Mechanisms Of Very Late Stent Thrombosis Research Articles

Very Late Stent Thrombosis in Drug-Eluting Stents New Observations and Clinical Implications.

Despite the reduction in stent failure with newer-generation drug-eluting stents, very late stent thrombosis (VLST) remains an unpredictable and potentially catastrophic complication of coronary revascularization procedures and is associated with high morbidity and mortality. Here, we present an updated overview of the latest advances in understanding the causes of VLST. Clinical studies that revealed potential risk factors and pathophysiologic studies on the mechanisms of VLST are discussed. Importantly, novel insights from recent advances in intravascular imaging are included. To date, there is no clinical guideline for VLST treatment. We propose an evidence-based recommendation that an intravascular-imaging-informed percutaneous coronary intervention strategy combined with optimized antiplatelet therapy is the foundation for successful VLST clinical management. Moreover, the future of VLST prevention, such as improved patient risk stratification and advances in addressing late stent failure, are also discussed.

Abstract 10073: Characteristics of Very Late Stent Thrombosis Assessed by Coronary Angioscopy and Histopathology of Aspirated Thrombus

Background: The mechanisms of very late stent thrombosis (VLST) have not been fully elucidated and may involve multiple factors. The aim of this study was to evaluate characteristics of VLST based on angioscopy and histopathology of aspirated thrombus. Methods: Coronary angioscopy was performed in all stent thrombosis cases to evaluate the culprit lesion. The mechanisms of VLST were divided according to two factors by angioscopic findings such as uncovered struts and neoatherosclerosis. Uncovered struts were defined as stent struts uncovered by neointima. Neoatherosclerosis was defined as stent struts covered by yellow neointima. Furthermore, aspirated material was collected for assessment of atherothrombotic characteristics in all cases. Results: From February 2011 to April 2015, emergency PCI for acute myocardial infarction was performed in 336 patients, with 13 of these cases due to stent thrombosis. Clinical characteristics of VLST patients are shown in Figure. In uncovered struts, all 3 cases were not on any antiplatelet therapy prior to VLST, whereas patients with neoatherosclerosis were taking at least one antiplatelet agents except for one case. In the presence of neoatherosclerosis, thrombus with atheroma material was aspirated in 5 of 10 cases despite there was no atheroma material in patients with uncovered strut. The time period of occurrence of VLST was significantly shorter in patients with uncovered strut compared with neoatherosclerosis (48.6±12.5 month vs. 84.3±6.9 month, p=0.03) In 13 case of VLST, peri stent contrast staining (PSS) was found in 1 case of each neoatherosclerosis and uncovered strut at the time of follow-up angiography. Conclusions: Discontinuation of dual anti platelet therapy was an important predictor for VLST, especially in patients with uncovered struts. However, most VLST weredue to neoatherosclerotic plaque rupture assessed by coronary angioscopy, which were also confirmed by histopathology of aspirated thrombus.

Very late stent thrombosis

Drug-eluting stents (DES) are effective in reducing neointimal proliferation and in-stent restenosis. However, the procedure is complicated by early and late stent thrombosis that is related to incomplete healing, leading to stent malapposition and incomplete reendothelialization. Stent restenosis results in significant mortality and morbidity and portends a poor long-term outcome. In this article, we review recent findings regarding the prevalence of late and very late stent thrombosis (VLST) and the mechanisms that may be at play. Long-term follow-up from large registry studies and randomized controlled trials of DES implantation have recently created an awareness of the persistence of VLST (0.26%/year) for up to at least 5 years. Recent findings utilizing intravascular ultrasound and optical coherence tomography have also provided important insights into the mechanism of VLST and suggest that delayed healing and neoatherosclerosis are important. Finally, the development of novel stent scaffolds and antiplatelet agents holds much promise for reducing the risk of VLST. DES implantation continues to be complicated by the risk of VLST. Recent insights into the mechanisms of this significant clinical problem have important implications in preventing VLST.