Evidence map›Paper›PMID 30995875›Full record

Observational studyJournal of the American Heart Association2019

Impaired Cholesterol-Uptake Capacity of HDL Might Promote Target-Lesion Revascularization by Inducing Neoatherosclerosis After Stent Implantation.

Yuichiro Nagano, Hiromasa Otake, Takayoshi Toba, Koji Kuroda, Yuto Shinkura, Natsuko Tahara, Yoshiro Tsukiyama, Kenichi Yanaka, Hiroyuki Yamamoto, Akira Nagasawa and 13 more

Abstract readObservational Study
In one paragraph

Observational study in Journal of the American Heart Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors.

Yuichiro Nagano1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Hiromasa Otake1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Takayoshi Toba1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Koji Kuroda1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Yuto Shinkura1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Natsuko Tahara1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Yoshiro Tsukiyama1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Kenichi Yanaka1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Hiroyuki Yamamoto1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Akira Nagasawa1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Hiroyuki Onishi1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Yoichiro Sugizaki1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Ryo Takeshige1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Amane Harada3 Central Research Laboratories Sysmex Corporation Kobe Japan.
Katsuhiro Murakami3 Central Research Laboratories Sysmex Corporation Kobe Japan.
Maria Kiriyama3 Central Research Laboratories Sysmex Corporation Kobe Japan.
Toshihiko Oshita1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Yasuhiro Irino2 Division of Evidence-based Laboratory Medicine Kobe University Graduate School of Medicine Kobe Japan.
Hiroyuki Kawamori1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Tatsuro Ishida1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Ryuji Toh2 Division of Evidence-based Laboratory Medicine Kobe University Graduate School of Medicine Kobe Japan.
Toshiro Shinke1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.
Ken-Ichi Hirata1 Division of Cardiovascular Medicine Department of Internal Medicine Kobe University Graduate School of Medicine Kobe Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background We evaluated the importance of high-density lipoprotein (HDL) functionality for target-lesion revascularization in patients treated with coronary stents using a rapid cell-free assay system to evaluate the functional capacity of HDL to accept additional cholesterol (cholesterol-uptake capacity; CUC). Methods and Results From an optical coherence tomography (OCT) registry of patients treated with coronary stents, 207 patients were enrolled and their HDL was functionally evaluated by measuring the CUC. Follow-up OCT was performed (median duration, 24.5 months after stenting) to evaluate the presence of neoatherosclerosis. Clinical follow-up was performed to assess target-lesion revascularization for a median duration of 42.3 months after stent implantation. Neoatherosclerosis was identified in 37 patients (17.9%). Multivariate logistic regression analysis revealed that a decreased CUC was independently associated with neoatherosclerosis (odds ratio, 0.799; P<0.001). The CUC showed a significant inverse correlation with incidence of target-lesion revascularization (odds ratio, 0.887; P=0.003) and with lipid accumulation inside stents, suggesting that neoatherosclerosis contributes to the association between CUC and target-lesion revascularization. Conclusions Impaired HDL functionality, detected as decreased CUC, might lead to future stent failure by provoking atherogenic changes of the neointima within stents. Both quantitative and qualitative assessments of HDL might enable the improved prediction of clinical outcomes after stent implantation.

Indexed as

Plaque, AtheroscleroticStentsAgedAged, 80 and overCholesterol, HDLCoronary Artery DiseaseCoronary VesselsFemaleHumansMacrophagesMaleMiddle AgedPercutaneous Coronary InterventionRegistriesTime FactorsTomography, Optical CoherenceCholesterol, HDLcholesterol‐uptake capacityhigh‐density lipoproteinneoatherosclerosisoptical coherence tomographytarget‐lesion revascularization

Identifiers

PMID30995875
PMCPMC6512103

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.