Key result
OCT identifies VLST causes in >97% of cases, commonly revealing stent malapposition or neoatherosclerosis rupture.
Why the study?
What are the pathophysiological mechanisms and predictive factors of very late stent thrombosis?
What are the pathophysiological mechanisms and predictive factors of very late stent thrombosis?
This review highlights that younger age, smoking, STEMI, and overlapping stents are predictors of very late stent thrombosis, with OCT identifying mechanisms like malapposition and neoatherosclerosis rupture in over 97% of cases.
Supports OCT-guided VLST evaluation; leaves open whether targeting malapposition or neoatherosclerosis reduces recurrence.
Very late stent thrombosis ( VLST ) represents a rare, but potentially lethal complication, in the era of percutaneous coronary intervention. Its etiology, pathogenesis, and predictive factors have not yet been established due to its relatively low prevalence and multifactorial nature. In this review article, after presenting the current definitions on stent thrombosis, we focus on the contemporary data on VLST , for both bare‐metal stents and drug‐eluting stents. Possible pathophysiological mechanisms and predictive factors are also illustrated, with data drawn from several multicenter studies. Factors such as younger patients, smokers at the time of initial DES implantation, STEMI or the presence of thrombus at the time of initial DES implantation, overlapping stents, seem to represent independent predictors of VLST . Finally, there is a special reference on cases of VLST , studied with optical coherence tomography ( OCT ). OCT managed to identify the cause of VLST in over 97% of the cases in these studies, whereas some of the most common mechanisms of VLST in these patients were stent malapposition, neoatherosclerosis rupture, uncovered struts, and stent underexpansion.
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Kafkas et al. (2018) conducted a review in Very late stent thrombosis. Optical coherence tomography identified the cause of very late stent thrombosis in over 97% of cases, with common mechanisms including stent malapposition and neoatherosclerosis rupture.
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