E. L. STANLEY, P. KEZDI AND R. K. KORDENAT 161 
Table II. — Hemodynamic Results Following Experimental Myocardial Infarction Produced by Helical Coil Insertion 
Anterior Descending (10 Dogs) 
Average Cardiac Output Lit/min. Heart Rate Stroke Volume MBP SCOT 
Control 4.2 115 B/min. 36 cc 127 mm Hg — 
8 hour 2.8 155* 18 cc* 115 mm Hg — 
24 hour 2.2* 195* 12 cc* 81 mm Hg 452 
48 hour 2.3» 177* 13 cc* 95 mm Hg 330 
Left Circumflex (11 Dogs) 
Cardiac Output Heart Rate Stroke Volume MBP SCOT 
Control 3.2 96 33 128 mm Hg — 
8 hour 2.4 170 14 cc* 90 mm Hg — 
24 hour 2.1 168* 13 cc* 91 mm Hg 152 
48 hour 2^8 158* 19 cc* 98 mm Hg 94^ 
♦ p < 0.02 
The hemodynamic values recorded in 21 dogs that survived at least 48 hours following the acute mycardial infarction produced by occlusion 
of the helical coil. 
Rapid Luminal Occlusion 
In eleven animals the effects of rapid occlu- 
sion v^^as evaluated by the infusion of a 0.1% so- 
lution of palmitic acid into the coronary artery 
shortly after release of the helical coil wive 
(Table III). One hundred mgms of the Crysta- 
line fatty acid* was dissolved in 100 cc of nor- 
mal saline heated to 50° centigrade. Two cc of 
the mixture were slowly injected (one min.) 
through the inner catheter just proximal to the 
helical coil while the ECG was continuously 
monitored. Small amounts of radio contrast 
media were used to determine the time of com- 
plete occlusion. 
In nine animals 2-4 cc of the palmitic acid, 
when injected proximal to the helical wire, pro- 
duced immediate occlusion at the wire site. 
Seven of the nine animals died immediately 
with acute dilatation of the heart in either ven- 
tricular fibrillation or electrical standstill. Two 
* Matheson, Coleman, and Bell — Norwood, Ohio 
Table III. — Rapid Occlusion of a Helical Wire with 
0.1 % Palmitic Acid 
Palmitic Acid 0.1% 
No. Dogs 
Anterior 
Descending 
Left 
Circumflex 
Total 
With wire 
Without wire 
Thrombosis 
Time of Death 
Immediate 
Later 
ECG Changes 
Ventricular Fibrillation 
AV Diassociation 
Asystole 
11 
9 
2 
9 
1 
4 
5 
1 
5 
4 
4 hr. 
3 
1 
2 
5 
30 min. 
Injection of 0.1% palmitic acid at the helical wire resulted in 
immediate occlusion and sudden death. Listed are the time of death 
and the terminal arrhythmia event. 
animals survived the acute occlusive procedure 
but died 30 minutes and four hours later, re- 
spectively. At post mortem examination the hel- 
ical wire was completely occluded while the ar- 
tery distal to the wire site was patent in all 
animals. 
In two animals the fatty acid solution was in- 
jected without a helical coil wire being present. 
After 20 cc total injection was made during a 
10 minute period, the ECG showed typical ST-T 
wave changes of acute ischemia progressing to 
arrhythmia and death. No occlusion of the 
major branches of the arteries was seen at post- 
mortem examination. 
Prolongation of Luminal Occlusion 
In 17 dogs the effect of preheparinization 
upon the time of luminal occlusion at the wire 
site was evaluated. The standard technique of 
cut down, double catheter placement, and wire 
releases were followed ; the only exception being 
the injection of 4,000 units of sodium heparin 
I.V. just prior to the release of the helical coil. 
The animals were evaluated by daily ECG's, 
SGOT levels, and visualization of the left coro- 
nary artery by injection of dye into the branch 
containing the helical coil. 
In ten animals the wire was placed in the an- 
terior descending branch and in seven animals 
into the circumflex branch (Table IV). The se- 
rial selective visualization of the coronary 
branch showed gradual narrowing of the ar- 
terial lumen at the site of the coil progressing 
to complete occlusion. In eight animals the 
blockade was complete within the first 24 hours 
after wire insertion. In seven animals the time 
