Evidence map›Paper›PMID 33986139›Full record

ArticleNeurology2021

Effect of Patent Foramen Ovale Closure After Stroke on Circulatory Biomarkers.

Wenjun Deng, David McMullin, Ignacio Inglessis-Azuaje, Joseph J Locascio, Igor F Palacios, Ferdinando S Buonanno, Eng H Lo, MingMing Ning

Open access · greenAbstract read
In one paragraph

Article in Neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Linking patent foramen ovale with atrial cardiomyopathy: a narrative review of clinical signals, electrophysiology, and translational opportunities.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2026
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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.

Wenjun DengFrom the Clinical Proteomics Research Center (W.D., D.M., F.S.B., E.H.L., M.M.N.), Cardio-Neurology Division (W.D., I.I.-A., J.J.L., I.F.P., F.S.B., E.H.L., M.M.N.), and Neuroprotection Research Laboratory (E.H.L., M.M.N.), Massachusetts General Hospital, Harvard Medical School, Boston.
David McMullinFrom the Clinical Proteomics Research Center (W.D., D.M., F.S.B., E.H.L., M.M.N.), Cardio-Neurology Division (W.D., I.I.-A., J.J.L., I.F.P., F.S.B., E.H.L., M.M.N.), and Neuroprotection Research Laboratory (E.H.L., M.M.N.), Massachusetts General Hospital, Harvard Medical School, Boston.
Ignacio Inglessis-AzuajeFrom the Clinical Proteomics Research Center (W.D., D.M., F.S.B., E.H.L., M.M.N.), Cardio-Neurology Division (W.D., I.I.-A., J.J.L., I.F.P., F.S.B., E.H.L., M.M.N.), and Neuroprotection Research Laboratory (E.H.L., M.M.N.), Massachusetts General Hospital, Harvard Medical School, Boston.
Joseph J LocascioFrom the Clinical Proteomics Research Center (W.D., D.M., F.S.B., E.H.L., M.M.N.), Cardio-Neurology Division (W.D., I.I.-A., J.J.L., I.F.P., F.S.B., E.H.L., M.M.N.), and Neuroprotection Research Laboratory (E.H.L., M.M.N.), Massachusetts General Hospital, Harvard Medical School, Boston.
Igor F PalaciosFrom the Clinical Proteomics Research Center (W.D., D.M., F.S.B., E.H.L., M.M.N.), Cardio-Neurology Division (W.D., I.I.-A., J.J.L., I.F.P., F.S.B., E.H.L., M.M.N.), and Neuroprotection Research Laboratory (E.H.L., M.M.N.), Massachusetts General Hospital, Harvard Medical School, Boston.
Ferdinando S BuonannoFrom the Clinical Proteomics Research Center (W.D., D.M., F.S.B., E.H.L., M.M.N.), Cardio-Neurology Division (W.D., I.I.-A., J.J.L., I.F.P., F.S.B., E.H.L., M.M.N.), and Neuroprotection Research Laboratory (E.H.L., M.M.N.), Massachusetts General Hospital, Harvard Medical School, Boston.
Eng H LoFrom the Clinical Proteomics Research Center (W.D., D.M., F.S.B., E.H.L., M.M.N.), Cardio-Neurology Division (W.D., I.I.-A., J.J.L., I.F.P., F.S.B., E.H.L., M.M.N.), and Neuroprotection Research Laboratory (E.H.L., M.M.N.), Massachusetts General Hospital, Harvard Medical School, Boston.
MingMing NingFrom the Clinical Proteomics Research Center (W.D., D.M., F.S.B., E.H.L., M.M.N.), Cardio-Neurology Division (W.D., I.I.-A., J.J.L., I.F.P., F.S.B., E.H.L., M.M.N.), and Neuroprotection Research Laboratory (E.H.L., M.M.N.), Massachusetts General Hospital, Harvard Medical School, Boston. mmning@mgh.harvard.edu.
MACOM (United States) · US

Funding

Statistics and Bioinformatics Core - WangU24DK097153 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BURANT, CHARLES F · 2012 to 2017
$10.1M
Proteomic Profiling of Patent Foramen Ovale Related Neurovascular InjuryR01NS067139 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI NING, MINGMING · 2010 to 2023
$3.7M
Thrombolysis Profiles in tPA ResponseR01NS093415 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI LO, ENG H., NING, MINGMING · 2015 to 2019
$1.9M
NIDDK NIH HHS U24 DK097153NINDS NIH HHS R01 NS067139NINDS NIH HHS R01 NS093415
6 · The paper itself

Abstract

objectiveTo determine the influence of patent foramen ovale (PFO) closure on circulatory biomarkers.

methodsConsecutive patients with PFO-related stroke were prospectively enrolled and followed with serial sampling of cardiac atrial and venous blood pre- and post-PFO closure over time. Candidate biomarkers were identified by mass spectrometry in a discovery cohort first, and lead candidates were validated in an independent cohort.

resultsPatients with PFO-related stroke (n = 254) were recruited and followed up to 4 years (median 2.01; interquartile range 0.77-2.54). Metabolite profiling in the discovery cohort (n = 12) identified homocysteine as the most significantly decreased factor in intracardiac plasma after PFO closure (false discovery rate 0.001). This was confirmed in a validation cohort (n = 181), where intracardiac total homocysteine (tHcy) was immediately reduced in patients with complete closure, but not in those with residual shunting, suggesting association of PFO shunting with tHcy elevation (β 0.115; 95% confidence interval [CI] 0.047-0.183;

conclusionsPFO shunting may contribute to circulatory tHcy elevation, which is renormalized by PFO closure. PFO is not just a door for clots, but may itself enhance clot formation and injure neurovasculature by clot-independent mechanisms. Biomarkers such as tHcy can potentially serve as cost-effective measures of residual shunting and neurovascular risk for PFO stroke.

Indexed as

AdultBiomarkersFemaleForamen Ovale, PatentHomocysteineHumansMaleMass SpectrometryMiddle AgedProspective StudiesStrokeBiomarkersHomocysteine

Identifiers

PMID33986139
PMCPMC8279569
OpenAlexW3160113889

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.