Evidence map›Paper›PMID 7500507›Full record

Trial reportJAMA1995

Effects of lowering elevated LDL cholesterol on the cardiovascular risk of lipoprotein(a).

V M Maher, B G Brown, S M Marcovina, L A Hillger, X Q Zhao, J J Albers

Registry-linked trialAbstract readClinical TrialRandomized Controlled Trial
PubMed
In one paragraph

Trial report in JAMA, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It reports registered trial NCT00000512. Cited by 68 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 4 pooled it
17.9field-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.

NCT00000512 phase3completed

Familial Atherosclerosis Treatment Study

Ran1984Enrolled146Registered outcomes1Posted comparisons0ConditionsCardiovascular Diseases, Coronary Arteriosclerosis, Coronary Disease, Heart DiseasesArmscolestipol, lovastatin, niacin, Placebo for colestipol, Placebo for lovastatin
Open the trial in the graph
3 · Its place in the literature

Who cites it

68 citing papers in PubMed, 4 syntheses or guidelines pooled it, 291 citations in OpenAlex.

  1. Niacin for primary and secondary prevention of cardiovascular events.The Cochrane database of systematic reviews · 2017 · on this map
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8 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

6 authors at 1 institution in 1 country.

V M MaherDepartment of Medicine, University of Washington School of Medicine, Seattle, USA.
B G Brown
S M Marcovina
L A Hillger
X Q Zhao
J J Albers
Seattle University · US

Funding

Serum Amyloid and Inflammation in AtherogenesisP01HL030086 · NHLBI · UNIVERSITY OF WASHINGTON · PI ALBERS, JOHN J · 1985 to 2009
$14.7M
FUNCTIONAL CHARACTERISTICS OF THE LEFT HEARTR01HL019451 · NHLBI · UNIVERSITY OF WASHINGTON · PI DODGE, HAROLD T · 1985 to 1990
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THROMBOLYSIS IN MYOCARDIAL ISCHEMIA-CORE APPLICATIONR01HL042419 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI ZARET, BARRY L · 1989 to 1991
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NHLBI NIH HHS P01 HL 30086NHLBI NIH HHS R01 HL 19451NHLBI NIH HHS R01 HL 42419
6 · The paper itself

Abstract

objectiveTo determine if lowering elevated low-density lipoprotein cholesterol (LDL-C) levels offsets the adverse effect of raised lipoprotein(a) (Lp[a]) levels on coronary artery disease (CAC) in men.

designRandomized, double-blind, placebo-controlled trial of lipid lowering for CAD.

settingPost hoc analysis of the Familial Atherosclerosis Treatment Study.

participantsA total of 146 men aged 62 years or younger with CAD and apolipoprotein B levels of at least 125 mg/dL.

interventionPatients received a Step II Diet and lovastatin (40 mg daily) plus colestipol (30 g daily), niacin (4 g daily) plus colestipol, or placebo (plus colestipol if LDL-C > 90th percentile) for 2.5 years. They were grouped by their LDL-C responses: "minimal" if LDL-C decreased by 10% or less from baseline (mean [SD] change, +6% [13%]) and "substantial" if LDL-C decreased more than 10% (mean [SD] change, -40% [16%]).

main outcome measureImpact of lowering elevated LDL-C on the cardiac event rate (death, myocardial infarction, and revascularization for refractory ischemia) and CAD change associated with elevated Lp(a).

resultsIn multivariate analyses, the best correlate of baseline CAD severity was Lp(a) (r = 0.30; P < .001). For 36 patients with minimal LDL-C reduction, CAD progression correlated only with in-treatment Lp(a) levels (r = 0.45; P < .01), but for 84 patients with substantial LDL-C reduction, disease regressed and its change correlated with in-treatment LDL-C (r = 0.24; P < .05) but not with Lp(a) (r = -0.05). Lipoprotein(a) levels were not significantly altered in either group. For 40 patients with Lp(a) at the 90th percentile or higher, events were frequent (39%) if reduction of LDL-C was minimal, but were few (9%) if reduction was substantial (relative risk, 0.23; 95% confidence interval, 0.06 to 0.99).

conclusionsIn men with CAD and elevated LDL-C, Lp(a) levels were dominant correlates of baseline disease severity, its progression, and event rate over 2.5 years. However, with substantial LDL-C reductions, persistent elevations of Lp(a) were no longer atherogenic or clinically threatening. This provides a possible direction for treatment in such patients with elevated Lp(a) and LDL-C.

Indexed as

AdultCholesterol, LDLCoronary DiseaseDisease ProgressionDouble-Blind MethodHumansLipoprotein(a)MaleMiddle AgedMyocardial InfarctionReoperationRisk FactorsSeverity of Illness IndexCholesterol, LDLLipoprotein(a)

Identifiers

PMID7500507
OpenAlexW2085713634

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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.