34 
CARDIAC MODELS 
this time. The peak A-V difference for GOT oc- 
curred 3 hours post-infarction. LDH activity in 
both the arterial blood and the cardiac venous 
blood exceeded upper normal limits at 2 hours 
post-infarction, but a definite A-V difference 
was not seen until 3 hours. The peak A-V dif- 
ference occurred at 6 hours, the last time for 
which venous samples were obtained. The ratio 
of observed peak values to baseline values of en- 
zyme activity for CPK, GOT and LDH were 55, 
22 and 5, respectively. 
All 33 experiments in which CPK activity in 
mixed venous or arterial blood rose to abnormal 
levels, showed myocardial infarcts at autopsy. 
Five experiments, during which CPK levels did 
not exceed upper normal limits and in which 
myocardial infarction was attempted, failed to 
show any evidence of infarction at autopsy. In 1 
experiment in which CPK activity rose to ab- 
normal levels, no myocardial infarction was 
found. The possibility that an infarction was 
missed cannot be excluded. With this one excep- 
tion it appeared that myocardial infarction and 
CPK elevation were either both present or both 
absent. 
Figure 1 correlates serum CPK levels with 
EKG changes. It was found that changes in re- 
polarization in the electrocardiograms preceded 
elevations in CPK activity, but that elevations 
in CPK activity preceded abnormalities in depo- 
larization. By the time depolarization changes 
were manifest, CPK levels had exceeded 500 
mU/ml. 
Lactate levels were determined in the arterial 
and coronary sinus blood of 7 dogs, 5 with acute 
myocardial infarction and 2 without. The con- 
trol dogs showed no appreciable change in lac- 
tate levels in either arterial or coronary sinus 
blood throughout the course of the experiment. 
The 5 dogs with myocardial infarction were in- 
distinguishable from the control group in that 
none showed any change in coronary sinus lac- 
tate during the post-infarction period, com- 
pared to the pre-infarction period. It is empha- 
sized that the venous samples were mixed 
myocardial venous blood. However, as in the case 
of studies of enzyme levels, the coronary sinus 
catheter was advanced far into the proximal 
great cardiac vein to enhance selective venous 
drainage from the anterior aspect of the left 
ventricle, where the infarcts were produced. 
The results of hemodynamic measurements in 
6 infarcted dogs and in 2 sham operated dogs 
are summarized in Figure 2. The CO, SV, EF, 
dp/dt, EDV and ConI all show a fall with re- 
spect to control values 2Vi hours post-infarc- 
tion, and at a comparable time in the sham op- 
erated dogs. At the same time both the 
infarcted group and the sham operated group 
demonstrated increases in HR and increases in 
LVEDP. The infarcted group, in general, 
showed these changes to a greater degree. The 
most distinct difference between the 2 groups, 
however, is seen in the data obtained 3 days fol- 
lowing myocardial infarction or sham opera- 
tion. In the former group there was a return 
toward normal but the preinfarction values 
were never achieved. In the sham group, these 
variables returned closer to or even beyond con- 
trol values. The single variable which became 
most abnormal 2V2 hours following infarction 
and which showed the least tendency to return to 
normal 3 days later was LVEDP. 
It can be seen that not only in the infarcted 
dogs but in the sham operated dogs, general de- 
terioration of hemodynamic state was apparent 
at the 2V2 hour point. Anesthesia, surgical ma- 
nipulations, withdrawal of blood samples and 
injection of Hypaque into the coronary arterial 
system were the major factors which the sham 
group shared with the infarcted group, and 
which were found to influence the hemodynamic 
state. Of interest is the observation that in this 
group of infarcted dogs where 15 to 25 percent 
of left ventricular mass was destroyed, the he- 
modynamic deterioration at 2V2 hours or at 3 
days was not more profound. 
Our pathologic findings consisted of two cate- 
gories — the myocardial, in which examination 
was oriented to mapping the size and location of 
the myocardial infarction, and the coronary ar- 
teries, in which presence and severity of vascu- 
lar damage and presence and extent of intra- 
vascular thrombosis were studied. The upper 
limit of the locations of infarcts was the ante- 
rior aspect of the left ventricle approximately 
midway between the coronary ostium and the 
apex of the heart. The lower limit was the apex 
proper, occasionally with involvement of the 
diaphragmatic surface of the apical region. The 
