Evidence map›Paper›PMID 32226783›Full record

ReviewFrontiers in bioengineering and biotechnology2020

Thrombogenic and Inflammatory Reactions to Biomaterials in Medical Devices.

Carlos A Labarrere, Ali E Dabiri, Ghassan S Kassab

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in bioengineering and biotechnology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 105 citations in OpenAlex.

  1. Review
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  11. Enhanced Hemocompatibility via Bivalirudin and Bicarbonate as Alternative to Heparin in a Catheter-Based Axial-Flow System.Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions · 2025
    Article
  12. Review
  13. Engineering the Immune Response to Biomaterials.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  14. Article
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  16. Article
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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

3 authors at 1 institution in 1 country.

Carlos A LabarrereCalifornia Medical Innovations Institute, San Diego, CA, United States.
Ali E DabiriCalifornia Medical Innovations Institute, San Diego, CA, United States.
Ghassan S KassabCalifornia Medical Innovations Institute, San Diego, CA, United States.
California Medical Innovations Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Blood-contacting medical devices of different biomaterials are often used to treat various cardiovascular diseases. Thrombus formation is a common cause of failure of cardiovascular devices. Currently, there are no clinically available biomaterials that can totally inhibit thrombosis under the more challenging environments (e.g., low flow in the venous system). Although some biomaterials reduce protein adsorption or cell adhesion, the issue of biomaterial associated with thrombosis and inflammation still exists. To better understand how to develop more thrombosis-resistant medical devices, it is essential to understand the biology and mechano-transduction of thrombus nucleation and progression. In this review, we will compare the mechanisms of thrombus development and progression in the arterial and venous systems. We will address various aspects of thrombosis, starting with biology of thrombosis, mathematical modeling to integrate the mechanism of thrombosis, and thrombus formation on medical devices. Prevention of these problems requires a multifaceted approach that involves more effective and safer thrombolytic agents but more importantly the development of novel thrombosis-resistant biomaterials mimicking the biological characteristics of the endothelium and extracellular matrix tissues that also ameliorate the development and the progression of chronic inflammation as part of the processes associated with the detrimental generation of late thrombosis and neo-atherosclerosis. Until such developments occur, engineers and clinicians must work together to develop devices that require minimal anticoagulants and thrombolytics to mitigate thrombosis and inflammation without causing serious bleeding side effects.

Indexed as

biomaterialsC-reactive proteininflammationmedical devicesmonomeric C-reactive proteinsulfated glycosaminoglycansthrombosistissue factor

Identifiers

PMID32226783
PMCPMC7080654
OpenAlexW3012532511

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.