This is from one of the Pauling/Rath US patents (# 5,278,189)
Essentially all human blood contains lipoprotein(a); however, there can a thousand-fold range in its plasma concentration between individuals. High levels of Lp(a) are associated with a high incidence of cardiovascular disease. Armstrong, V. W., et al. (1986) Atherosclerosis 62: 249-257; Dahlen, G., et al. (1986) Circulation 74: 758-765; Miles, L. A., et al. (1989) Nature 339: 301-302; Zenker, G., et al. (1986). Stroke 17: 942-945 (The term occlusive cardiovascular disease will be used hereafter as including all pathological states leading to a narrowing and/or occlusion of blood vessels throughout the body, but particularly atherosclerosis, thrombosis and other related pathological states, especially as occurs in the arteries of the heart muscle and the brain.)
Prevention and treatment of occlusive cardiovascular disease with ascorbate and substances that inhibit the binding of lipoprotein (A)
http://patft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO2&Sect2=HITOFF&p=1&u=%2Fnetahtml%2FPTO%2Fsearch-bool.html&r=1&f=G&l=50&co1=AND&d=PTXT&s1=5278189.PN.&OS=PN/5278189&RS=PN/5278189
Now, the Pauling/Rath guinea pig experiments illustrated that Lp(a) (really apo(a)) rises in these vitamin C deficient animals after being deprived of their ordinary dietary vitamin C - leading to atherosclerosis, based on the sticky Lp(a). The latest Rath-team work with GULO-knockout mice (mice that cannot make their own vitamin C) illustrates the same thing. Lp(a) adapts the body for low vitamin C by increasing and thus strengthening otherwise weak arteries.