AbstractIt is gratifying to report the first observation of the amelioration of effort angina by the use ofhigh-dose L-lysine and ascorbate in a man with severe coronary artery disease (CAD). Thisregimen 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 postulatedmechanism correlates with the findings that apoliprotein(a) [apo(a)] has a striking homologyto plasminogen, and the Lp(a) accumulates in atherosclerotic lesions in the arteries of man (Rathet al., 1989) and the hypoascorbic guinea pig (Rath and Pauling, 1990a, 1990b) and in occludedbypass venous grafts (Gushing et al., 1989). It is hoped that the remarkable outcome in this singlecase will motivate clinicians to examine the efficacy of lysine and ascorbate in additional casesof refractory angina.