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Vol. 66. Issue 4.
Pages 317-319 (April 2013)
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Vol. 66. Issue 4.
Pages 317-319 (April 2013)
Scientific letter
DOI: 10.1016/j.rec.2012.09.007
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Role of Intravascular Ultrasound in Stent Thrombosis
Valor de la ecografía intracoronaria en la trombosis de stent
Leire Unzué Vallejo
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Corresponding author:
, Felipe Hernández Hernández, María Teresa Velázquez Martín, Julio García Tejada, Agustín Albarrán González-Trevilla, Juan Tascón Pérez
Unidad de Hemodinámica y Cardiología Intervencionista, Hospital 12 de Octubre, Madrid, Spain
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Table. Intravascular Ultrasound Findings in Enrolled Patients and Therapeutic Management
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To the Editor,

Despite ongoing development in stent design and the greater efficacy of antiplatelet therapy, stent thrombosis (ST) continues to be a widely recognized and much dreaded adverse event, with an incidence of 1% to 5%1,2 and a mortality that exceeds 10% in all series.3,4 In ST, the implantation of an additional stent has been related to an adverse outcome, higher risk of rethrombosis, and increased mortality.1,2 Intravascular ultrasound (IVUS) is an essential tool to identify the causal mechanism of ST; however, IVUS is rarely used to investigate ST in our setting.1,5

We describe IVUS findings obtained in definitive STs referred between 2008 and 2011 to our hospital and compare the therapeutic management of patients who underwent IVUS to that of patients not examined with IVUS.

A total of 2028 patients with 3004 stents were treated and 45 definitive STs were reported, 18 (40%) of them investigated with IVUS (Table). IVUS was more likely to be used in acute and subacute ST than late or very late ST. In most cases, several ST-related mechanisms were identified: in patients with early ST (acute and subacute), underexpansion and lesion at the stent border were the most common echographic findings, whereas patients with late and very late thrombosis were most likely to show in-stent proliferation with severe stenosis and, in 1 case, malapposition due to positive vessel remodeling. The 4 ST mechanisms observed are shown in the Figure.


Intravascular Ultrasound Findings in Enrolled Patients and Therapeutic Management

Patient  Age  Vessel  Stent  Time, d  Angiographic findings  Intravascular ultrasound findings  Therapeutic management 
68  ADA  DES  Complete occlusion at proximal stent border  Underexpansion and adherent thrombus  Thrombus aspiration, abiximab, and postdilation 
70  RCA  BMS  Complete occlusion at proximal stent border  Intimal flap at proximal stent border  Thrombus aspiration and implantation of new BMS 
69  RCA  BMS  Image of organized stent thrombus, with TIMI 1 distal flow  Slight underexpansion. Severe lesion at distal stent border  Thrombus aspiration and implantation of new BMS 
72  ADA  DES  Complete stent occlusion at overlap of tandem stents  Considerable underexpansion (360° calcium ring in vessel) (Figure BHigh-pressure postdilation with balloons of increasing size 
63  ADA  DES  Complete occlusion at proximal stent border  Intimal flap at distal stent border, malapposition  Thrombus aspiration, abiximab, and implantation of a new DES 
69  ADA  DES  Complete occlusion at proximal stent border  Stent underexpansion and malapposition  Thrombus aspiration, abiximab, and postdilation 
47  RCA  DES  Complete stent occlusion (distal border)  Intimal flap at distal stent border with portal entrance distally visible but proximally trapped by stent; 60-90° arch  Thrombus aspiration, abiximab, and new DES 
76  Cx  DES  Complete occlusion at proximal stent border  Severe underexpansion, malapposition  Thrombus aspiration, abiximab, and postdilation 
72  RCA  BMS  V-shaped stents at bifurcation, with occlusion from stent origin in posterolateral artery  Underexpansion of posterolateral artery stent  Abciximab and postdilation 
10  40  ADA  BMS  Complete occlusion anterior to stent with ruptured plaque image at proximal stent border  Intimal flap at proximal stent border. Adherent thrombus (Figure AThrombus aspiration, abiximab, and new DES 
11  83  Dx  BMS  Complete occlusion from stent origin in first Dx  Stent struts adjusted to Dx ostium, protruding into ADA; underexpansion  Thrombus aspiration toward ADA, abiximab, and postdilation 
12  64  RCA  BMS  14  Stent thrombosis in middle RCA with TIMI 0 flow  Stent underexpansion  Thrombus aspiration, abiximab, and postdilation 
13  71  GSV  DES  240  Critical focal in-stent restenosis at distal border of bridge (anastomosis toward OM) with TIMI 1 distal flow  Severe concentric hyperplasia  Thrombus aspiration, abiximab, and new DES 
14  58  OM  DES  290  Image of stent thrombus with aneurysmal vessel dilatation at proximal stent border  Malapposition by positive vessel remodeling (Figure CThrombus aspiration, abiximab, and postdilation; IVUS confirmation of outcome 
15  49  RCA  DES  350  Complete occlusion at proximal stent border  Good stent apposition with no proliferation; adherent thrombus  Thrombus aspiration and abiximab 
16  69  PIV  DES  683  Complete occlusion of stent (middle segment) implanted in distal RCA toward posterior descending artery  Underexpansion and adherent thrombus  Abciximab and postdilation 
17  70  ADA  DES  1858  Image of organized stent thrombus with TIMI 1 distal flow  Stent underexpansion, malapposition, and residual thrombus  Thrombus aspiration, abiximab, and postdilation 
18  51  RCA  BMS  2221  Complete occlusion of proximal border of first stent (2 overlapping stents)  Diffuse stent proliferation (probable neoatherosclerosis) with severe stenosis (Figure DAbciximab and DES implant 
  Therapeutic management in both groupsP 
  IVUS (n=18)  No IVUS (n=27)   
Early thrombosis  12 (66.7)  5 (3.7)  .01* 
Late thrombosis  6 (33.3)  14 (51.8)  .22 
Bare-metal stents  7 (38.9)  9 (33.3)  .71 
Drug-eluting stents  11 (61.1)  18 (66.7)  .71 
Aspiration  14 (77.8)  13 (48.2)  .05* 
Abciximab  15 (83.3)  14 (51.8)  .03* 
New stent implantation  6 (33.3)  17 (62.9)  .05* 
Mortality  4 (22.2)  4 (14.8)  .52 
Rethrombosis  1 (5.5)  3 (11.1)  .52 

ADA, anterior descending artery; BMS, bare-metal stent; Cx, circumflex artery; DES, drug eluting stent; Dx, diagonal artery; GSV, great saphenous vein; IVUS, intravascular ultrasound; OM, obtuse marginal artery; PIV, posterior interventricular artery; RCA, right coronary artery; TIMI: Thrombolysis in Myocardial Infarction.

Malapposition is defined as 1 or more stent struts separated from the vessel wall, except at the origin of a secondary branch. Underexpansion is defined as minimal stent area <80% of the mean proximal and distal reference area.

* Statistically significant results.


Four main mechanisms of stent thrombosis. The upper row shows the coronary angiographies once distal flow is recovered, the middle row provides a zoomed view of the stent, and the bottom row contains intravascular ultrasound cross-sectional images. A: Intimal flap at the stent border. B: Stent underexpansion. C: Malapposition due to positive vessel remodeling. D: Neointimal proliferation with severe stenosis.


In terms of therapeutic management, patients with late thrombosis most often required balloon predilation to advance the IVUS probe, which could overestimate the minimum stent area. In 17 patients, IVUS identified the definitive cause of thrombosis. The symptoms were related to discontinuation of dual antiplatelet therapy in only 1 patient with late thrombosis, and IVUS study revealed no pathologic findings. The use of glycoprotein IIb-IIIa inhibitors and thrombosis aspiration devices was more common in the group of patients assessed with IVUS. STs examined by IVUS were treated less often with implantation of a second stent. In fact, IVUS study made it possible to orient and optimize treatment in all patients. No significant differences were detected in angiographic outcome, mortality, or rethrombosis.

The IVUS findings of early and late ST in our series presented different profiles, which could indicate that these entities have different pathophysiologic mechanisms. The relationship between early thrombosis and mechanical factors during the implant procedure has already been reported in previous studies. Cheneau et al.6 found that subacute ST and inadequate outcome in the implantation procedure was related to significantly smaller stent areas and other echographic findings, such as dissection, residual thrombus, or tissue prolapse between the struts. In the largest published register, Amstrong et al.4 identified multiple clinical, angiographic, and prognostic factors based on the point in time of the STs, which would indicate that each entity must correspond to a different etiologic mechanism. Additionally, these authors observed a stronger tendency toward stent implantation in very late thrombosis than in early thrombosis.

Implantation of an additional stent in thrombosis conditions was identified as an independent predictive factor of mortality and ST recurrence in the ESTROFA register.1 In our series, patients who underwent IVUS were less likely to receive a second stent as part of thrombosis management, but no differences in mortality or rethrombosis were observed. However, IVUS was more often used in early than late thrombosis, which could overestimate the value of IVUS in preventing implantation of a second stent.

IVUS is highly useful for investigating the causal mechanism of thrombosis symptoms, as it reveals pathophysiologic factors underestimated by conventional angiography and identifies patients who may benefit from implantation of an additional stent.


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Drug-eluting stent thrombosis: results from the multicenter Spanish registry ESTROFA (Estudio Español sobre TROmbosis de stents FArmacoactivos).
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Predictors of coronary stent thrombosis: the Dutch Stent Thrombosis Registry.
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Copyright © 2012. Sociedad Española de Cardiología
Revista Española de Cardiología (English Edition)

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