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Circulation. 2001;103:1051-1056

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(Circulation. 2001;103:1051.)
© 2001 American Heart Association, Inc.


Clinical Investigation and Reports

The Impact of Calcification on the Biomechanical Stability of Atherosclerotic Plaques

Hayden Huang, SM; Renu Virmani, MD; Hesham Younis, MA; Allen P. Burke, MD; Roger D. Kamm, PhD; Richard T. Lee, MD

From the Cardiovascular Division (R.T.L.), Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass; the Center for Biomedical Engineering (H.Y., R.D.K., R.T.L.), Massachusetts Institute of Technology, Cambridge, Mass; the Health Sciences and Technology Division of the Massachusetts Institute of Technology (H.H.), Cambridge, Mass; and the Department of Cardiovascular Pathology (R.V., A.P.B.), Armed Forces Institute of Pathology, Washington, DC.

Correspondence to Richard T. Lee, MD, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115. Email rlee{at}rics.bwh.harvard.edu

Background—Increased biomechanical stresses in the fibrous cap of atherosclerotic plaques contribute to plaque rupture and, consequently, to thrombosis and myocardial infarction. Thin fibrous caps and large lipid pools are important determinants of increased plaque stresses. Although coronary calcification is associated with worse cardiovascular prognosis, the relationship between atheroma calcification and stresses is incompletely described.

Methods and Results—To test the hypothesis that calcification impacts biomechanical stresses in human atherosclerotic lesions, we studied 20 human coronary lesions with techniques that have previously been shown to predict plaque rupture locations accurately. Ten ruptured and 10 stable lesions derived from post mortem coronary arteries were studied using large-strain finite element analysis. Maximum stress was not correlated with percentage of calcification, but it was positively correlated with the percentage of lipid (P=0.024). When calcification was eliminated and replaced with fibrous plaque, stress changed insignificantly; the median increase in stress for all specimens was 0.1% (range, 0% to 8%; P=0.85). In contrast, stress decreased by a median of 26% (range, 1% to 78%; P=0.02) when lipid was replaced with fibrous plaque.

Conclusions—Calcification does not increase fibrous cap stress in typical ruptured or stable human coronary atherosclerotic lesions. In contrast to lipid pools, which dramatically increase stresses, calcification does not seem to decrease the mechanical stability of the coronary atheroma.


Key Words: atherosclerosis • plaque • stress • calcification • lipids




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