Document Detail


A mechanistic analysis of the role of microcalcifications in atherosclerotic plaque stability: potential implications for plaque rupture.
MedLine Citation:
PMID:  22777419     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The role of microcalcifications (μCalcs) in the biomechanics of vulnerable plaque rupture is examined. Our laboratory previously proposed (Ref. 44), using a very limited tissue sample, that μCalcs embedded in the fibrous cap proper could significantly increase cap instability. This study has been greatly expanded. Ninety-two human coronary arteries containing 62 fibroatheroma were examined using high-resolution microcomputed tomography at 6.7-μm resolution and undecalcified histology with special emphasis on calcified particles <50 μm in diameter. Our results reveal the presence of thousands of μCalcs, the vast majority in lipid pools where they are not dangerous. However, 81 μCalcs were also observed in the fibrous caps of nine of the fibroatheroma. All 81 of these μCalcs were analyzed using three-dimensional finite-element analysis, and the results were used to develop important new clinical criteria for cap stability. These criteria include variation of the Young's modulus of the μCalc and surrounding tissue, μCalc size, and clustering. We found that local tissue stress could be increased fivefold when μCalcs were closely spaced, and the peak circumferential stress in the thinnest nonruptured cap (66 μm) if no μCalcs were present was only 107 kPa, far less than the proposed minimum rupture threshold of 300 kPa. These results and histology suggest that there are numerous μCalcs < 15 μm in the caps, not visible at 6.7-μm resolution, and that our failure to find any nonruptured caps between 30 and 66 μm is a strong indication that many of these caps contained μCalcs.
Authors:
Natalia Maldonado; Adreanne Kelly-Arnold; Yuliya Vengrenyuk; Damien Laudier; John T Fallon; Renu Virmani; 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.; Webcasts     Date:  2012-07-09
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  303     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-09-03     Completed Date:  2012-11-07     Revised Date:  2013-09-03    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H619-28     Citation Subset:  IM    
Affiliation:
Department of Biomedical Engineering, The City College of New York, The City University of New York, New York, New York 10031, USA.
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MeSH Terms
Descriptor/Qualifier:
Aged
Biomechanics
Computer Simulation
Coronary Artery Disease / complications,  physiopathology,  radiography*
Coronary Vessels / pathology*,  physiopathology
Elastic Modulus
Female
Fibrosis
Finite Element Analysis
Humans
Imaging, Three-Dimensional*
Male
Middle Aged
Models, Cardiovascular
Plaque, Atherosclerotic
Radiographic Image Interpretation, Computer-Assisted*
Rupture, Spontaneous
Stress, Mechanical
Vascular Calcification / complications,  physiopathology,  radiography*
X-Ray Microtomography / methods*
Grant Support
ID/Acronym/Agency:
AG034198/AG/NIA NIH HHS; RCI HL101151/HL/NHLBI NIH HHS
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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