Document Detail


The explosive growth of small voids in vulnerable cap rupture; cavitation and interfacial debonding.
MedLine Citation:
PMID:  23218838     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Natalia Maldonado; Adreanne Kelly-Arnold; Luis Cardoso; Sheldon Weinbaum
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2012-12-06
Journal Detail:
Title:  Journal of biomechanics     Volume:  46     ISSN:  1873-2380     ISO Abbreviation:  J Biomech     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-01-21     Completed Date:  2013-07-04     Revised Date:  2014-05-14    
Medline Journal Info:
Nlm Unique ID:  0157375     Medline TA:  J Biomech     Country:  United States    
Other Details:
Languages:  eng     Pagination:  396-401     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Ltd. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Acute Coronary Syndrome* / pathology,  physiopathology
Humans
Models, Cardiovascular*
Plaque, Atherosclerotic* / pathology,  physiopathology
Stress, Physiological*
Grant Support
ID/Acronym/Agency:
AG034198/AG/NIA NIH HHS; HL101151/HL/NHLBI NIH HHS; RC1 HL101157/HL/NHLBI NIH HHS; SC2 AG034198/AG/NIA NIH HHS
Comments/Corrections

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