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

Nicolas Amabile, MD, PhD

Service de Cardiologie, Institut Mutualiste Montsouris, Paris

OCT : toute la lumière sur l’angioplastie

Comprendre la thrombose grâce à l’OCT

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 ?

Procedure related / Mechanical Primary PCI Complex lesion morphology Residual dissection Malapposition Stent underexpansion

ST is a multifaceted process

Patient-related / Clinical Diabetes Impaired LVEF Poor compliance to APT High-on APT platelet reactivity Malignancy Genetic traits Stent type related Early DES (vs. newer DES/BMS)

Stent Thrombosis

OCT +++

Adapted from Byrne R et al. , Eur Heart Journal 2015

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

IVUS vs. OCT

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

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

The PESTO French multicentre registry

Mechanisms of stent thrombosis according to clinical presentation

Global (n=120) Acute+ Subacute ST (n=23) Late+ Very Late ST (n=97) p Malapposition (%) 34 48 32 0.12 Ruptured NA (%) 23 28 0.004 Underexpansion (%) 11 26 7 0.02 Coronary Evagination (%) 8 10 0.11 ER disease progression (%) 8 4 8 0.45 Isolated uncovered struts (%) 8 10 0.11 Neointimal hyperplasia (%) 4 5 0.34 Edge dissection (%) 1 4 0.19 No cause identified (%) 3 18 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 (%) 1.4 0.61 No cause identified (%) 5.6 0.13 Souteyrand et al., Eur Heart Journal 2016

The Bern Copenhagen VLST STUDY

2010-2014 88 patients @ 4 centers 64 patients with DES 58 patients analysed 38 Early gen. DES 20 New gen. DES 24 BMS 6 poor quality

BERN VLST STUDY

Consensus among 5 investigators

Study flow OCT-detected causes of VLST

Taniwaki M et al. Circulation 2016

PRESTIGE

Consecutive pts presenting with ST Angiographic confirmation of definite ST* Blood sampling Thrombus aspiration, ev. small balloon predil OCT of the target vessel PCI according to local practice Histopathogy of thrombus 1

OCT substudy

• 29 Centers with OCT capability
• Pts prospectively enrolled using a

centralized telephone registration system

• Data collected according to a

standardized protocol

• OCT before interventions

(recommended)

• OCT immediately after emergent

PCI (suggested)

• 217 patients comprised the primary

study cohort for the current analysis. Restore an effective flow

* according to Academic Research Consortium (ARC) criteria.

1 J. Riegger et al Eur H J 2015:ESC FASTTRACK

N =231 N =675

ClinicalTrials.gov NCT01300507

OVERVIEW Adriaenssens T et al. Circulation 2017

Malapposed struts Edge dissection No dominant cause identifiable Underexpansion

Acute ST Subacute ST

21.4% 78.6% 59.6% 6.4% 25.5% 2.1% 4.3%

PRESTIGE

Uncovered struts

Acute ST Subacute ST

Adriaenssens T et al. Circulation 2017

Late ST VLST

Uncovered struts Malapposed struts Restenosis Other Underexpansion

31.8

13.6% 13.6% 18.2% 9.1% 13.6

No dominant cause identifiable Neoatherosclerosis 20.2% 14.2% 4.5% 12.7% 8.2 % 8.9%

31.3%

PRESTIGE

Adriaenssens T et al. Circulation 2017

Can OCT help to provide a better ST management ?

Can OCT impact treatment ?

10 20 30 40 50 60 Completely identified Probably identified Unidentified Before OCT analysis After OCT analysis Souteyrand et al., Eur Heart Journal 2016

Percentage (%)

Identification of ST underlying mechanism in clinical practice The investigators reported that OCT analysis influenced their management strategy in 55% of cases

10 20 30 40 50 60 70 POBA Stenting Medical therapy Redo ThrASP CathPCI series (angio guided/n=7060) PESTO cohort (OCT guided/n=120)

Can OCT impact treatment ?

Souteyrand et al., Eur Heart Journal 2016

Definite Stent Thrombosis

Ruptured NA Neointimal hyperplasia ER disease progression Severe underexpansion Malapposition (Coronary evagination) Edge dissection Isolated uncovered struts No underlying mechanical cause

STENT (DES ++) Drug eluting balloon ? POBA Medical therapy Culprit lesion deocclusion (Deferred) OCT analysis

N Amabile/M Radu ESC 2015