38 
CARDIAC MODELS 
FiGUEE 4. — Section of 3-day old lesion. Arrow indi- 
cates area of bleeding and cellular infiltration into 
medial layer of artery. Epicardial aspect of artery is 
seen in upper left. 
one or neither of these factors. The mechanism 
by which electric current caused the arterial le- 
sion remains unexplained, although thermal ef- 
fects were excluded to our satisfaction. The de- 
pendence upon degree of blood flow reduction 
thwarted our ability to prescribe a specific 
amount of total electrical energy necessary to 
cause thrombosis. 
The sequence of the evolution of the electro- 
cardiographic pattern of myocardial infarction 
followed the classical changes, but at a much ac- 
celerated rate, and was stabilized in the so- 
called chronic pattern within 12 hours. Two 
kinds of arrhythmias, always ventricular, were 
found. The early group subsided within 2 hours, 
were potentially lethal, but were easily con- 
trolled with intravenous lidocaine. The group of 
late ventricular arrhythmias appeared after 
about 1 hours of quiescence and lasted for as 
long as 8 days, were typically innocuous, and 
were also extremely resistant to control with in- 
travenous lidocaine. The segregation of ar- 
rhythmias into early and late with a definite 
quiescent period between them was observed 
very frequently, and remained unexplained. It 
was not related to the size of the myocardial in- 
farction. 
Comparison of 3 cellular enzymes, released 
into the circulation, LDH, GOT and CPK, re- 
vealed the CPK to be the most sensitive accom- 
paniment of infarction from the standpoint of 
the ratio of peak levels to baseline levels. Fur- 
thermore, whenever myocardial infarction was 
found, serum CPK activity rose to abnormal 
levels. Reversible myocardial injury, as judged 
Figure 5. — Section of 4-day old lesion. Epicardial as- 
pect of artery is seen in upper left. 
