Evidence map›Paper›PMID 27216845›Full record

ReviewCurrent cardiology reports2016

Future Lipid-Altering Therapeutic Options Targeting Residual Cardiovascular Risk.

Michel Farnier

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current cardiology reports, 2016. 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
3.8field-weighted citation impact, top 7% 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, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Vaccine against arteriosclerosis: an update.Therapeutic advances in vaccines · 2017
    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

1 author at 1 institution in 1 country.

Michel FarnierLipid Clinic, Point Medical, 21000, Dijon, France. michelfarnier@nerim.net.
NVH Medicinal (France) · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Low-density lipoproteins (LDL) play a causal role in the development of atherosclerosis, and reduction of LDL cholesterol with a statin is a cornerstone in prevention of cardiovascular disease. However, it remains an unmet need to reduce the residual risk on maximally tolerated statin alone or in combination with other drugs such as ezetimibe. Among the new LDL-lowering therapies, PCSK9 inhibitors appear the most promising class. Genetic studies suggest that triglyceride-rich lipoproteins are associated with cardiovascular risk and several promising triglyceride-lowering therapies are at various stages of development. At the opposite end, high-density lipoprotein (HDL) cholesterol seems to not be causally associated with cardiovascular risk, and thus far, trials designed to reduce cardiovascular risk by mainly raising HDL cholesterol levels have been disappointing. Nevertheless, new drugs targeting HDL are still in development. This review describes the new drugs reducing LDL, apolipoprotein(a), and triglyceride-rich lipoproteins, and the strategies to modulate HDL metabolism.

Indexed as

Antibodies, MonoclonalCardiovascular DiseasesCholesterol, HDLHumansHypolipidemic AgentsMolecular Targeted TherapyPCSK9 InhibitorsProprotein Convertase 9Antibodies, MonoclonalCholesterol, HDLHypolipidemic AgentsPCSK9 InhibitorsPCSK9 protein, humanProprotein Convertase 9Antisense oligonucleotideCardiovascular riskHDL metabolismLDL cholesterolPCSK9 inhibitorsTriglyceride-rich lipoproteins

Identifiers

PMID27216845
OpenAlexW2398065281

What OpenQuestion holds

Texttitle and abstract
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.