Evidence map›Paper›PMID 31354010›Full record

ArticleJournal of the American Heart Association2019

Extracellular Vesicles Promote Arteriogenesis in Chronically Ischemic Myocardium in the Setting of Metabolic Syndrome.

Laura A Scrimgeour, Brittany A Potz, Ahmad Aboul Gheit, Guangbin Shi, Melissa Stanley, Zhiqi Zhang, Neel R Sodha, Nagib Ahsan, M Ruhul Abid, Frank W Sellke

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  5. Cardioprotection in cardiovascular surgery.Basic research in cardiology · 2024
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  19. Review
  20. Extracellular Vesicles and Ischemic Cardiovascular Diseases.Advances in experimental medicine and biology · 2023
    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

10 authors at 2 institutions in 1 country.

Laura A ScrimgeourDivision of Cardiothoracic Surgery Department of Surgery Cardiovascular Research Center Rhode Island Hospital Warren Alpert Medical School of Brown University Providence RI.
Brittany A PotzDivision of Cardiothoracic Surgery Department of Surgery Cardiovascular Research Center Rhode Island Hospital Warren Alpert Medical School of Brown University Providence RI.
Ahmad Aboul GheitDivision of Cardiothoracic Surgery Department of Surgery Cardiovascular Research Center Rhode Island Hospital Warren Alpert Medical School of Brown University Providence RI.
Guangbin ShiDivision of Cardiothoracic Surgery Department of Surgery Cardiovascular Research Center Rhode Island Hospital Warren Alpert Medical School of Brown University Providence RI.
Melissa StanleyDivision of Cardiothoracic Surgery Department of Surgery Cardiovascular Research Center Rhode Island Hospital Warren Alpert Medical School of Brown University Providence RI.
Zhiqi ZhangDivision of Cardiothoracic Surgery Department of Surgery Cardiovascular Research Center Rhode Island Hospital Warren Alpert Medical School of Brown University Providence RI.
Neel R SodhaDivision of Cardiothoracic Surgery Department of Surgery Cardiovascular Research Center Rhode Island Hospital Warren Alpert Medical School of Brown University Providence RI.
Nagib AhsanCenter of Biomedical Research Excellence Center for Cancer Research Development Proteomics Core Facility Rhode Island Hospital Providence RI.
M Ruhul AbidDivision of Cardiothoracic Surgery Department of Surgery Cardiovascular Research Center Rhode Island Hospital Warren Alpert Medical School of Brown University Providence RI.
Frank W SellkeDivision of Cardiothoracic Surgery Department of Surgery Cardiovascular Research Center Rhode Island Hospital Warren Alpert Medical School of Brown University Providence RI.
Rhode Island Hospital · USBrown University · US

Funding

Effect of Cardioplegia and Cardiopulmonary Bypass on Coronary Microvascular ReactivityR01HL046716 · NHLBI · RHODE ISLAND HOSPITAL · PI SELLKE, FRANK W · 1997 to 2023
$8.5M
Vascular Dysfunction in Myocardial Ischemia and Metabolic SyndromeR01HL128831 · NHLBI · RHODE ISLAND HOSPITAL · PI SELLKE, FRANK W, USHEVA-SIMIDJIYSKA, ANNY · 2016 to 2025
$5.7M
Trauma and Inflammation Research TrainingT32GM065085 · NIGMS · RHODE ISLAND HOSPITAL · PI Alfred Ayala · 2004 to 2026
$3.2M
Sub-cellular Targeting of Endothelial ROS in Myocardial IschemiaR01HL133624 · NHLBI · RHODE ISLAND HOSPITAL · PI ABID, RUHUL · 2017 to 2020
$1.6M
NHLBI NIH HHS R01 HL046716NHLBI NIH HHS R01 HL128831NHLBI NIH HHS R01 HL133624NIGMS NIH HHS T32 GM065085
6 · The paper itself

Abstract

Background Ischemic heart disease continues to be a leading cause of mortality in patients. Extracellular vesicles (EVs) provide a potential for treatment that may induce collateral vessel growth to increase myocardial perfusion. Methods and Results Nineteen male Yorkshire pigs were given a high-fat diet for 4 weeks, then underwent placement of an ameroid constrictor on the left circumflex artery to induce chronic myocardial ischemia. Two weeks later, the pigs received either intramyocardial vehicle (n=6), EVs (high-fat diet with myocardial EV injection [HVM]; n=8), or HVM and calpain inhibition (n=5). Five weeks later, myocardial function, perfusion, coronary vascular density, and cell signaling were examined. Perfusion in the collateral-dependent myocardium was increased during rapid ventricular pacing in the HVM group in both nonischemic (P=0.04) and ischemic areas of the ventricle (P=0.05). Cardiac output and stroke volume were significantly improved in the HVM group compared with the control group during ventricular pacing (P=0.006). Increased arteriolar density was seen in the HVM group in both nonischemic and ischemic myocardium (P=0.003 for both). However, no significant changes in the capillary density were observed between the control, HVM, and HVM and calpain inhibition groups (P=0.07). The group that received EVs with oral calpain inhibition had neither increased vessel density (P>0.99) nor improvement in blood flow or cardiac function (P=0.48) when compared with the control group. Conclusions These findings suggest that EVs promote angiogenesis in areas of chronic myocardial ischemia and improve cardiac function under conditions of diet-induced metabolic syndrome.

Indexed as

Neovascularization, PhysiologicAnimalsChronic DiseaseDisease Models, AnimalExtracellular VesiclesMaleMetabolic SyndromeMyocardial IschemiaSwineangiogenesiscardiovascular diseasecoronary vesselsextracellular vesicles

Identifiers

PMID31354010
PMCPMC6761642
OpenAlexW2966835530

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.