Failure Mechanisms and Neoatherosclerosis Patterns in Very Late Drug-Eluting and Bare-Metal Stent Thrombosis

Nakamura, Daisuke; Attizzani, Guilherme F.; Toma, Catalin; Sheth, Tej; Wang, Wei; Soud, Mohamad; Aoun, Reem; Tummala, Ramyashree; Leygerman, Milana; Fares, Anas; Mehanna, Emile; Nishino, Seiji; Fung, Anthony; Costa, Marco A.; Bezerra, Hiram G.

doi:10.1161/circinterventions.116.003785

Cited by 66 publications

(44 citation statements)

References 30 publications

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“…OCT analysis in patients with DES‐ISR demonstrated a wide variety of abnormal findings, such as thin cap fibroatheroma‐containing neointima, in‐stent neointimal rupture, and intraluminal thrombi . Neoatherosclerosis has been reported to be more frequently observed and exhibit more longitudinal extension in BMS compared with DES . On the other hand, lipid‐rich neoatherosclerosis is considered to develop inside stents earlier in DES than BMS …”

Section: Discussionmentioning

confidence: 99%

Vulnerable neoatherosclerosis in coronary artery with whole circumference showing intravascular echo attenuation

Hirota

Nomura

Ono

et al. 2019

Clinical Case Reports

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Section: Discussionmentioning

confidence: 99%

Vulnerable neoatherosclerosis in coronary artery with whole circumference showing intravascular echo attenuation

Hirota

Nomura

Ono

et al. 2019

Clinical Case Reports

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“…Taniwaki et al reported that the mechanisms for VLST in 58 patients receiving DES (20 next‐ and 38 first‐generation) were malapposition (34.5%), neoatherosclerosis (27.6%), uncovered struts (12.1%), and stent underexpansion (6.9%) . Three other OCT studies also investigated the mechanisms of stent thrombosis but also included bare metal stent thrombosis or late DES thrombosis that might act as confounders . These studies were not performed exclusively with patients with very late DES thrombosis.…”

Section: Discussionmentioning

confidence: 99%

“…Third, malapposition was consistently observed regardless of VLST 8 Three other OCT studies also investigated the mechanisms of stent thrombosis but also included bare metal stent thrombosis or late DES thrombosis that might act as confounders. 6,7,9 These studies were not performed exclusively with patients with very late DES thrombosis. The results of our study differed slightly from those of Taniwaki et al 8 in the types and frequencies of VLST mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…A retrospective study and 3 prospective multicenter registry studies using optical coherence tomography (OCT) showed that the morphological features of thrombosed DES include stent malapposition, uncovered DES struts, in-stent neoatherosclerosis, and stent underexpansion. [6][7][8][9] Nevertheless, data on these OCT features remain insufficient, especially for patients with very late DES thrombosis. Using OCT, this study investigated the morphological characteristics of very late DES thrombosis and changes in causative OCT findings over time.…”

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confidence: 99%

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Characteristics of Earlier Versus Delayed Presentation of Very Late Drug‐Eluting Stent Thrombosis: An Optical Coherence Tomographic Study

Lee

Ahn

Mintz

et al. 2017

JAHA

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BackgroundThe pathophysiology underlying very late drug‐eluting stent (DES) thrombosis is not sufficiently understood. Using optical coherence tomography, we investigated characteristics of very late stent thrombosis (VLST) according to different onset times.Methods and ResultsA total of 98 patients from 10 South Korean hospitals who underwent optical coherence tomography for evaluation of very late DES thrombosis were retrospectively included in analyses. VLST occurred at a median of 55.1 months after DES implantation. All patients were divided into 2 equal groups of earlier versus delayed presentation of VLST, according to median onset time. In total, 27 patients were treated with next‐generation DES and 71 with first‐generation DES. Based on optical coherence tomography findings at thrombotic sites, main VLST mechanisms were as follows, in descending order: neoatherosclerosis (34.7%), stent malapposition (33.7%), and uncovered struts without stent malapposition or evagination (24.5%). Compared with patients with earlier VLST, patients with delayed VLST had lower frequency of uncovered struts without stent malapposition or evagination (34.7% versus 14.3%, respectively; P=0.019). Conversely, the frequency of neoatherosclerosis was higher in patients with delayed versus earlier VLST (44.9% versus 24.5%, respectively; P=0.034). The frequency of stent malapposition was not different between patients with earlier and delayed VLST (34.7% versus 32.7%, respectively; P=0.831). The frequency of stent malapposition, evagination, and uncovered struts was still half of delayed VLST.ConclusionsThe pathological mechanisms of very late DES thrombosis changed over time. Delayed neointimal healing remained a substantial substrate for VLST, even long after DES implantation.

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“…Noteworthily, BMS and first-generation DES were designed to reduce the incidence of intra-stent restenosis (ISR) by delaying re-endothelization process up to 6-7 months in BMS and over 40 months in first-generation DES (sirolimus-and paclitaxeleluting stents) (Joner et al, 2006;Simard et al, 2014 (Yamaji et al, 2017). Especially neoatherosclerosis, defined as calcified or lipid neointima is another critical point to be considered as occurring more frequently and with increased longitudinal extension in BMS than DES occurring (Lee et al, 2013;Nakamura et al, 2016;Nakazawa et al, 2011). In line with this evidence, the pathophysiology of ISR and ISCT seems diametrically opposed.…”

Section: Intrastent Coronary Thrombosismentioning

confidence: 99%

Update on pathological platelet activation in coronary thrombosis

Elia

Montecucco

Portincasa

et al. 2018

Journal Cellular Physiology

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Although coronary thrombosis (CT) is integral to cardiovascular outcomes, the underlying pathophysiological mechanisms remain unclear. CT may occur in case of atherosclerotic plaque erosion/rupture, or even after stenting implantation. Platelets (PLT) activation is the keystone of atherothrombosis and depends on many dysregulated elements, including endothelial dysfunction, oxidized lipoproteins, and immune response. Besides the classical view of PLT as an effector of hemostatic response, a new repertoire of PLT activities is emerging. PLT lipidome oxidation is a self‐maintaining process which promotes PLT reactivity, coagulation cascade, and inflammatory cell activation. PLT‐innate immune cell interaction is also sustained by neutrophil extracellular traps and NLRP3 inflammasome pathways. Other noteworthy emerging mechanisms are implicated in the crosstalk between PLT and surrounding cells. Especially, microvesicles (MVs) released from PLT may extend their signaling network far beyond the classical cell−cell interactions. Moreover, the recognition of noncoding RNA in PLT MVs introduce another layer of complexity in terms of intercellular signaling by a direct regulation of messenger RNA profile and gene expression in the recipient cells. The aim of this narrative review is to update the recent advance in CT and intracoronary stent thrombosis, including causal factors and potential translation of experimental evidence into the clinical setting.

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Failure Mechanisms and Neoatherosclerosis Patterns in Very Late Drug-Eluting and Bare-Metal Stent Thrombosis

Abstract: Background-There are few clinical studies on the pathophysiological mechanisms of very late stent thrombosis (VLST).We report optical coherence tomography findings in patients with VLST and compare the findings between bare-metal stents (BMS) and drug-eluting stents (DES

Cited by 66 publications

References 30 publications

Vulnerable neoatherosclerosis in coronary artery with whole circumference showing intravascular echo attenuation

Vulnerable neoatherosclerosis in coronary artery with whole circumference showing intravascular echo attenuation

Characteristics of Earlier Versus Delayed Presentation of Very Late Drug‐Eluting Stent Thrombosis: An Optical Coherence Tomographic Study

Update on pathological platelet activation in coronary thrombosis

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