Evidence map›Paper›PMID 28703931›Full record

Trial reportClinical cardiology2017

Rationale and design of a randomized trial of apixaban vs warfarin to evaluate atherosclerotic calcification and vulnerable plaque progression.

Kazuhiro Osawa, Rine Nakanishi, Theingi Tiffany Win, Dong Li, Sina Rahmani, Negin Nezarat, Nasim Sheidaee, Matthew J Budoff

Open access · bronzeAbstract readComparative StudyRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Clinical cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% of its field
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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Warfarin involvement, in comparison to NOACs, in the development of systemic atherosclerosis.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2022
    Review
  6. Review
  7. Review
  8. Calcification of the heart: mechanisms and therapeutic avenues.Expert review of cardiovascular therapy · 2018
    Review
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

8 authors at 2 institutions in 1 country.

Kazuhiro OsawaLos Angeles Biomedical Research Institute at Harbor University of California-Los Angeles.
Rine NakanishiLos Angeles Biomedical Research Institute at Harbor University of California-Los Angeles.
Theingi Tiffany WinDivision of Cardiology, Department of Medicine, University of New Mexico, Albuquerque.
Dong LiLos Angeles Biomedical Research Institute at Harbor University of California-Los Angeles.
Sina RahmaniLos Angeles Biomedical Research Institute at Harbor University of California-Los Angeles.
Negin NezaratLos Angeles Biomedical Research Institute at Harbor University of California-Los Angeles.
Nasim SheidaeeLos Angeles Biomedical Research Institute at Harbor University of California-Los Angeles.
Matthew J BudoffLos Angeles Biomedical Research Institute at Harbor University of California-Los Angeles.ORCID http://orcid.org/0000-0002-9616-1946
University of California, Los Angeles · USUniversity of New Mexico · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vitamin K antagonists (VKAs) are known to increase vascular calcification, suggesting increased cardiovascular disease events. Apixaban is an oral direct factor Xa inhibitor superior to warfarin at preventing stroke or systemic embolism and may stabilize coronary atherosclerosis. The potential benefits of avoiding VKA therapy and the favorable effects of factor Xa inhibitors could contribute to cardiovascular disease event reduction. We hypothesized that apixaban inhibits vascular calcification and coronary atherosclerosis progression compared with warfarin in patients with atrial fibrillation (AF). This study is a single-center, prospective, randomized, open-label study. From May 2014 to December 2015, 66 patients with nonvalvular AF who experienced VKA therapy were enrolled. Patients were randomized into either warfarin or apixaban cohorts and followed for 52 weeks. The primary objective is to compare the rate of change in coronary artery calcification (CAC) from baseline to follow-up in apixaban vs warfarin cohorts. The key secondary objective is to compare the rate of incident plaques and quantitative changes in plaque types between patients randomized to either warfarin or apixaban cohorts using serial coronary computed tomography angiography. Expert readers will blindly assess CAC and coronary artery plaques. It is thought that this trial will result in significant differences in CAC and coronary artery plaque progression between the VKA and apixaban. The results are anticipated to provide a novel insight into treatment selection for AF patients. The study is registered at http://www.clinicaltrials.gov (NCT 02090075).

Indexed as

Plaque, AtheroscleroticAdolescentAdultAgedAged, 80 and overAnticoagulantsAtrial FibrillationClinical ProtocolsComputed Tomography AngiographyCoronary AngiographyCoronary Artery DiseaseCoronary VesselsDisease ProgressionElectrocardiographyFactor Xa InhibitorsFemaleAnticoagulantsapixabanFactor Xa InhibitorsPyrazolesPyridonesWarfarinapixabancoronary artery plaquecoronary artey calciumwarfarin

Identifiers

PMID28703931
PMCPMC6490550
OpenAlexW2736911896

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.