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STENT THROMBOSIS AND IN STENT RESTENOSIS
stent failure constitutes stent thrombosis and instent restenosis. Presentation includes SCAI consensus document and management of two cases
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STENT THROMBOSIS AND IN STENT RESTENOSIS
- 1. Stent Thrombosis and In-stentRestenosis – Prevention And Management
- 2. Agenda Background StentThrombosis (ST) Classification Management – Interventional and Pharmaceutical In-Stent Restenosis (ISR) Mechanisms, Classification and Imaging Management Prevention Take Home Message
- 3. Introduction • Stent failureremains the major drawback to the use of coronary stents as a revascularisation strategy. • Stent failure constitutes stent thrombosis(ST) and In-stent restenosis (ISR). • Recent advances in imaging have substantially improved our understanding of the mechanisms underlying the stent failure. • Both have in common numerous clinical risk factors and mechanical elements at the time of stent implantation.
- 4.
- 5. Background • ST isan acute or subacute thrombotic occlusion that usually presents as an acute MI or acute coronary syndrome and is associated with high rates of morbidity and mortality. Incidence: 0.5-1% in the first year 0.2-0.6% in every subsequent year Higher incidence with STEMI Lower incidence with elective stent placement
- 6. Risk factors forstent thrombosis Clinical ACS (STEMI/NSTEMI) Left ventricular dysfunction Chronic kidney disease Diabetes mellitus COVID -19 Procedural Stent length Stent underexpansion No reflow Residual stenosis Dissection Multiple stents Bifurcation stenting Lesion related Necrotic core Bifurcation lesions Prior brachytherapy Multivessel disease Inflow and outflow obstruction Stent related Biocompatible polymers Polymer/stent thickness Drug dosage Antiplatelet related adherence CYP2C19 polymorphisms High- on treatment platelet activity Antiplatelet type DAPT duration
- 7. Early ST (<30 days) Late ST (1-12 months) Very Late ST (>12 months) Platelet rich thrombi formation Mainly due to Inadequate procedural result Impaired neointimal healing Acute < 24 hours Predisposing factors: Stenting across major branches Bifurcations Overlapped areas Exaggerated response to healing in DES Stents are placed in stenosed segments with high lipid core Predisposing factors Malapposition Uncovered struts Neoatherosclerosis Stent underexpansion Sub acute – 24 hours to 30 days Emergency PCI – when presentation is acute Optimal reperfusion only in 2/3rds Types of ST
- 8. Image guidance :a must to explore cause and decide on management SCAI Expert Consensus Statement on Management of In-Stent Restenosis and Stent Thrombosis, JSCAI. 2023 Early restenosis due to protrusion of a calcified nodule (white arrows). After Stent thrombosis, the repeat OCT showed protruding calcified nodule within the stent.
- 9. Management Algorithm • Mostare dealt with balloon dilatation (NC, Scoring, Cutting) • Thrombus aspiration if the clot burden is large • Address stent-related mechanical issues • Additional stent implantation should ordinarily be limited to significant residual dissections, especially if recent DAPT has been discontinued. • Optimise pharmacotherapy • Assess the aetiology of stent closure after the establishment of flow
- 10. SCAI Expert ConsensusStatement on Management of In-Stent Restenosis and Stent Thrombosis, JSCAI. 2023
- 11. Pharmacologic Management • Evaluatethe compliance with DAPT • Restart or intensify dual antiplatelet therapy (DAPT) • More potent drugs: prasugrel/ticagrelor • Sustained administration of 150mg Clopidogrel if platelet aggregation studies reveal insufficient (<50%) inhibition of platelet aggregation • Consider prolonged therapy in high-risk patients. • Glycoprotein IIb/IIIa antagonists – prolonged infusions up to 72 hours: to prevent distal embolisation • Long-term anticoagulation – rare; for recurrent ST
- 12. Case • 52 F •Diabetes, hypertension • IWMI • CHB • Cardiogenic shock • CAG – Distal RCA total occlusion, 90 % stenosis in LAD and LCX • Primary PCI to the distal RCA • Had chest pain with in 24 hours • ST elevation in inferior leads
- 13. Final Result Negotiated run-throughwire 1.25*6 mm balloon dilation Heavy thrombus burden After 3.0*15 NC balloon dilation Acute Stent Thrombosis
- 14.
- 15. Background • Recurrent diameterstenosis at the stent segment >50% of the vessel diameter. • The rate of ISR is higher in patients with Diabetes (5.7% vs 8.7%). • Recurrent ISR is seen in approximately 20% of all cases. • Recurrence is independently predicted by the number of stents placed at the location. (43.1% increase in TLR ). • A third layer of metal should be avoided as associated with underexpansion. Incidence of ISR – 10% 25% cases present with Acute MI 30-day mortality (AMI)- 10%-25%.
- 16. Mechanisms of ISR Biological Neointimal tissue proliferationor hyperplasia Neoatherosclero sis Mechanical Stent underexpansion – primary cause MSA IVUS > 5.0mm2 OCT -> 4.5mm2 Target MSA > 90% of the reference segment Stent fracture Edge dissection >60 °, > 3 mm in length, penetrating the media Late acquired malapposition
- 17. Classification • Temporally • EarlyISR (<30 days) • Late ISR (30 days – 1 year) • Very Late ISR (>1 year) • Coronary angiography remains the standard diagnostic method. • IVUS and OCT provide a detailed assessment of the native artery and stented segment
- 18. Morphological classification MEHRAN CLASSIFICATION- •based on coronary angiography 1. Class I-focal involvement 2. Class II-diffuse intrastent 3. Class III-diffuse proliferative 4. Class IV-total occlusion. This was highly relevant to bare metal stenting (BMS), but its applicability to DES ISR is uncertain.
- 19. Imaging in ISR •IVUS and OCT are essential • Determines the cause of failure • IVUS (better penetration) for stent underexpansion • OCT ( high resolution) for neoatherosclerosis • Guide re-intervention strategy
- 21. THE WAKSMAN ISRCLASSIFICATION • Based on intracoronary imaging. • Type I -Mechanical TYPE 1 A- UNDEREXPANTION TYPE 1 B- STENT FRACTURE OCT OCT IVUS IVUS
- 22. • Type II- •Type III-mixed pattern • Type IV-chronic total occlussions • Type V-lesions previously treated with > 2 stents TYPE 2 A-NEOINTIMAL HYPERPLASIA TYPE 2B-NEOATHEROSCLEROIS NONCALCIFED AND CALCIFIED (TYPE 2C) OCT IVUS OCT IVUS
- 23. SCAI Algorithm ofISR Mx Critical principle Obtain the largest acute lumen gain as possible by maximising the immediate postprocedural MLA
- 24. Treatment Modalities Balloon Angioplasty Forunderdeployed stent, focal ISR, short DAPT Underexpansion, focal stent gap, stent fracture – high NC pressure balloons Hyperplasia – scoring/ cutting balloon Drug coated balloons Class I indication (ESC) Inflation time > 60 sec Balloon: artery ratio > 0.91 New DES After appropriate sizing and expansion of original DES Minimise stent coverage Atherectomy Orbital/ rotational Arc of calcium > 270°, > 0.67 mm in thickness Risk of entrapment ELCA Brachytherapy IVL For highly calcific neoatherosclerosis
- 25. Considerations for CABGin refractory or recurrent ISR • Multivessel CAD especially LM or proximal LAD involvement • Prior CABG • Suitability of distal vessel for grafting (including diffuseness of CAD, extent of “metal jacket,” and size of vessel) • Global and regional LV function including viability (especially the segment subtended by the involved vessel) • Comorbid conditions (including age, frailty, life expectancy, and activity level) • Anticipated completeness of revascularization • Response to optimal medical therapy
- 26. Prevention of Stentfailure • Adequate bed preparation – plaque modification • Optimisation of the stent by imaging modality • Addressing the post-stent complications • Compliance with the drug therapy (DAPT)
- 27. Case • 55-year-old male •Hypertensive, Diabetic • H/o PTCA in 2010 • Noncompliant with medications after a year of PCI • Presented with unstable angina • CAG – DVD – RCA ISR, mid LAD 90% stenosis
- 28. OCT images ofISR Neointimal hyperplasia of BMS in mid RCA MLA 3.06mm² After NC balloon dilation Increase in MLA to 4.9 mm²
- 29. Post DES 3.0*32mm stent, MLA 7.87mm², 95% expansion
- 30. Take Home Message Stentfailure remains the major drawback to the use of coronary stents as a revascularisation strategy. Incidence of Stent Thrombosis is 0.5 to 1.0%; higher incidence in STEMI. Incidence of ISR is 10%. It is higher in diabetics, patients on hemodialysis and those with multiple stents. Recurrence of ISR is seen in almost 20% cases. Imaging-guided PCI is needed to establish the cause and management strategy. Optimise the vessel preparation, especially in complex lesions. Drug Compliance must be revisited in all cases of stent thrombosis.
Editor's Notes
- #5 The rate is lower for elective stent placement (0.3%-0.5%) but higher in acute coronary syndrome (3.4%) and MI In contemporary practice, the observed mortality rate (~30%) is high, although recent clinical trials and studies requiring au topsy confirmation suggest a better survival, with an average rate of <10%. The ST rate is higher in ST-elevation myocardial infarction presentations treated with primary stenting. Approximately 20% of patients with a first ST expe rience a recurrent ST episode within 2 years.
- #7 Stent thrombosis is classified by the Academic Research Consortium criteria based on the presenting clinical scenario and timing after initial stent placement.
- #8 Early restenosis due to re-protrusion of a calcified nodule. This patient underwent percutaneous coronary intervention to treat lesions in the distal and mid right coronary ar tery. Optical coherence tomography (OCT) showed an eruptive calcified nodule (white ar rows)inbothlesions. A calcified noduleischaracterized byanaccumulationofsmallcalcium fragmentstypically with strong signalattenuation duetoaccompanyingandoverlyingfibrin. The patient came back for staged procedure of LAD (left anterior descending artery) 6 weeks later. OCTshowed reprotruding calcified nodules within the stent.
- #11 Prevention of ST is dependent on optimal stent implantation and the duration and compliance with DAPT. Congenital or acquired hyporesponder DAPT status seen with clopidogrel is uncommon with prasugrel or ticagrelor. Prior generation stents were susceptible to ST with discontinuation of DAPT out to 5 years and longer in anecdotal cases. With the newest generation of stents, the duration of treatment can be decreased safely to 3 months or 1 month.
- #15 Additional criteria for clinically relevant ISR include: recurrent angina, objective signs of ischemia, or abnormal fractional flow reserve Second-generation drug-eluting stents (DES) have a 5.7% ISR rate in patients without diabetes, and 8.7% rate in those with diabetes. Beyond 1 year, there is a gradual increase in major adverse cardiovascular events (MACE); the 5-year ISR rate is 9% to 12% in noncomplex lesions. Recurrent ISR occurs in approximately 20% of all ISR cases. Recurresnt ISR is independently predicted by the number of stents placed at the location. The 1-year MACE (43.1%) and target lesion revascularization (41.2%) rates were significantly higher in the 3 stent layer group than in the 1-stent-layer and 2-stent-layer groups. The number of metallic layers and hemodialysis requirement were identified as independent predictors of MACE. A third layer of metal is almost always associated with underexpansion and should be avoided.
- #16 Waksman ISR Classification – type II Neointima – SMCs and ECM Neoatherosclerosis – Inhibition of endothelialization by DES allows LDL into vessel wall. So at later stages, the healed neointima is prone to atherosclerosis.
- #17 Early – undersizing, underexpansion, stent fracture Late – delayed healing, uncovered stent struts, intimal hyperplasia Very late – neoatherosclerosis, , intimal hyperplasia, stent fracture
- #19 The most common treatment approach for the first episode of ISR is to implant a second DES, based on the rationale that DES therapy has superior efficacy over balloon angioplasty alone. However, this is not always necessary and may not be the bestsolution,particularly when the reference vessel and the resultant minimal lumen area are small. If the underlying etiology is not directly addressed and corrected, there is a high likelihood of recurrent ISR, and the rate of ISR in second layer DES is high: 12% to 16% at 12 months and 33% at 3 to 5 years.56–58
- #24 ELCA – Debulks neointimal hyperplasia; for breaking peri-stent calcium IVL – for breaking calcium Focal ISR – Balloon angioplasty; ELCA or atherectomy may be beneficial in selected cases For diffuse ISR, atherectomy or scoring/cutting balloon angioplasty followed by repeat DES implantation is typically advised For focal calcific nodule – double layer NC super high pressure balloons sustaining pressures of 30-35 mm Hg