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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Prof. J. Wouter Jukema
View the Slides from this session in ESC Congress 365
This session on past and current stent failure, chaired by J.W. Jukema (Leiden, NL) and F. Alfonse Manterola (Madrid, ES), included interactive presentations that combined the latest preclinical and clinical data relevant for the daily practise of (interventional) cardiologists.
First, Prof. Michael Joner (CV Path Institute,USA and Deutsches Herzzentrum Muenchen, DE), presented a lecture on “Stent thromboisis: is it still a problem?” He clearly demonstrated that stent thrombosis (ST) is multifactorial in nature and represents a clinical manifestation of differential failure modes such as early ST – most recently related to procedural failure modes and increased acute thrombogenicity (e.g device-related, procure related or patient related) andlate ST. Delayed arterial healing plays a central role here and is also the cause of neoatherosclerosis, vasomotor dysfunction and late restenosis.
This lecture was followed by Prof. A. Colombo (Milan, IT), who highlighted a number of structural stent issues, both for drug-eluting stents (DES) and for the newly developed biodegradable scaffolds. He discussed how you should and should not combine these devices, based current knowledge and practical experience. It clear that new biodegradable scaffolds at present cannot fully replace drug-eluting stents, certainly not for complex (e.g bifurcation) lesions and that the need for adequate dual antiplatelet therapy persists with these new scaffolds.
Next, R.A. Byrne (Deutsches Herzzentrum, Technische Universitat, Munich, DE) presented his data on “can we predict who is at risk for stent failure”. He clearly showed that:• patient, procedural/vessel and stent-related risk (e.g first generation DES) factors exist for ST; • for early stent ST, procedural/vessel-related factors dominate; • for late ST stent-related and patient related (e.g. DM, low LVEF, presence of malignancy) factors dominate; • premature discontinuation of P2Y12 receptor antagonists is one of the most prominent predictors; • newer imaging methods (e.g. combined OCT/NIRF) offer potential to better risk stratify and tailor treatment.
In the final lecture G. Guagliumi (Bergamo, IT), highlighted the differences of in-stent-restenosis (ISR) and (peri)stent neoatherosclerosis (SNA). SNA is now with the second generation DES becoming more and more apparent and sometimes presents us with clinical sequel, such as plaque rupture and new myocardial infarctions. How much this new problem of SNA can be influenced/stopped by profound lipid lowering is a matter of ongoing debate and research.
All in all this was an interesting and very well attended interactive session that provided us with evidence and practical guidelines on how to prevent, recognise, and influence stent (scaffold) failure of past and new devices in daily practice.
Stent failure: update on mechanisms and treatment
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