Evidence map›Paper›PMID 33257928›Full record

ReviewClinical chemistry2021

Residual Cardiovascular Risk at Low LDL: Remnants, Lipoprotein(a), and Inflammation.

Ron C Hoogeveen, Christie M Ballantyne

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Clinical chemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 174 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
174citing papers in PubMed, 7 pooled it
25.1field-weighted citation impact, top 1% 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

174 citing papers in PubMed, 7 syntheses or guidelines pooled it, 293 citations in OpenAlex.

  1. Pooled it
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  8. Trial
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  10. Features of Lipid Disorders in Cardiovascular-Kidney-Metabolic Syndrome.International journal of molecular sciences · 2026
    Review
  11. Article
  12. Article
  13. Review
  14. Uric acid and subclinical atherosclerosis: distinct associations across coronary and carotid arteries.Clinical research in cardiology : official journal of the German Cardiac Society · 2026
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

114 more citing papers are in PubMed but not listed here.

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.

Ron C HoogeveenSection of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, TX.
Christie M BallantyneSection of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, TX.
Baylor College of Medicine · US

Funding

Profiling Cardiovascular Events and Biomarkers in the Very Old to Improve Personalized Approaches for the Prevention of Cardiac and Vascular DiseaseR01HL134320 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI BALLANTYNE, CHRISTIE MITCHELL, SELVIN, ELIZABETH · 2016 to 2019
$3.1M
NHLBI NIH HHS R01 HL134320
6 · The paper itself

Abstract

backgroundCurrent guidelines target low-density lipoprotein cholesterol (LDL-C) concentrations to reduce atherosclerotic cardiovascular disease (ASCVD) risk, and yet clinical trials demonstrate persistent residual ASCVD risk despite aggressive LDL-C lowering. CONTENT: Non-LDL-C lipid parameters, most notably triglycerides, triglyceride-rich lipoproteins (TGRLs), and lipoprotein(a), and C-reactive protein as a measure of inflammation are increasingly recognized as associated with residual risk after LDL-C lowering. Eicosapentaenoic acid in statin-treated patients with high triglycerides reduced both triglycerides and ASCVD events. Reducing TGRLs is believed to have beneficial effects on inflammation and atherosclerosis. High lipoprotein(a) concentrations increase ASCVD risk even in individuals with LDL-C < 70 mg/dL. Although statins do not generally lower lipoprotein(a), proprotein convertase subtilisin/kexin type 9 inhibitors reduce lipoprotein(a) and cardiovascular outcomes, and newer approaches are in development. Persistent increases in C-reactive protein after intensive lipid therapy have been consistently associated with increased risk for ASCVD events. SUMMARY: We review the evidence that biochemical assays to measure TGRLs, lipoprotein(a), and C-reactive protein are associated with residual risk in patients treated to low concentrations of LDL-C. Growing evidence supports a causal role for TGRLs, lipoprotein(a), and inflammation in ASCVD; novel therapies that target TGRLs, lipoprotein(a), and inflammation are in development to reduce residual ASCVD risk.

Indexed as

AtherosclerosisBiomarkersCholesterol, LDLC-Reactive ProteinHeart Disease Risk FactorsHumansHypolipidemic AgentsInflammationLipoprotein(a)LipoproteinsTriglyceridesBiomarkersCholesterol, LDLC-Reactive ProteinHypolipidemic AgentsLipoprotein(a)Lipoproteinslipoprotein triglycerideTriglycerides

Identifiers

PMID33257928
PMCPMC7793228
OpenAlexW3106601080

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.