title: How does calcification influence plaque vulnerability? Insights from fatigue analysis.
abstract: BACKGROUND
  Calcification is commonly believed to be associated with cardiovascular disease burden. But whether or not the calcifications have a negative effect on plaque vulnerability is still under debate.
  
  
  RESULTS
  Fatigue rupture analysis and the fatigue life were used to evaluate the rupture risk. An idealized baseline model containing no calcification was first built. Based on the baseline model, we investigated the influence of calcification on rupture path and fatigue life by adding a circular calcification and changing its location within the fibrous cap area. Results show that 84.0% of calcified cases increase the fatigue life up to 11.4%. For rupture paths 10D far from the calcification, the life change is negligible. Calcifications close to lumen increase more fatigue life than those close to the lipid pool. Also, calcifications in the middle area of fibrous cap increase more fatigue life than those in the shoulder area.
  
  
  CONCLUSIONS
  Calcifications may play a positive role in the plaque stability. The influence of the calcification only exists in a local area. Calcifications close to lumen may be influenced more than those close to lipid pool. And calcifications in the middle area of fibrous cap are seemly influenced more than those in the shoulder area.
authors: Department of Engineering Mechanics, Southeast University, Nanjing 210096, China.
authors: Baijian
authors: B
authors: Wu
authors: School of Biological Science & Medical Engineering, Southeast University, Nanjing 210096, China.
authors: Xuan
authors: X
authors: Pei
authors: School of Biological Science & Medical Engineering, Southeast University, Nanjing 210096, China ; University Department of Radiology, University of Cambridge, Cambridge CB2 0QQ, UK.
authors: Zhi-Yong
authors: ZY
authors: Li
mesh_terms: D002114:Calcinosis / Q000378:metabolism* / Q000503:physiopathology*; D002318:Cardiovascular Diseases / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D008962:Models, Theoretical; D058226:Plaque, Atherosclerotic / Q000378:metabolism* / Q000503:physiopathology*; D013314:Stress, Mechanical