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Prof. Robert Gabor Kiss,
View the Slides from this session in ESC Congress 365
Read the ESC Practice Guidelines on Myocardial Revascularisation
Historically, Barcelona has been a hot spot for "breaking news" about drug-eluting stents (DES): Increased rates of late stent thrombosis were first reported at the ESC Congress held here in 2006. Fortunately, things have changed significantly and we now have a safe, new DES generation of new antiplatelet agents.
Pathophysiology of stent thrombosis was presented by Steffen Massberg (Munich, DE). The current view of intra-arterial thrombus formation is not far from the “fatal triad,” according to Virchow. However, some new aspects have emerged; immunothrombosis, the inflammatory face of thrombotic processes, and the NET matrix, based on externalized DNA coming into the extracellular space. This DNA-based net induces contact activation, platelet aggregation, inactivates local effect of anticoagulants, etc. In thrombi taken directly from a stent thrombosis, a large amount of neutrophil is trapped. Probably some forms of stent polymers are important in activating neutrophils as pivotal players in immunothrombotic mechanisms of stent thrombosis. Additionally, hypersensitivity reactions and eosinophilic leukocytes may play a role via direct coagulation activation and fibrin formation. Finally, a chronic inflammatory process can cause an accelerated local form of atherosclerosis called a neoatherosclerosis. Early stent thrombosis is a procedure related to bifurcation stenting, strut fracture, stent strut thickeness etc. Late stent thrombosis can be caused by delayed healing, malapposition and uncovered struts. Very late stent thrombosis might be caused by an abnormal local vascular response: neoatherosclerosis.
Stefan James (Uppsala, SE) elegantly covered stent thrombosis registry datasets from 2006 to the current SCAAR results presented by Christoph Varenhorst two days ago also here in Barcelona. Previously, the Bern/Rotterdam, the BASKET/LATE and the SCAAR 2006 results pointed out the true risk of late and very late stent thrombosis. First generagion DES, as we call them now, had small but relevant risk. Among them, Paclitaxel-coated stents performed worse than Sirolimus-based DES.The game has changed significantly since 2006. New anti-thrombotics came into practice after some pivotal trials in which the rate of developing stent thrombosis decreased significantly. Lessons learned from PLATO, TRITO-TIMI 38 and ATLAS-TIMI 51 trials revealed Ticagrelor, Prasugrel, Rivaroxaban as better options than Clopidogrel in this fight. We know have new generation DES with biodegradable polymers, better metallic structure and smaller vascular footprints. According to the SCAAR 2014 registry, the risk of any stent thrombosis of G2 DES groups are well below the risk of BMS implantations and G1 DES forms. On the other hand, completely biodegradable vascular scaffolds might face a rate of stent thrombosis as 0.9-3%.
Maria Radu (Copenhagen, DK) led us into stent imaging. Possible triggers of stent thrombis, such as stent thrombus, strut malapposition, vascular wall evagination/bulging, uncovered areas, positive remodelling or neoatherosclerosis can be visible with IVUS or OCT. Edge dissection was believed to be a major factor of stent thrombosis, but in a longitudinal follow-up series, late and very late stent thrombosis is very rare in this situation (1 in 256). By OCT, edge dissection is frequently detected at the time of the intervention, (26-46%). By angio, it could be seen in 1.7-6.4%, and in 7.8-19.3% by IVUS. One malapposed strut can be seen in 25-75% of the cases, but after 6 months, those healed completely in >35% of the cases. Neoatheroscleros is described in 30% of the cases examined by OCT at 420 days. It was overwhelmingly seen in Paclitaxel-eluting stents. In the contrary, major evaginations and bulging was seen almost exclusively in Sirolimus stents.
Stefanie Schulz from Munich summarized the current landscape of dual antiplatelet therapy (DAPT) duration issues in stented patients. She noted that we might not know the ideal length of DAPT even in BMS cases, there are not enough study results supporting the current guideline of one month DAPT. In DES the average stent thrombosis onset was 9 days after DAPT discontinuation, mirroring platelet turnover physiology. After more than 6-months, stent thrombosis occurred 104 days following the APD discontinuation, and mechanisms of early and late stent thrombosis must therefore be different.
In conclusion, using the current DES generation, stent thrombosis is rare and practically will not develop after one year.
New insights in stent thrombosis
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