JACOB I. HIRSCH, FRITZ STREULI AND FRED GORSTEIN 
33 
human clinical cases. We also observed a mark- 
edly accelerated course of evolution of the pat- 
tern of infarction compared to clinical human 
cases. Q waves of diagnostic dimensions were 
typically well established in 3 to 4 hours follow- 
ing myocardial infarction, and by 8 to 12 hours 
all remnants of injury currents had usually dis- 
appeared. In none of our experiments did my- 
ocardial infarction produce supraventricular 
arrhythmias, atrio-ventricular block or intra- 
venticular block. 
A number of interesting and somewhat puz- 
zling observations should be mentioned. In 6 
experiments S-T segments were observed to re- 
main elevated for 3 hours until the time of sac- 
rifice, and no myocardial infarction was found 
at a time when early changes of infarction 
should have been evident. In 5 of these 6 cases 
serum enzyme levels did not exceed normal lim- 
its, lending further support to the anatomic ob- 
servation. Continued S-T segment elevation for 
3 hours is therefore not necessarily an indica- 
tion that acute infarction has occurred. In 1 ex- 
periment, only, a large transmural infarct was 
unaccompanied by any changes in ventricular 
depolarization. On the other hand, 2 cases in 
which scattered focal myocardial necrosis was 
found were accompanied by pathological Q 
waves. In the most interesting and inexplicable 
case, diagnostic Q waves appeared despite the 
absence of infarction pathologically and the ab- 
sence of rise above normal of the CPK. 
Ventricular arrhythmias ranged from prema- 
ture contractions to ventricular fibrillation. 
These arrhythmias were clearly separable into 
two groups, early and late. The early arrhyth- 
mias characteristically made their appearance 
15 to 30 minutes after the appearance of injury 
currents and subsided in IV2 to 2 hours. These 
were found to be potentially lethal, but typically 
were easily suppressed by prompt administra- 
tion of intravenous lidocaine. The group of late 
ventricular arrhythmias typically made their 
appearance about 2V2 to 3 hours following coro- 
nary occlusion after an intervening quiescent 
period of a V2 to IV2 hours. These arrhythmias 
persisted for 1 to 3 days, were extremely resist- 
ant to control with intravenous lidocaine but 
with 2 exceptions were non-lethal and well 
tolerated.^-'' 
In our initial experiments, the levels of 3 en- 
zymes, creatine phosphokinase, glutamic 0x0- 
loacetic transaminase, and lactic dehydrogenase 
were measured in the arterial blood and in the 
myocardial venous drainage. The latter samples 
were obtained from catheters in the proximal 
great cardiac vein to favor insofar as possible 
venous drainage from the region of infarction. 
Table I demonstrates the average levels of en- 
zyme activity of 6 dogs that sustained large my- 
ocardial infarctions. The time of onset of acute 
myocardial infarction in this table and in all 
our experiments was defined as that time in 
which the electrocardiogram first showed a cur- 
rent of injury which persisted. CPK activity in 
the cardiac venous blood showed a small but 
definite rise 1 hour following zero time, thus de- 
fined. From 2 hours onward the arterial blood 
levels were elevated well into the abnormal 
range. Maximum A-V difference across the my- 
ocardium occurred at 3 hours. In contrast, the 
GOT level in cardiac venous blood had risen sig- 
nificantly by 2 hours post-infarction. Arterial 
blood levels were also minimally elevated by 
Table 
I. — Enzymes 
(mil /ml) 
(Average of 6 
chronic 
dogs with large 
myocardial infarction) 
CPK 
GOT 
LDH 
TIME 
TO MI 
ART. 
cs 
CS-A 
ART. 
cs 
CS-A 
ART. 
CS 
CS-A 
—3 hrs. 
67 
60 
— 7 
10.1 
12.9 
+ 2.8 
197 
198 
+ 1 
-IV2 " 
56 
52 
— 4 
13.4 
12.7 
— 0.7 
150 
190 
+ 40 
-Vz " 
55 
53 
— 2 
13.0 
15.7 
+ 2.7 
154 
168 
+ 14 
0 
ACUTE MYOCARDIAL INFARCTION 
+1 " 
74 
98 
+ 24 
19.0 
20.5 
+ 1.5 
166 
192 
+ 26 
+2 " 
323 
514 
+191 
46.0 
61.0 
+ 15.0 
276 
290 
+ 4 
+3 " 
1221 
1678 
+457 
114 
140.0 
+26.0 
471 
573 
+102 
+4% " 
2166 
2320 
+154 
180 
200.0 
+20.0 
764 
868 
+104 
+6 " 
2578 
2823 
+245 
247 
254.0 
+ 7.0 
788 
930 
+142 
+7% " 
2814* 
253 * 
831* 
+9 " 
3326* 
264 * 
841* 
+24 " 
1750* 
146 * 
382* 
* Mixed venous (instead of arterial) samples 
