138 
CARDIAC MODELS 
Dr. Stanley : What was the pressure during 
and before pulsation in the aortic route? Do 
you happen to remember the diastolic pressure? 
This is quite critical as far as coronary flow is 
concerned. 
Dr. Chatterjee: Yes. Well I don't remember 
it exactly right now. 
P. N. Sawyer, State University of New York, 
Downstate Medical Center, N.Y. : As I guess 
all of you know. Dr. Dennis and a number of 
his confreres have studied the dog and other 
animals as cardiogenic shock preparations. 
We've been asked to attempt to salvage fifty 
humans using counterpulsation techniques. 
About twenty different parameters of cardiac 
output and performance were studied following 
their going into cardiogenic shock. We found 
that there is the following angiography in this 
group of patients : First, by the time a human 
has gone into cardiogenic shock, he has, in es- 
sence, no functioning coronary artery left. Sec- 
ondly, any support mechanism that we have 
tested (including partial left heart total by- 
pass, or inter-artery balloon pumping) im- 
mediately resulted in an improvement in pa- 
tients for whom this modality was successfully 
instituted. In this group of patients and in our 
combined group study with the cooperation of 
ten schools, there has still been an 80% mor- 
tality and, in our hands, a 95% short-term 
mortality, and nearly a 100% long-term mor- 
tality. This gives rise to the basic conflict of 
interest here insofar as our experimental ani- 
mals give us some basic information, but we 
still do not have an animal preparation that 
corresponds in any way to the human prepara- 
tion. I believe this leads to another obvious 
comment. At this point, I think almost every- 
body has reached the conclusion, as has Dr. 
LaFarge, that some form of permanent left 
ventricular replacement or support should take 
the load permanently off from the essentially 
non-functioning human left ventricle. This will 
be necessary to save the majority of human 
patients whom we see in cardiogenic shock. 
Dr. Chatterjee : I don't wish to comment. 
Chairman : I would like to comment on this 
since Dr. Chatterjee does not wish to. I call 
your attention to an article, which I cannot cite 
exactly for you, by Alexander Leaf at the Mas- 
sachusetts General Hospital, that appeared in 
the American Journal of Medicine last year 
and is concerned with the mechanism of cell 
death due to ischemia and edema. It discusses 
the mechanism that you suggested, i.e., the con- 
cept of a critical opening pressure in a vessel 
which is occluded both by the disease process 
and by the edema which results in transient 
ischemia following that process. It is compar- 
able to some sort of self-perpetuating decreased 
coronary flow. It has also been clinically ob- 
served at the Massachusetts General Hospital 
where the Kantrowitz or rather the Avco bal- 
loon counterpulsation was repeatedly used 
(and is used now in a number of patients) that 
the same phenomenon occurs, although I don't 
know the effect on coronary collateral circula- 
tion in humans. It is certainly evident that the 
same kind of long-term unexpected and unex- 
plained benefit occurs in terms of decreased 
lactate production and increased coronary flow. 
It certainly results in clinical improvement, i.e., 
restoration of what one would consider to be 
clinical parameters of recovery. Now this is 
not always obtained, but it suggests that at 
least the critical opening pressure reoxygena- 
tion of areas which are in borderline ischemia 
and suffering thereby, together with a sort of 
self-perpetuating process, may indeed be part 
of the mechanism. How this affects coronary 
collateral circulation has yet to be seen. 
Dr. Sawyer: I concede that, but why do 80% 
of them die? That is, I concede, since that is 
exactly what we have found. They all display 
improved lactate metabolism, they all display 
improved cardiac output, they all display im- 
proved systolic pressures, they all have effective 
increased workloads and decreased diastolic 
pressures and they all die. 
Chairman La Farge : Well, that is true. They 
don't all die, but a very significant percentage 
are assisted for a very short period of time and 
this is why there is the considerable interest in 
using this technique. First of all, it gives you 
the time to deal with a patient — time which 
was not available previously. Secondly, in that 
period of time not only standard or newer meth- 
ods of drug treatment can be applied, but cor- 
onary angiography can be done as well, and the 
differential diagnosis between small vessel dis- 
