Appeal No. 94-4009 Paper No. 32
Application No. 07/953,716 Page 11
increase in thickness. At this stage, the lipid composition
of the intima consists mainly of phospholipids (lecithins,
cephalins and sphingomyelins; [cited pages not of record]).
Some cholesterol is present, but cholesterol esters are
generally absent.
We find nothing in Bowman that shows that atherosclerotic
intimal thickening necessarily precedes other contributors to
atherosclerosis like hyperlipidemia or hypercholesterolemia.
We do, however, find a reasonable suggestion that it was
conventional to delay both the development and the progression
of atherosclerosis by treating hypercholesterolemia and
hyperlipidemia (Bowman at 23.62, col. 2 ("Treatment of
atherosclerosis")).
Even if we accepted Appellants' narrower construction
that treatment must occur before any atherosclerotic intimal
thickening had occurred, Appellants identify hyperlipidemia as
a promoter of smooth muscle cell activation (Paper No. 1
(Spec.) at 2). Consequently, Fujikawa's hyperlipidemia
patients would inherently be treated for atherosclerotic
intimal thickening. Note that, since the claimed treatment
begins prior to atherosclerotic intimal thickening, the
patients are still healthy in terms of intimal thickening.
Consequently, the clinician would have to have had some reason
to suspect that the patient would benefit from prophylactic
treatment for intimal thickening. At the hearing, we asked
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