JACOB I. HIRSCH, FRITZ 
Figure 6. — Metallic salts appear as irregular black 
granules throughout thrombus mass. 
by the electrocardiogram, was not accompanied 
by CPK release. CPK release was deemed to be 
a clinical sine qua non for myocardial necrosis. 
Shell et al. have compared quantitatively the 
size of myocardial infarction in the dog with 
the total CPK released, and these were found to 
agree closely.^ 
SUMMARY 
In summary, our hemodynamic measure- 
ments in anesthetized dogs revealed a general 
depression of cardiac function immediately fol- 
lowing myocardial infarction. This did not re- 
turn completely to the pre-infarction status 
after 3 days, in contrast to sham operated ani- 
mals. The most markedly disturbed of these 
variables was the LVEDP, which, after 3 days, 
STREULI AND FRED GORSTEIN 39 
I remained clearly beyond normal limits. This is 
in agreement with the observation made by 
i Kumar et al. in conscious dogs.^*' It is of inter- 
est that with a substantial loss of left ventricu- 
lar mass, cardiac function at rest returned to 
near pre-infarction levels, and that the eleva- 
tion of LVEDP was the result of a reduction in 
left ventricular compliance. 
Pathologic examination of the myocardial in- 
farctions which were produced revealed a wide 
variation in their size, despite the fact that the 
site of occlusion was fairly circumscribed 
around the mid LAD coronary artery, and de- 
spite the fact that these arteries were of quite 
similar size. Under these circumstances, the 
single most important determinant of infarct 
size from one animal to another seemed to be 
the unique anatomy of the coronary arterial 
Figure 7. — Thirty-minute old thrombus. Epicardial as- 
pect of artery is in upper left corner. 
