162 
CARDIAC MODELS 
Table IV. — Heparin Induced Prolongation of Helical 
Wire Occlusion Time of Occlusion (Day after Wire 
Insertion) 
Day of Occlusion 
1st 2nd 
Number of Dogs 
No 
3rd 4th Bth Occlusion 
Total 
Anterior Descending 
5 1 
12 0 
1 
10 
Left Circumflex 
3 1 
10 1 
1 
7 
Total 
8 2 
2 2 1 
2 
17 
% of Total 
47% 12% 
12% 12% 
5% 
Delay of the onset of the occlusion at the helical coil site by 4000 
units of heparin injected at the time of wire implant. No heparin 
given following the initial dosage. 
of blockade and infarction was delayed up to 
the fifth post-insertion day, while in two ani- 
mals no occlusion developed and the arterial 
lumen was patent up to ten days. 
In one of the animals which failed to demon- 
strate clot formation at the wire site the long 
chain free fatty acid (palmitic acid) was in- 
jected. After 4-6 cc of 0.1% palmitic acid solu- 
tion there was complete occlusion at the wire 
site, the ECG demonstrated hyperacute is- 
chemic changes, and the animal promptly fibril- 
lated (Figure 3). Resuscitation efforts were to 
no avail. At postmortem examination the clot 
was easily dissected from the helical coil wire 
but remained intact when placed in formalin. 
Histologic sectioning of the specimen showed 
the same type fibrin and platelet immeshed clot 
as was present in clots that formed under the 
more natural condition of gradual occlusion 
over 12-24 hours. 
Anatomical 
The postmortem examination of the hearts 
closely resembled the human condition. The hel- 
ical coil wire was completely occluded with clot 
but the vessel both proximal and distal to the 
blockade was patent. While the clot was firm 
and did not break up when manipulated by for- 
ceps, it could be easily teased away from the 
arterial wall. After 8-10 days the magnesium 
alloy began to disintegrate but at no time was 
the intima of the coronary artery involved in 
the pathologic process. Microscopic examination 
of the clot revealed mostly fibrin and platelets 
in a haphazard arrangement which never dem- 
onstrated the concentric laminar appearance of 
slowly progressive thrombosis formation. 
The myocardial infarction distal to the ar- 
terial occlusion involved the entire wall thick- 
ness with the wedge shaped distribution of that 
particular vessel. The animals dying early had 
only hemorrhagic changes of the myocardium 
while those sacrificed 10-14 days after infarc- 
tion showed thinning of the ventricular wall 
plus scar formation which permitted the infarc- 
tion to be easily demarcated from the viable 
surrounding myocardium. 
DISCUSSION 
Several authors have described methods for 
experimental production of acute myocardial 
infarction in the closed chest animals in order 
to attempt close resemblance of the human con- 
dition. Gensini et al. used microspheres to selec- 
tively occlude the left anterior branch, pro- 
ducing distal myocardial infarction with both 
hemodynamic and ECG changes.^ More recently 
Lluch et al. have injected a single dose of metal- 
lic mercury into the circumflex branch to pro- 
duce cardiogenic shock.*' Both of these models 
approximate human myocardial infarction; 
however the multiple blockade of small pe- 
ripheral vessels is anatomically different from 
the large vessel, gradually occlusive, process 
seen in the clinical condition. In 1968 Nakhja- 
van described a technique for insertion of a 
stainless steel cylinder into a branch of the left 
coronary artery.'^ Blood flow continued through 
the orifice for several hours if immediate clot- 
ting was prevented by anticoagulation. Signifi- 
cant arrhythmias, intra-ventricular conduction 
defects, and a 50% early mortality character- 
ized this model. Hood, in 1970, described their 
results in a method of coronary occlusion which 
employed a balloon cuff" device implanted about 
the coronary artery. They noted moderate left 
ventricular failure, a decline in cardiac output, 
and a 20% incidence of ventricular fibrillation.® 
The thrombogenic properties of several met- 
als has been recognized earlier and in 1951 
Stone and Lord suggested the use of magnesium 
alloys threaded into saccular abdominal aneu- 
rysms to promote thrombosis and thereby pre- 
vent leakage or rupture. Utilizing these ob- 
servations, Blair et al. in 1964 proposed a model 
of experimental myocardial infarction using 
magnesium alloys to promote thrombus forma- 
