Ruptured Neoatherosclerosis as Source of Late Stent Thrombosis

Summary

Neoatherosclerosis has been termed to define neointimal atherosclerotic changes occurring within a coronary stent [1,2]. Based on histological [2] and angioscopic studies [3], rupture within the neointima has been reported in the long-term after coronary stent implantation and has been proposed to be responsible for late and very late stent thrombosis. More recently, optical coherence tomography (OCT) with high discriminating power has been proposed to characterise this phenomenon in daily practice [4,5].

Case Report

We report the case of a 72-year-old man presenting with anterior ST-elevation myocardial infarction 2,833 days after bare-metal stent implantation (Multi-link Vision, Abbott Vasc, 3.5 × 28 mm) in the mid portion of the left anterior descending coronary artery. The coronary angiogram (Figure 1A) demonstrated an occlusion at stent (S) entrance. Percutaneous coronary intervention was readily performed and the aspiration thrombectomy permitted a restoration to a normal coronary blood flow (Figure 1B). Subsequently, an OCT imaging (DragonFly catheter, LightLab Imaging, St. Jude Medical) demonstrated “spongiform” neoatherosclerosis due to redundant intraintimal neovascularisation (Figure 1D–G) with ruptured thin-cap fibroatheroma, and reactive “cauliflower” thrombosis (Figure 1H–I). Histology of the aspirate demonstrated area of nicely delineated neointimal hyperplasia attached to the thrombus (Figure 1K–L, Movat pentachrom staining). Some sparse foamy macrophages are present within the restenotic area, close to the thrombus area and in larger number in the weak part of the plaque (Figure 1M, HRP Anti Macrophage [MAC387] staining). The lesion was then treated with balloon angioplasty with nice angiographic end-result (Figure 1C).

Stent thrombosis is a rare but devastating event. Very late stent thrombosis (>1 year after stent implantation) is a specific entity, mainly encountered after implantation of first-generation drug eluting stents with an observed rate at 0.6% events/year [6]. This rare condition is usually due to hypersensitivity reaction associated with delayed endothelial healing, exaggerated positive vessel remodeling and incomplete stent apposition [7]. Nevertheless, some cases might be due to the rupture of the neointimal tissue. Indeed, and although in-stent restenosis is generally considered as a stable process, growing evidence—as illustrated here—tends to challenge this concept. In this case and in analogy to de novo atherosclerotic plaque, the presence of abundant microvessels seems to be a key player in the neointimal plaque vulnerability.