164 
CARDIAC MODELS 
tion in the coronary artery-^*^ At thoracotomy, 
a magnesium aluminum coil was threaded into 
the left anterior descending artery of dogs. 
Complete occlusion occurred in 5-7 days. This 
occlusion resembled the human process in that 
the intimal layer of the arterial wall was in- 
volved in the laminar thrombosis. Kezdi et al. 
reported that this myocardial infarction model 
was associated with a decrease in arterial blood 
pressure, cardiac output and maximum acceler- 
ation of aortic flow.^^ These hemodynamic pa- 
rameters returned toward the normal in several 
days. The slowly developing arterial occlusion 
permitted collateral circulation to develop 
which decreased the resultant myocardial in- 
farction size. 
While the helical coil model of Blair resem- 
bled the human condition, a prolonged interval 
until complete occlusion occurred and the peri- 
cardiotomy with its resulting ECG changes were 
undesirable. Selective release of the helical coil 
wire into a branch of the left coronary artery 
under fluoroscopic control by the described 
catheter technique removed the need for an 
open-chest procedure. By this technique the oc- 
clusive process, instead of gradual thrombosis 
over several days, proceeds rapidly within 24 
hours. The clot, while firmly attached to the 
wire, is not adherent to the intimal wall of the 
artery. Apparently injury to the arterial wall 
by wire penetration (Blair technique) results 
in gradual thrombosis while intra-arterial in- 
sertion develops rapid clotting. 
The time of arterial obstruction could be al- 
tered by drugs which prolong the clotting mech- 
anism. Single injections of Na heparin were 
effective in our model, whereas continuous anti- 
coagulation with heparin was required by Na- 
khjavan et al. in their study to retard the occlu- 
sive process. The steel cylinder sleeve used in 
their study permits less flow, has a greater sur- 
face area exposed to the blood elements, and has 
a different thrombogenic quality than magne- 
sium. The helical coil wire with its small sur- 
face area, nominal obstruction to flow, and slow 
tendency to clot requires little anticoagulation 
to prolong the time of obstruction. However im- 
mediate complete obstruction of the helical coil 
site can be achieved, when desired, by the use of 
long chain fatty acids. 
The phenomena of rapidly induced intravas- 
cular thrombosis by fatty acids is well recog- 
nized and has been visualized in the living ex- 
tracorporeal eye. Seaman et al.^- demonstrated 
the deposition of platelet aggregates with fibrin 
on both arteries and veins. In fact, a 0.1% solu- 
tion of sodium stearate may cause clotting in 
the syringe by precipitation of the contact acti- 
vation phase of the water fall sequence of 
coagulation. 13 These platelet aggregates may 
occur in less than one minute, require calcium 
ions, and are not inhibited by heparin. This 
very rapid occlusion was noted in our study. 
The consequences of immediate free fatty acid 
induced occlusion were catastrophic and en- 
tirely different from the gradual process of 
thrombosis. Mechanical contractions immedi- 
ately ceased, cardiac dilatation progressed rap- 
idly and mechanical electrical dissociation was 
noted. Sinus rhythm and the hyperacute is- 
chemic changes of the ST-T wave were present 
in the ECG for several seconds after absence of 
mechanical systole was noted on the fluoro- 
scopic screen. Either ventricular fibrillation or 
electrical asystole, neither of which responded 
to resuscitative measjres, was the terminal 
event. 
The association of elevated free fatty acids, 
arrhythmias and a high incidence of death has 
been reported in patients with acute myocardial 
infarction.^* The same authors (Oliver et al.) 
demonstrated that the elevation of plasma free 
fatty acids through activation of lipoprotein li- 
pase by heparin was associated with serious 
ventricular arrhythmias in dogs with acute my- 
ocardial infarction. 1^ More recently, Henderson 
et al. have studied the effects of free fatty acids 
on myocardial contractility during anoxia.^" 
While free fatty acids had no significant effect 
on isolated rat muscle strips under normal oxy- 
gen pressure, both hypoxic and anoxic muscles 
had a gradual decrease of contractility to S0% 
of the control level. This decrease of force de- 
velopment could be partially restored by addi- 
tion of calcium to the media, suggesting that 
the calcium available for the contractility proc- 
ess had been bound by the free fatty acid. These 
observations may partially explain the observed 
electrical-mechanical disassociation occurring 
in our model ; the suddenly hypoxic heart with 
