Comprendre la thrombose grce lOCT Nicolas Amabile, MD, PhD Service - PowerPoint PPT Presentation

OCT : toute la lumière sur l’angioplastie Comprendre la thrombose grâce à l’OCT Nicolas Amabile, MD, PhD Service de Cardiologie, Institut Mutualiste Montsouris, Paris

DÉCLARATION DE LIENS D'INTÉRÊT AVEC LA PRÉSENTATION Intervenant : Nicolas AMABILE, Paris ☑ Je déclare les liens d'intérêt suivants : Bourse de Recherche : Abbott Honoraires : Abbott, Biosensors, Boston Scientific

• A 69 year old man is referred to our centre for acute inferior STEMI + VF x 2. • Previous Medical History: – Previous PCIs on RCA (2013: BES x 2 / Mid & p-Prox RCA ; 2014 : BES x 2 for RIS) – Severe PAD – Paroxysmal AF – Antiplatelet therapy : clopidogrel 75mg/d + VKA

Initial Coronary Angiography

Initial Coronary Angiography What is the mechanism for ST ? What is your management ?

• Stent thrombosis : infrequent cause of acute coronary syndrome • Yet its incidence decreased over time , ST still carries out high mortality • ST remains a challenge for interventional cardiologist, who needs: – To identify the ST mechanism – To apply the appropriate management

Can OCT help to identify the ST underlying cause ?

ST is a multifaceted process OCT +++ Patient-related / Clinical Diabetes Procedure related / Mechanical Impaired LVEF Primary PCI Poor compliance to APT Complex lesion morphology High-on APT platelet reactivity Residual dissection Malignancy Malapposition Genetic traits Stent underexpansion Stent Thrombosis Stent type related Early DES (vs. newer DES/BMS) Adapted from Byrne R et al. , Eur Heart Journal 2015

Definite stent thrombosis Culprit lesion deocclusion IC imaging Analysis Ruptured neoatheroma Malapposition Severe underexpansion Edge dissection Isolated uncovered struts Coronary evaginations ISR without neoatherosclerosis Edge related disease progression No morphological abnormalities

IVUS vs. OCT Maehara A et al., JACC: CARDIOVASCULAR IMAGING 2017, 10(12):1487-503

Ruptured Malapposition NIH with thrombus Neoatherosclerosis Severe underexpansion Isolated uncovered struts Edge related Edge dissection plaque progression Coronary evaginations

The PESTO French multicentre registry

Mechanisms of stent thrombosis according to clinical presentation Global Acute+ Subacute ST Late+ Very Late ST p (n=120) (n=23) (n=97) Malapposition (%) 34 48 32 0.12 Ruptured NA (%) 23 0 28 0.004 Underexpansion (%) 11 26 7 0.02 Coronary Evagination (%) 8 0 10 0.11 ER disease progression (%) 8 4 8 0.45 Isolated uncovered struts (%) 8 0 10 0.11 Neointimal hyperplasia (%) 4 0 5 0.34 Edge dissection (%) 1 4 0 0.19 No cause identified (%) 3 18 0 0.001 Souteyrand et al., Eur Heart Journal 2016

Type & mechanisms of stent thrombosis according to stent type BMS (n=47) DES (n=71) p Acute + Subacute ST (%) 19.1 18.3 0.91 Late + Very Late ST (%) 80.9 81.7 0.91 Index PCI to ST delay (y) 6.5±0.9 3.1±0.4 <0.001 Malapposition (%) 31.9 35.2 0.71 Ruptured Neoatherosclerosis (%) 36.2 14.1 0.005 Underexpansion (%) 6.4 12.7 0.22 Coronary Evagination (%) 2.1 12.7 0.04 Edge related disease progression (%) 12.8 4.2 0.09 Isolated uncovered struts (%) 4.3 11.3 0.16 Neointimal hyperplasia (%) 4.3 4.2 1.0 Edge dissection (%) 0 1.4 0.61 No cause identified (%) 0 5.6 0.13 Souteyrand et al., Eur Heart Journal 2016

The Bern Copenhagen VLST STUDY

BERN VLST STUDY Study flow OCT-detected causes of VLST 2010-2014 Consensus among 5 investigators 88 patients @ 4 centers 24 BMS 64 patients with DES 6 poor quality 58 patients analysed 38 Early gen. DES 20 New gen. DES Taniwaki M et al. Circulation 2016

PRESTIGE OCT substudy Consecutive pts presenting with ST • 29 Centers with OCT capability • Pts prospectively enrolled using a N =675 Angiographic confirmation of definite ST* centralized telephone registration system • Data collected according to a OVERVIEW Blood sampling standardized protocol • OCT before interventions Histopathogy of (recommended) Thrombus aspiration, ev. small balloon predil thrombus 1 • OCT immediately after emergent PCI (suggested) Restore an effective flow • 217 patients comprised the primary N =231 OCT of the target vessel study cohort for the current analysis. PCI according to local practice * according to Academic Research Consortium (ARC) criteria. 1 J. Riegger et al Eur H J 2015:ESC FASTTRACK ClinicalTrials.gov NCT01300507 Adriaenssens T et al. Circulation 2017

PRESTIGE Subacute ST Acute ST Acute ST Subacute ST 78.6% 4.3% 2.1% 21.4% 59.6% 25.5% 6.4% Uncovered struts Edge dissection Malapposed struts No dominant cause identifiable Underexpansion Adriaenssens T et al. Circulation 2017

PRESTIGE Late ST VLST 20.2% 13.6 9.1% 31.3% 31.8 14.2% 4.5% 8.9% 18.2% 13.6% 12.7% 8.2 13.6% % Uncovered struts Restenosis Neoatherosclerosis Malapposed struts Other Underexpansion No dominant cause identifiable Adriaenssens T et al. Circulation 2017

Can OCT help to provide a better ST management ?

Can OCT impact treatment ? 60 Identification of ST underlying mechanism in clinical practice 50 Percentage (%) 40 30 Before OCT analysis After OCT analysis 20 10 0 Completely Probably identified Unidentified identified The investigators reported that OCT analysis influenced their management strategy in 55% of cases Souteyrand et al., Eur Heart Journal 2016

Can OCT impact treatment ? 70 60 50 40 30 20 10 0 POBA Stenting Medical therapy Redo ThrASP CathPCI series (angio guided/n=7060) PESTO cohort (OCT guided/n=120) Souteyrand et al., Eur Heart Journal 2016

Definite Stent Thrombosis Culprit lesion deocclusion N Amabile/M Radu ESC 2015 (Deferred) OCT analysis Ruptured NA Severe underexpansion Isolated uncovered struts Neointimal hyperplasia Malapposition No underlying ER disease progression (Coronary evagination) mechanical cause Edge dissection STENT (DES ++) POBA Medical therapy Drug eluting balloon ?