Evidence map›Paper›PMID 26671971›Full record

ArticleCirculation. Cardiovascular interventions2016

Natural IgM Blockade Limits Infarct Expansion and Left Ventricular Dysfunction in a Swine Myocardial Infarct Model.

Smita Sihag, Michael S Haas, Karen M Kim, J Luis Guerrero, Jonathan Beaudoin, Elisabeth M Alicot, Franziska Schuerpf, James D Gottschall, Robyn J Puro, Joren C Madsen and 4 more

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

Article in Circulation. Cardiovascular interventions, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 33% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Increasing the efficacy and safety of a human complement inhibitor for treating post-transplant cardiac ischemia reperfusion injury by targeting to a graft-specific neoepitope.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2021
    Article
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

14 authors at 4 institutions in 1 country.

Smita SihagFrom the Transplantation Biology Research Center, Massachusetts General Hospital, Charlestown (S.S., J.D.G., J.C.M., D.H.S., J.S.A.); Cardiac Surgery Research Laboratory, Massachusetts General Hospital, Boston, (J.L.G., J.B., J.S.A.); DecImmune Therapeutics, Cambridge, MA (M.S.H., E.M.A., F.S., R.J.P., W.N.); Program in Cellular and Molecular Medicine, Boston Children's Hospital, MA (M.C.C.); Department of Pediatrics, Harvard Medical School, Boston, MA (M.C.C.); and Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (K.M.K.).
Michael S HaasFrom the Transplantation Biology Research Center, Massachusetts General Hospital, Charlestown (S.S., J.D.G., J.C.M., D.H.S., J.S.A.); Cardiac Surgery Research Laboratory, Massachusetts General Hospital, Boston, (J.L.G., J.B., J.S.A.); DecImmune Therapeutics, Cambridge, MA (M.S.H., E.M.A., F.S., R.J.P., W.N.); Program in Cellular and Molecular Medicine, Boston Children's Hospital, MA (M.C.C.); Department of Pediatrics, Harvard Medical School, Boston, MA (M.C.C.); and Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (K.M.K.).
Karen M KimFrom the Transplantation Biology Research Center, Massachusetts General Hospital, Charlestown (S.S., J.D.G., J.C.M., D.H.S., J.S.A.); Cardiac Surgery Research Laboratory, Massachusetts General Hospital, Boston, (J.L.G., J.B., J.S.A.); DecImmune Therapeutics, Cambridge, MA (M.S.H., E.M.A., F.S., R.J.P., W.N.); Program in Cellular and Molecular Medicine, Boston Children's Hospital, MA (M.C.C.); Department of Pediatrics, Harvard Medical School, Boston, MA (M.C.C.); and Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (K.M.K.).
J Luis GuerreroFrom the Transplantation Biology Research Center, Massachusetts General Hospital, Charlestown (S.S., J.D.G., J.C.M., D.H.S., J.S.A.); Cardiac Surgery Research Laboratory, Massachusetts General Hospital, Boston, (J.L.G., J.B., J.S.A.); DecImmune Therapeutics, Cambridge, MA (M.S.H., E.M.A., F.S., R.J.P., W.N.); Program in Cellular and Molecular Medicine, Boston Children's Hospital, MA (M.C.C.); Department of Pediatrics, Harvard Medical School, Boston, MA (M.C.C.); and Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (K.M.K.).
Jonathan BeaudoinFrom the Transplantation Biology Research Center, Massachusetts General Hospital, Charlestown (S.S., J.D.G., J.C.M., D.H.S., J.S.A.); Cardiac Surgery Research Laboratory, Massachusetts General Hospital, Boston, (J.L.G., J.B., J.S.A.); DecImmune Therapeutics, Cambridge, MA (M.S.H., E.M.A., F.S., R.J.P., W.N.); Program in Cellular and Molecular Medicine, Boston Children's Hospital, MA (M.C.C.); Department of Pediatrics, Harvard Medical School, Boston, MA (M.C.C.); and Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (K.M.K.).
Elisabeth M AlicotFrom the Transplantation Biology Research Center, Massachusetts General Hospital, Charlestown (S.S., J.D.G., J.C.M., D.H.S., J.S.A.); Cardiac Surgery Research Laboratory, Massachusetts General Hospital, Boston, (J.L.G., J.B., J.S.A.); DecImmune Therapeutics, Cambridge, MA (M.S.H., E.M.A., F.S., R.J.P., W.N.); Program in Cellular and Molecular Medicine, Boston Children's Hospital, MA (M.C.C.); Department of Pediatrics, Harvard Medical School, Boston, MA (M.C.C.); and Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (K.M.K.).
Franziska SchuerpfFrom the Transplantation Biology Research Center, Massachusetts General Hospital, Charlestown (S.S., J.D.G., J.C.M., D.H.S., J.S.A.); Cardiac Surgery Research Laboratory, Massachusetts General Hospital, Boston, (J.L.G., J.B., J.S.A.); DecImmune Therapeutics, Cambridge, MA (M.S.H., E.M.A., F.S., R.J.P., W.N.); Program in Cellular and Molecular Medicine, Boston Children's Hospital, MA (M.C.C.); Department of Pediatrics, Harvard Medical School, Boston, MA (M.C.C.); and Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (K.M.K.).
James D GottschallFrom the Transplantation Biology Research Center, Massachusetts General Hospital, Charlestown (S.S., J.D.G., J.C.M., D.H.S., J.S.A.); Cardiac Surgery Research Laboratory, Massachusetts General Hospital, Boston, (J.L.G., J.B., J.S.A.); DecImmune Therapeutics, Cambridge, MA (M.S.H., E.M.A., F.S., R.J.P., W.N.); Program in Cellular and Molecular Medicine, Boston Children's Hospital, MA (M.C.C.); Department of Pediatrics, Harvard Medical School, Boston, MA (M.C.C.); and Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (K.M.K.).
Robyn J PuroFrom the Transplantation Biology Research Center, Massachusetts General Hospital, Charlestown (S.S., J.D.G., J.C.M., D.H.S., J.S.A.); Cardiac Surgery Research Laboratory, Massachusetts General Hospital, Boston, (J.L.G., J.B., J.S.A.); DecImmune Therapeutics, Cambridge, MA (M.S.H., E.M.A., F.S., R.J.P., W.N.); Program in Cellular and Molecular Medicine, Boston Children's Hospital, MA (M.C.C.); Department of Pediatrics, Harvard Medical School, Boston, MA (M.C.C.); and Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (K.M.K.).
Joren C MadsenFrom the Transplantation Biology Research Center, Massachusetts General Hospital, Charlestown (S.S., J.D.G., J.C.M., D.H.S., J.S.A.); Cardiac Surgery Research Laboratory, Massachusetts General Hospital, Boston, (J.L.G., J.B., J.S.A.); DecImmune Therapeutics, Cambridge, MA (M.S.H., E.M.A., F.S., R.J.P., W.N.); Program in Cellular and Molecular Medicine, Boston Children's Hospital, MA (M.C.C.); Department of Pediatrics, Harvard Medical School, Boston, MA (M.C.C.); and Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (K.M.K.).
David H SachsFrom the Transplantation Biology Research Center, Massachusetts General Hospital, Charlestown (S.S., J.D.G., J.C.M., D.H.S., J.S.A.); Cardiac Surgery Research Laboratory, Massachusetts General Hospital, Boston, (J.L.G., J.B., J.S.A.); DecImmune Therapeutics, Cambridge, MA (M.S.H., E.M.A., F.S., R.J.P., W.N.); Program in Cellular and Molecular Medicine, Boston Children's Hospital, MA (M.C.C.); Department of Pediatrics, Harvard Medical School, Boston, MA (M.C.C.); and Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (K.M.K.).
Walter NewmanFrom the Transplantation Biology Research Center, Massachusetts General Hospital, Charlestown (S.S., J.D.G., J.C.M., D.H.S., J.S.A.); Cardiac Surgery Research Laboratory, Massachusetts General Hospital, Boston, (J.L.G., J.B., J.S.A.); DecImmune Therapeutics, Cambridge, MA (M.S.H., E.M.A., F.S., R.J.P., W.N.); Program in Cellular and Molecular Medicine, Boston Children's Hospital, MA (M.C.C.); Department of Pediatrics, Harvard Medical School, Boston, MA (M.C.C.); and Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (K.M.K.).
Michael C CarrollFrom the Transplantation Biology Research Center, Massachusetts General Hospital, Charlestown (S.S., J.D.G., J.C.M., D.H.S., J.S.A.); Cardiac Surgery Research Laboratory, Massachusetts General Hospital, Boston, (J.L.G., J.B., J.S.A.); DecImmune Therapeutics, Cambridge, MA (M.S.H., E.M.A., F.S., R.J.P., W.N.); Program in Cellular and Molecular Medicine, Boston Children's Hospital, MA (M.C.C.); Department of Pediatrics, Harvard Medical School, Boston, MA (M.C.C.); and Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (K.M.K.).
James S AllanFrom the Transplantation Biology Research Center, Massachusetts General Hospital, Charlestown (S.S., J.D.G., J.C.M., D.H.S., J.S.A.); Cardiac Surgery Research Laboratory, Massachusetts General Hospital, Boston, (J.L.G., J.B., J.S.A.); DecImmune Therapeutics, Cambridge, MA (M.S.H., E.M.A., F.S., R.J.P., W.N.); Program in Cellular and Molecular Medicine, Boston Children's Hospital, MA (M.C.C.); Department of Pediatrics, Harvard Medical School, Boston, MA (M.C.C.); and Division of Cardiovascular Surgery, Hospital of the University of Pennsylvania, Philadelphia (K.M.K.).
Boston Children's Hospital · USDecImmune Therapeutics (United States) · USHarvard University · USMassachusetts General Hospital · US

Funding

XENOGENIC TOLERANCE IN MICEP01HL018646 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI ALLAN, JAMES S. · 1985 to 2019
$37.5M
Therapeutic to Reduce Acute Inflammation Following Cardiac IschemiaR44HL084821 · NHLBI · DECIMMUNE THERAPEUTICS, INC · PI NEWMAN, WALTER · 2010 to 2014
$3.2M
RES FACIL CONST: XENOTRANSPLANTATION, LUNG ALLOGRAFT REJECTION IN SWINEC06RR020135 · NCRR · MASSACHUSETTS GENERAL HOSPITAL · PI SLAVIN, PETER L · 2004 to 2004
$2.7M
Therapeutic to Reduce Acute Inflammation Following Cardiac IschemiaR43HL084821 · NHLBI · DECIMMUNE THERAPEUTICS, INC · PI ALICOT-CARROLL, ELISABETH M · 2006 to 2006
$129k
NCI NIH HHS CO6RR020135-01NCRR NIH HHS C06 RR020135NHLBI NIH HHS HL084821NHLBI NIH HHS P01 HL018646NHLBI NIH HHS P01HL018646NHLBI NIH HHS R43 HL084821NHLBI NIH HHS R44 HL084821
6 · The paper itself

Abstract

backgroundAcute coronary syndrome is the leading cause of mortality worldwide. However, treatment of acute coronary occlusion inevitably results in ischemia-reperfusion injury. Circulating natural IgM has been shown to play a significant role in mouse models of ischemia-reperfusion injury. A highly conserved self-antigen, nonmuscle myosin heavy chain II, has been identified as a target of pathogenic IgM. We hypothesized that a monoclonal antibody (m21G6) directed against nonmuscle myosin heavy chain II may inhibit IgM binding and reduce injury in a preclinical model of myocardial infarction. Thus, our objective was to evaluate the efficacy of intravenous m21G6 treatment in limiting infarct expansion, troponin release, and left ventricular dysfunction in a swine myocardial infarction model. METHODS AND

resultsMassachusetts General Hospital miniature swine underwent occlusion of the midleft anterior descending coronary artery for 60 minutes, followed by 1 hour, 5-day, or 21-day reperfusion. Specificity and localization of m21G6 to injured myocardium were confirmed using fluorescently labeled m21G6. Treatment with m21G6 before reperfusion resulted in a 49% reduction in infarct size (P<0.005) and a 61% reduction in troponin-T levels (P<0.05) in comparison with saline controls at 5-day reperfusion. Furthermore, m21G6-treated animals recovered 85.4% of their baseline left ventricular function as measured by 2-dimensional transthoracic echocardiography in contrast to 67.1% in controls at 21-day reperfusion (P<0.05).

conclusionsTreatment with m21G6 significantly reduced infarct size and troponin-T release, and led to marked preservation of cardiac function in our study. Overall, these findings suggest that pathogenic IgM blockade represents a valid therapeutic strategy in mitigating myocardial ischemia-reperfusion injury.

Indexed as

AnimalsAntibodies, Anti-IdiotypicAntibodies, MonoclonalCoronary VesselsDisease Models, AnimalDisease ProgressionEchocardiographyFollow-Up StudiesImmunoglobulin MMyocardial InfarctionMyocardiumMyosin Heavy ChainsSwineSwine, MiniatureTroponin TVentricular Dysfunction, LeftAntibodies, Anti-IdiotypicAntibodies, MonoclonalImmunoglobulin MMyosin Heavy ChainsTroponin Timmunologyinflammationleft ventricular functionmyocardial infarctiontroponin T

Identifiers

PMID26671971
PMCPMC4687758
OpenAlexW2206135428

What OpenQuestion holds

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Registered trials

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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.