Although retrospective case-control studies continue to indicate that plasma lipoprotein(a) [Lp(a)] concentrations are associated with coronary heart disease (CHD), several large population-based prospective studies have failed to confirm that Lp(a) is an independent risk factor. However, evidence exists from several studies to suggest that elevated plasma Lp(a) increases the CHD risk associated with more traditional risk factors. Although identification of the functional role of Lp(a) in atherogenesis has been thwarted by the physical, chemical, and genetic complexity of Lp(a), the structural similarity of Lp(a) to both the fibrinolytic proenzyme plasminogen and low-density lipoprotein (LDL) has suggested a prothrombotic or atherogenic role (or both) for this lipoprotein. Because the clinical determination and application of plasma Lp(a) concentration poses several challenges, we cannot recommend its routine measurement at this time. Rather, plasma Lp(a) determinations should be limited to either patients at high risk for the development of CHD or patients at borderline risk for the development of CHD in whom uncertainty may exist about how aggressively to treat modifiable risk factors such as elevated LDL cholesterol.