The link between impaired fibrinolytic function and CHD has been reinforced considerably in the past couple of years. This has been achieved by a combination of epidemiological, clinical, cell biological and molecular biological studies. The molecular mechanisms for the identified associations between more established risk factors for atherosclerotic disease and impaired fibrinolytic function now need to be disentangled to promote the design of specific drugs that may pave the way for intervention. The possibility that some of the observed relations are epiphenomena should also not be disregarded. The concept of genotype-specific differences in the susceptibility of the individual to common metabolic disturbances needs to be examined in greater detail. Basic research on the role of fibrinolysis in atherosclerosis and its thrombotic complications should be given high priority, because the modulation of fibrinolytic function is likely to become an important approach to prevention.