Evidence map›Paper›PMID 35977831›Full record

Trial reportNeurology2022

Association of Blood Pressure Lowering Intensity With White Matter Network Integrity in Patients With Cerebral Small Vessel Disease.

Chris Patrick Pflanz, Marco S Egle, John T O'Brien, Robin G Morris, Thomas R Barrick, Andrew M Blamire, Gary A Ford, Daniel Tozer, Hugh S Markus, PRESERVE study group

Open access · hybridAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
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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

10 authors at 1 institution in 1 country.

Chris Patrick PflanzFrom the Stroke Research Group (C.P.P., M.S.E., D.T., H.S.M.), Department of Clinical Neuroscience, University of Cambridge; Department of Psychiatry (J.T.O.B.), University of Cambridge; Kings College Institute of Psychiatry (R.G.M.), Psychology and Neurosciences, London, UK; Molecular and Clinical Science Research Institute (T.R.B.), St George's, University of London, UK; Magnetic Resonance Centre (A.M.B.), Institute of Cellular Medicine, Newcastle University, UK; and Oxford University Hospitals NHS Foundation Trust & University of Oxford (G.A.F.).
Marco S EgleFrom the Stroke Research Group (C.P.P., M.S.E., D.T., H.S.M.), Department of Clinical Neuroscience, University of Cambridge; Department of Psychiatry (J.T.O.B.), University of Cambridge; Kings College Institute of Psychiatry (R.G.M.), Psychology and Neurosciences, London, UK; Molecular and Clinical Science Research Institute (T.R.B.), St George's, University of London, UK; Magnetic Resonance Centre (A.M.B.), Institute of Cellular Medicine, Newcastle University, UK; and Oxford University Hospitals NHS Foundation Trust & University of Oxford (G.A.F.).
John T O'BrienFrom the Stroke Research Group (C.P.P., M.S.E., D.T., H.S.M.), Department of Clinical Neuroscience, University of Cambridge; Department of Psychiatry (J.T.O.B.), University of Cambridge; Kings College Institute of Psychiatry (R.G.M.), Psychology and Neurosciences, London, UK; Molecular and Clinical Science Research Institute (T.R.B.), St George's, University of London, UK; Magnetic Resonance Centre (A.M.B.), Institute of Cellular Medicine, Newcastle University, UK; and Oxford University Hospitals NHS Foundation Trust & University of Oxford (G.A.F.).
Robin G MorrisFrom the Stroke Research Group (C.P.P., M.S.E., D.T., H.S.M.), Department of Clinical Neuroscience, University of Cambridge; Department of Psychiatry (J.T.O.B.), University of Cambridge; Kings College Institute of Psychiatry (R.G.M.), Psychology and Neurosciences, London, UK; Molecular and Clinical Science Research Institute (T.R.B.), St George's, University of London, UK; Magnetic Resonance Centre (A.M.B.), Institute of Cellular Medicine, Newcastle University, UK; and Oxford University Hospitals NHS Foundation Trust & University of Oxford (G.A.F.).
Thomas R BarrickFrom the Stroke Research Group (C.P.P., M.S.E., D.T., H.S.M.), Department of Clinical Neuroscience, University of Cambridge; Department of Psychiatry (J.T.O.B.), University of Cambridge; Kings College Institute of Psychiatry (R.G.M.), Psychology and Neurosciences, London, UK; Molecular and Clinical Science Research Institute (T.R.B.), St George's, University of London, UK; Magnetic Resonance Centre (A.M.B.), Institute of Cellular Medicine, Newcastle University, UK; and Oxford University Hospitals NHS Foundation Trust & University of Oxford (G.A.F.).
Andrew M BlamireFrom the Stroke Research Group (C.P.P., M.S.E., D.T., H.S.M.), Department of Clinical Neuroscience, University of Cambridge; Department of Psychiatry (J.T.O.B.), University of Cambridge; Kings College Institute of Psychiatry (R.G.M.), Psychology and Neurosciences, London, UK; Molecular and Clinical Science Research Institute (T.R.B.), St George's, University of London, UK; Magnetic Resonance Centre (A.M.B.), Institute of Cellular Medicine, Newcastle University, UK; and Oxford University Hospitals NHS Foundation Trust & University of Oxford (G.A.F.).ORCID 0000-0002-8749-1257
Gary A FordFrom the Stroke Research Group (C.P.P., M.S.E., D.T., H.S.M.), Department of Clinical Neuroscience, University of Cambridge; Department of Psychiatry (J.T.O.B.), University of Cambridge; Kings College Institute of Psychiatry (R.G.M.), Psychology and Neurosciences, London, UK; Molecular and Clinical Science Research Institute (T.R.B.), St George's, University of London, UK; Magnetic Resonance Centre (A.M.B.), Institute of Cellular Medicine, Newcastle University, UK; and Oxford University Hospitals NHS Foundation Trust & University of Oxford (G.A.F.).ORCID 0000-0001-8719-4968
Daniel TozerFrom the Stroke Research Group (C.P.P., M.S.E., D.T., H.S.M.), Department of Clinical Neuroscience, University of Cambridge; Department of Psychiatry (J.T.O.B.), University of Cambridge; Kings College Institute of Psychiatry (R.G.M.), Psychology and Neurosciences, London, UK; Molecular and Clinical Science Research Institute (T.R.B.), St George's, University of London, UK; Magnetic Resonance Centre (A.M.B.), Institute of Cellular Medicine, Newcastle University, UK; and Oxford University Hospitals NHS Foundation Trust & University of Oxford (G.A.F.).ORCID 0000-0002-0404-3214
Hugh S MarkusFrom the Stroke Research Group (C.P.P., M.S.E., D.T., H.S.M.), Department of Clinical Neuroscience, University of Cambridge; Department of Psychiatry (J.T.O.B.), University of Cambridge; Kings College Institute of Psychiatry (R.G.M.), Psychology and Neurosciences, London, UK; Molecular and Clinical Science Research Institute (T.R.B.), St George's, University of London, UK; Magnetic Resonance Centre (A.M.B.), Institute of Cellular Medicine, Newcastle University, UK; and Oxford University Hospitals NHS Foundation Trust & University of Oxford (G.A.F.). hsm32@medschl.cam.ac.uk.ORCID 0000-0002-9794-5996
PRESERVE study group
St George's, University of London · GB

Funding

British Heart FoundationBritish Heart Foundation TSA BHF 2010/01Medical Research Council MR/L023784/1Medical Research Council MR/L023784/2
6 · The paper itself

Abstract

BACKGROUND AND

objectivesDiffusion tensor imaging (DTI) networks integrate damage from a variety of pathologic processes in cerebral small vessel disease (SVD) and may be a sensitive marker to detect treatment effects. We determined whether brain network analysis could detect treatment effects in the PRESERVE trial data set, in which intensive vs standard blood pressure (BP) lowering was compared. The primary end point of DTI had not shown treatment differences.

methodsParticipants with lacunar stroke were randomized to standard (systolic 130-140 mm Hg) or intensive (systolic ≤ 125 mm Hg) BP lowering and followed for 2 years with MRI at baseline and at 2 years. Graph theory-based metrics were derived from DTI data to produce a measure of network integrity weighted global efficiency and compared with individual MRI markers of DTI, brain volume, and white matter hyperintensities.

resultsData were available in 82 subjects: standard n = 40 (mean age 66.3 ± 1.5 years) and intensive n = 42 (mean age 69.6 ± 1.0 years). The mean (SD) systolic BP was reduced by 13(14) and 23(23) mm Hg in the standard and intensive groups, respectively ( DISCUSSION: Brain network analysis may be a sensitive surrogate marker in trials in SVD. This work suggests that measures of brain network efficiency may be more sensitive to the effects of BP control treatment than conventional DTI metrics. TRIAL REGISTRATION INFORMATION: The trial is registered with the ISRCTN Registry (ISRCTN37694103; doi.org/10.1186/ISRCTN37694103) and the NIHR Clinical Research Network (CRN 10962; public-odp.nihr.ac.uk/QvAJAXZfc/opendoc.htm?document=crncc_users%5Cfind%20a%20clinical%20research%20study.qvw&lang=en-US&host=QVS%40crn-prod-odp-pu&anonymous=true). CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that intensive BP lowering in patients with SVD results in improved brain network function when assessed by DTI-based brain network metrics.

Indexed as

Cerebral Small Vessel DiseasesWhite MatterAgedBlood PressureBrainCytochrome P-450 CYP2B1Diffusion Tensor ImagingHumansMagnetic Resonance ImagingMiddle AgedCytochrome P-450 CYP2B1

Identifiers

PMID35977831
PMCPMC9620809
OpenAlexW4292148875

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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.