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lead to further right-heart stress and a lack of improvement in TV pa-

thology. We also examined the type of MR (degenerative vs functional)

and LV dimensions but did not ﬁnd that baseline pathology of the mitral

valve or LV was associated with TR reduction.

This study found that elevated PASP was not associated with re-

sidual TR, similar to previous publications.

However, this study did not

differentiate the etiology of pulmonary hypertension. Future studies

would beneﬁt from, using invasive hemodynamics, evaluating the type

of pulmonary hypertension (precapillary, postcapillary, or mixed) and its

subsequent association with TR reduction. To our knowledge, this is the

ﬁrst publication to demonstrate a relationship between dilated right

atrium with residual TR. The RA size was not evaluated in previous

studies.

5-7

The explanation of larger RA size resulting in higher rates of

residual TR may imply that atrial functional TR is less likely to improve. It

could also mean that the chronicity of TR plays a role, with longstanding

TR associated with RA dilation.

Although previous studies found that RV systolic dysfunction in-

creases the chances of residual TR after M-TEER, neither RV dimensions

and/or function correlated with residual TR in this study.

RV ﬁndings

such as RV area, TAPSE, and TAD were also not predictors of TR

improvement. These data warrant further investigation with magnetic

resonance imaging and/or strain imaging to understand what RV size/-

function will limit TR improvement. Previous surgical and transcatheter

literature has found that larger TAD is less likely to show TR improvement,

but this study found that TAD was not associated with residual TR. Future

studies will have to examine this relationship, to understand the differ-

ence in surgical versus transcatheter TR improvement.

TR has long been associated with the presence of a CIED; however,

this study did not ﬁnd whether patients with a CIED experienced a more

residual TR than those without. Theoretically, patients with CIED-

mediated TR (ie, lead impingement on the TV) would not show TR

improvement despite successful MR reduction.

It is unclear how many

patients in this study experienced CIED-mediated TR because the pri-

mary focus on transesophageal echocardiography was the mitral valve.

Previous publications also found that, after M-TEER, the presence of

CIED does not affect TR improvement.

5-7

Therefore, thorough TV im-

aging is required in such cases to rule out CIED-mediated TR. In cases

with no lead impingement, we can expect that TR improvement is as

common for patients without CIED.

Clinical applicability

Reliably predicting which patients with concomitant MR and TR will

improve after isolated MR therapy is becoming increasingly important.

Current trials are evaluating the use of M-TEER versus surgery in pa-

tients with intermediate and low surgical risk: for example, REPAIR MR

(NCT04198870) and PRIMARY (NCT05051033). When guidelines

expand to offer lower-risk patients transcatheter mitral therapies, it must

be considered that TR may not improve. Until transcatheter tricuspid

therapies are more established, patients with concomitant TR must then

be strongly considered for surgery.

Our ﬁndings indicate that the degree of MR reduction was the only

reliable predictor of TR reduction. However, it is difﬁcult to anticipate

which patients will have unsuccessful M-TEER. With transcatheter mitral

valve replacement technologies on the horizon, a greater reduction of

MR may be anticipated with replacement devices. If the abolishment of

MR is the most effective for TR reduction, isolated MR therapy that yield

greater MR reduction (ie, transcatheter mitral valve replacement) may

be favored in patients with concomitant MR and TR.

Limitations

This study was a retrospective study. Six echocardiographic spe-

cialists interpreted the TR severity and echocardiographic parameters,

so variability among readers may exist. The follow-up period was any-

where from 1 month to 6 months. Most of them were within 2 months,

and a longer-term follow-up was poor because many 1-year echocar-

diograms were not performed. Ideally, a longer-term follow-up would

provide more time for remodeling and reassessment of TR. However,

previous data show that TR improvement is an early phenomenon

(primarily occurring within the ﬁrst months).

TR is a dynamic process and volume shifts may affect the degree of

TR. Follow-up echocardiograms occurred at ~1 month postoperatively,

and volume status of the patients was not reported.

Conclusion

There are few clinical and echocardi ographic predictors of severe

TR after M-TEER. Overall, severe residual TR is common after M -TEER

and difﬁcult to predict. This study highlights the importance of

establishing transcatheter TV therapies for such patients.

Declaration of competing interest

Chad A. Kliger is a consultant and receives speaking honoraria from

Edwards Lifesciences and Medtronic. Luigi Pirelli is a consultant and

receives speaking honoraria from Edwards Lifesciences and Medtronic.

Azhar Supariwala is a consultant and receives speaking honoraria from

Abbott. Bruce Rutkin is a consultant and receives speaking honoraria

from Edwards Lifesciences and Medtronic. None of the other authors

have anything to disclose.

Funding

This research did not receive any speciﬁc grant from funding

agencies in the public, commercial, or not-for-proﬁt sectors.

Ethics statement and patient consent

This study was approved by the institutional review board at the

Northwell Health and adhered to relevant ethical guidelines. No patient

consent was required because all data were retrospective.

References

1. Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the

management of patients with valvular heart disease: executive summary: a report of

the American College of Cardiology/American Heart Association Joint Committee

on Clinical Practice Guidelines. Circulation. 2021;143(5):e35–e71. Erratum in:

Circulation. 2021;143(5):e228; Circulation. 2021;143(10):e784. https://doi.org/10

.1161/CIR.0000000000000932.

2. Boerlage-van Dijk K, Wiegerinck EM, Araki M, et al. Predictors of outcome in

patients undergoing MitraClip implantation: an aid to improve patient selection.

Int J Cardiol. 2015;189:238–243.

3. Pavasini R, Ruggerini S, Grapsa J, et al. Role of the tricuspid regurgitation after

mitraclip and transcatheter aortic valve implantation: a systematic review and

meta-analysis. Eur Heart J Cardiovasc Imaging. 2018;19(6):654–659.

4. Geyer M, Keller K, Bachmann K, et al. Concomitant tricuspid regurgitation severity

and its secondary reduction determine long-term prognosis after transcatheter

mitral valve edge-to-edge repair. Clin Res Cardiol. 2021;110(5):676–688. https://

doi.org/10.1007/s00392-020-01798-4

5. Meijerink F, Koch K T, de Winter RJ, et al. Tricuspi d regurgitation after

transcatheter mitral valve repair: clinical course and impact on outcome.

Catheter Cardiovasc Interv. 2021;98(3):E427–E435. Jan 18. https://doi.org/

10.1002/ccd.29464.

6. Toyama K, Ayabe K, Kar S, et al. Postprocedural changes of tricuspid

regurgitation after MitraClip therapy for mitral regurgitation. Am J Cardiol.

2017;120(5):857–861.

7. Kavsur R, Iliadis C, Spieker M, et al. Predictors and prognostic relevance of tricuspid

alterations in patients undergoing transcatheter edge-to-edge mitral valve repair.

EuroIntervention. 2021;17(10):827–834. https://doi.org/10.4244/EIJ-D-20-01094

8. Feldman T, Kar S, Rinaldi M, et al; EVEREST Investigators. Percutaneous

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the initial EVEREST (Endovascular Valve Edge-to-Edge REpair Study) cohort.

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2009.03.077

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ehjci/jex139

10. Mehr M, Karam N, Taramasso M, et al; TriValve and TRAMI Investigators. Combined

tricuspid and mitral versus isolated mitral valve repair for severe MR and TR: an

analysis from the TriValve and TRAMI registries. J Am Coll Cardiol Intv. 2020;

13(5):543–550. https://doi.org/10.1016/j.jcin.2019.10.023

11. Mutlak D, Khalil J, Lessick J, Kehat I, Agmon Y, Aronson D. Risk factors for the

development of functional tricuspid regurgitation andtheir population-attributable

fractions. J Am Coll Cardiol Img. 2020;13(8):1643– 1651.

12. Addetia K, Harb SC, Hahn RT, Kapadia S, Lang RM. Cardiac implantable electronic

device lead-induced tricuspid regurgitation. J Am Coll Cardiol Img. 2019;12(4):

622–636. https://doi.org/10.1016/j.jcmg.2018.09.028

C. Basman et al. / Journal of the Society for Cardiovascular Angiography & Interventions 2 (2023) 100612 5

Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/

Editorial

Residual Tricuspid Regurgitation After Mitral Transcatheter Edge-to-Edge

Repair: Accomplice or Bystander?

Vikrant Jagadeesan, MD

, John Blair, MD

West Virginia Heart and Vascular Institute, West Virginia University School of Medicine, Morgantown, West Virginia;

Section of Cardiology, Department of

Medicine, University of Chicago Pritzker School of Medicine, Chicago, Illinois

Tricuspid regurgitation (TR) has been associated with worse out-

comes with increasing severity. Community-based echocardiographic

studies of asymptomatic patients demonstrated the prevalence of at

least moderate TR or greater can range from 3% to 8%, with 1-

year–adjusted mortality rates for moderate TR at 29.5% and severe TR

at 45.6%.

1,2

The 2020 ACC/AHA guidelines deﬁne a staging system for

TR with 3 principal stages: progressive TR (stage B), asymptomatic se-

vere TR (stage C), and symptomatic severe TR (stage D).

It is a class I

recommendation that concomitant tricuspid valve surgery be per-

formed in patients with stage C or D TR undergoing left-sided valvular

surgery. Progressive stage B TR by deﬁnition is clinically asymptomatic

with no hemodynamic consequences. A study examining patients with

stage B TR who underwent isolated left-sided valvular surgery showed

that those with a tricuspid annular diastolic diameter of >40.0 mm (or

>21.0 mm/m

) who did not undergo concomitant tricuspid annulo-

plasty had worse New York Heart Association functional class and

worsening TR by more than 2 grades in 5-10 years of follow-up.

This

supported a class 2a recommendation for patients with stage B TR to

undergo concomitant tricuspid valve surgery at the time of left-sided

valve surgery.

For patients who are not suitable conventional surgical candidates

for concomitant mitral and tricuspid valve repair/replacement, trans-

catheter therapies may be considered. Currently, no commercially

available FDA-approved transcatheter therapy exists for TR in the

United States. Therefore, these patients are often evaluated for isolated

mitral transcatheter edge-to-edge repair (m-TEER) with the goal of

improving TR by reducing pulmonary arterial (PA) pressures due to

severe mitral regurgitation (MR). Unlike the strength of recommenda-

tions guiding surgical intervention, rigorous evidence on the trans-

catheter management of coexisting MR and TR is lacking.

Approximately 60% of patients undergoing m-TEER also have moder-

ate or greater TR with signiﬁcantly decreased 1-year survival in patients

with residual severe TR compared with those with lesser degrees of TR

after m-TEER.

This is consistent with subgroup analyses from the

Transcatheter Mitral Valve Interventions (TRAMI) and Getting Reduction

of Mitral Insufﬁciency by Percutaneous Clip Implantation (GRASP) reg-

istries that showed worse 12-month outcomes of mortality, rehospital-

ization for heart failure, and major adverse cardiovascular and

cerebrovascular events.

6,7

Basman et al

present prospectively collected registry data analyzed

retrospectively in a single-hospital system comprising 4 high volume

m-TEER centers. Their goal was to identify predictors of severe TR at the

1-month follow-up transthoracic echocardiography (TTE) after m-TEER.

TR improvement was deﬁned as a reduction in TR grade by at least 1þ

resulting in moderate (2þ) or less TR. Approximately half of the patients

who underwent successful MR reduction also experienced signiﬁcant

TR reduction. Multivariate analyses showed MR reduction of 3þ as the

only predictor of signiﬁcant TR reduction. Univariate predictors of se-

vere residual TR were right atrial area and unsuccessful m-TEER. Other

factors such as atrial arrhythmia, previous cardiac implantable electronic

device, mechanism of MR, tricuspid annular dilation, right ventricular

(RV) function, PA systolic pressure, and left ventricular (LV) dimensions

did not reach statistical signiﬁcance.

The authors should be commended on their report of the largest

analysis to date on signiﬁcant predictors of severe TR after m-TEER.

However, several limitations should be noted. First, methodologic chal-

lenges and the small sample size in a single-system limit the study’spo-

tentiallarger scale effect. The numberof operators and their experience is

not known, which may affect procedural success and outcomes. In addi-

tion, all baseline covariates were TTE-based parameters although all pa-

tients underwent transesophageal echocardiography (TEE) guidance for

m-TEER. Baseline TEE mitral and tricuspid valve parameters were a po-

tential valuable missed repository of important analyzable predictors. For

example,baselinetricuspid coaptation gap, althoughnot directly studied

in this context, has been shown to affect tricuspid-TEER procedural strat-

egyand success.

Because>90% of the TRpathologyin thestudy Basman

et al was functional, baseline coaptation gap and its correlation with ulti-

mate TR reduction could be very relevant. In addition, other pertinent

baselineTEE covariates could have been examined such as quantiﬁcation

of TR by proximal isovelocity surface area and tricuspid annular

DOI of original article: https://doi.org/10.1016/j.jscai.2023.100612.

Keywords: mitral regurgitation; tricuspid regurgitation.

* Corresponding author: Vikrant.jagadeesan@wvumedicine.org (V. Jagadeesan).

https://doi.org/10.1016/j.jscai.2023.100999

Received 21 March 2023; Received in revised form 14 April 2023; Accepted 17 April 2023

Available online 19 May 2023

CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Journal of the Society for Cardiovascular Angiography & Interventions 2 (2023) 100999

measurements. For degenerative MR, qualitative and quantitative char-

acterization of the MR pathology on TEE such as myxomatousdiseaseand

ﬂail width/gap are important to understand the severity of degenerative

MR in this cohort andcontextualize the observedoutcomes. Even though

45% of the cohort had functional MR, thedegreeof LV systolicdysfunction

was not quantiﬁed. Rather, LV dysfunction was analyzed as a binary vari-

able that does not accurately capture the effect of varying degrees of

baselinecardiomyopathy on MR reduction after m-TEER and consequent

TR outcomes. Procedural informationis alsonot available such as average

number of clips per case, type of clip(s), and end-procedural/short-term

follow-up mitral mean gradient. Iatrogenic mitral stenosis from m-TEER

could signiﬁcantly increaseresultant TR. Regarding the span of the study,

only30-dayfollow-upwas analyzed when12-monthoutcomeswouldhave

had more signiﬁcance. Pre-procedure and post-procedure brain natri-

uretic peptide levelsand TTE inferior vena cava assessment could also be

an important gauge of volume status that could affect follow-up TR

assessment. Finally, quantifying TR based on the ACC/AHA staging sys-

tem instead of the routinely cited 5-grade system may have more rele-

vance in future guideline derivation.

The authors’ primary conclusion of signiﬁcant MR reduction as a

predictor of signiﬁcant TR reduction is intuitive but not necessarily ad-

ditive. Physiologically, it can be explained by the effective reduction of

left atrial pressure leading to consequent reduction in mean PApressure

and TR reduction. The authors acknowledge the inability to account for

the presence of intrinsic PA hypertension. Although PA systolic pressure

was not found to be a signiﬁcant risk factor for severe residual TR, TTE-

derived pulmonary vascular resistance could have been explored as an

important covariate. The authors also report that right atrial area was a

predictor of severe residual TR in univariate analyses, but not RV

dysfunction. RV dysfunction, similar to the LV, was also treated cate-

gorically (moderate or severe). Quantiﬁcation of RV ejection fraction, RV

area, and tricuspid annular dilation assessed by pre- and post-cardiac

magnetic resonance imaging may help reﬁne our understanding on the

role of right atrioventricular remodeling on TR reduction. Strain analyses

could have also strengthened the study ﬁndings. One study demon-

strated improvement in RV free-wall global longitudinal strain at 12

months after m-TEER, but not LV strain.

This may suggest that the RV

may be more able to reverse remodel in response to improvements in

PA pressure. Longitudinal changes in RV strain may play an important

role in predicting residual TR after m-TEER.

The recently published 5-year COAPT trial data and the ongoing

REPAIR-MR and PRIMARY trials may expand m-TEER to larger patient

populations.

If m-TEER in the future reaches a comparable ubiquity

with transcatheter aortic valve replacement, studies similar to the one

reported by Basman et al are warranted to identify salient predictors of

signiﬁcant TR reduction in patients with severe MR treated with

m-TEER. The generalizability of this study is conﬁned by the sample size

and single-system experience. Limited clinical and TTE-based

covariates and the absence of longer-term follow-up cap the study’s

ability to be practice-changing. Despite these limitations, Basman et al

provide essential insight into predicting severe TR after m-TEER. Future

studies in larger cohorts using hemodynamic parameters and multi-

modality imaging will help elucidate in which patients residual TR after

m-TEER is a bystander responsive to reduction in PA pressure or an

accomplice to severe MR that will continue to portend a poor prognosis

even after successful m-TEER.

Declaration of competing interest

The author(s) declared no potential conﬂicts of interest with respect

to the research, authorship, and/or publication of this article.

Funding sources

This research did not receive any speciﬁc grant from funding

agencies in the public, commercial, or not-for-proﬁt sectors.

References

1. d'Arcy JL, Coffey S, Loudon MA, et al. Large-scale community echocardiographic

screening reveals a major burden of undiagnosed valvular heart disease in older

people: the OxVALVE Population Cohort Study. Eur Heart J. 2016;37(47):

3515–3522.

2. Chorin E, Rozenbaum Z, Topilsky Y, et al. Tricuspid regurgitation and long-term

clinical outcomes. Eur Heart J Cardiovasc Imaging. 2020;21(2):157–165.

3. Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the

management of patients with valvular heart disease: a report of the American

College of Cardiology/American Heart Association joint committee on clinical

practice guidelines. Circulation. 2020;143(5):e72–e227.

4. Dreyfus GD, Corbi PJ, Chan KM, Bahrami T. Secondary tricuspid regurgitation or

dilatation: which should be the criteria for surgical repair? Ann Thorac Surg. 2005;

79(1):127–132.

5. Geyer M, Keller K, Bachmann K, et al. Concomitant tricuspid regurgitation severity

and its secondary reduction determine long-term prognosis after transcatheter

mitral valve edge-to-edge repair. Clin Res Cardiol. 2021;110(5):676–688.

6. Ohno Y, Attizzani GF, Capodanno D, et al. Association of tricuspid regurgitation

with clinical and echocardiographic outcomes after percutaneous mitral valve

repair with the MitraClip System: 30-day and 12-month follow-up from the

GRASP Registry. Eur Heart J Cardiovasc Imag. 2014;15(11):1246–1255.

7. Kalbacher D, Sch

€

afer U, von Bardeleben RS, et al. Impact of tricuspid valve

regurgitation in surgical high-risk patients undergoing MitraClip implantation:

results from the TRAMI registry. EuroIntervention. 2017;12(15):e1809–e1816.

8. Basman C, Kodra A, Pirelli L, et al. Predictors of residual tricuspid regurgitation after

transcatheter mitral valve repair. J Soc Cardiovasc Angiogr Interv. 2023;2(4):100612.

9. Donal E, Sitges M, Panis V, et al. Impact of coaptation gap location on procedural

strategy and outcomes following tricuspid transcatheter edge-to-edge repair:

insights from the TriClip bRIGHT study. Eur Heart J. 2022;43(2):2127.

10. Peters AP, Leya M, Baldridge A, et al. Temporal trends in left and right heart

remodeling following transcatheter edge-to-edge mitral repair for degenerative

mitral regurgitation. Struct Heart. 2021;5(6):634–636.

11. Stone GW, Abraham W, Lindenfeld J, et al. Five-year follow-up after transcatheter

repair of secondary mitral regurgitation. N Engl J Med. Published online March 5,

2023. https://doi.org/10.1056/NEJMoa2300213

2 Editorial / Journal of the Society for Cardiovascular Angiography & Interventions 2 (2023) 100999

Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/

Letter to the Editor

Response to Letter to the Editor regarding the article “Comparison of

Large-Bore Thrombectomy With Catheter-Directed Thrombolysis for the

Treatment of Pulmonary Embolism”

We appreciate the additional information from Giunio et al

regarding the feasibility of antecubital access pigtail catheter for me-

chanical thrombus fragmentation and adjunctive catheter-directed

thrombolysis (CDT) based on their previously published retrospective

review of 27 consecutive patients. Indeed, ultrasound-assisted CDT has

been studied against pigtail catheter CDT in a small cohort previously,

which demonstrated similar mortality outcomes and similar reductions

in pulmonary artery pressure and Miller score, but with decreased

infusion times and lower total tissue plasminogen activator (tPA) infu-

sion rates in the ultrasound-assisted CDT cohort.

In a recent

meta-analysis assessing ultrasound-assisted versus standard catheter

CDT, no difference was noted in major outcomes between the 2 mo-

dalities, including mortality and major bleeding.

Moreover, the dose of

tPA and duration of infusion were noted to be lower in this larger

analysis but was not statistically signiﬁcant. We recognize the potential

economic advantages of using either a standard catheter or pigtail

catheter for CDT, although propose that potential decreased infusion

times and tPA doses may reduce overall hospital costs in minimizing

intensive care unit stay, decreasing bleeding risks, and improving pa-

tient satisfaction. Cost-analysis factoring these other components into

consideration may be of interest.

Our initial analysis

evaluated the outcomes of CDT in comparison

with large-bore thrombectomy (LBT) in our institution’s experience,

given the lack of randomized data comparing the 2 different modal-

ities to date. Because there is no difference in major outcomes be-

tween ultrasound-assisted CDT and standard catheter CDT, we

believe our ﬁndings may still be translated to facilities using standard

catheter CDT as t he primary modality of endovascular therapy. Given

the nonrandomized nature of our patient cohort and the increasing

ability to treat more hemodynamically unstable p atients with

venoarterial-extracorporea l membrane oxygenation followed by

adjunctive LBT, we recognize there a re intrinsic differences in be-

tween our patient po pulation. Nonetheless, regardless of the differ-

ences between our coh orts, mortality outcomes were not statistically

different ba sed on univariate, multivariate, and inverse propensity

weighting. We look forward to ongoing trials evaluating outcomes of

CDT and LBT to help further our understanding of matching optimal

modality to patient selection.

Declaration of competing interest

Jun Li is a member of the Advisory board for Boston Scientiﬁc, Inari

Medical, and Medtronic and consultant for Abbott Vascular, Endovas-

cular Engineering, and Philips. Mehdi Shishehbor is a member of the

Global Advisory Board for Abbott Vascular, Medtronic, Terumo, Phillips,

Boston Scientiﬁc, ANT, and Inquis Medical.

Funding sources

This letter did not receive any speciﬁc grant from funding agencies

in the public, commercial, or not-for-proﬁt sectors.

Jun Li, MD

, Mehdi H. Shishehbor, DO, MPH, PhD

Harrington Heart and Vascular Institute, University Hospitals Cleveland

Medical Center, Cleveland, Ohio

* Corresponding author:

jun.li@uhhospitals.org (J. Li).

References

1. Giunio L, Lozo M, Borovac JA, Bradaric A, Zanchi J, Miric D. Feasibility and safety of

catheter-directed thrombolysis via superﬁcial cubital vein for the treatment of acute

massive and submassive pulmonary embolism. Postepy Kardiol Interwencyjnej.

2021;17(4):389–397.

2. Graif A, Grilli CJ, Kimbiris G, et al. Comparison of ultrasound-accelerated versus

pigtail catheter-directed thrombolysis for the treatment of acute massive and

submassive pulmonary embolism. J Vasc Interv Radiol. 2017;28(10):1339–1347.

3. Sun B, Yang JX, Wang ZK, et al. Clinical efﬁcacy and safety of ultrasound-assisted

thrombolysis vs. standard catheter-directed thrombolysis in patients with acute

pulmonary embolism: a study level meta-analysis of clinical trials. Front Cardiovasc

Med. 2022;9:967786.

4. Feroze R, Arora S, Tashtish N, et al. Comparison of large-bore thrombectomy with

catheter-directed thrombolysis for the treatment of pulmonary embolism. J Soc

Cardiovasc Angiogr Interv. 2023;2, 100453.

DOI of original article: https://doi.org/10.1016/j.jscai.2023.100613.

https://doi.org/10.1016/j.jscai.2023.101034

Received 20 April 2023; Accepted 25 April 2023

Available online 16 May 2023

the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Journal of the Society for Cardiovascular Angiography & Interventions 2 (2023) 101034

Standards and Guidelines

SCAI Expert Consensus Statement on Management of In-Stent Restenosis

and Stent Thrombosis

Lloyd W. Klein, MD, MSCAI

, Sandeep Nathan, MD, MSc, FSCAI

, Akiko Maehara, MD,

FSCAI

, John Messenger, MD, SCAI

, Gary S. Mintz, MD

, Ziad A. Ali, MD, DPhil, FSCAI

Jennifer Rymer, MD, FSCAI

, Yader Sandoval, MD, FSCAI

, Karim Al-Azizi, MD, FSCAI

Roxana Mehran, MD, MSCAI

, Sunil V. Rao, MD, FSCAI

, Amir Lotﬁ, MD, FRCP, FSCAI

Division of Cardiology, University of California, San Francisco, San Francisco, California;

Section of Cardiology, Department of Medicine, University of

Chicago, Chicago, Illinois;

Center for Interventional Vascular Therapy, Division of Cardiology, Columbia University College of Physicians and Surgeons, New

York, New York;

Division of Cardiology, University of Colorado Anschutz Medical Campus, Aurora, Colorado;

Clinical Trials Center, Cardiovascular

Research Foundation, New York, New York;

DeMatteis Cardiovascular Institute, St. Francis Hospital & Heart Center, Roslyn, New York;

Division of

Cardiology, Duke University School of Medicine, Durham, North Carolina;

Allina Health Minneapolis Heart Institute, Minneapolis, Minnesota;

Department

of Interventional Cardiology, Baylor Scott & White Health – The Heart Hospital, Plano, Texas;

Zena and Michael A. Wiener Cardiovascular Institute, Mount

Sinai Medical Center, New York, New York;

Division of Cardiology, NYU Langone Health System, New York, New York;

Division of Cardiology, University of

Massachusetts Chan Medical School – Baystate, Springﬁeld, Massachusetts

ABSTRACT

Stent failure remains the major drawback to the use of coronary stents as a revascularization strategy. Recent advances in imaging have substantially

improved our understanding of the mechanisms underlying these occurrences, which have in common numerous clinical risk factors and mechanical ele-

ments at the time of stent implantation. In-stent restenosis remains a common clinical problem despite numerous improvements in-stent design and polymer

coatings over the past 2 decades. It generates signiﬁcant health care cost and is associated with an increased risk of death and rehospitalization. Stent

thrombosis causes abrupt closure of the stented artery and therefore carries a high risk of myocardial infarction and death. This Society for Cardiovascular

Angiography & Interventions (SCAI) Expert Consensus Statement suggests updated practical algorithmic approaches to in-stent restenosis and stent

thrombosis. A pragmatic outline of assessment and management of patients presenting with stent failure is presented. A new SCAI classiﬁcation that is time-

sensitive with mechanistic implications of in-stent restenosis is proposed. Emphasis is placed on frequent use of intracoronary imaging and assessment of

timing to determine the precise etiology because that information is crucial to guide selection of the best treatment option. SCAI recommends image-

guided coronary stenting at the time of initial implantation to minimize the occurrence of stent failure. When in-stent restenosis and stent thrombosis are

encountered, imaging should be strongly considered to optimize the subsequent approach.

Table of Contents

Introduction. . . ...................................... 2

Methodology . . . ................................. 2

In-stent restenosis . . . ................................. 2

Risk factors ...................................... 2

Pathogenesis and contributory factors. . . ................ 2

Deﬁnition and classiﬁcation .......................... 3

Imaging adjuncts to diagnosis . . ...................... 3

Physiologic assessment . . ........................... 3

Proposed treatment strategies . . ...................... 3

Stent thrombosis ..................................... 7

Incidence and clinical presentation . . . .................. 7

Classiﬁcation . . ................................... 7

Pathogenesis. . ................................... 7

Correlates of timing of ST and mechanism . . .............10

Diagnostic imaging modalities ........................10

Mechanical and pharmacologic treatment of ST ...........12

Conclusion . ........................................13

Peer review statement .................................13

Declaration of competing interest . ........................13

Funding sources . . ...................................13

Supplementary material . . . .............................13

References . ........................................13

Abbreviations: BMS, bare metal stents; DAPT, dual antiplatelet therapy; DCB, drug-coated balloons; DES, drug-eluting stents; ISR, in-stent restenosis; IVUS, intravascular ultra-

sound; MACE, major adverse cardiovascular events; OCT, optical coherence tomography; RCT, randomized clinical trial; ST, stent thrombosis.

Keywords: coronary stenting; in-stent restenosis; major adverse cardiovascular events; stent thrombosis; target vessel failure.

* Corresponding author: Amir.LotﬁMD@baystatehealth.org (A. Lotﬁ).

https://doi.org/10.1016/j.jscai.2023.100971

Available online 18 May 2023

CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Journal of the Society for Cardiovascular Angiography & Interventions 2 (2023) 100971

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Introduction

Coronary stenting has transformed revascularization strategy, pro-

ducing excellent procedural and clinical outcomes in myriad clinical

settings. Despite proven short and long-term beneﬁts, in-stent reste-

nosis (ISR) and stent thrombosis (ST) continue to be limitations. There

remains no deﬁnitive management approach for either condition

despite a greater understanding of the underlying mechanisms ensuing

from advances in intracoronary imaging.

In this Society for Cardiovascular Angiography & Interventions (SCAI)

Expert Consensus Statement, practical algorithmic approaches to ISR

and ST are offered. A pragmatic outline of assessment and management

of patients presenting with stent failure is presented. A new SCAI clas-

siﬁcation that is time-sensitive with mechanistic implications of ISR is

proposed. Emphasis is placed on frequent use of intracoronary imaging

and assessment of timing to determine the precise etiology, as that in-

formation is crucial to guide selection of the best treatment option.

Methodology

This statement has been developed according to SCAI Publications

Committee policies for writing group composition, disclosure and

management of relationships with industry, internal and external review,

and organizational approval. Detailed author disclosures are included

as Supplemental Table 1. The work of the writing committee was

supported exclusively by SCAI, a nonproﬁt medical specialty society,

without commercial support. Writing group members contributed to

this effort on a volunteer basis and did not receive payment from SCAI.

Group members in each section performed literature searches, and the

section leads in collaboration authored initial section drafts with other

members of the writing group. The draft manuscript was peer reviewed

in February 2023 and the document was revised to address pertinent

comments. The writing group unanimously approved the ﬁnal version

of the document. The SCAI Publications Committee and Executive

Committee endorsed the document as ofﬁcial society guidance in

March 2023. SCAI statements are primarily intended to help clinicians

make decisions about treatment alternatives. Clinicians also must

consider the clinical presentation, setting, and preferences of individual

patients to make judgments about the optimal approach.

In-stent restenosis

ISR remains a common clinical problem despite numerous im-

provements in-stent design and polymer coatings over the past 2 de-

cades. ISR generates signiﬁcant health care cost and is associated with

an increased risk of death and rehospitalization. The incidence of ISR is

10%; 25% of ISR cases present with acute myocardial infarction (MI) with

a 30-day mortality rate of 10% to 25%.

1–4

Risk factors

Clinical. The incidence of ISR varies depending on individual pa-

tient, angiographic and procedural characteristics as listed in

Table 1.

1–15

Second-generation drug-eluting stents (DES) have a 5.7%

ISR rate in patients without diabetes, and 8.7% rate in those with dia-

betes.

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 is not unusual in contemporary practice. The failure to

appreciate and address the original mechanism of ISR underlies re-

fractory cases of recurrence. As in ﬁrst ISR, the use of intracoronary

imaging may provide insights into the underlying mechanisms. Recur-

rent ISR occurs in approximately 20% of all ISR cases.

7,8

Recurrence is

independently predicted by the number of stents placed at the loca-

tion.

9,10

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. Importantly, on multivari-

able analysis, the number of metallic layers and hemodialysis require-

ment were identiﬁed as independent predictors of MACE. A third layer

of metal is almost always associated with underexpansion and should

be avoided.

Pathogenesis and contributory factors

The preferred treatment strategy depends on a precise diagnosis

and understanding of the cause. Consequently, identifying the mech-

anism in each case using intracoronary imaging and optimizing the

interventional result are critical steps (Table 1).

Biologic factors. The primary biologic mechanism of ISR is neointimal

tissue proliferation or hyperplasia, an exaggerated homeostatic healing

response to arterial wall damage sustained during stent implantation.

The distribution of neointimal tissue proliferation may be focal or diffuse

along the length of the stent. Causative factors are local inﬂammation

resulting from mechanical disruption of the intima/media leading to

aggressive neointimal hyperplasia/proliferation that consists of smooth

muscle cells and extracellular matrix. Hypersensitivity reactions to the

metal and/or the polymer of early-generation DES are also recognized

mechanisms of neointimal hyperplasia.

Neoatherosclerosis is an increasingly recognized mechanism of

stent failure seen with current generation DES. It is characterized by

accumulation of lipid-laden foamy macrophages sometimes with

necrotic core formation within stented segments.

Injury to the vessel

by balloon inﬂation and stent deployment stimulates neointima for-

mation. The subsequent intimal and medial damage leads to prolifer-

ation and migration of vascular smooth muscle cells, macrophages, and

extracellular matrix formation. These activate the coagulation cascade

and an inﬂammatory response. This combination of events, along with

elution of antiproliferative drug, inhibits endothelialization. The lack of

endothelium allows incorporation of low-density lipoprotein into the

artery wall early after DES implantation. At later stages, the healed

in-stent neointima is prone to atherosclerosis development.

Additional mechanisms of ISR include elastic recoil and relocation/

subluxation of axially transmitted plaque (tissue intrusion) (especially

early) and reorganization of thrombus, neointima formation, and

remodeling (especially late).

6–16

Mechanical factors. The primary mechanical cause of ISR is under-

expansion. This may result from stent undersizing, low deployment

pressures, or underlying calciﬁed lesions. Other mechanical causes

include stent recoil, longitudinal stent deformation, stent fracture,

crushed stents, dislocated stents, and geographic miss. Geographic

miss results from incorrect placement of the stent so that it does not fully

Table 1. In-stent restenosis risk factors

1–15

Patient factors Angiographic factors Procedural factors

 Diabetes

mellitus

 Renal

insufﬁciency

 ACS

presentation

 Female

 Recurrent ISR

 Lesion length >20 mm

 Diameter <3mm

 Chronic total occlusion

 Ostial location

 Bifurcation

 Saphenous vein graft

 Severe Calciﬁcation

 Multivessel CAD

 Underexpansion

 Stent fracture

 Bare metal stent

 Stenoses proximal and distal

to stent

 Major arterial dissection

involving media or >3mm

length

 Multiple stent layers

ACS, acute coronary syndrome; CAD, coronary artery disease; ISR, in-stent

restenosis.

2 L.W. Klein et al. / Journal of the Society for Cardiovascular Angiography & Interventions 2 (2023) 100971

cover the diseased segment. Stent fracture may be seen at hinge points

in the coronary artery and after stenting a calciﬁed nodule. Other

ﬁndings, such as early-stent malapposition, tissue prolapse, and

asymmetry/eccentricity have little or no prognostic value. Stent

underexpansion may occur as a result of undersizing, low deployment

pressures, or heavily calciﬁed lesions.

9–13

Some interventional cardiologists favor routine poststent placement

dilation with high-pressure balloons; while this can be an effective

strategy, it can also lead to edge dissections. Instead, postprocedural

imaging might be a more effective use of time and effort.

Deﬁnition and classiﬁcation

In-stent restenosis is established angiographically as a binary event,

deﬁned as recurrent diameter stenosis at the stent segment >50% of

the vessel diameter.

Additional criteria for clinically relevant ISR

include: recurrent angina, objective signs of ischemia, or abnormal

fractional ﬂow reserve.

17–19

Morphologic patterns. Coronary angiography remains the standard

diagnostic method to determine ISR severity and morphologic pattern:

Mehran. The Mehran System

classiﬁes restenotic lesions on the basis

of morphology and extent of disease, with 4 subclasses based on

location within the stented segment. Lesions were classiﬁed as focal

(class I), diffuse intrastent (class II), diffuse proliferative (class III), and

total occlusion (class IV). This schema was highly relevant to bare metal

stenting (BMS), but its applicability to DES ISR is uncertain.

Waksman. The Waksman ISR Classiﬁcation

is based on mechanistic

considerations informed by intracoronary imaging. There are 5 groups

of DES ISR identiﬁed: mechanical (type I; underexpansion I A, stent

fracture I B), biologic (type II; intimal hyperplasia II A, neoatherosclerosis

noncalciﬁed II B, neoatherosclerosis calciﬁed II C), mixed pattern (type

III), chronic total occlusions (type IV), and lesions previously treated with

>2 stents (type V).

Intravascular ultrasound- and optical coherence tomography-based

classiﬁcations. Kang et al

has proposed an intravascular ultrasound

(IVUS)-based classiﬁcation that incorporates length of the restenosis as

well as minimal luminal area. Gonzalo et al

and Ali et al

have pro-

posed optical coherence tomography (OCT) classiﬁcations that rely on

both quantitative and qualitative parameters.

Timing. Table 2 is the proposed new SCAI classiﬁcation incorporating

the cause of ISR based on time from implantation. SCAI recommends

that early (<30 days), late (30 days to 1 year), and very late (>1 year)

timing categories be adopted for all future diagnostic and therapeutic

studies. By integrating mechanistic etiology with timing, this classiﬁ-

cation will be useful to determine best treatment options.

Imaging adjuncts to diagnosis

SCAI strongly recommends routine evaluation by intravascular im-

aging to determine the cause of ISR, to inform therapeutic strategy, and

to conﬁrm effective treatment after percutaneous coronary intervention

(PCI).

24–29

Identifying the mechanism of stent failure is paramount

because the causative factors will inﬂuence the selection of treatment

and devices to manage the ISR, ultimately impacting the durability of

the repeat revascularization. Despite being the primary means of

assessing ISR in clinical practice, angiography alone is usually inade-

quate because of limited resolution and inherent deﬁciency in quanti-

fying vessel size, stent size, stent expansion, number of stent layers,

in-stent calciﬁc neoatherosclerosis, and extrastent calciﬁc disease.

Identifying the mechanism of ISR depends on visualizing the stent and

its relation to the arterial wall, rather than the lumen itself.

In contrast to angiography, IVUS and OCT provide detailed

assessment of the native artery and stented segment (Figure 1A, B).

Recent intravascular imaging studies demonstrate that suboptimal stent

deployment is common—occurring in 31% to 58% of patients—and

that suboptimal stent deployment confers an increased risk of adverse

events.

30–33

The relative advantages of IVUS and OCT are summarized

in Table 3.

34,35

Suboptimal minimal stent area (MSA) is a major predictor of stent

failure, and an IVUS optimized MSA of >5.0 mm

or OCT optimized

MSA of >4.5 mm

are optimal goals. Another useful criterion is to

achieve a target MSA >90% of the closest proximal or distal reference

segment. In addition, intraluminal diagnostic imaging should be per-

formed to ensure that there are no inﬂow or outﬂow obstructions within

5 mm of the proximal or distal stent edge. In particular, any major edge

dissections (deﬁned as >60



, >3 mm in length, or penetrating the

media) should be stented.

33–35

Physiologic assessment

Patients with ISR of intermediate range severity on coronary angi-

ography present a clinical challenge because of potential short and

long-term complications, and it is recommended that objective evi-

dence of myocardial ischemia is demonstrated prior to proceeding with

repeat intervention. Even though there are no randomized clinical trials

(RCTs) assessing coronary physiology to guide management of ISR,

there are several retrospective observational trials that suggest that it

may assist in clinical decision-making.

36,37

Deferral of coronary revas-

cularization in patients with ISR and fractional ﬂow reserve >0.80 was

associated with similar outcomes over 36 months to patients with de

novo coronary stenosis.

Further studies may deﬁne the value of cor-

onary physiology assessment in developing decision strategy before

and after intervention.

Proposed treatment strategies

A summary of existing RCTs and registries,

20,38–51

including clinical

situations in which particular treatment modalities have been shown to

be advantageous, are presented in Table 4.

52–55

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 best solution, 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

General strategic approach. The critical principle is to obtain the

largest acute lumen gain as possible by maximizing the immediate

Table 2. SCAI classiﬁcation of in-stent restenosis: a system based on time

interval and causative factor

Classiﬁcation Time interval Morphologic substrates

Early <30 d  Undersizing

 Underexpansion

 Stent fracture

Late 30 d to 1 y  Delayed healing (including drug induced)

 Uncovered stent struts

 Intimal hyperplasia (especially in BMS ISR)

Very late >1y  Neoatherosclerosis

 Intimal hyperplasia

 Stent fracture

BMS, bare metal stent; ISR, in-stent restenosis.

L.W. Klein et al. / Journal of the Society for Cardiovascular Angiography & Interventions 2 (2023) 100971 3

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postprocedural minimal luminal area. To operationalize this concept, a

complete diagnostic evaluation of the cause of ISR must be pursued.

An algorithmic approach is provided in Figure 2. Repeat PCI should be

routinely performed following intracoronary imaging assessment. The

mechanism of the initial ISR should be determined, with correction of

any underlying mechanical factors with image guidance to ensure

optimal sizing and expansion. A second stent should be image-guided

to ensure correct stent expansion to ensure appropriate stent

expansion.

Besides repeat DES, a number of adjunct treatments exist that may

be highly effective.

58–69

If there is signiﬁcant underexpansion, it is

critical to increase expansion by applying high-pressure balloons. If

there is additional hyperplasia, perhaps preparation with scoring/cut-

ting balloons, rotational atherectomy (RA), orbital atherectomy (OAS),

drug-coated balloons (DCBs), vascular brachytherapy (VBT), excimer

laser coronary angioplasty (ELCA), or intravascular lithotripsy (IVL) may

be useful.

When ISR is predominantly because of neointimal hyperplasia,

treatment is dependent on the pattern of ISR. For focal ISR, a high-

pressure or scoring/cutting balloon may be sufﬁcient; ELCA or athe-

rectomy may be beneﬁcial in selected cases. For diffuse ISR, atherec-

tomy or scoring/cutting balloon angioplasty followed by repeat DES

implantation is typically advised.

If stent underexpansion is not because of calciﬁcation, atheroa-

blation should be used only if signiﬁcant neointimal hyperplasia is also

present. RA, OAS, and ELCA may debulk neointima hyperplasia,

although mechanistic evaluations fail to demonstrate this effect. In

cases where intravascular imaging identiﬁes an arc of calcium >270



>0.67 mm in thickness, atherectomy vessel preparation should be

considered to optimize lesion and stent expansion.

60–69

If stent underexpansion is due to signiﬁcant peri-stent calcium

(>90



), RA, OAS, and ELCA may be employed to improve stent

underexpansion by disrupting the calciﬁed plaque behind the stent.

IVL may also be useful. These techniques are associated with cal-

cium modiﬁcation and/or fracture, and when followed by high-

pressure inﬂations may reduce stent underexpansion. However, if

unsuccessful, coronary artery bypass grafting may be necessary (see

Figure 3).

Balloon angioplasty. Balloon angioplasty should be the initial step in

focal lesions or if short dual antiplatelet therapy (DAPT) duration is

required. In the setting of stent underexpansion, high-pressure non-

compliant balloon inﬂations are the preferred strategy.

Super high-pressure balloons. Double layer, noncompliant coronary

balloons (OPN NC, SIS Medical) capable of inﬂation pressures ranging

from 35 to 55 atm have recently become available in the United States.

This class of percutaneous transluminal coronary angioplasty balloon

has performed favorably in severely calciﬁed de novo lesions and may

be a consideration in ISR secondary to an underexpanded stent.

Neointimal HyperplasiaStent Under-expansion Stent Fracture Neoatherosclerosis

Minimum Stent Area 2.95 mm

Neointima Lumen AreaLipidic Neoatherosclerosis Old Stent StrutsCalcium

ABCD

Ac Bc Cc Dc

Acc Bcc Ccc Dcc

Coronary

Angiogram

OCT

Mechanism of

Stent Failure

Top

Neointimal HyperplasiaStent Under-expansion Stent Fracture Neoatherosclerosis

Neointima Lumen AreaCalcified Neoatherosclerosis Old Stent Struts

de novo Plaque

Minimum Stent Area 3.2 mm

ABCD

Ac Bc Cc Dc

Acc Bcc Ccc Dcc

Coronary

Angiogram

IVUS

Mechanism of

Stent Failure

Bottom

In-Stent Restenosis

Figure 1.

Mechanisms of in-stent restenosis evaluated by intravascular

imaging. A

-D

are optical coherence tomography (OCT) or intra-

vascular ultrasound (IVUS) images corresponding to the in-stent

restenosis seen in the angiographic images (A-D, white arrows).

-D

are representative diagrams provided to clarify the intra-

coronary images, A

-D

. Top . Mechanisms of in-stent restenosis

evaluated by OCT. (A) A patient experienced recurrent in-stent

restenosis (ISR), and OCT visualized a severely underexpanded

stent because of circumferential thick calcium behind stent with only

a minimum amount of neointimal hyperplasia. (B) This patient was

treated with a single drug-eluting stent. At the time of ISR, the OCT

image showed a lack of stent struts over half of the arterial

circumference (double headed arrow) while stents struts were

overlapped at 7 to 9 o’clock. These are typical features of stent

fracture. (C) Excess amount of neointimal hyperplasia within a well-

expanded stent. (D) Lipidic neointima (strong signal attenuation)

within the stent struts indicating neoatherosclerosis. Bottom.

Mechanisms of in-stent restenosis evaluated by IVUS (A) IVUS visu-

alized an underexpanded stent with a minimum amount of neo-

intimal hyperplasia. By looking at the adjacent segment, the cause

of underexpansion was a small vessel with a myocardial bridge. (B)

IVUS delineates overlapped struts within a single stent at 7 to 10

o’clock indicating stent fracture. (C) Excess amount of neointimal

hyperplasia within a well-expanded old stent. (D) Calciﬁed plaque

(superﬁcial hyperintensity with acoustic shadow from 8 to 12 o’clock)

within the stent indicates neoatherosclerosis.

4 L.W. Klein et al. / Journal of the Society for Cardiovascular Angiography & Interventions 2 (2023) 100971

Repeat DES. In general, repeat DES implantation has historically

shown superior results compared with balloon angioplasty alone.

However, this approach should only be undertaken once appropriate

sizing and expansion of the original stent has been assured using

intravascular imaging. A second stent may not be necessary if the

original stent was underdeployed and can be corrected.

If focal edge restenosis, stent gap, or stent fracture is identiﬁed,

conventional or high-pressure balloon dilation at the site of the me-

chanical complication should be the initial treatment. This should then

be followed by repeat DES implantation when the ISR is focal. Repeat

DES to cover the entire diseased segment can be performed when the

ISR is diffuse or proliferative, but care should be taken to minimize the

stent coverage as much as possible.

44–52

There is no deﬁnitive evidence

regarding which type of DES should be used to treat ISR of a previously

implanted DES, and there is no consensus on whether a different stent

type or drug should be used when an additional DES is implanted.

However, the RIBS III trial

assessed the impact of selecting a different

DES for treatment of ISR and demonstrated better angiographic and

clinical outcomes at 9-month follow-up in the cohort that received a

different DES than the ﬁrst implanted stent.

Cutting and scoring balloons. The use of balloons incorporating

cutting or scoring elements has been shown in very small series to result

Table 3. Applications of OCT vs IVUS

34,35

IVUS OCT

Assessing lesion severity in left main disease þþþ þ

Assessing de novo lesion characteristics

Thin cap ﬁbroatheroma  þþþ

Thrombus þ þþþ

Plaque rupture þþ þþþ

Calciﬁed nodule þ þþþ

Dissection þþ þþþ

Positive remodeling þþþ þ

Plaque burden þþþ þ

Aorto-ostial disease þþþ 

Stent optimization

Expansion þþ þþþ

Apposition þþ þþþ

Stent failure

Neointimal hyperplasia þþþ

Underexpansion þþ þþþ

Malapposition þþ þþþ

Renal impairment þþþ þ

þþþ Excellent; þþ Good; þ Poor;  Not advised

IVUS, intravascular ultrasound; OCT, optical coherence tomography.

Table 4. Summary of in-stent restenosis and stent thrombosis management strategies

Modalities of

treatment

When to consider Other considerations

In-stent restenosis

1,2,20,38–51

Balloon angioplasty  Focal, discrete lesions

 Stent underexpansion

 Need for short DAPT

 Risk of recurrence and edge dissection high

 Use of DCB associated with lower risk of TLR and binary restenosis

Repeat DES  If only one prior layer, may consider over balloon

angioplasty alone

 Focal edge restenosis, stent gap, stent fracture

 Reduction in need for target revascularization compared with angioplasty alone

 No deﬁnitive consensus for change in-stent type but RIBS III trial showed reduction of

restenosis rate and improved event-free survival in cohort receiving a different DES

platform

Cutting and scoring

balloons

 May modify neointimal growth

 May help to avoid additional stent layer

 Scoring balloon angioplasty superior to PTA alone at 6-8 mo (improved angiographic

outcomes and reduced stenosis)

Atheroablation  Should be considered if mode of stent underexpansion

calciﬁcation and resistant to high-pressure balloons

 Should be considered when signiﬁcant neointimal

hyperplasia present

 Clinical trials for use of atheroablation for ISR negative

DCB  May help to avoid additional stent layer  Treatment with DCB non-inferior to DES in terms of 6-mo MLD

Vascular

brachytherapy

 Refractory ISR

 Limited availability

 Due to delay in endothelialization, patients may need lifelong DAPT

 Treatment can be repeated every 12 mo

Intravascular

lithotripsy

 May be considered when there is highly calciﬁed

neoatherosclerosis

 Limited data to suggest proper case selection

Stent thrombosis

52–55

Balloon angioplasty  May be needed in addition to repeat DES and/or

aspiration thrombectomy to restore coronary blood ﬂow

Repeat DES  May be needed in addition to PTA and/or aspiration

thrombectomy to restore coronary blood ﬂow

 Should normally limit to signiﬁcant residual dissections

after PTA

 No stent type associated with reduction in ST

Aspiration

thrombectomy

 Consider when heavy thrombus burden present

 Consider adjunctive glycoprotein IIb/IIIa inhibitors if

persistent heavy thrombus burden after aspiration

 Associated with improved microvascular perfusion during STEMI because of ST

 Majority of patients undergoing aspiration thrombectomy had successful recanalization

Pharmacologic

therapies

 Consider glycoprotein IIb/IIIa inhibitor infusion

 Assess compliance and consider switch to higher

potency antiplatelet therapy if the patient was compliant

and still taking DAPT

 May consider drug resistance testing and prolonged

DAPT duration

 Consider patient’s renal function and bleeding risk when continuing glycoprotein IIb/IIIa

inhibitor after PCI

 Prolonged anticoagulation and antiplatelet therapy may be beneﬁcial when residual

thrombus is detected following intervention

DAPT, dual antiplatelet therapy; DCB, drug-coated balloon; DES, drug-eluting stent; ISR, in-stent restenosis; MLD, minimal lumen diameter; PCI, percutaneous coronary

intervention; PTA, percutaneous transluminal angioplasty; STEMI, ST-elevation myocardial infarction; TLR, target lesion revascularization.

Avoid when there are already 2 layers of stent

L.W. Klein et al. / Journal of the Society for Cardiovascular Angiography & Interventions 2 (2023) 100971 5

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