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Br Heart J 1984; 51: 399-406
Myocardial infarction related to coronary artery bypass
graft surgery
C G A McGREGOR,* A L MUIR, A F SMITH, H C MILLER, W J HANNAN, E W J CAMERON,
D J WHEATLEYt
From the Departments of Clinical Surgery, Medicine, Clinical Chemisny, and Medical Physics, University of
Edinburgh, and the Departments of Cardiology and Cardiac Surgery, Royal Infirmary, Edinburgh
SUMMARY Fifty consecutive patients undergoing coronary artery bypass grafting for chronic stable
angina were assessed by serial electrocardiography, preoperative and postoperative myocardial scanning
with technetium-99m pyrophosphate, gated radionuclide ventriculography, and serial measurement
of creatine kinase, aspartate aminotransferase, urea stable lactic dehydrogenase, and
creatine kinase isoenzyme (MB) to assess the incidence of perioperative myocardial infarction and
identify the most appropriate diagnostic techniques. The correlation between myocardial scanning
and the measurement of peak enzyme and isoenzyme activity was excellent in the diagnosis of
perioperative infarction, although electrocardiography proved less helpful. There appeared to be no
advantage in measuring creatine kinase MB rather than the more routinely measured enzymes.
There were two deaths and evidence of myocardial infarction in five other patients, an incidence of
14%. Perioperative infarction was associated with a significant reduction in resting ejection fraction
in two cases. In those patients without evidence of perioperative infarction the mean increase in
ejection fraction of 7.80/o was statistically significant.
Myocardial infarction related to coronary artery
bypass graft surgery is associated with increased mortality
and morbidity and accounts for most deaths
perioperatively and within the first month of operation.
‘ The incidence of this complication is difficult to
estimate, and figures of 4-40% have been reported.2-4
The varying incidence can be attributed to variations
in operative expertise, techniques of myocardial protection,
case selection, and particularly to the diagnostic
indices of myocardial infarction applied in different
series.5-7
The assessment of chest pain and interpretation of
the electrocardiogram in the diagnosis of myocardial
infarction after cardiac surgery are difficult.8-’0 An
increase in the activity of enzymes, including the rela-
Requests for reprints to Dr C G A McGregor, Department of Cardiovascular
Surgery, Stanford University School of Medicine, Stanford
University Medical Center, Stanford, California 94305, USA.
*Present address: Department of Cardiovascular Surgery, Stanford University
School of Medicine, Stanford University Medical Center, Stanford, CA 94305,
USA.
tPresent address: Department of Cardiac Surgery, University of Glasgow, Royal
Infirmary, Glasgow.
Accepted for publication 27 October 1983
tively cardiospecific MB isoenzyme of creatine kinase
(CKMB), occurs after cardiac surgery, and the ability
of plasma enzyme measurements to distinguish those
patients who have had a myocardial infarction related
to coronary surgery remains uncertain.” - ‘3 Other
diagnostic techniques include radionuclide imaging
with technetium-99m pyrophosphate, which in a
non-surgical context is a sensitive and specific indicator
of myocardial infarction.14 15 Furthermore, this
technique may be the only method of making the
diagnosis after coronary surgery in some
patients. 16- 18
Severe myocardial infarction is likely to be associated
with impairment of left ventricular function, and
a comparison of left ventricular performance before
and after operation using radionucide ventriculography
is a further method of assessing myocardial
injury.
In the present study the above techniques were
used in 50 patients undergoing coronary artery bypass
surgery. Our aim was to identify the most appropriate
techniques for diagnosing perioperative myocardial
infarction. Once the incidence of perioperative infarction
and the most accurate methods of diagnosis have
been determined, the effect of improved methods of
399
McGregor, Muir, Smith, Miller, Hannan, Cameron, Wheatley
myocardial preservation may be assessed.
Patients and methods
Fifty consecutive patients undergoing coronary artery
bypass graft surgery as the sole procedure were
studied. All underwent operation for the treatment of
chronic stable angina uncontrolled by optimum medical
treatment. All patients were being treated with
beta blockers. Their age range was 36-68 (mean 52)
years.
OPERATIVE TECHNIQUES
Standard cardiopulmonary bypass techniques were
used at flow rates of 2*4 1/M2. The mean bypass time
was 114 minutes (range 53-224 minutes), and the
mean aortic cross clamping time 36 minutes (range
0-72 minutes). The mean number of grafts performed
was 2-1 per patient (range 1-4). Intermittent aortic
cross clamping with systemic hypothermia to 28°C
was used in 24 patients and cold potassium cardioplegic
arrest with topical cardiac cooling and systemic
hypothermia to 28°C in 26. The method of myocardial
protection used was based on the current practice of
the surgeon performing the operation.
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ELECTROCARDIOGRAPHY
Electrocardiograms were recorded preoperatively and
daily postoperatively until discharge and were assessed
blind by a cardiologist. The appearance of new Q
waves of 0-04 s or more duration was regarded as
indicating myocardial infarction.
ENZYME MEASUREMENT
Creatine kinase and aspartate aminotransferase were
measured by standard techniques. ‘9 The upper limit
of normal for non-ambulant healthy subjects is 150
U/I and 30 U/I respectively.
Creatine kinase MB was measured using a slight
modification of the chromatographic method of
Mercer,20 using kit reagents supplied by Boehringer
Corporation, Lewes. The upper limit of normal for
non-ambulant healthy subjects is 10 U/1.
Urea stable lactate dehydrogenase was measured
using a slight modification of a previously published
method.2′ The upper limit of normal for healthy
adults is 300 U/1.
Analytical precision was 5% (coefficient of variation)
for enzyme activities for each enzyme in the
ranges encountered in this study. The above enzymes
were measured preoperatively and on seven subse-
P <0001
a
A6
P<0 001
a
a
P<0.001
a
a
A
:1
a Pc<0001
~~~~~ -Ml
Normcil
I 1-~~~’ range
CKMB CK AST USLD
Fig. 1 Peak serum enzyme activities (expressed as a multiple ofthe upper limit ofnormal)
for creatine kinase MB (CKMB), creatine kinase (CK); aspartate aminotransferase
(AS7), and urea stable lactate dehydrogenase (USLD).
A, patients with both positive myocardial scan and positive enzyme activity; 0, remainder
ofpatients. p values refer to comparison of individual enzymelisoenzyme activities between
five patients with both positive myocardial scans and positive enzymeslisoenzyme activity
and the remaining patients.
400
*0 *
Myocardial infarction related to coronary artery bypass graft surgery
quent occasions in the first 48 hours postoperatively:
immediately and at 3, 6, 9, 12, 24, and 48 hours after
operation.
STATISTICAL ANALYSIS OF DATA
The definition of a normal response of plasma enzyme
activity to coronary artery surgery is difficult. Fig. 1
shows that of the peak measurements for each enzyme
a few were higher than the rest. To obtain an objective
but, purely arbitrary, definition of normal and
abnormal increases in enzyme activity, the following
procedure was adopted for each enzyme:
(1) All enzyme values were log transformed
(since even the central and left hand portions of the
frequency distribution curves showed a log normal
rather than a normal distribution).
(2) The central symmetrical portion of the distribution
curve (trimmed) was used to yield provision
estimates of mean and standard deviation
(SD).22
(3) Means and standard deviations for each
enzyme were calculated using all enzyme measurements
except for those which were more than 2
SD above the trimmed mean (from (2)).
Any enzyme measurement more than 2 SD above
the mean was classed as being abnormally high. This
figure was 109 U/I for creatine kinase MB, 2600 U/I
for creatine kinase, 190 U/I for aspartate aminotransferase,
and 800 U/I for urea stable lactate dehydrogenase.
MYOCARDIAL SCANNING
Analogue and digital images were obtained two hours
after an intravenous injection of 400 MBq (10-8 mCi)
of technetium-99m pyrophosphate in the anterior, 300
and 600 left anterior oblique, and left lateral projections
with the patient supine using a Nuclear Enterprises
Mk 5 HR gamma camera.
Forty eight patients who were available for study
had scans performed between two and five days postoperatively,
and in 34 patients scans were also performed
preoperatively. All scans were assessed blind
by two observers and were graded into: (a) those
showing no activity (-), (b) those showing increased
activity over the region of the heart but of less intensity
than surrounding bone (+), and (c) those with
increased activity over the heart of equal or greater
intensity than bone (+). Only category (c) was
accepted as a true positive for myocardial infarction
and had to be present in two of the four views.
RADIONUCLIDE VENTRICULOGRAPHY
Radionuclide ventriculography was carried out
preoperatively and one week postoperatively at rest in
34 of the 50 patients. All studies were carried out with
patients supine using a 30° left anterior oblique projection
with a 100 caudal tilt on a Nuclear Enterprises
Mk 5 HR gamma camera. The method of analysis has
been described in detail elsewhere.23
Results
All 34 preoperative technetium myocardial scans were
negative. Preoperative enzyme activity was not
appreciably increased in any of the 50 patients. Two
deaths occurred in the immediate postoperative
period of low cardiac output. Both patients were considered
to have suffered myocardial injury at the time
of operation which was incompatible with maintaining
circulation. Of the 48 patients surviving operation,
36 had no evidence of myocardial infarction
when any of the criteria used in the study were
applied.
Table 1 shows the results for the remaining 12
patients who had evidence of myocardial infarction by
at least one criterion. Table 2 summarises the positive
Table 1 Evidence ofmyocardial infarction in 50 patients after coronary artery bypass graft(s) using technetium-99mpyrophosphate
scanning, electrocardiography, and enzyme measurements
Case No Myocardial scanning Electrocardiography Enzyme activity
CKMB CK AST USLD
1 + + + + + +
2 + + + + + _
3 + - + + + +
4 + - _ _ _ _
5 - + _ _ _ _
6 - + - - - +
7 + - + + + +
8 - - + _ _ _
9 - + _ _ _ _
10 + + + + + +
11 - - + - - -
12 - - - - + -
CKMB, creatine kinase MB; AST, aspartate aminotransferase; USLD, urea stable lactate dehydrogenase; -, negative; +, positive; +, scans
showing increased activity over-the region of the heart but of less intensity than surrounding bone.
401
McGregor, Muir, Smith, Miller, Hannan, Cameron, Wheatley
Table 2 Swmary of results of myocardial scanning, measurement ofenzme actitity, and electrocardiography in 12 patients with
evidence of myocardial infarction after coronary artmy bypass grafting
No ofpositive results ECG changes
Scans Enzymes
CKMB AST USLD Total
Myocardial sans 5 5 5 4 5 3
Electrcardiographic
changes 3 3 3 3 3 6
Enzyme measurements 5 6 4
CK, creatine kinase; AST, aspartate aminotransferase; USLD, urea stable lactate dehydrogenase.
findings of the diagnostic tests used. In Tables 2 and 3
the results in those patients with isolated increases in
activity of only one enzyme and in whom there was no
evidence of infarction by any other criterion were
omitted.
Five patients had positive myocardial scans. All five
had enzymatic evidence of infarction in at least three
of the four enzyme measurements including creatine
kinase MB isoenzyme. Three of the five patients
fulfilled the electrocardiographic criterion of infarction.
One further patient had a scan of diffuse appearance
(giving a ± result) which did not correlate with
the other criteria.
Six patients had electrocardiographic changes indicating
myocardial infarction, but in only three (the
same three as above) did this correlate with scanning
and enzymatic evidence of infarction. Six patients had
enzymatic evidence of myocardial infarction. Five of
these patients had positive scans. Four of the patients
had positive electrocardiographic evidence, but in one
(case 6) the enzymatic evidence consisted of an isolated
increase in urea stable lactate dehydrogenase
activity.
Table 3 outlines the changes in resting ejection fraction
during the operative period in those patients with
evidence of infarction. Of the five patients with both
scanning and enzymatic evidence of infarction, the
ejection fraction remained the same in three and
decreased by 0.1 and 0*18 in the remaining two
patients, the greatest reductions in the entire group.
In the two patients in this group with negative electrocardiograms
the ejection fraction decreased by 0-1
in one and was the same in the other (+0.01). The
mean reduction in ejection fraction in these patients
was 12-1%, although this was not statistically
significant compared with the preoperative value in
this small group of patients. In the two patients with
isolated positive creatine kinase MB activity and a
negative scan and negative electrocardiogram ejection
fraction increased by 0-1 and 0 12 respectively. In the
two patients with positive electrocardiograms and
both negative scan and negative enzyme/isoenzyme
activity ejection fraction increased in one and was the
same in the other. In the one patient with a positive
electrocardiogram and isolated positive urea stable
lactate dehydrogenase activity ejection fraction was
Table 3 Changes in resting ejection fraction assessed by radionuclide ventriculography in 11 patients with evidence of infarction by
myocardial scanning, measurement ofenzymatic activity, and electrocardiography
Case No Before surgery After surgery Change
Positive scans and positive enzyme activiy
1 0-49 0.5 +0-01
2 0-49 0.45 -0-04
3 0-4 0-41 +0-01
7 0-38 0.28 -0.1
10 0.59 0-41 -0-18
Positive enzyme activty, negative scans, and negative ECG
8 0-53 0-63 +0-1
11 0-4 0.52 +0-12
Positive ECG, negative scans, and negative enzyne activity
5 0-4 0-52 +0-12
9 0-4 0-44 +0-04
Positive enezye (USLD) activity, positive ECG, and negative scan
6 0-63 0-57 -0-06
Equivocal scan, negative ECG, negative enzyme activity
4 0.52 0-57 +0.05
402
Myocardial infarction related to coronary artery bypass graft surgery
0)
C,
0 3 6 9 12 24 36 48
t L Hours after discontinuation of bypass J
Before
operation
Fig. 2 Mean (geometric) activity of creatine kinase MB at
t’arious times in the postoperative period for patients with infarcts
(A) and those without (*).
reduced by 0-06. When the five patients with positive
scans and positive enzymes are excluded, there was a
significant mean increase in ejection fraction in the
remaining patients of 7.80/o in relation to preoperative
values (p<0-05). Improved detection of wall motion
abnormalities by phase analysis may be helpful in
diagnosing perioperative infarction, but this method
was not available to us at the time of the study.
Measurements of activity of each of the four
enzymes in the five patients with both positive scans
and positive enzymes were compared with those in the
remaining patients using the Mann-Whitney U test of
ranking (Fig. 1). There was no difference between the
enzymes in their ability to differentiate between these
five patients and the remainder. The timing as well as
the magnitude of creatine kinase MB release were different
in these five patients compared with those in
the remaining patients (Fig. 2). Peak creatine kinase
MB release occurred between nine and 12 hours after
operation in these five patients but at about three
hours in the others. Only creatine kinase MB has this
notable qualitative difference in the shape of the
release curve.
There was no significant difference between these
five patients with positive myocardial scans and positive
enzymes and isoenzymes activity and the remainder
of the group in age, cross clamping time, cardiopulmQnary
bypass time, number of coronary grafts
performed, or, with one exception, length of stay in
hospital.
Discussion
Myocardial infarction after coronary artery bypass
graft surgery may result from early graft closure,
technical failure, or embolisation from the site of
anastomosis or from global myocardial ischaemia
secondary to cross clamping at the aorta and inadequate
myocardial protection. Coronary artery surgery
can, therefore, result in myocardial injury which varies
in both magnitude and type-that is, whether
transmural or global or a mixture of both.
Coronary surgery may improve left ventricular
function by restoring circulation to ischaemic
myocardium but if complicated by perioperative
myocardial infarction may compromise left ventricular
function. A balance of the two effects may be present
in any individual patient. For this reason we performed
ventriculography. Our own observations in
non-surgical myocardial infarction2425 and that of
others26-28 suggest that, although left ventricular
ejection fraction may fluctuate in the acute stages
(0-24 h) of myocardial infarction, cardiac performance
thereafter changes little but, in general, gradually
improves over the next three to six months. As
the patients in the present study were haemodynamically
stable without taking any positive inotropic
agent at the time of either ejection fraction determination
it was appropriate to image at this time and use
the observation to correlate with the other diagnostic
criteria of severe myocardial injury.
The likelihood of one particular test yielding a positive
diagnosis will depend on whether the infarction is
transmural or global and on the diagnostic threshold
applied to that test. Transmural infarction is more
likely to result in a positive electrocardiogram and
myocardial scan than a more diffuse lesion, whereas
measurements of increased enzyme and isoenzyme
activity should be obtained in both. There is, therefore,
no clinical gold standard for the diagnosis of
perioperative myocardial infarction. In this study the
criteria for a positive scan were set high purposefully
to avoid false positive results, but by doing this we
may have missed very small infarcts. Although we
attempted to be objective, the enzymatic and isoenzymatic
criteria of infarction are (as discussed) arbitrary.
In this study a good correlation was found between
radionuclide scintigraphic and enzymatic and isoenzymatic
evidence of myocardial injury. All five
patients with positive myocardial scans had enzymatic
and isoenzymatic evidence of injury. Agreement between
the positive scanning and positive enzymatic
criteria applied in the study was regarded as diagnostic
of myocardial infarction, and, therefore, these five
patients were considered to have had an infarction.
In two of these patients infarction was associated
403
McGregor, Muir, Smith, Miller, Hannan, Cameron, Wheatley
with a pronounced reduction in resting ejection fraction
as assessed non-invasively by radionuclide ventriculography.
In three patients there was little change
in ejection fraction, and this is consistent with reports
questioning the functional importance of perioperative
infarction in some patients.29 30 Nevertheless, in
two cases perioperative infarction resulted in a pronounced
deterioration in cardiac function with a
reduced ejection fraction, and in one case the patient
was in hospital for three months because of low cardiac
output and subsequent renal failure. In the other
four patients with myocardial infarction hospital stay
was not prolonged. These results agree with those of
previous reports showing early and late reduction in
ventricular function in patients who have had a
perioperative myocardial infarction.3′ 32 In contrast,
those patients in the study who were not considered to
have had a perioperative infarction had a significant
increase in ejection fraction of 7-8%. It is difficult to
assess how much the withdrawal of beta blockade
affected the postoperative measurement of ejection
fraction, but some effect was present in patients both
with and without infarcts. In the two patients with
isolated isoenzymatic evidence of infarction and negative
enzymes, a negative myocardial scan, and negative
electrocardiogram no functional deterioration
occurred, and the results support the findings of
others that isoenzyme activity may be too sensitive in
assessing perioperative myocardial infarction when
used alone.3334 The one patient with an equivocal (±
result) scan had a diffuse increase in uptake over the
precordium, which was of lower intensity than that in
surrounding bone, and the importance of this appearance
is uncertain.6 15 Patients without coronary disease
may show such an appearance. Simultaneous
measurement of perioperative enzyme activity helps
to elucidate this problem. There were no positive
preoperative scans, and this may reflect the fact that
our patients had chronic stable angina. Provided that
agreement between scanning and enzymatic evidence
is accepted as proof of myocardial infarction, in this
study there were no false positive scans, which is similar
to the results of other workers.’ 33 Such patients
with chronic stable angina do not seem to need to be
studied preoperatively in contrast to other groups of
patients-that is, those with unstable angina, in
whom the incidence of positive preoperative scans
may be as high as 400/o.16 35
The measurement of peak isoenzyme activity
proved to be a valuable adjunct to myocardial scanning
in this study and has been shown to correlate
well with other indices of myocardial injury, but its
sensitivity and relative advantages over the more
commonly measured enzymes are unclear.3 3637 An
important aspect of our study was the finding that
there was no advantage in measuring creatine kinase
MB isoenzyme rather than the more routinely measured
enzymes. For our laboratory we suggest that
measurements of creatine kinase total of 2600 U/I,
aspartate aminotransferase of 190 U/1, and urea stable
lactate dehydrogenase of 800 U/I represent myocardial
infarction, although the frequency and timing of sampling
must be taken into account. These findings will
vary for different types of cardiac operations and between
centres. The time of peak activity of creatine
kinase MB in this study differed between patients
with and without infarcts, being nine to 12 hours after
operation in those with infarcts and three hours in
those without. For routine purposes, it is difficult to
justify the requirement for measuring creatine kinase
MB.
The electrocardiogram was positive in three of the
five patients with scanning and isoenzymatic evidence
of injury. Of the other three patients who developed
new Q waves, their appearance was transitory in two
and persisted in one. These findings are consistent
with previous reports of Q waves which do not persist
and false positives which have been attributed to
unmasking of old infarcts by restoring a normal circulation
to an ischaemic contralateral ventricular wall.38
Q waves also occur in patients in whom an improvement
in regional wall motion in the relevant area has
been observed,39 although others have found no evidence
that the appearance of new Q waves was not
due to myocardial infarction.3′
Many surgical considerations may affect the incidence
of perioperative myocardial infarction. In this
study both techniques of myocardial protection were
used in the group with an infarction. There was one
death and one infarct in patients in whom cold cardioplegia
was used and one death and four infarcts in
the group who had aortic cross clamping with systemic
hypothermia. In the present study there was no
relation between the incidence of perioperative
myocardial infarction and cardiopulmonary bypass
times or number of coronary grafts performed, which
agrees with some previous reports4041 but contrasts
with others.3042
As well as resulting in an increase in operative mortality
perioperative myocardial infarction has been
shown in a recent report from the Coronary Artery
Surgery Study42 to result in a significant reduction in
the three year cumulative survival rate. In that study
perioperative infarction was diagnosed by the
development of new postoperative Q waves, and these
workers acknowledge that this may represent an
underestimate of the true incidence. Accepting that
the concordance of scanning and enzymatic evidence
is indicative of myocardial infarction, the incidence of
perioperative infarction in the current study was 14%,
including the two patients who died in the immediate
postoperative period. It is crucial to estimate the inci-
404
Myocardial infarction related to coronary artery bypass graft surgery
dence of perioperative myocardial infarction in order
to assess the early and late results of coronary artery
surgery and to allow surgeons to monitor the effectiveness
of currently used methods of myocardial protection.
The combination of myocardial scanning and
the measurement of enzyme activity can give a high
degree of accuracy in this sometimes difficult diagnostic
problem.
This study was carried out with the support of
research grants from the Lothian Health Board and
Scottish Hospital Endowment Research Trust.
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