836 
ANATOMY AND PATHOLOGY 
developing diet-induced atherosclerosis appli- 
cable to the more leisurely course of spontane- 
ous disease? 
A partial answer to the first question may 
of course be found in surveys of the vessels of 
animals which have reached middle and old 
age on diets which are not bizarre.'^ But this 
answer is not easy to attain. Wild-caught ani- 
mals are always of uncertain age, and probably 
only a few reach anything near their potential 
lifespan. Breeding of captive animals has been 
achieved on a significant scale only in the last 
few years, and the pressure for terminal experi- 
mental use and expense of maintenance will en- 
sure that few captive-born animals will live out 
a life of the order of 40 years. 
Furthermore, wild diets and inexpensive lab- 
oratory chows probably differ, in the opposite 
direction with respect to fat and cholesterol, 
from the average Western human diet as much 
as do laboratory atherogenic diets. 
A partial answer to the first question which 
may be drawn from our own files is equivocal. 
We have not seen a single instance of damage 
to heart, brain or kidneys which could be attrib- 
uted to atherosclerotic vascular insufficiency. 
However, the aorta and renal and coronary ar- 
teries do show cellular intimal thickening which 
increases with age (Fig. 12). The internal elas- 
tic lamella becomes fragmented and duplicated, 
but foam cells, lipid deposits, necrosis and cal- 
cification have not occurred. We can therefore 
conclude, from a very small sample, that rhesus 
monkeys do in time develop arterial intimal 
thickening similar in some respects to that seen 
in human vessels. The documentation of the full 
natural history of this thickening will require 
many years and many animals. We have so far 
had the opportunity to examine only 8 post- 
pubertal rhesus monkeys of known age, the 
oldest of which was 14 and the rest 7 or less ! 
As Dr. Stout has indicated,^ case reports of 
clinically significant atherosclerosis in zoo pri- 
mates will remain for some time our source of 
confidence that monkeys and apes are appropri- 
ate models. 
The answer to the second question about modi- 
fying the course of spontaneous atherosclerosis 
lies too far in the future for consideration here. 
Congenital cardiac anomalies 
The utility of congenital heart disease in ex- 
perimental animals as a model lies rather more 
in identification of causes rather than docu- 
mentation of anatomical variations and ex- 
perimental manipulations of the disordered 
dynamics of flow. Malformations do occur in 
nonhuman primates, but descriptions of only 
eleven naturally occurring cases have been pub- 
lished, all unexpected findings at postmortem.'^ 
Wild animals with clinically important anom- 
alies probably do not survive long, and more 
cases will doubtless be found as the population 
of captive-born animals increases. 
At the Oregon Center only one spontaneous 
anomaly has been noted. A wild-born Japanese 
macaque (Macaca fuscata), 6 years in residence 
and the mother of 2 infants, recently died in 
severe right heart failure. She had almost no 
interatrial septum (failure of the septum pri- 
mum) (Fig. 13). An enlarged heart had been 
noted radiographically 6 years before death. 
There was nothing in a routine autopsy to sug- 
gest a generalized genetic syndrome, but no 
biochemical or chromosomal studies were made. 
The two children are fortunately available for 
further observation. 
Figure 12. — Intimal thickening, with elastosis, in the 
aorta of an adult female rhesus monkey. Verhoeff-van 
Gieson, 50x. 
