E. L. STANLEY, P. KEZDI AND R. K. KORDENAT 
165 
an excess of free fatty acids and depression of 
muscle contractility undergoes rapid dilatation, 
complete pump failure, and terminal arrhyth- 
mias. 
Cardiac arrhythmias, particularly those of 
ventricular origin, have been recognized in the 
experimental infarction in the dog since Harris 
noted the delayed development of ventricular 
ectopic rhythms. 1^ In the studies of Berglund 
et al., hemodynamic measurements prior to the 
ventricular fibrillation have not shov^^n any sin- 
gle pattern in the experimental coronary 
occlusion. Primary fibrillation without pump 
failure occurred in 50%, gradual failure with 
terminal arrhythmia in 20%, and combined 
failure and dysrhythmia in 30% of the series. 
However, not all ventricular arrhythmias are 
precursors to ventricular fibrillation (at least in 
the experimental animal). Idioventricular 
tachycardia, complicating ligation of the anter- 
ior descending coronary artery in the dog, oc- 
curred in 48% of the study by Logic. In no 
instance was spontaneous ventricular fibrilla- 
tion noted, probably since idioventricular tachy- 
cardia is not associated with early, closely cou- 
pled extrasystoles. Joison at al., using the bal- 
loon cuff model of coronary occlusion, noted the 
development of a multifocal ventricular tachy- 
cardia 1-3 days after experimental dog myocar- 
dial infarction ; only a small number of animals 
died of ventricular fibrillation and sinus rhythm 
was later restored.-*' These findings are similar 
to our results with the closed chest wire tech- 
nique. Also the idioventricular tachycardia, un- 
like other ventricular arrhythmias, rarely causes 
hemodynamic embarrassment since loss of 
atrial drive rarely becomes significant. 
The hemodynamic changes in experimental 
myocardial infarction will vary depending upon 
the technique utilized and the total left ventric- 
ular mass involved. Selective embolization of 
the circumflex artery with 0.2 cc mercury pro- 
duces a shock-like state and death of the animal 
within 48 hours. Misra et al. reported a de- 
crease of 40% in the systemic blood pressure, 
54% of cardiac output, and an increase of 28% 
in the heart rate with this technique.-- The 
magnesium helical wire method of Blair was 
used by Kezdi et al. to produce gradual obstruc- 
tion of the left anterior descending artery. This 
method resulted in a decrease in cardiac output 
of 15% , blood pressure of 12%, and a heart 
rate increase of 5%." The present myocardial 
infarction model resulted in greater hemody- 
namic alterations (CO. decrease 42% ) than our 
previous open-chest model, but does not result 
in shock and early death as the Lluch mercury 
model. Return toward control values occurs in 
the hemodynamic variables over several days in 
hearts with 26% of the left ventricle involved 
in the infarction. This is similar to the experi- 
ence of Hood et al. who demonstrated a de- 
creased response to inotropic stimulation and 
increased left ventricular end-diastolic pres- 
sures in spite of normal hemodynamics four 
days after acute anterior descending ligation. 
SUMMARY 
A small myocardial infarction while demon- 
strating significant hemodynamic deterioration 
is compatible with survival. The initial 48-hour 
mortality rate of 16% is similar to the more re- 
cent experience of coronary care units. The 
hemodynamic and electrophysiologic similari- 
ties of this experimental infarction model to the 
human conditions are noteworthy. Gradual in- 
tracoronary occlusion in the awake intact ani- 
mal, predictability of myocardial infarction, 
and the anatomical resemblance contribute to 
its usefulness in the study of drug effects on the 
electrical and hemodynamic alterations during 
infarction. Adaptation of this technique in the 
experimental laboratory should increase the 
knowledge of the pathophysiologic state exist- 
ing with acute myocardial infarction. 
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