Evidence map›Paper›PMID 12793968›Full record

ReviewCurrent atherosclerosis reports2003

Homocysteine and atherothrombosis: diagnosis and treatment.

Diane E Handy, Joseph Loscalzo

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current atherosclerosis reports, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 18% 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, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Imbalance of Homocysteine and HOxidative medicine and cellular longevity · 2019
    Review
  8. Article
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

2 authors at 1 institution in 1 country.

Diane E HandyWhitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA.
Joseph Loscalzo
Boston University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperhomocysteinemia has long been recognized as a risk factor for cardiovascular disease. Many cross-sectional and retrospective case-control studies have shown an association between elevated total homocysteine levels and coronary, peripheral, and cerebral vascular disease; prospective studies, however, have been inconsistent. Overall, there is evidence to suggest a modest association between elevated homocysteine levels and cardiovascular disease risk. Folate supplementation has been shown to reduce plasma homocysteine even when levels are in the normal range. Clinical studies suggest that lowering plasma homocysteine may improve endothelial dysfunction, a marker of atherothrombotic risk. The long-term effects of folate supplementation on homocysteine levels and cardiovascular disease risk await the results of ongoing clinical trials. However, several recent studies suggest a benefit for reduction of plasma homocysteine levels, as individuals with lower homocysteine have reduced cardiovascular event rates.

Indexed as

ArteriosclerosisCoronary DiseaseEndothelium, VascularFolic AcidHematinicsHomocysteineHumansHyperhomocysteinemiaMethylenetetrahydrofolate Reductase (NADPH2)Oxidative StressPolymorphism, GeneticThrombosisFolic AcidHematinicsHomocysteineMethylenetetrahydrofolate Reductase (NADPH2)

Identifiers

PMID12793968
OpenAlexW2011770824

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.