Abstract 10073: Characteristics of Very Late Stent Thrombosis Assessed by Coronary Angioscopy and Histopathology of Aspirated Thrombus

Background: The mechanisms of very late stent thrombosis (VLST) have not been fully elucidated and may involve multiple factors. The aim of this study was to evaluate characteristics of VLST based on angioscopy and histopathology of aspirated thrombus. Methods: Coronary angioscopy was performed in all stent thrombosis cases to evaluate the culprit lesion. The mechanisms of VLST were divided according to two factors by angioscopic findings such as uncovered struts and neoatherosclerosis. Uncovered struts were defined as stent struts uncovered by neointima. Neoatherosclerosis was defined as stent struts covered by yellow neointima. Furthermore, aspirated material was collected for assessment of atherothrombotic characteristics in all cases. Results: From February 2011 to April 2015, emergency PCI for acute myocardial infarction was performed in 336 patients, with 13 of these cases due to stent thrombosis. Clinical characteristics of VLST patients are shown in Figure. In uncovered struts, all 3 cases were not on any antiplatelet therapy prior to VLST, whereas patients with neoatherosclerosis were taking at least one antiplatelet agents except for one case. In the presence of neoatherosclerosis, thrombus with atheroma material was aspirated in 5 of 10 cases despite there was no atheroma material in patients with uncovered strut. The time period of occurrence of VLST was significantly shorter in patients with uncovered strut compared with neoatherosclerosis (48.6±12.5 month vs. 84.3±6.9 month, p=0.03) In 13 case of VLST, peri stent contrast staining (PSS) was found in 1 case of each neoatherosclerosis and uncovered strut at the time of follow-up angiography. Conclusions: Discontinuation of dual anti platelet therapy was an important predictor for VLST, especially in patients with uncovered struts. However, most VLST weredue to neoatherosclerotic plaque rupture assessed by coronary angioscopy, which were also confirmed by histopathology of aspirated thrombus.

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Abstract 5992: Comparison of 4 Years Efficacy and Durability of Sirolimus-Eluting Stent and Paclitaxel- Eluting Stent Deployment in Patients with Very Long Coronary Lesions: Multicenter Registry in Asia

Circulation ◽

10.1161/circ.118.suppl_18.s_1041-a ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Sunao Nakamura ◽

Hisao Ogawa ◽

Jang-Ho Bae ◽

Yeo Hans Cahyadi ◽

Wasan Udayachalerm ◽

...

Keyword(s):

Myocardial Infarction ◽

Stent Thrombosis ◽

Late Stent Thrombosis ◽

Cardiac Events ◽

Stent Deployment ◽

Very Late Stent Thrombosis ◽

Coronary Lesion ◽

Coronary Lesions ◽

Sirolimus Eluting Stent

Aim : The aim of this study is to compare the 4 years safety and durability of Sirolimus-eluting stent (SES) and Paclitaxel-eluting stent (PES) deployment on the outcome of patients with very long coronary lesions (VLL). Methods : A prospective analysis of 656 patients 730 lesions (male 70.4%, mean age 66.9 yrs) with very long coronary lesion (≥40mm) (368 SES and 288 PES) in five high volume Asian centers after successful stenting in VLL was performed. Lesion locations of VLL were LAD 48.2% (SES 50.2%, PES 45.7%), LCX 18.5%, RCA 33.3%. Complete clinical follow-up to 4 years is being analyzed for all patients. Results : The baseline clinical characteristics between 2 groups were similar. At 4 years overall cardiac events of SES (16.3%) were lower than PES (24.0%) (p=0.03). See table for clinical results. Conclusion : The use of SES and PES in patients with very long coronary lesion was safe and feasible with low acute complication and low incidence of restenosis. SES showed lesser incidence of cardiac events (death, myocardial infarction, CABG and PCI) at 4 years clinical follow-up. SAT (sub acute stent thrombosis), LAST (late stent thrombosis: ~1year), VLAST (very late stent thrombosis: 1year~ 4years) MACE (death, myocardial infarction, CABG and PCI).

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Neoatherosclerosis, plaque rupture and very late stent thrombosis of a first generation drug eluting stent treated with aspiration thrombectomy and newer generation drug eluting stent implantation

International Journal of Cardiology ◽

10.1016/j.ijcard.2014.12.118 ◽

2015 ◽

Vol 201 ◽

pp. 648-649 ◽

Cited By ~ 1

Author(s):

Ahmad Mustafa ◽

Safa Daghem ◽

Vasim Farooq ◽

Farzin Fath-Ordoubadi ◽

Bernard Clarke

Keyword(s):

Stent Thrombosis ◽

Stent Implantation ◽

First Generation ◽

Plaque Rupture ◽

Drug Eluting Stent ◽

Late Stent Thrombosis ◽

Aspiration Thrombectomy ◽

Very Late Stent Thrombosis ◽

Drug Eluting

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Acute Coronary Syndrome after 17 Years of Bare Metal Stent Implantation: “Very” Very Late Stent Thrombosis

Case Reports in Cardiology ◽

10.1155/2020/9628719 ◽

2020 ◽

Vol 2020 ◽

pp. 1-5

Author(s):

Raghavendra Rao K ◽

S. Reddy ◽

J. R. Kashyap ◽

K. Vikas ◽

Hithesh Reddy ◽

...

Keyword(s):

Acute Coronary Syndrome ◽

Stent Thrombosis ◽

Plaque Rupture ◽

Bare Metal Stents ◽

Metal Stents ◽

Bare Metal ◽

Late Stent Thrombosis ◽

Very Late Stent Thrombosis ◽

Mortality And Morbidity ◽

Coronary Syndrome

Very late stent thrombosis (VLST) is a catastrophic and life-threatening complication after percutaneous coronary intervention which presents as an acute coronary syndrome with significantly high mortality and morbidity. VLST is a rare entity with drug-eluting stents and even rarer with bare metal stents. The exact pathophysiologic mechanism of VLST after BMS implantation is not known although various mechanisms have been proposed. Recently, in-stent neoatherosclerosis with intimal plaque rupture has been proposed as a potential mechanism of VLST after BMS. We report a rare case of VLST occurring 17 years after BMS implantation with angiographic and intravascular imaging evidence which provides insight into the mechanisms of VLST.

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The Association Between S100A8/A9 and the Development of Very Late Stent Thrombosis in Patients With Acute Myocardial Infarction

Clinical and Applied Thrombosis/Hemostasis ◽

10.1177/1076029620943295 ◽

2020 ◽

Vol 26 ◽

pp. 107602962094329

Author(s):

Xiang Wang ◽

Meng Guan ◽

Xiuhang Zhang ◽

Taiyuan Ma ◽

Muli Wu ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Stent Thrombosis ◽

High Sensitivity ◽

Coronary Intervention ◽

Serum Levels ◽

Late Stent Thrombosis ◽

Very Late Stent Thrombosis ◽

Hs Crp

Very late stent thrombosis (VLST) is a rare but serious complication following percutaneous coronary intervention (PCI). S100A8/A9 plays an important role in thrombosis through modulating the inflammatory response. This observational study aimed to reveal the association between S100A8/A9 and VLST. Continuous blood samples were collected from patients at both the time of index PCI for acute myocardial infarction (AMI) and the time of PCI for VLST (VLST group) or follow-up coronary angiography (AMI group). In all, 56 patients were selected in each group from a cohort of 8476 patients and other 112 individuals who underwent health checkups (normal control [NC] group) were selected as controls. Serum levels of S100A8/A9 and high sensitivity C-reactive protein (hs-CRP) were tested and compared. The mean level of S100A8/A9 was 3754.4 ± 1688.9 ng/mL during index PCI and increased to 5517.8 ± 2650.9 ng/mL at the time of VLST; in the AMI group, S100A8/A9 level was 2434.9 ± 1243.4 ng/mL during index PCI and decreased to 1568.2 ± 772.1 ng/mL during follow-up, similar to that detected in the NC group (1618.2 ± 641.4 ng/mL). Of note, S100A8/A9 levels showed significant increases during VLST when compared to its own levels during index PCI, which was different from the changes of hs-CRP. Higher serum levels of S100A8/A9 are associated with the development of VLST.

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Very late stent thrombosis caused by neoatherosclerotic plaque rupture

EuroIntervention ◽

10.4244/eijv10i12a251 ◽

2015 ◽

Vol 10 (12) ◽

pp. e1-e3 ◽

Cited By ~ 1

Author(s):

Mikkel Hougaard ◽

Per Thayssen ◽

Henrik Steen Hansen ◽

Lisette Okkels Jensen

Keyword(s):

Stent Thrombosis ◽

Plaque Rupture ◽

Late Stent Thrombosis ◽

Very Late Stent Thrombosis

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Very late stent thrombosis and neointimal plaque rupture after implantation of sirolimus-eluting stents: observations with angiography, IVUS and OCT

Cardiovascular Intervention and Therapeutics ◽

10.1007/s12928-011-0064-1 ◽

2011 ◽

Vol 26 (3) ◽

pp. 263-268 ◽

Cited By ~ 2

Author(s):

Nobuo Sakamoto ◽

Kazuhiko Nakazato ◽

Tomofumi Misaka ◽

Hiroyuki Mizukami ◽

Hiroyuki Kunii ◽

...

Keyword(s):

Stent Thrombosis ◽

Plaque Rupture ◽

Late Stent Thrombosis ◽

Very Late Stent Thrombosis

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Coronary Aneurysm Occurring Late after Drug-Eluting Stent Implantation

ISRN Cardiology ◽

10.5402/2011/367512 ◽

2011 ◽

Vol 2011 ◽

pp. 1-3 ◽

Cited By ~ 2

Author(s):

Etan Abergel ◽

Ariel Roguin

Keyword(s):

Case Report ◽

Stent Thrombosis ◽

Stent Implantation ◽

Healing Process ◽

Late Stent Thrombosis ◽

Very Late Stent Thrombosis ◽

Coronary Stent Implantation ◽

Increased Risk ◽

Drug Eluting

Drug-eluting stents may affect the normal healing process of the vessel wall and the remodeling process and may lead to late stent malapposition (LSM). The known incidence of this phenomen originates from short-term angiographic follow-up studies. We describe a case report of very late stent malapposition and marked positive vessel remodeling 3 years after sirolimus-eluting coronary stent implantation. Angiography performed one year after stent implantation was normal. Thus, the abnormalities developed sometime between years 1 and 3. The cause is unknown, but it is reasonable to suggest a local effect of the medication/polymer of the stent. LSM rate and aneurysmal formation is higher in DES than in BMS and may be associated with increased risk for late stent thrombosis. Currently, the risk of very late stent thrombosis after DES implantation is of major concern. As observed in this case report, LSM might occur and develop very late. This has significant consequences especially to the many asymptomatic patients with DES implanted many years ago and the recommendation of dual antiplatelet therapy. More studies with late and very late follow up are needed to better define this finding, its mechanism, how to avoid it, and how to treat it properly.

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