In-Stent Atherosclerosis at a Crossroads

• DOI: 10.1161/circulationaha.116.025129
• Publication Date: 2016-11-07T21:42:35Z
• Authors: Ioannis Andreou; Peter H. Stone
• Keywords: Drug-Eluting Stents; Coronary Artery Disease; Prosthesis Design; Coronary Vessels; Plaque, Atherosclerotic; 3. Good health; 03 medical and health sciences; Percutaneous Coronary Intervention; Treatment Outcome; 0302 clinical medicine; Metals; Risk Factors; Neointima; Humans; Stents

Accumulating histopathologic and intravascular imaging studies indicate that atherosclerosis development inside a coronary stent is a complication that may be identified as the substrate in a considerable proportion of late/very late stent thrombosis and restenosis cases.1 The frequency of in-stent atherosclerosis-related very late stent thrombosis is similar between early and new-generation drug-eluting stents but with considerably shorter implantation-to-thrombosis interval in the latter.2 Although in-stent atherosclerosis has recently been the subject of continued concern and investigation, the mechanisms of its development remain unknown. The prevailing hypothesis is that it occurs due to the formation of de novo atherosclerosis within the neointima, which has led to the widespread adoption of the term “neoatherosclerosis.” However, the underlying native atherosclerotic plaque might as well contribute to the pathogenesis of this disease entity, a hypothesis largely overlooked in recent reports. Our current understanding of in-stent atherosclerosis derives solely from pathological and retrospective observational clinical studies, which only provide a single snapshot of atherosclerotic lesion evolution. The term “neoatherosclerosis” has been adopted on the assumption that the atherosclerotic tissue within the stent does not communicate with the underlying native atherosclerotic plaque (ie, de novo atherosclerosis). However, whereas in autopsy studies it may be feasible to identify lesions without evidence of direct communication between the …