Several treatment strategies, including lowering low-density lipoprotein cholesterol with intensive statin therapy, reducing triglycerides with fibrates, and raising high-density lipoprotein cholesterol with nicotinic acid, have the potential to induce atherosclerosis regression. Atherosclerosis imaging techniques including intravascular ultrasound, carotid ultrasound to measure carotid intima-media thickness, and cardiovascular MRI are established modalities for describing longitudinal changes in the quantity and quality of atherosclerotic plaque. An increasing number of clinical trials are using radiologic measures of subclinical atherosclerosis as surrogate end points in lieu of the traditional "hard" end points of myocardial infarction and death. This approach has great appeal, as improvements in atherosclerosis imaging now enable the characterization of early atheromas and positive remodeling within the vessel wall before the plaque becomes obstructive. Additional prospective data correlating these surrogate end points with hard outcomes are needed to determine whether atherosclerosis regression will be the major determinant of future treatment strategies.