Evidence map›Paper›PMID 27320173›Full record

Trial reportAtherosclerosis2016

Relationship of baseline HDL subclasses, small dense LDL and LDL triglyceride to cardiovascular events in the AIM-HIGH clinical trial.

John J Albers, April Slee, Jerome L Fleg, Kevin D O'Brien, Santica M Marcovina

Abstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Atherosclerosis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

50 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  12. Atherogenic circulating lipoproteins in ischemic stroke.Frontiers in cardiovascular medicine · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

John J AlbersUniversity of Washington, Northwest Lipid Metabolism and Diabetes Research Laboratories, 401 Queen Anne Ave N, Seattle, WA 98109, USA. Electronic address: jja@uw.edu.
April SleeAIM-HIGH Coordinating Center, Axio Research, 2601 Fourth Ave, Ste 200, Seattle, WA 98121, USA. Electronic address: AprilS@axioresearch.com.
Jerome L FlegNational Heart, Lung, and Blood Institute, Division of Cardiovascular Diseases, 6701 Rockledge Dr, Rm 8150, Bethesda, MD 20892, USA. Electronic address: flegj@nhlbi.nih.gov.
Kevin D O'BrienUniversity of Washington, Division of Cardiology, Department of Medicine, 1959 NE Pacific Ave, Box 356422, Seattle, WA 98195-6422, USA. Electronic address: cardiac@uw.edu.
Santica M MarcovinaUniversity of Washington, Northwest Lipid Metabolism and Diabetes Research Laboratories, 401 Queen Anne Ave N, Seattle, WA 98109, USA. Electronic address: smm@uw.edu.

Funding

AIM HIGH: Niacin Plus Statin to Prevent Vascular EventsU01HL081616 · UNIVERSITY OF WASHINGTON · 2005 to 2005
$663k
AIM-HIGHU01HL081649 · AXIO RESEARCH, LLC · 2005 to 2005
$0k
NHLBI NIH HHS U01 HL081616NHLBI NIH HHS U01 HL081649
6 · The paper itself

Abstract

BACKGROUND AND

aimsPrevious results of the AIM-HIGH trial showed that baseline levels of the conventional lipid parameters were not predictive of future cardiovascular (CV) outcomes. The aims of this secondary analysis were to examine the levels of cholesterol in high density lipoprotein (HDL) subclasses (HDL2-C and HDL3-C), small dense low density lipoprotein (sdLDL-C), and LDL triglyceride (LDL-TG) at baseline, as well as the relationship between these levels and CV outcomes.

methodsIndividuals with CV disease and low baseline HDL-C levels were randomized to simvastatin plus placebo or simvastatin plus extended release niacin (ERN), 1500 to 2000 mg/day, with ezetimibe added as needed in both groups to maintain an on-treatment LDL-C in the range of 40-80 mg/dL. The primary composite endpoint was death from coronary disease, nonfatal myocardial infarction, ischemic stroke, hospitalization for acute coronary syndrome, or symptom-driven coronary or cerebrovascular revascularization. HDL-C, HDL3-C, sdLDL-C and LDL-TG were measured at baseline by detergent-based homogeneous assays. HDL2-C was computed by the difference between HDL-C and HDL3-C. Analyses were performed on 3094 study participants who were already on statin therapy prior to enrollment in the trial. Independent contributions of lipoprotein fractions to CV events were determined by Cox proportional hazards modeling.

resultsBaseline HDL3-C was protective against CV events (HR: 0.84, p = 0.043) while HDL-C, HDL2-C, sdLDL-C and LDL-TG were not event-related (HR: 0.96, p = 0.369; HR: 1.07, p = 0.373; HR: 1.05, p = 0.492; HR: 1.03, p = 0.554, respectively).

conclusionsThe results of this secondary analysis of the AIM-HIGH Study indicate that levels of HDL3-C, but not other lipoprotein fractions, are predictive of CV events, suggesting that the HDL3 subclass may be primarily responsible for the inverse association of HDL-C and CV disease.

Indexed as

AgedAnticholesteremic AgentsCardiovascular DiseasesCardiovascular SystemCholesterol, HDLCohort StudiesCoronary Artery DiseaseEzetimibeFemaleHumansHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteins, HDLLipoproteins, LDLMaleMiddle AgedMyocardial InfarctionAnticholesteremic AgentsCholesterol, HDLEzetimibeHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteins, HDLLipoproteins, LDLlow density lipoprotein triglycerideNiacinSimvastatinTriglyceridesCardiovascular riskHDL2-cholesterolHDL3-cholesterolHomogeneous assaysLDL-triglycerideSmall dense LDL

Identifiers

PMID27320173
PMCPMC4983241

What Socratic holds

Texttitle and abstract
LicenceTDM
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 Socratic graph.