Evidence map›Paper›PMID 28676061›Full record

ArticleJournal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance2017

Hemorrhage promotes inflammation and myocardial damage following acute myocardial infarction: insights from a novel preclinical model and cardiovascular magnetic resonance.

Nilesh R Ghugre, Mihaela Pop, Reuben Thomas, Susan Newbigging, Xiuling Qi, Jennifer Barry, Bradley H Strauss, Graham A Wright

Open access · goldAbstract read
In one paragraph

Article in Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. SCMR Position Paper (2020) on clinical indications for cardiovascular magnetic resonance.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2020
    Guideline
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Journal of Cardiovascular Magnetic Resonance: 2017/2018 in review.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2019
    Review
  16. Omnipolarity applied to equi-spaced electrode array for ventricular tachycardia substrate mapping.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2019
    Article
  17. Article
  18. Journal of Cardiovascular Magnetic Resonance 2017.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2018
    Review
  19. Review
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

8 authors at 4 institutions in 1 country.

Nilesh R GhugrePhysical Sciences Platform, Sunnybrook Research Institute, 2075 Bayview Avenue, Room M7-510, Toronto, ON, M4N 3M5, Canada. nghugre@sri.utoronto.ca.
Mihaela PopPhysical Sciences Platform, Sunnybrook Research Institute, 2075 Bayview Avenue, Room M7-510, Toronto, ON, M4N 3M5, Canada.
Reuben ThomasPhysical Sciences Platform, Sunnybrook Research Institute, 2075 Bayview Avenue, Room M7-510, Toronto, ON, M4N 3M5, Canada.
Susan NewbiggingThe Toronto Centre for Phenogenomics, Mount Sinai Hospital, Toronto, ON, Canada.
Xiuling QiPhysical Sciences Platform, Sunnybrook Research Institute, 2075 Bayview Avenue, Room M7-510, Toronto, ON, M4N 3M5, Canada.
Jennifer BarryPhysical Sciences Platform, Sunnybrook Research Institute, 2075 Bayview Avenue, Room M7-510, Toronto, ON, M4N 3M5, Canada.
Bradley H StraussSchulich Heart Research Program, Sunnybrook Health Sciences Centre, Toronto, ON, Canada.
Graham A WrightPhysical Sciences Platform, Sunnybrook Research Institute, 2075 Bayview Avenue, Room M7-510, Toronto, ON, M4N 3M5, Canada.
Sunnybrook Health Science Centre · CASunnybrook Research InstituteHealth Sciences Centre · CAToronto Centre for Phenogenomics · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyocardial hemorrhage is a frequent complication following reperfusion in acute myocardial infarction and is predictive of adverse outcomes. However, it remains unsettled whether hemorrhage is simply a marker of a severe initial ischemic insult or directly contributes to downstream myocardial damage. Our objective was to evaluate the contribution of hemorrhage towards inflammation, microvascular obstruction and infarct size in a novel porcine model of hemorrhagic myocardial infarction using cardiovascular magnetic resonance (CMR).

methodsMyocardial hemorrhage was induced via direct intracoronary injection of collagenase in a novel porcine model of ischemic injury. Animals (N = 27) were subjected to coronary balloon occlusion followed by reperfusion and divided into three groups (N = 9/group): 8 min ischemia with collagenase (+HEM); 45 min infarction with saline (I-HEM); and 45 min infarction with collagenase (I+HEM). Comprehensive CMR was performed on a 3 T scanner at baseline and 24 h post-intervention. Cardiac function was quantified by cine imaging, edema/inflammation by T2 mapping, hemorrhage by T2* mapping and infarct/microvascular obstruction size by gadolinium enhancement. Animals were subsequently sacrificed and explanted hearts underwent histopathological assessment for ischemic damage and inflammation.

resultsAt 24 h, the +HEM group induced only hemorrhage, the I-HEM group resulted in a non-hemorrhagic infarction, and the I+HEM group resulted in infarction and hemorrhage. Notably, the I+HEM group demonstrated greater hemorrhage and edema, larger infarct size and higher incidence of microvascular obstruction. Interestingly, hemorrhage alone (+HEM) also resulted in an observable inflammatory response, similar to that arising from a mild ischemic insult (I-HEM). CMR findings were in good agreement with histological staining patterns.

conclusionsHemorrhage is not simply a bystander, but an active modulator of tissue response, including inflammation and microvascular and myocardial damage beyond the initial ischemic insult. A mechanistic understanding of the pathophysiology of reperfusion hemorrhage will potentially aid better management of high-risk patients who are prone to adverse long-term outcomes.

Indexed as

Magnetic Resonance Imaging, CineAnimalsContrast MediaCoronary CirculationDisease Models, AnimalEdema, CardiacFemaleGadolinium DTPAHemorrhageMicrocirculationMyocardial InfarctionMyocarditisMyocardiumPredictive Value of TestsSus scrofaTime FactorsContrast MediaGadolinium DTPAcardiovascular magnetic resonanceHemorrhageInflammationIschemia reperfusion injuryMicrovascular obstructionMyocardial infarctionT2T2*

Identifiers

PMID28676061
PMCPMC5496389
OpenAlexW2733996821

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.