Evidence map›Paper›PMID 27215419›Full record

ReviewHerz2016

[Impact of lipid metabolism parameters on the development and progression of coronary artery disease : An update].

D Sinning, D M Leistner, U Landmesser

Abstract readReview
PubMed Publisher
In one paragraph

Review in Herz, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. [Serum annexin A2 level is significantly elevated in patients with coronary heart disease].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
    Article
  5. 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

3 authors at 3 institutions in 1 country.

D SinningKlinik für Kardiologie, Charité - Universitätsmedizin Berlin (Campus Benjamin Franklin), Hindenburgdamm 30, 12203, Berlin, Deutschland.
D M LeistnerKlinik für Kardiologie, Charité - Universitätsmedizin Berlin (Campus Benjamin Franklin), Hindenburgdamm 30, 12203, Berlin, Deutschland.
U LandmesserKlinik für Kardiologie, Charité - Universitätsmedizin Berlin (Campus Benjamin Franklin), Hindenburgdamm 30, 12203, Berlin, Deutschland. ulf.landmesser@charite.de.
Berlin Institute of Health at Charité - Universitätsmedizin Berlin · DECharité - Universitätsmedizin Berlin · DEGerman Centre for Cardiovascular Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disorders of lipid metabolism play a major role in the development and progression of coronary artery disease. Dyslipidemia therefore plays a central role in therapeutic approaches for prevention and treatment of cardiovascular events associated with coronary artery disease. Epidemiological studies have shown an association between various lipid metabolism parameters, the risk of developing coronary artery disease and progression of a pre-existing disease. In particular, increased levels of low-density lipoprotein cholesterol (LDL-C), reduced levels of HDL cholesterol (HDL-C), as well as high levels of triglycerides and increased lipoprotein(a) [Lp(a)] levels can be taken into account when assessing the risk stratification of patients for primary prevention of coronary artery disease. Lifestyle and dietary changes, intensified statin therapy and possibly the addition of ezetimibe remain the major interventions in both primary and secondary prevention of coronary artery disease, as they improve the prognosis particularly by lowering levels of LDL-C. Recently, genetic studies have contributed to extending our understanding of the relationship between lipid metabolism and coronary artery disease. A causal role for progression of coronary artery disease could be demonstrated for LDL-C, Lpa and triglyceride-rich lipoproteins (TRL), which could not be demonstrated for HDL-C in various studies. Furthermore, the effect of reduction of LDL-C by proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition and by the cholesteryl ester transfer protein (CETP) inhibitor anacetrapib on cardiovascular events is currently being investigated in large clinical outcome study programs.

Indexed as

Lipid MetabolismAnticholesteremic AgentsCoronary Artery DiseaseDisease ProgressionEvidence-Based MedicineHumansLipidsPCSK9 InhibitorsPrevalenceProprotein Convertase 9Reproducibility of ResultsRisk FactorsSensitivity and SpecificityTreatment OutcomeAnticholesteremic AgentsLipidsPCSK9 InhibitorsPCSK9 protein, humanProprotein Convertase 9Coronary artery diseaseLipid metabolismLipoprotein(a)Proprotein covertase subtilisin-kexin type 9, humanTriglycerides

Identifiers

PMID27215419
OpenAlexW2472446175

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.