Most cardiovascular events result from a thrombotic complication of an atherosclerotic lesion. Inflammation plays a central role in both the pathogenesis of atherosclerosis and the progression of its complications (especially plaque rupture). Fibrinogen, on the one hand a marker of inflammation and on the other a major determinant in thrombosis and haemorrheology, plays a central role in atherosclerosis and its thrombotic complications. The clinical data are in agreement with epidemiological data, and show that increased plasma fibrinogen levels (compared with values in paired controls) are predictive of the risk of cardiovascular events - both primary cardiovascular events in the general population and recurrence in patients. Determining the plasma fibrinogen level in terms of genetic predisposition and environmental factors provides a good example of the interrelationship between genes and the environment. It must be recognised that a minimal increase in the fibrinogen level (within the plasma reference values) is an indicator of a significantly increased risk. This shows why epidemiological data are not useful for determining cardiovascular risk in individual patients in daily clinical practice (with the exception of the very high levels that are infrequently observed).