Evidence map›Paper›PMID 26395041›Full record

ArticleThe Journal of thoracic and cardiovascular surgery2015

Effects of small platform catheter-based left ventricular assist device support on regional myocardial signal transduction.

Keshava Rajagopal, Progyaparamita Saha, Isa Mohammed, Pablo G Sanchez, Tieluo Li, Zhongjun J Wu, Bartley P Griffith

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

Article in The Journal of thoracic and cardiovascular surgery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Keshava RajagopalDivision of Cardiac Surgery, Department of Surgery, University of Maryland School of Medicine and Medical Center, Baltimore, Md. Electronic address: Keshava.Rajagopal@uth.tmc.edu.
Progyaparamita SahaDivision of Cardiac Surgery, Department of Surgery, University of Maryland School of Medicine and Medical Center, Baltimore, Md.
Isa MohammedDivision of Cardiac Surgery, Department of Surgery, University of Maryland School of Medicine and Medical Center, Baltimore, Md.
Pablo G SanchezDivision of Cardiac Surgery, Department of Surgery, University of Maryland School of Medicine and Medical Center, Baltimore, Md.
Tieluo LiDivision of Cardiac Surgery, Department of Surgery, University of Maryland School of Medicine and Medical Center, Baltimore, Md.
Zhongjun J WuDivision of Cardiac Surgery, Department of Surgery, University of Maryland School of Medicine and Medical Center, Baltimore, Md.
Bartley P GriffithDivision of Cardiac Surgery, Department of Surgery, University of Maryland School of Medicine and Medical Center, Baltimore, Md.
University of Maryland, Baltimore · US

Funding

First-in-Human Use of an Artificial Lung for Ambulatory Respiratory SupportR01HL118372 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI GRIFFITH, BARTLEY P, WU, ZHONGJUN JON · 2013 to 2023
$7.9M
Strain Controlled LVAD Unloading and Post MI RemodelingR01HL081106 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI GRIFFITH, BARTLEY P · 2006 to 2010
$3.4M
Shear-Induced Hemostatic Dysfunction and Bleeding in CF-VAD PatientsR01HL124170 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI GRIFFITH, BARTLEY P, WU, ZHONGJUN JON · 2015 to 2018
$2.0M
NHLBI NIH HHS 1R01 HL 118372NHLBI NIH HHS 1R01 HL 124170NHLBI NIH HHS R01 HL081106NHLBI NIH HHS R01 HL118372NHLBI NIH HHS R01 HL124170
6 · The paper itself

Abstract

objectivesLeft ventricular (LV) assist device (LVAD) support reduces pathological loading. However, load-induced adaptive responses may be suppressed. Pathological loading dysregulates cardiac G protein-coupled receptor (GPCR) signaling. Signaling through G proteins is deleterious, whereas beta (β)-arrestin-mediated signaling is cardioprotective. We examined the effects of pathological LV loading/LV dysfunction and treatment via LVAD, on β-arrestin-mediated signaling, and genetic networks downstream of load.

methodsAn ovine myocardial infarction (MI) model was used. Sheep underwent sham thoracotomy (n = 3), mid-left anterior descending coronary artery ligation to produce MI (n = 3), or MI with placement of a small-platform catheter-based LVAD (n = 3). LVAD support was continued for 2 weeks. Animals were maintained for a total of 12 weeks. Myocardial specimens were harvested and analyzed.

resultsMI induced β-arrestin activation. Increased interactions between epidermal growth factor receptor and β-arrestins were observed. LVAD support inhibited these responses to MI (P < .05). LVAD support inhibited the activation of cardioprotective signaling effectors Akt (P < .05), and, to a lesser extent, extracellular regulated kinase 1/2 (P not significant); however, MI resulted in regional activation of load-induced GPCR signaling via G proteins, as assessed by the induction of atrial natriuretic peptide mRNA expression in the MI-adjacent zone relative to the MI-remote zone (P < .05). MI-adjacent zone atrial natriuretic peptide expression was renormalized with LVAD support.

conclusionsLVAD support inhibited cardioprotective β-arrestin-mediated signaling. However, net benefits of normalization of load-induced GPCR signaling were observed in the MI-adjacent zone. These findings may have implications for the optimal extent and duration of unloading, and for the development of adjunctive medical therapies.

Indexed as

Cardiac CathetersHeart-Assist DevicesSignal TransductionVentricular Function, LeftAnimalsArrestinsAtrial Natriuretic Factorbeta-ArrestinsCardiac CatheterizationDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesMaterials TestingMyocardial InfarctionMyocardiumPhosphorylationProsthesis DesignArrestinsAtrial Natriuretic Factorbeta-ArrestinsExtracellular Signal-Regulated MAP KinasesProto-Oncogene Proteins c-aktReceptors, G-Protein-CoupledRNA, Messengerintracellular signalingleft ventricular dysfunctionmechanical circulatory supportmechanotransductionmyocardial infarction

Identifiers

PMID26395041
PMCPMC4637226
OpenAlexW1171720707

What OpenQuestion holds

Textmetadata
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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.