Atherosclerosis is a chronic inflammatory disease of the arterial intima, characterized by accumulation of lipoproteins and accompanying inflammation, leading to the formation of plaques that eventually trigger occlusive thrombotic events, such as myocardial infarction and ischemic stroke. Although many aspects of plaque development have been elucidated, the role of extracellular vesicles (EVs), which are lipid bilayer-delimited vesicles released by cells as mediators of intercellular communication, has only recently come into focus of atherosclerosis research. EVs comprise several subtypes that may be differentiated by their size, mode of biogenesis, or surface marker expression and cargo. The functional effects of EVs in atherosclerosis depend on their cellular origin and the specific pathophysiological context. EVs have been suggested to play a role in all stages of plaque formation. In this review, we highlight the known mechanisms by which EVs modulate atherogenesis and outline current limitations and challenges in the field.