Cerebrovascular and cardiovascular diseases constitute the most substantial disease burden worldwide and are only increasing in importance. Understanding how individuals with atherosclerosis may be better assessed for risk of stroke and myocardial infarction will have immense importance in deciding on therapeutic options. Carotid atherosclerosis is frequently portrayed as an orderly progression from asymptomatic plaque formation that enlarges with aging and culminates in either stable, calcified plaque or vulnerable, ruptured and inflamed plaque. New evidence suggests that atherosclerosis is better described as an equilibrium between synthetic and degradative processes. Putatively, plaques heal and decrease in size through processes such as efferocytosis in individuals unlikely to experience symptoms, whereas individuals who experience symptoms lack reparative mechanisms. Present clinically employed imaging strategies overlook plaque healing mechanisms. Other approaches that examine the downstream effects of plaque, rather than static plaque measurement, such as ultrasound emboli signal detection may address the gap between plaque that is vulnerable in appearance and that which is actually likely to cause symptoms. To ascertain the clinical risk of atherosclerosis optimally, both sides of the equation must be examined instead of relying on a unidirectional accumulative approach to atherosclerosis.