European Heart Journal – Cardiovascular Imaging (2015) 16, 110–111 doi:10.1093/ehjci/jeu199
EDITORIAL
Why are we so concerned with acute incomplete stent apposition? Gary S. Mintz* Cardiovascular Research Foundation, 111 East 59th Street – 11th Floor, New York 10022 NY, USA Online publish-ahead-of-print 23 October 2014
Cook et al.7 the late ISA area in their 13 very late stent thrombosis patients measured 8.3 + 7.5 mm2) or frank aneurysm formation11—is most related to stent thrombosis. While late ISA is frequently seen at the time of very late DES thrombosis,7,12 incidentally detected late ISA during routine follow-up studies of DES-treated patients is not associated with an increased frequency of subsequent adverse events.5,6,13,14 Furthermore, the cause-andeffect relationship between late ISA and very late stent thrombosis has been challenged by studies relating late ISA, very late stent thrombosis, and inflammation;9 studies reporting a high prevalence of strut fracture in very late stent thrombosis lesions;12 and most recently OCT studies indicating that neoatherosclerosis may be a more important cause of very late stent thrombosis than late ISA.15 What does this mean clinically? Adequately powered clinical studies—such as definitive, large registries with careful and systematic follow-up—should be undertaken to determine whether acute ISA is or is not predictive of stent thrombosis and, if so, how large an area, diameter, or volume is problematic. To the contrary, in the largest OCT study available to date in 351 patients,5 acute ISA was detected in 62% of stents post-PCI, measured 1.16 + 0.69 mm2 (similar to SES in the current study), persisted in half (but decreasing to 0.88 + 0.71 mm2), and was not associated with any adverse events at 28.6 + 10.3 months follow-up. Until information is available to the contrary, the misguided emphasis on avoiding ISA should be replaced with renewed attention to what is known to be important—stent expansion and proper lesion coverage.3 Conflict of interest: G.S.M. reports the following relationships with industry: consultant, BostonScientific; grant support and consultant, Volcano; grant support, St Jude; grant support and consultant, InfraReDx; consultant, ACIST.
References 1. Shimamura K, Kubo T, Akasaka T, Kozuma K, Kimura K, Kawamura M et al. Outcomes of everolimus-eluting stent incomplete stent apposition: a serial optical coherence tomography analysis. Eur Heart J Cardiovasc Imaging 2015;16:41 –6. 2. Ziada KM, Nissen SE. Intravascular ultrasound imaging. Chapter 27. In: Moliterno DJ (ed.) Cardiac Catheterization and Interventional Cardiology Self-Assessment Program, Version 3. Bethesda, MD: American College of Cardiology Foundation, 2008; 297 –311.
The opinions expressed in this article are not necessarily those of the Editors of EHJCI, the European Heart Rhythm Association or the European Society of Cardiology.
* Corresponding author. Tel: +646 434 4133; fax: +646 434 4715. Email: [email protected] Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2014. For permissions please email: [email protected].
Downloaded from by guest on April 10, 2016
In their article, Shimamura et al. report that incomplete stent apposition (ISA) was observed in all 38 everolimus-eluting stents (EES) and all 39 sirolimus-eluting stents (SES) post-percutaneous coronary intervention (PCI) (measuring 315 + 94 mm and 0.50 + 0.24 mm2 in EES and 308 + 119 mm and 0.95 + 0.70 mm2 in SES), that it persisted in 26% of EES and 38% of SES at 8–12 months although the size of the ISA significantly decreased during follow-up in both groups (to 110 + 165 mm and 0.17 + 0.27 mm2 in EES and 143 + 175 mm and 0.41 + 0.66 mm2 in SES), and that the best post-stenting optical coherence tomographic (OCT)measured ISA distance that predicted late-persistent ISA was .355 mm in EES and .285 mm in SES.1 The authors concluded: ‘OCT can predict late-persistent ISA after DES implantation and provide useful information to optimize PCI’. Why are we so concerned with acute ISA? Despite the lack of supporting evidence, the most recent Cardiac Catheterization and Interventional Cardiology Self-Assessment Program (CathSAP) stated, ‘stent apposition may be the most important determinant of freedom from subacute stent thrombosis with DES’.2 To the contrary, the predictors of early ST that have been identified with intravascular imaging are primarily stent underexpansion and secondarily inflow/ outflow problems such as a larger plaque burden, a small lumen area, and/or a large dissection at either stent edge.3 Depending on the sensitivity of the methodology used, ISA after DES implantation is observed in up to 40% by IVUS in patients undergoing primary PCI4 and 60– 100% in stable patients by OCT.1,5 Given the nearly ubiquitous finding of acute ISA, it is not surprising that studies using IVUS2,6 or OCT5 have shown no relationship between acute ISA and early, late, or very late stent thrombosis after DES implantation. Then there is the second misconception that acute ISA is important because it can persist; and late ISA has been linked to very late stent thrombosis.7 – 9 However, not all late ISA are equal in terms of prognosis; pathoanatomic pathways leading to late ISA also include positive remodelling causing an increase in vessel dimensions that is greater than any increase in abluminal tissue growth and abluminal thrombus dissolution or plaque regression without positive remodelling. Positive remodelling is responsible for approximately one-third of late ISA;4 and late ISA in the setting of positive remodelling10—especially large areas of malapposition (in the initial report by
111
Editorial
3. Mintz GS. Clinical utility of intravascular imaging and physiology in coronary artery disease. J Am Coll Cardiol 2014;64:207 –22. 4. Guo N, Maehara A, Mintz GS, He Y, Xu K, Wu X et al. Incidence, mechanisms, predictors, and clinical impact of acute and late stent malapposition after primary intervention in patients with acute myocardial infarction: an intravascular ultrasound substudy of the Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction (HORIZONS-AMI) trial. Circulation 2010;122: 1077– 84. 5. Im E, Kim BK, Ko YG, Shin DH, Kim JS, Choi D et al. Incidences, predictors, and clinical outcomes of acute and late stent malapposition detected by optical coherence tomography after drug-eluting stent implantation. Circ Cardiovasc Interv 2014;7: 88 – 96. 6. Steinberg DH, Mintz GS, Mandinov L, Yu A, Ellis SG, Grube E et al. Long-term impact of routinely detected early and late incomplete stent apposition: an integrated intravascular ultrasound analysis of the TAXUS IV, V, and VI and TAXUS ATLAS workhorse, long lesion, and direct stent studies. JACC Cardiovasc Interv 2010;3:486 –94. 7. Cook S, Wenaweser P, Togni M, Billinger M, Morger C, Seiler C et al. Incomplete stent apposition and very late stent thrombosis after drug-eluting stent implantation. Circulation 2007;115:2426 – 34. 8. Hassan AK, Bergheanu SC, Stijnen T, van der Hoeven BL, Snoep JD, Plevier JW et al. Late stent malapposition risk is higher after drug-eluting stent compared with baremetal stent implantation and associates with late stent thrombosis. Eur Heart J 2010; 31:1172 –80.
9. Cook S, Eshtehardi P, Kalesan B, Ra¨ber L, Wenaweser P, Togni M et al. Impact of incomplete stent apposition on long-term clinical outcome after drug-eluting stent implantation. Eur Heart J 2012;33:1334 –43. 10. Guagliumi G, Sirbu V, Musumeci G, Gerber R, Biondi-Zoccai G, Ikejima H et al. Examination of the in vivo mechanisms of late drug-eluting stent thrombosis: findings from optical coherence tomography and intravascular ultrasound imaging. JACC Cardiovasc Interv 2012;5:12–20. 11. Alfonso F, Pe´rez-Vizcayno MJ, Ruiz M, Sua´rez A, Cazares M, Herna´ndez R et al. Coronary aneurysms after drug-eluting stent implantation: clinical, angiographic, and intravascular ultrasound findings. J Am Coll Cardiol 2009;53:2053 –60. 12. Kosonen P, Vikman S, Jensen LO, Lassen JF, Harnek J, Olivecrona GK et al. Intravascular ultrasound assessed incomplete stent apposition and stent fracture in stent thrombosis after bare metal versus drug-eluting stent treatment the Nordic Intravascular Ultrasound Study (NIVUS). Int J Cardiol 2013;168:1010 –6. 13. Hong MK, Mintz GS, Lee CW, Park DW, Lee SW, Kim YH et al. Impact of late drug-eluting stent malapposition on 3-year clinical events. J Am Coll Cardiol 2007; 50:1515 –6. 14. Hoffmann R, Morice MC, Moses JW, Fitzgerald PJ, Mauri L, Breithardt G et al. Impact of late incomplete stent apposition after sirolimus-eluting stent implantation on 4-year clinical events: intravascular ultrasound analysis from the multicentre, randomised, RAVEL, E-SIRIUS and SIRIUS trials. Heart 2008;94:322–8. 15. Kang SJ, Lee CW, Song H, Ahn JM, Kim WJ, Lee JY et al. OCT analysis in patients with very late stent thrombosis. JACC Cardiovasc Imaging 2013;6:695 –703.
IMAGE FOCUS
doi:10.1093/ehjci/jeu164 Online publish-ahead-of-print 3 September 2014
.............................................................................................................................................................................
Late thrombosis of thoracic aortic stent graft 1 Cardiology Department, Vall d’Hebron Hospital, Passeig de la Vall D’Hebron, 119-129, Barcelona 08035, Spain and 2Radiology Department, Vall d’Hebron Hospital, Barcelona, Spain
* Corresponding author. Tel: +34 722109406, Email: [email protected]
A 17-year-old motorcycle accident victim underwent urgent successful thoracic endovascular aortic repair (TEVAR) of blunt thoracic aortic rupture. On computed tomography (CT), the rupture was distal to the origin of the subclavian artery and was treated with a custom-made, 24 mm, 6.6 cm TX2 stent. The stent graft was inserted via the femoral artery and positioned at the level of the area of aortic rupture. One year later, the patient was admitted to the emergency department for sudden onset of severe dyspnoea, abdominal pain, and paraparesis of the legs. Transoesophageal echocardiography revealed severe circumferential thrombosis of the distal part of the stent (Panels A and B, and see Supplementary data online, Movie S1) producing significant stenosis. Thoracoabdominal CT showed in-stent thrombosis causing severe stenosis of the distal descending thoracic aorta, without signs of stent degeneration, endoleaks, and/or collapse of the scaffold (Panel C). Emergency open aortic bypass surgery was performed with an extra-anatomical Dacron graft connecting the ascending aorta to the supracoeliac abdominal aorta, as seen on the postoperative CT (Panel D). The patient was discharged with no additional complications. Late thrombosis of the stent was an unusual complication of TEVAR. A possible mechanism of this complication may be a tiny intimal lesion secondary to graft delivery that could initiate a stepwise thrombosis process. Aortic stent thrombosis can determine different clinical settings: distal emboli or an increase in afterload with resistant high blood pressure leading to heart failure. If the patient is haemodynamically stable, anticoagulants can be indicated. When signs of severe stenosis and haemodynamic compromise appear, emergency surgery must be performed. Supplementary data are available at European Heart Journal – Cardiovascular Imaging online. Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2014. For permissions please email: [email protected].
Downloaded from by guest on April 10, 2016
Valentina Galuppo1*, Domenico Gruosso1, Giuliana Maldonado1, Hug Cuellar2, and Arturo Evangelista1
EDITORIAL
Why are we so concerned with acute incomplete stent apposition? Gary S. Mintz* Cardiovascular Research Foundation, 111 East 59th Street – 11th Floor, New York 10022 NY, USA Online publish-ahead-of-print 23 October 2014
Cook et al.7 the late ISA area in their 13 very late stent thrombosis patients measured 8.3 + 7.5 mm2) or frank aneurysm formation11—is most related to stent thrombosis. While late ISA is frequently seen at the time of very late DES thrombosis,7,12 incidentally detected late ISA during routine follow-up studies of DES-treated patients is not associated with an increased frequency of subsequent adverse events.5,6,13,14 Furthermore, the cause-andeffect relationship between late ISA and very late stent thrombosis has been challenged by studies relating late ISA, very late stent thrombosis, and inflammation;9 studies reporting a high prevalence of strut fracture in very late stent thrombosis lesions;12 and most recently OCT studies indicating that neoatherosclerosis may be a more important cause of very late stent thrombosis than late ISA.15 What does this mean clinically? Adequately powered clinical studies—such as definitive, large registries with careful and systematic follow-up—should be undertaken to determine whether acute ISA is or is not predictive of stent thrombosis and, if so, how large an area, diameter, or volume is problematic. To the contrary, in the largest OCT study available to date in 351 patients,5 acute ISA was detected in 62% of stents post-PCI, measured 1.16 + 0.69 mm2 (similar to SES in the current study), persisted in half (but decreasing to 0.88 + 0.71 mm2), and was not associated with any adverse events at 28.6 + 10.3 months follow-up. Until information is available to the contrary, the misguided emphasis on avoiding ISA should be replaced with renewed attention to what is known to be important—stent expansion and proper lesion coverage.3 Conflict of interest: G.S.M. reports the following relationships with industry: consultant, BostonScientific; grant support and consultant, Volcano; grant support, St Jude; grant support and consultant, InfraReDx; consultant, ACIST.
References 1. Shimamura K, Kubo T, Akasaka T, Kozuma K, Kimura K, Kawamura M et al. Outcomes of everolimus-eluting stent incomplete stent apposition: a serial optical coherence tomography analysis. Eur Heart J Cardiovasc Imaging 2015;16:41 –6. 2. Ziada KM, Nissen SE. Intravascular ultrasound imaging. Chapter 27. In: Moliterno DJ (ed.) Cardiac Catheterization and Interventional Cardiology Self-Assessment Program, Version 3. Bethesda, MD: American College of Cardiology Foundation, 2008; 297 –311.
The opinions expressed in this article are not necessarily those of the Editors of EHJCI, the European Heart Rhythm Association or the European Society of Cardiology.
* Corresponding author. Tel: +646 434 4133; fax: +646 434 4715. Email: [email protected] Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2014. For permissions please email: [email protected].
Downloaded from by guest on April 10, 2016
In their article, Shimamura et al. report that incomplete stent apposition (ISA) was observed in all 38 everolimus-eluting stents (EES) and all 39 sirolimus-eluting stents (SES) post-percutaneous coronary intervention (PCI) (measuring 315 + 94 mm and 0.50 + 0.24 mm2 in EES and 308 + 119 mm and 0.95 + 0.70 mm2 in SES), that it persisted in 26% of EES and 38% of SES at 8–12 months although the size of the ISA significantly decreased during follow-up in both groups (to 110 + 165 mm and 0.17 + 0.27 mm2 in EES and 143 + 175 mm and 0.41 + 0.66 mm2 in SES), and that the best post-stenting optical coherence tomographic (OCT)measured ISA distance that predicted late-persistent ISA was .355 mm in EES and .285 mm in SES.1 The authors concluded: ‘OCT can predict late-persistent ISA after DES implantation and provide useful information to optimize PCI’. Why are we so concerned with acute ISA? Despite the lack of supporting evidence, the most recent Cardiac Catheterization and Interventional Cardiology Self-Assessment Program (CathSAP) stated, ‘stent apposition may be the most important determinant of freedom from subacute stent thrombosis with DES’.2 To the contrary, the predictors of early ST that have been identified with intravascular imaging are primarily stent underexpansion and secondarily inflow/ outflow problems such as a larger plaque burden, a small lumen area, and/or a large dissection at either stent edge.3 Depending on the sensitivity of the methodology used, ISA after DES implantation is observed in up to 40% by IVUS in patients undergoing primary PCI4 and 60– 100% in stable patients by OCT.1,5 Given the nearly ubiquitous finding of acute ISA, it is not surprising that studies using IVUS2,6 or OCT5 have shown no relationship between acute ISA and early, late, or very late stent thrombosis after DES implantation. Then there is the second misconception that acute ISA is important because it can persist; and late ISA has been linked to very late stent thrombosis.7 – 9 However, not all late ISA are equal in terms of prognosis; pathoanatomic pathways leading to late ISA also include positive remodelling causing an increase in vessel dimensions that is greater than any increase in abluminal tissue growth and abluminal thrombus dissolution or plaque regression without positive remodelling. Positive remodelling is responsible for approximately one-third of late ISA;4 and late ISA in the setting of positive remodelling10—especially large areas of malapposition (in the initial report by
111
Editorial
3. Mintz GS. Clinical utility of intravascular imaging and physiology in coronary artery disease. J Am Coll Cardiol 2014;64:207 –22. 4. Guo N, Maehara A, Mintz GS, He Y, Xu K, Wu X et al. Incidence, mechanisms, predictors, and clinical impact of acute and late stent malapposition after primary intervention in patients with acute myocardial infarction: an intravascular ultrasound substudy of the Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction (HORIZONS-AMI) trial. Circulation 2010;122: 1077– 84. 5. Im E, Kim BK, Ko YG, Shin DH, Kim JS, Choi D et al. Incidences, predictors, and clinical outcomes of acute and late stent malapposition detected by optical coherence tomography after drug-eluting stent implantation. Circ Cardiovasc Interv 2014;7: 88 – 96. 6. Steinberg DH, Mintz GS, Mandinov L, Yu A, Ellis SG, Grube E et al. Long-term impact of routinely detected early and late incomplete stent apposition: an integrated intravascular ultrasound analysis of the TAXUS IV, V, and VI and TAXUS ATLAS workhorse, long lesion, and direct stent studies. JACC Cardiovasc Interv 2010;3:486 –94. 7. Cook S, Wenaweser P, Togni M, Billinger M, Morger C, Seiler C et al. Incomplete stent apposition and very late stent thrombosis after drug-eluting stent implantation. Circulation 2007;115:2426 – 34. 8. Hassan AK, Bergheanu SC, Stijnen T, van der Hoeven BL, Snoep JD, Plevier JW et al. Late stent malapposition risk is higher after drug-eluting stent compared with baremetal stent implantation and associates with late stent thrombosis. Eur Heart J 2010; 31:1172 –80.
9. Cook S, Eshtehardi P, Kalesan B, Ra¨ber L, Wenaweser P, Togni M et al. Impact of incomplete stent apposition on long-term clinical outcome after drug-eluting stent implantation. Eur Heart J 2012;33:1334 –43. 10. Guagliumi G, Sirbu V, Musumeci G, Gerber R, Biondi-Zoccai G, Ikejima H et al. Examination of the in vivo mechanisms of late drug-eluting stent thrombosis: findings from optical coherence tomography and intravascular ultrasound imaging. JACC Cardiovasc Interv 2012;5:12–20. 11. Alfonso F, Pe´rez-Vizcayno MJ, Ruiz M, Sua´rez A, Cazares M, Herna´ndez R et al. Coronary aneurysms after drug-eluting stent implantation: clinical, angiographic, and intravascular ultrasound findings. J Am Coll Cardiol 2009;53:2053 –60. 12. Kosonen P, Vikman S, Jensen LO, Lassen JF, Harnek J, Olivecrona GK et al. Intravascular ultrasound assessed incomplete stent apposition and stent fracture in stent thrombosis after bare metal versus drug-eluting stent treatment the Nordic Intravascular Ultrasound Study (NIVUS). Int J Cardiol 2013;168:1010 –6. 13. Hong MK, Mintz GS, Lee CW, Park DW, Lee SW, Kim YH et al. Impact of late drug-eluting stent malapposition on 3-year clinical events. J Am Coll Cardiol 2007; 50:1515 –6. 14. Hoffmann R, Morice MC, Moses JW, Fitzgerald PJ, Mauri L, Breithardt G et al. Impact of late incomplete stent apposition after sirolimus-eluting stent implantation on 4-year clinical events: intravascular ultrasound analysis from the multicentre, randomised, RAVEL, E-SIRIUS and SIRIUS trials. Heart 2008;94:322–8. 15. Kang SJ, Lee CW, Song H, Ahn JM, Kim WJ, Lee JY et al. OCT analysis in patients with very late stent thrombosis. JACC Cardiovasc Imaging 2013;6:695 –703.
IMAGE FOCUS
doi:10.1093/ehjci/jeu164 Online publish-ahead-of-print 3 September 2014
.............................................................................................................................................................................
Late thrombosis of thoracic aortic stent graft 1 Cardiology Department, Vall d’Hebron Hospital, Passeig de la Vall D’Hebron, 119-129, Barcelona 08035, Spain and 2Radiology Department, Vall d’Hebron Hospital, Barcelona, Spain
* Corresponding author. Tel: +34 722109406, Email: [email protected]
A 17-year-old motorcycle accident victim underwent urgent successful thoracic endovascular aortic repair (TEVAR) of blunt thoracic aortic rupture. On computed tomography (CT), the rupture was distal to the origin of the subclavian artery and was treated with a custom-made, 24 mm, 6.6 cm TX2 stent. The stent graft was inserted via the femoral artery and positioned at the level of the area of aortic rupture. One year later, the patient was admitted to the emergency department for sudden onset of severe dyspnoea, abdominal pain, and paraparesis of the legs. Transoesophageal echocardiography revealed severe circumferential thrombosis of the distal part of the stent (Panels A and B, and see Supplementary data online, Movie S1) producing significant stenosis. Thoracoabdominal CT showed in-stent thrombosis causing severe stenosis of the distal descending thoracic aorta, without signs of stent degeneration, endoleaks, and/or collapse of the scaffold (Panel C). Emergency open aortic bypass surgery was performed with an extra-anatomical Dacron graft connecting the ascending aorta to the supracoeliac abdominal aorta, as seen on the postoperative CT (Panel D). The patient was discharged with no additional complications. Late thrombosis of the stent was an unusual complication of TEVAR. A possible mechanism of this complication may be a tiny intimal lesion secondary to graft delivery that could initiate a stepwise thrombosis process. Aortic stent thrombosis can determine different clinical settings: distal emboli or an increase in afterload with resistant high blood pressure leading to heart failure. If the patient is haemodynamically stable, anticoagulants can be indicated. When signs of severe stenosis and haemodynamic compromise appear, emergency surgery must be performed. Supplementary data are available at European Heart Journal – Cardiovascular Imaging online. Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2014. For permissions please email: [email protected].
Downloaded from by guest on April 10, 2016
Valentina Galuppo1*, Domenico Gruosso1, Giuliana Maldonado1, Hug Cuellar2, and Arturo Evangelista1
