The domestic cat has not been used in studies of atherosclerosis, with
the exception of a single study published in 1970. We have further ev
aluated the susceptibility of the domestic cat to diet-induced atheros
clerosis, the ultimate intent being to discern the atherogenic risk du
e to lipoprotein lipase deficiency in an affected feline kindred with
a phenotype very similar to that of the human form of this condition.
We subjected a group of normal domestic oats to a moderately high-fat,
cholesterol-enriched diet (30% fat and 3% cholesterol) for a period o
f 2 to 8 months. Plasma lipid levels were monitored monthly. At the ti
me of killing, all organs and the entire vascular tree were removed, s
ectioned, processed, and stained with hematoxylin and eosin. The entir
e vascular tree was also stained with Movat's pentachrome and oil red
O (ORO) and assessed semiquantitatively (0 to 5+/5+) and quantitativel
y (mean intimal area and ORO positivity, mm(2)). Both blood lipid meas
urements (total cholesterol, high-density lipoprotein-cholesterol, tri
glycerides, and low-density lipoprotein-cholesterol) and vessel wall l
esion assessment (intimal area, mm(2)) were statistically elevated (p
< 0.05) in the cholesterol-fed cats as compared to those on a normal d
iet. The highest correlations obtained between blood lipid components
and vessel wall measures were the percent increase in triglyceride fro
m base line versus the ORO measurement or foam cell grade (r = 0.86),
and percent increase in triglycerides versus the intimal area in the l
ower abdominal aorta (r = 0.91). Similar relationships were found when
the intimal area in the brachiocephalic/subclavian vessels was correl
ated with the absolute triglyceride values (r = 0.85) or with the perc
ent increase in triglycerides (r = 0.83). Thus, we produced atheroscle
rotic lesions in the cat within 2 to 4 months on a cholesterol-enriche
d diet; blood lipid levels were highly correlated with lesional measur
ements in the vessel wall. This study will provide the basis for evalu
ation of the susceptibility of New Zealand lipoprotein lipase-deficien
t cats to diet-induced atherosclerosis.