Evidence map›Paper›PMID 27164693›Full record

ArticleNeurology2016

Subacute decline in serum lipids precedes the occurrence of primary intracerebral hemorrhage.

Chia-Ling Phuah, Miriam R Raffeld, Alison M Ayres, Anand Viswanathan, Steven M Greenberg, Alessandro Biffi, Jonathan Rosand, Christopher D Anderson

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

Article in Neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Observational
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Chia-Ling PhuahFrom the Division of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., A.V., S.M.G., J.R., C.D.A.), and Hemorrhagic Stroke Research Group (A.M.A., A.V., S.M.G., A.B., J.R., C.D.A.), Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Miriam R RaffeldFrom the Division of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., A.V., S.M.G., J.R., C.D.A.), and Hemorrhagic Stroke Research Group (A.M.A., A.V., S.M.G., A.B., J.R., C.D.A.), Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Alison M AyresFrom the Division of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., A.V., S.M.G., J.R., C.D.A.), and Hemorrhagic Stroke Research Group (A.M.A., A.V., S.M.G., A.B., J.R., C.D.A.), Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Anand ViswanathanFrom the Division of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., A.V., S.M.G., J.R., C.D.A.), and Hemorrhagic Stroke Research Group (A.M.A., A.V., S.M.G., A.B., J.R., C.D.A.), Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Steven M GreenbergFrom the Division of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., A.V., S.M.G., J.R., C.D.A.), and Hemorrhagic Stroke Research Group (A.M.A., A.V., S.M.G., A.B., J.R., C.D.A.), Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Alessandro BiffiFrom the Division of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., A.V., S.M.G., J.R., C.D.A.), and Hemorrhagic Stroke Research Group (A.M.A., A.V., S.M.G., A.B., J.R., C.D.A.), Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Jonathan RosandFrom the Division of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., A.V., S.M.G., J.R., C.D.A.), and Hemorrhagic Stroke Research Group (A.M.A., A.V., S.M.G., A.B., J.R., C.D.A.), Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA.
Christopher D AndersonFrom the Division of Neurocritical Care and Emergency Neurology (C.-L.P., J.R., C.D.A.), Center for Human Genetic Research (C.-L.P., M.R.R., A.B., J.R., C.D.A.), The J. Philip Kistler Stroke Research Center (A.M.A., A.V., S.M.G., J.R., C.D.A.), and Hemorrhagic Stroke Research Group (A.M.A., A.V., S.M.G., A.B., J.R., C.D.A.), Massachusetts General Hospital, Boston; and Program in Medical and Population Genetics (C.-L.P., A.B., J.R., C.D.A.), Broad Institute, Cambridge, MA. cdanderson@mgh.harvard.edu.
Broad Institute · US

Funding

The NINDS International Stroke Genetics Consortium StudyU01NS069208 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI KITTNER, STEVEN J · 2010 to 2013
$9.4M
Vascular Dysfunction in Cerebral Amyloid AngiopathyR01AG026484 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI GREENBERG, STEVEN M · 2005 to 2019
$7.5M
Gene Discovery for Warfarin-Related Intracerebral HemorrhageR01NS059727 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ROSAND, JONATHAN · 2008 to 2012
$4.2M
Early Detection of Cerebral Amyloid AngiopathyR01NS070834 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI GREENBERG, STEVEN M · 2010 to 2014
$2.3M
Harvard Partners Neurology NEXT Clinical Trial SiteU10NS077360 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI GREENBERG, STEVEN M · 2011 to 2017
$2.3M
SCORE-IT: The CTA Spot Sign Score in Acute Cerebral HemorrhageR01NS073344 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ROSAND, JONATHAN · 2011 to 2015
$2.2M
Genetic Analyses of Lipids in Cerebral Hemorrhage and Small Vessel DiseaseK23NS086873 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ANDERSON, CHRISTOPHER DAVID · 2014 to 2018
$951k
Effect of White Matter Disease on Gait and Balance in Cerebral Amyloid AngiopathyK23AG028726 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI VISWANATHAN, ANAND · 2010 to 2014
$823k
NIA NIH HHS K23 AG028726NIA NIH HHS R01 AG026484NINDS NIH HHS K23 NS086873NINDS NIH HHS R01 NS059727NINDS NIH HHS R01 NS070834NINDS NIH HHS R01 NS073344NINDS NIH HHS U01 NS069208NINDS NIH HHS U10 NS077360
6 · The paper itself

Abstract

objectiveWe aimed to describe the temporal variation in circulating lipid levels among patients with intracerebral hemorrhage (ICH) and investigate their association with ICH risk.

methodsThis was a single-center, retrospective, longitudinal, case-control analysis using cases drawn from an ongoing cohort study of primary ICH and controls drawn from a hospital-based clinical data registry. Piecewise linear mixed-effect random coefficient models were used to determine the significance of changes in serum lipid trends on ICH risk.

resultsTwo hundred twelve ICH cases and 301 control individuals were analyzed. Overall trends in serum total cholesterol (TC) and low-density lipoprotein (LDL) levels differed between ICH cases and non-ICH controls (p = 0.00001 and p = 0.0092, respectively). Patients with ICH experience accelerated decline in serum TC and LDL levels during 6 months immediately preceding ICH, compared with levels between 6 and 24 months pre-ICH (TC: -29.25 mg/dL, p = 0.001; LDL: -21.48 mg/dL, p = 0.0038), which was not observed in non-ICH controls. Subgroup analysis confirmed that this phenomenon cannot be attributed to statin or alcohol exposure. Serum triglycerides and high-density lipoprotein trends did not differ between groups.

conclusionsLongitudinal lipid levels differ between ICH cases and non-ICH controls, most notably for a decline in serum TC and LDL levels within 6 months preceding primary ICH, independent of statin or alcohol use. These changes in serum TC and LDL trends suggest a biological pathway that precipitates ICH occurrence. Further studies are needed to replicate these results and characterize rate of change in serum lipids as a potential biomarker of impending acute cerebral injury.

Indexed as

AgedBiomarkersCase-Control StudiesCerebral HemorrhageCholesterolFemaleHumansLongitudinal StudiesMalePrognosisRegistriesRetrospective StudiesTime FactorsTriglyceridesBiomarkersCholesterolTriglycerides

Identifiers

PMID27164693
PMCPMC4891207
OpenAlexW2343791809

What OpenQuestion holds

Textmetadata
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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.