Post-intervention IVUS is not predictive for very late in-stent thrombosis in drug-eluting stents

Abstract

Immediate post-intervention IVUS showing no malapposition does not guarantee an uneventful course after DES implantation.

Detection of Stent Underdeployment by StentBoost Imaging

“…Indeed, the underexpansion of the stent probably plays a more important role in restenosis and adverse clinical outcomes than stent malapposition itself. Prospective studies have shown that stent malapposition assessed by IVUS immediately following DES implantation was not associated with increased adverse clinical events . In addition, the frequency of stent underexpansion appears much higher than malapposition when assessed by IVUS (40% vs. 1–7%, respectively) .…”

Late acquired stent malapposition: why, when and how to handle?

“…A reasonable approach to avoid this conflict is to perform an IVUS guided post-dilatation, especially with DES, of lesions at high risk of suboptimal stent deployment; in such cases, a non-compliant balloon dilatation, using a balloon size that matches the media-to-media IVUS measurement, is recommended. w54 However, a post-intervention IVUS showing no SM cannot guarantee LASM with subsequent stent thrombosis 6. This may be appropriate for acute malapposition where, in most cases, the malapposition degree is mild.…”

“…w2 w3 Its clinical significance, that will be further discussed later, is related to the incomplete endothelialisation of the unapposed stent struts that may result in fibrin deposits and eventually stent thrombosis 5 . w4 w5 Although the exact role of SM in this potentially fatal complication is still unclear, there are enough data to support the proposal that SM is implicated in at least some of the cases 6 7…”

Genetic determinants of adverse outcome (restenosis, malapposition and thrombosis) after stent implantation

“…Subacute and acute ST are classically related to procedure Genetic determinants of adverse outcome after stent implantation REVIEW parameters such as stent underdeployment (acute SM) [67,68] or procedure-related complications such as coronary dissections [69,70]. By contrast, (very) late ST appears to be an active phenomenon associated with late SM (persistent or acquired) [9,71], stent type [9], duration of dual antiplatelet therapy [66] and inflammation [58]. Gene variations in the platelet aggregation pathway, responsiveness to clopidogrel or presence of inherited thrombophilic disorders were a ssociated with both acute and late ST.…”