Evidence map›Paper›PMID 23218838›Full record

ArticleJournal of biomechanics2013

The explosive growth of small voids in vulnerable cap rupture; cavitation and interfacial debonding.

Natalia Maldonado, Adreanne Kelly-Arnold, Luis Cardoso, Sheldon Weinbaum

Open access · greenAbstract read
In one paragraph

Article in Journal of biomechanics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
  2. Biomechanics of Plaque Rupture and Cardiovascular Calcification.Advances in experimental medicine and biology · 2026
    Review
  3. The Pathophysiology of Coronary Artery Disease.The International journal of angiology : official publication of the International College of Angiology, Inc · 2025
    Review
  4. Article
  5. Considerations on the Development of Therapeutics in Vascular Calcification.Journal of cardiovascular development and disease · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. The Time-Dependent Role of Bisphosphonates on Atherosclerotic Plaque Calcification.Journal of cardiovascular development and disease · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

4 authors at 2 institutions in 1 country.

Natalia MaldonadoDepartment of Biomedical Engineering, The City College of New York of The City University of New York, NY, USA.
Adreanne Kelly-Arnold
Luis Cardoso
Sheldon Weinbaum
City College of New York · USCity University of New York · US

Funding

Predicting Cardiovascular Risk in Vulnerable Plaque RuptureRC1HL101157 · NHLBI · CITY COLLEGE OF NEW YORK · PI WEINBAUM, SHELDON · 2009 to 2010
$765k
Age Related Bone Loss Assessed by Ultrasound Tomography: Bone Quality Beyond BMDSC2AG034198 · NIA · CITY COLLEGE OF NEW YORK · PI CARDOSO, LUIS · 2009 to 2011
$434k
NHLBI NIH HHS HL101151NHLBI NIH HHS RC1 HL101157NIA NIH HHS AG034198NIA NIH HHS SC2 AG034198
6 · The paper itself

Abstract

While it is generally accepted that ruptures in fibrous cap atheromas cause most acute coronary deaths, and that plaque rupture occurs in the fibrous cap at the location where the tissue stress exceeds a certain critical peak circumferential stress, the exact mechanism of rupture initiation remains unclear. We recently reported the presence of multiple microcalcifications (μCalcs) <50 μm diameter embedded within the fibrous cap, μCalcs that could greatly increase cap instability by introducing up to a 5-fold increase in local tissue stress. Here, we explore the hypothesis that, aside from cap thickness, μCalc size and interparticle spacing are principal determinants of cap rupture risk. Also, we propose that cap rupture is initiated near the poles of the μCalcs due to the presence of tiny voids that explosively grow at a critical tissue stress and then propagate across the fibrous cap. We develop a theoretical model based on classic studies in polymeric materials by Gent (1980), which indicates that cavitation as opposed to interfacial debonding is the more likely mechanism for cap rupture produced by μCalcs <65 μm diameter. This analysis suggests that there is a critical μCalc size range, from 5 μm to 65 μm, in which cavitation should be prevalent. This hypothesis for cap rupture is strongly supported by our latest high resolution μCT studies in which we have observed trapped voids in the vicinity of μCalcs within fibrous caps in human coronaries.

Indexed as

Acute Coronary SyndromeModels, CardiovascularPlaque, AtheroscleroticStress, PhysiologicalHumans

Identifiers

PMID23218838
PMCPMC4019735
OpenAlexW2075879509

What OpenQuestion holds

Textmetadata
LicenceTDM
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.