110 
CARDIAC MODELS 
tion showed that this pattern corresponds to in- 
farction of the anterior, lateral, and septal part 
of the left ventricle as well as of the posterior 
part of the apex and a small part of the right 
ventricular wall, (b) Only one animal diifered 
from pattern (a) although the ECG changes 
had a similar time sequence (see Figure 3) : the 
S-T segment was elevated in leads I, II, aVL, 
V.s, and Vy and depressed in leads III, aVR, and 
Vi. A Q wave was observed in leads I and V5, 
whereas the amplitude of the R wave decreased 
in Vi and V3. This pattern, corresponding to an 
infarction of the lateral aspect of the free wall 
of the left ventricle, was confirmed at autopsy. 
At 3 days an inverted T wave was observed in 
leads II, III, and aVF; however, since it was 
also seen in the control tracing, it may be unre- 
lated to ischemia and may represent an abnor- 
mal repolarization pattern sometimes seen in a 
small number of intact rhesus monkeys. 
Right bundle branch block (RBBB) was ob- 
served in 18 animals after snare ligation. Ap- 
parently the conduction defect did not aifect 
survival and occurred about equally in both the 
"Alive" and "Dead" groups. In most cases, it 
was evident in the one-hour recording after in- 
farction; however, a few animals did not de- 
velop RBBB for several hours. 
Premature ventricular beats v/ere common 
immediately after coronary occlusion, but the 
most serious and frequent arrhythmia was ven- 
tricular fibrillation, 1 to 9 episodes of which oc- 
curred in 18 animals. Ventricular fibrillation 
was noted in 2 animals about 24 hours after li- 
gation; the other 57 episodes were observed 
within 40 minutes after coronary occlusion. 
These arrhythmias were successfully termi- 
nated with D.C. countershocks. Ventricular fib- 
rillation did not appear to affect survival; 35 
episodes occurred in 11 of the 15 (73%) surviv- 
ing monkeys and 24 episodes in 7 of the 11 
(63%) animals of Group I. 
Hemodynamics. The hemodynamic changes 
were more severe in the animals in Group I 
than in Group II (Figure 4). The aortic flow 
dropped to 45% of the control values shortly 
after coronary ligation and did not rise above 
50% of the control values throughout the sur- 
vival period. The aortic mean pressure fell to 
about 60% of the control values, rose in some 
cases to within 75 % of the control values about 
one hour after ligation, and then progressively 
declined until death. In Group II animals, the 
aortic flow dropped to about 65 % of the control 
values immediately after coronary ligation but 
generally never below 55% at any time during 
the experiment. The aortic mean blood pressure 
fell initially to about 75 % of the control values ; 
afterwards, it rose earlier and more rapidly 
than in Group I animals to about 80 to 85% of 
the control values and remained relatively sta- 
ble thereafter. 
The values of pulse pressure, left atrial pres- 
sure, and heart rate considerably overlapped in 
Groups I and II animals with no significant dif- 
ferences between the two. Of interest was the 
heart rate observed in the "control" period, 214 
± 15 and 211 ± 14 (mean ± S.D.) in monkeys 
of Groups I and II, respectively. 
Systolic, diastolic, and mean blood pressure 
and aortic flow were utilized in the discriminant 
analysis. Ten data arrangements were analyzed 
(Table I). In data arrangement #1, all values 
were selected at the time of the lowest diastolic 
blood pressure recording during the 30-minute 
post-ligation period with blood pressure values 
expressed in mm. Hg. The function obtained for 
the "Alive" and "Dead" groups was, respec- 
tively : 
La = -21.400 + .296W + .44X - .302Y 
+ .320Z 
Ld = -10.156 + .233W + .128X - .178Y 
+ .186Z 
(see Methods for symbols) . 
Data arrangement #1 correctly predicted 
100% (11 out of 11) of the monkeys dying 
from myocardial infarction with shock and 
93% (14 out of 15) of the monkeys surviving 
more than 12 hours. 
Pathology. A large myocardial infarct was 
found in every animal that survived at least 12 
hours after ligation. The distribution of ne- 
crosis was fairly constant ; nearly all of the apex 
and higher sections up to the level of the liga- 
tion in the anterior and the lateral walls of the 
left ventricle, the anterior half to two-thirds of 
the septum, and a small part of the anterior 
right ventricular wall. Generally a narrow zone 
of subendocardial muscle remained viable. How- 
ever, in one case the necrosis extended to the 
