mean survival time was 80-43+21-54 hours
(SD 220-72 hours); maximum survival time
was 1968 hours. Survival was very short in 41
(39%) subjects. Mean postmortem interval was
45A44+2-82 hours (SD 28-91 hours, range 3
to 168 hours). Cardiopulmonary resuscitation
was performed in 10 subjects.
Samples of serum from femoral vein blood,
pericardial fluid, and vitreous humour were
obtained using standard techniques. All
samples were stored at -40°C before analysis
and transported from Coimbra to Murcia in dry
ice (transit time 10 hours). Serum, pericardial
fluid, and vitreous humour samples were tested
in duplicate for myoglobin, total creatine kinase
(CK) activity, and creatine kinase MB iso-
enzyme (CK-MB). Lactate dehydrogenase

Table 1 Mean, SD, median, and range values for the biochemical parameters in groups 1 and 2
Death from definite myocardial infarction Cardiac disease-chest trauma
(n = 24) (n = 8)
Biochemical parameter Mean (SD) Median Range Mean (SD) Median Range
Myosin (pU/l) s 420 (550) 208 72-2339 1395 (1431) 802 205-3704
p 1970 (2958) 630 91-9844 1536 (1953) 741 171-5920
Myoglobin (ng/ml) s 3537 (6066) 954 22-24415 5251 (4246) 5062 323-10800
p 7337 (6763) 4566 596-24606 10743 (11501) 7815 408-36220
vh 142 (211) 60 0-896 81 (105) 42 6-323
CK (U/1) s 12335 (7989) 9049 2941-32400 12335 (12351) 9388 2800-42100
p 21259 (21891) 11801 314-76960 4396 (3724) 3719 201-9773
vh 95 (335) 7 1-1639 14 (17) 6 0-46
CK-MB (U/i) s 3183 (3393) 1891 147-15265 1353 (996) 883 620-3529
p 4792 (5843) 2064 267-19560 1017 (1045) 827 132-3420
vh 26 (75) 2 0-348 6(8) 1 0-21
LDH (U/I) s 3726 (4085) 3022 14-17245 3599 (4029) 2548 49-13226
p 13244 (18791) 4033 5-56020 1287 (1274) 760 87-3013
Cathepsin D (UAbs/g protein) p 2630 (2190) 2060 50-9440 2430 (1590) 2130 230-4990
s=serum; p =pericardial fluid; vh =vitreous humour.

Table 2 Mean, SD, median, and range values for the biochemical parameters in groups 3 and 4
Cardiac disease-violent death (excluding chest trauma) Cardiac disease-natural death
(n =27) (n= 12)
Biochemical parameter Mean (SD) Median Range Mean (SD) Median Range
Myosin (pU/i) s 673 (466) 638 58-1878 458 (537) 260 30-1881
p 498 (547) 345 22-2040 314 (202) 310 9-715
Myoglobin (ng/ml) s 4811 (4083) 4050 221-14625 4929 (5697) 4212 15-20400
p 6722 (7811) 4465 80-31500 4000 (5795) 1612 32-19896
vh 329 (1243) 36 0-6500 158 (217) 68 10-720
CK (U/I) s 7991 (6976) 6381 96-25620 7185 (5331) 4428 2165-19744
p 819 (9058) 2604 70-42230 11905 (15973) 6862 49-46287
vh 33 (80) 5 0-402 134 (428) 5 0-1493
CK-MB (U/i) s 1517 (1441) 1161 61-5668 3157 (4701) 1549 189-17170
p 2265 (3614) 495 30-13200 2496 (3116) 1314 21-10040
vh 22 (57) 1 0-273 25 (68) 2 0-240
LDH (U/i) s 7386 (10193) 2762 1-34320 5754 (9021) 3392 164-33140
p 2212 (2506) 1812 3-12925 5208 (6072) 2355 643-17800
Cathepsin D (UAbs/g protein) p 3470 (3120) 2670 60-12700 3440 (4490) 1450 70-13940
s=serum; p = pericardial fluid; vh vitreous humour.

Table 3 Mean, SD, median, and range values for the biochemical parameters in groups 5 and 6
No cardiac disease-death due to trauma No cardiac disease-violent death excluding trauma
(n=21) (n = 7)
Biochemical parameter Mean (SD) Median Range Mean (SD) Median Range
Myosin (pU/i) s 795 (1008) 438 63-4671 410 (376) 311 42-988
p 519 (968) 128 10-3496 340 (412) 249 22-1181
Myoglobin (ng/ml) s 5453 (4823) 4752 212-16875 4722 (6595) 2172 77-18750
p 10408 (11678) 5231 60-36120 4899 (5911) 3060 65-15720
vh 64 (111) 30 3-501 119 (193) 36 4-536
CK (U/i) s 8968 (10300) 6869 888-36390 10299 (12807) 3780 310-33020
p 3195 (4216) 520 88-14460 10840 (16553) 3124 16-42650
vh 22 (69) 5 0-324 10 (10) 8 2-32
CK-MB (U/i) s 2051 (1902) 1357 107-7343 2004 (1968) 772 245-4798
p 1090 (1345) 366 22-4513 1629 (3124) 288 8-8530
vh 7 (20) 1 0-92 3 (5) 1 0-15
LDH (U/i) s 4157 (4851) 3078 23-16718 1438 (1072) 1444 244-3501
p 2362 (3899) 1285 49-18512 1357 (1464) 1046 6-4268
Cathepsin D (UAbs/g protein) p 3220 (5460) 1610 80-24770 1050 (840) 980 20-2160
s=serum; p=pericardial fluid; vh=vitreous humour.
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126 Perez-Ctrceles, Osuna, Vieira, Martinez, Luna

Table 4 Mean, SD, median, and range valuesfor the biochemicalparameters in group 7 formed using the following BMDP (biomedical
No cardiac disease-natural death computer) programs: simple analysis of fre-
(n = 6) quencies, one-way analysis of variance, mul-
Biochemical parameter Mean (SD) Median Range tivariate analysis, and discriminant analysis.
Myosin (giU/1) s
p
143
201
(96)
(248)
121
248
24-291
40-699
Myoglobulin (ng/ml) s 2112 (1564) 2025 452-4275 Results
p 2334 (1844) 2548 86-4425
vh 16 (18) 11 0-40 On staining with haematoxylin and eosin, 36
CK (U/1) s 5857 (5845) 5459 59-13100 (34.3%) cases showed no morphological signs
p 8515 (7476) 6780 220-18875
vh 14 (9) 11 7-32 of myocardial ischaemia. In 37 (35 5%) cases,
CK-MB (U/I) s 893 (871) 577 14-2328 specific signs of myocardial necrosis were pres-
p 3508 (3844) 2585 180-10100
vh 5 (4) 3 0-12 ent, while in 32 (305%) cases there were non-
LDH (U/I) s 5676 (8455) 1443 1-21010 specific signs, principally congestion and in-
p 4131 (5959) 2275 6-15820
Cathepsin D (UAbs/g protein) p 1730 (1570) 1540 130-4000 terfibrillar oedema. On staining with acridine
orange, 18 (17*1%) cases were classified as
s = serum; p = pericardial fluid; vh = vitreous humour.
strongly positive (+ +), six (5 7%) as positive
(+), and six (5 7%) as unclear.
The values (mean, SD, median, and range)
of the biochemical parameters in the seven
(LDH) was measured in serum and pericardial diagnostic subgroups are presented in tables
fluid. Myosin was measured in serum and peri- 1-4. The highest concentrations of CK, CK-
cardial fluid, but not in vitreous humour, as MB, myosin, and LDH in pericardial fluid
the first 50 determinations in this material were were seen in subjects who had died exclusively
negative. Cathepsin D was measured in peri- of cardiac causes. We also found elevated
cardial fluid. When initial determinations myosin and myoglobin concentrations in serum
showed concentrations of markers above the and pericardial fluid of subjects with no mor-
clinical range, the samples were diluted with phological signs of cardiac disease who died of
saline and stabilised with 3% albumin to adjust extensive multiple injuries.
the concentrations to within the clinical ranges One-way analysis of variance was used to
in serum. compare the mean values for the biochemical
Myosin was analysed by radioimmunoassay parameters in the groups. Postmortem interval,
(RIA) using monoclonal antibodies (sandwich the myosin concentration in serum, total CK,
method) purchased from Sanofi Diagnostic CK-MB, myosin, and LDH concentrations in
Pasteur (Marnes la Coquette, France); my- pericardial fluid were significantly different
oglobin was tested by RIA using Biomerica (table 5). Table 6 shows statistically significant
(Newport Beach, California, USA) myoglobin associations between the following variables:
kits; total CK and LDH activities were meas- age, sex, postmortem interval, survival time,
ured with ultraviolet spectrophotometry and and the diagnostic category, graded according
commercial kits (Boehringer Mannheim, to the groups described in Methods (lowest
Mannheim, Germany); CK-MB was assayed score assigned to subjects who died of definite
with an immunoinhibition technique using myocardial infarction; highest score assigned
commercial kits (Boehringer Mannheim); and to subjects who died of natural non-cardiac
cathepsin D activity was tested according to causes). The correlation matrix showed stat-
the method of Yamamoto et al"5; total proteins istically significant correlations between the
were measured by Biuret's reaction with re- diagnostic category and age (r = 0 508), post-
-

agents from Boehringer Mannheim. mortem interval (r= -0 272), findings on

Statistical treatment of the data was per- staining with haematoxylin and eosin (r=
-0-616), staining with acridine orange (r=
0709), and variables from the biochemical
investigations as follows: serum CK-MB: peri-
cardial fluid CK-MB ratio (r = 0 233) and con-
Table 5 One-way analysis of variance centrations of myosin (r = -0*33 1), total CK
Variable DF F (experimental) Probability (r= -0275), and LDH (r= -0292) in peri-
cardial fluid.
Age 6 13-3991 0-0000
Postmortem interval 6 3-4737 0 0037
Myosin (serum) 6 2-6932 0-0184
Myosin (p) 6 3-0129 0-0096 Discussion
Total CK (p) 6 4-2738 0-0007
CK-MB (p) 6 2-2951 0-0408 Before presenting a detailed analysis of our
LDH (p) 6 3-8971 0-0016 results, we will describe the relation between
p = pericardial fluid. the diagnostic subgroups. This relation was
defined by factors that influenced the results
of the biochemical test-that is, the degree of
myocardial ischaemia and variables such as
age, survival time, and postmortem interval.
Table 6 Statistically significant associations As expected, we found that age was closely
Variables X2 DF Probability related to the diagnostic subgroup, as most
7-90 2 0-0192
violent deaths occurred in young subjects. The
Age-sex
Postnortem interval-diagnostic category 31-54 12 0-0016 postmortem interval was also closely related to
Survival time-diagnostic category 49-30 12 0-0000 the diagnosis, representing an important source
Age-diagnostic category 43-76 12 0-0000 of bias. This was probably because legal nec-
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Biochemical assessment of acute myocardial ischaemia
ropsies were performed sooner after the patient
had died in a hospital or another centre than
after sudden death in the home, when a long
interval can ensue between the time of death
and discovery of the body.
Because biochemical markers reach the vit-
reous humour by simple diffusion from serum,
the concentrations in the former depend on
the persistence of markers in serum and their
molecular weight. In the present study we
found no significant differences between diag-
nostic subgroups with respect to the con-
centrations of some markers in serum, nor
were there differences in these markers in the
vitreous humour.
The highest concentrations of the markers
in pericardial fluid were found in subjects with
morphological evidence of myocardial isch-
aemia. This confirms one of our initial hy-
potheses: because biochemical markers reach
the pericardial fluid via passive diffusion and
ultrafiltration due to the pressure gradient,10 11 16
markers are detectable in this fluid before they
are detectable in serum in subjects with myo-
cardial ischaemia. Other factors are the release
kinetics of myoglobin, the myosin heavy chain,
and CK-MB. It takes at least one hour,'7-19 48
hours,20 and four to eight hours,'2 respectively,
for these markers to become detectable in
serum. Because of its large molecular weight,
myosin is characterised by delayed release in
contrast to other biochemical markers.
No significant differences in myoglobin con-
centrations were detected between the groups
on analysis of variance. This may have been
because myocardial ischaemia occurred con-
comitantly with agonal processes.2' A large in-
crease in this protein may also have been the
result of multiple injuries and general hyp-
oxia.22 24In these processes the amount of myo-
globin released by heart tissue appears to be
elevated in pericardial fluid, whereas the myo-
globin concentration in serum is elevated only
after skeletal muscle injury. The lowest con-
centrations were found in subjects who died
of natural, non-cardiac causes, a finding that
confirms the negative predictive capacity of
the myoglobin concentration.7 Any alterations
related to agonal, or to general traumatic or
non-traumatic, processes is reflected as an in-
crease in the concentration of this protein.
Therefore, the concentration of myoglobin
alone does not reliably distinguish between
cardiac and skeletal muscle damage.
Myosin concentrations increase in serum
when death is due to myocardial injury, or
following trauma involving massive destruction
of skeletal muscle. The lowest concentrations
of myosin are recorded after non-cardiac death,
whereas the highest concentrations in peri-
cardial fluid occur after sudden cardiac death.
Thus, myosin concentration in pericardial fluid
appears to be a suitable postmortem marker
for the diagnosis of myocardial damage. This
can be explained by the release kinetics of
myosin, as noted above. We found no myosin
in the vitreous humour, probably because of
the large size and molecular weight of this
protein.
Total CK and CK-MB isoenzyme activities
127
in the different fluids investigated were com-
patible with the findings reported in earlier
studies.8'-02526 Elevated concentrations of both
markers were observed, with greater increases
occurring in the pericardial fluid of subjects
who died of heart related causes. The activity
of CK-MB in pericardial fluid differed sig-
nificantly between subjects in whom the cause
of death was definite myocardial infarction and
subjects with signs of cardiac disease but who
died of violent causes. Other authors found
that an increase in MB isoenzyme activities
may occur after multiple injuries,810 27-32 or after
intense cardiac resuscitation.25 We concur with
Lachica et al8 that the determination of CK-
MB isoenzyme in pericardial fluid is helpful in
routine practice, in cases where there is doubt
as to whether death was non-violent and in
cases in which myocardial infarction needs to
be excluded.
The significant correlation between LDH
concentration in pericardial fluid and the post-
mortem interval (r=0-306) is consistent with
the results of Luna et al,33 who found an increase
in the CK and LDH activities in pericardial
fluid after death. These authors, however,
noted that during the first 34 hours after death,
the increase in enzymatic activity does not
interfere with the diagnostic value of the ana-
lysis. Survival time and cause of death give rise
to significant variations, which are not large
enough to interfere with the diagnosis of the
cause of death.
Stewart et al" measured CK, LDH, and
their isoenzyme activities in pericardial fluid at
necropsy to determine the efficacy of these
values in postmortem studies of myocardial
ischaemia. These authors established diag-
nostic categories based on the cause of death
and the degree of cardiac change. They found
raised cardiac enzyme activities in cases of
cardiac compared with non-cardiac death. En-
zyme activities were not statistically different
between cardiac cases with and without his-
tological evidence of infarction (occlusive cor-
onary artery atheroma only). However, when
all groups in the study were compared, the
highest values were found in subjects who died
violently, with intense agonal distress. This was
in agreement with previous reports by Luna et
al,910 who analysed pericardial fluid from 144
cadavers and found elevated CK and CK-MB
activities in subjects who had died of myo-
cardial infarction and who had a violent death.
Our results suggest that biochemical markers
are useful in cases in which the diagnosis is
made difficult by the non-specificity or lack
of morphological data; these markers are also
useful in ruling out myocardial ischaemia. Peri-
cardial fluid is the sample material of choice
for biochemical tests for the diagnosis of myo-
cardial infarction after death.
We thank Ms K Shashok for translating the original manuscript
into English.
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Biochemical assessment of acute myocardial

ischaemia.
M D Perez-Cárceles, E Osuna, D N Vieira, A Martínez and A Luna

J Clin Pathol 1995 48: 124-128

doi: 10.1136/jcp.48.2.124

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