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    Fatigue Crack Propagation Analysis of Plaque Rupture

    Source: Journal of Biomechanical Engineering:;2013:;volume( 135 ):;issue: 010::page 101003
    Author:
    Pei, Xuan
    ,
    Wu, Baijian
    ,
    Li, Zhi
    DOI: 10.1115/1.4025106
    Publisher: The American Society of Mechanical Engineers (ASME)
    Abstract: Rupture of atheromatous plaque is the major cause of stroke or heart attack. Considering that the cardiovascular system is a classic fatigue environment, plaque rupture was treated as a chronic fatigue crack growth process in this study. Fracture mechanics theory was introduced to describe the stress status at the crack tip and Paris' law was used to calculate the crack growth rate. The effect of anatomical variation of an idealized plaque crosssection model was investigated. The crack initiation was considered to be either at the maximum circumferential stress location or at any other possible locations around the lumen. Although the crack automatically initialized at the maximum circumferential stress location usually propagated faster than others, it was not necessarily the most critical location where the fatigue life reached its minimum. We found that the fatigue life was minimum for cracks initialized in the following three regions: the midcap zone, the shoulder zone, and the backside zone. The anatomical variation has a significant influence on the fatigue life. Either a decrease in cap thickness or an increase in lipid pool size resulted in a significant decrease in fatigue life. Comparing to the previously used stress analysis, this fatigue model provides some possible explanations of plaque rupture at a low stress level in a pulsatile cardiovascular environment, and the method proposed here may be useful for further investigation of the mechanism of plaque rupture based on in vivo patient data.
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      Fatigue Crack Propagation Analysis of Plaque Rupture

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    http://yetl.yabesh.ir/yetl1/handle/yetl/151097
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    contributor authorPei, Xuan
    contributor authorWu, Baijian
    contributor authorLi, Zhi
    date accessioned2017-05-09T00:56:48Z
    date available2017-05-09T00:56:48Z
    date issued2013
    identifier issn0148-0731
    identifier otherbio_135_10_101003.pdf
    identifier urihttp://yetl.yabesh.ir/yetl/handle/yetl/151097
    description abstractRupture of atheromatous plaque is the major cause of stroke or heart attack. Considering that the cardiovascular system is a classic fatigue environment, plaque rupture was treated as a chronic fatigue crack growth process in this study. Fracture mechanics theory was introduced to describe the stress status at the crack tip and Paris' law was used to calculate the crack growth rate. The effect of anatomical variation of an idealized plaque crosssection model was investigated. The crack initiation was considered to be either at the maximum circumferential stress location or at any other possible locations around the lumen. Although the crack automatically initialized at the maximum circumferential stress location usually propagated faster than others, it was not necessarily the most critical location where the fatigue life reached its minimum. We found that the fatigue life was minimum for cracks initialized in the following three regions: the midcap zone, the shoulder zone, and the backside zone. The anatomical variation has a significant influence on the fatigue life. Either a decrease in cap thickness or an increase in lipid pool size resulted in a significant decrease in fatigue life. Comparing to the previously used stress analysis, this fatigue model provides some possible explanations of plaque rupture at a low stress level in a pulsatile cardiovascular environment, and the method proposed here may be useful for further investigation of the mechanism of plaque rupture based on in vivo patient data.
    publisherThe American Society of Mechanical Engineers (ASME)
    titleFatigue Crack Propagation Analysis of Plaque Rupture
    typeJournal Paper
    journal volume135
    journal issue10
    journal titleJournal of Biomechanical Engineering
    identifier doi10.1115/1.4025106
    journal fristpage101003
    journal lastpage101003
    identifier eissn1528-8951
    treeJournal of Biomechanical Engineering:;2013:;volume( 135 ):;issue: 010
    contenttypeFulltext
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