Most people of old age in the western society have atherosclerosis to a greater or lesser extent; the condition can almost be regarded as a normal consequence of aging.1 Therefore, the clinical problem of atherosclerosis may be better described by the term “accelerated” atherosclerosis, which reflects the fact that some patients suffer earlier than most from an atherosclerotic process. It is this acceleration of atherosclerotic disease progression that is usually the subject of investigation.

Establishing the rate of progression of coronary atherosclerosis in patients is important as progression of the disease is one of the major factors that determines clinical prognosis.2 ,3 Therefore, identifying patients at risk for increased progression of coronary artery disease (CAD) is important as these patients might benefit from early (lipid lowering) treatment. Thus far, it has proved difficult to identify patients at increased risk when lipoprotein disturbances are moderate, which is the case for most patients seen in daily practice.

Another problem is that, although lipid lowering appears to retard progression of coronary atherosclerosis, not every patient benefits to the same extent from treatment—for example, in spite of intensive low density lipoprotein (LDL) cholesterol reduction and high density lipoprotein (HDL) cholesterol augmentation, a substantial percentage of the treated patients in the familial atherosclerosis treatment study,4 experienced progression of coronary atherosclerosis over 2.5 years. Even the introduction of a powerful class of lipid lowering agents, HMGCoA reductase inhibitors or “statins”, has not led to complete control of progression and its clinical sequelae.5 ,6

Consequently, we have two problems to face: how to identify patients at increased risk for progression of CAD; and how …