Incidence, clinical presentation, and predictors of early neoatherosclerosis after drug-eluting stent implantation

Kim, Choongki; Kim, Byeong Keuk; Lee, Seung Yul; Shin, Dong Ho; Kim, Jung Sun; Ko, Young Guk; Choi, Donghoon; Jang, Yangsoo; Hong, Myeong Ki

doi:10.1016/j.ahj.2015.06.005

Cited by 30 publications

(16 citation statements)

References 25 publications

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“…From the Kobe University Hospital OCT registry (175 patients, 314 lesions), Kuroda et al (27) found that C-reactive protein (CRP) level (OR, 1.022; P = 0.001) and LDL cholesterol (OR, 1.022; P = 0.008) at follow-up were independently associated with the presence of NA. Although the exact mechanisms need to be investigated further, these results additionally support the postulated mechanism of NA; that is to say, oxidative stress and inflammation lead to atherosclerotic changes inside neointima (1226). These findings support the importance of secondary prevention after stent implantation.…”

Section: Oct and Nasupporting

confidence: 53%

“…Although one of the strongest risk factors of NA is a longer time interval to follow-up, when we used OCT to evaluate the incidence of NA that developed after short post-DES implantation durations, early NA was also observed in 6.4% of 482 DES-treated lesions within 12 months after stent implantation (at a median post-implantation follow-up of 9.1 months) (26). Independent predictors of early NA were hypertension (OR, 3.20; P = 0.010) and pre-stent low-density lipoprotein (LDL) cholesterol ≥ 130 mg/dL at the time of index procedure (OR, 3.89; P = 0.002).…”

Section: Oct and Namentioning

confidence: 99%

“…Moreover, the incidence of stent thrombosis (definite/probable) was significantly higher in patients with NA (6.5% vs. 0%, P = 0.017) (27). Patients with early NA (within 12 months after stent implantation) also had a higher incidence of clinical symptoms (13% vs. 57%, P < 0.001) and had undergone a higher frequency of TLR (9% vs. 55%, P < 0.001) at the time of OCT follow-up (26). …”

Section: Clinical Implication Of Na: Isr and Stent Thrombosismentioning

confidence: 99%

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Clinical Implication of Optical Coherence Tomography-Based Neoatherosclerosis

2017

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Recent research has indicated neoatherosclerosis (NA), the de novo development of atherosclerosis within the neointimal region of the stented segment after coronary stent implantation, as a mechanism of late/very late stent thrombosis (VLST) and restenosis. This research is based on histologic and intravascular imaging studies. Optical coherence tomography (OCT) is an imaging tool that is superior with regard to resolution capacity, and can be used to visualize detailed information about distinct morphological characteristics of the restenotic tissue. Thus, OCT is a valuable imaging tool for examining NA, such as macrophage infiltration, lipid accumulation, in-stent calcification, or neointimal rupture. This article discusses the prevalence, predictors, and clinical implications of NA that can be observed by OCT.

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Section: Oct and Nasupporting

confidence: 53%

Section: Oct and Namentioning

confidence: 99%

Section: Clinical Implication Of Na: Isr and Stent Thrombosismentioning

confidence: 99%

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Clinical Implication of Optical Coherence Tomography-Based Neoatherosclerosis

2017

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“…Many pathological factors have been elucidated as indicators of NA, such as delayed arterial healing [ 12 ], hypersensitivity [ 26 ], stent types, stent age, and patient characteristics [ 31 , 32 ], including current smoking and chronic kidney disease. Antiproliferative drugs-induced incomplete reendothelialization plays a key role in neoatherosclerotic development.…”

Section: Cellular Mechanisms Of Neoatherosclerosismentioning

confidence: 99%

Neoatherosclerosis after Drug‐Eluting Stent Implantation: Roles and Mechanisms

Cui

Liu

Zhao

et al. 2016

Oxidative Medicine and Cellular Longevity

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In-stent neoatherosclerosis (NA), characterized by a relatively thin fibrous cap and large volume of yellow-lipid accumulation after drug-eluting stents (DES) implantation, has attracted much attention owing to its close relationship with late complications, such as revascularization and late stent thrombosis (ST). Accumulating evidence has demonstrated that more than one-third of patients with first-generation DES present with NA. Even in the advent of second-generation DES, NA still occurs. It is indicated that endothelial dysfunction induced by DES plays a critical role in neoatherosclerotic development. Upregulation of reactive oxygen species (ROS) induced by DES implantation significantly affects endothelial cells healing and functioning, therefore rendering NA formation. In light of the role of ROS in suppression of endothelial healing, combining antioxidant therapies with stenting technology may facilitate reestablishing a functioning endothelium to improve clinical outcome for patients with stenting.

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“…This feature was also confirmed in ST registries, in which ruptured neoatherosclerosis, as well as stent malapposition, was a frequent OCT finding in patients suffering from late or very late ST (3,6). Although the pathophysiology of neoatherosclerosis has remained unknown, several OCT studies suggested that specific factors such as stent type, stent age, patients' characteristics including current smoking, chronic kidney disease, usage of angiotensin-converting enzyme inhibitors/angiotensin II receptor blockade, and the concentration of low-density lipoprotein cholesterol were associated with the presence of neoatherosclerosis at follow-up (13)(14)(15). Accordingly, the continued medical care for the inhibition of neoatherosclerosis may be warranted in patients receiving coronary stents.…”

Section: Neoatherosclerosismentioning

confidence: 99%