Case report: Lysine/ascorbate-related amelioration of angina pectoris

Abstract
It is gratifying to report the first observation of the amelioration of effort angina by the use of
high-dose L-lysine and ascorbate in a man with severe coronary artery disease (CAD). This
regimen was based on the hypothesis that, in thrombotic atherosclerosis, lipoprotein(a) [Lp(a)]
— size-heterogeneous, LDL-like particles displaying independent risk activity for CAD —
initiates plaque formation by binding to fibrin in the damaged arterial wall. This postulated
mechanism correlates with the findings that apoliprotein(a) [apo(a)] has a striking homology
to plasminogen, and the Lp(a) accumulates in atherosclerotic lesions in the arteries of man (Rath
et al., 1989) and the hypoascorbic guinea pig (Rath and Pauling, 1990a, 1990b) and in occluded
bypass venous grafts (Gushing et al., 1989). It is hoped that the remarkable outcome in this single
case will motivate clinicians to examine the efficacy of lysine and ascorbate in additional cases
of refractory angina.