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J Am Coll Cardiol, 2005; 45:1600-1602, doi:10.1016/j.jacc.2005.02.058
© 2005 by the American College of Cardiology Foundation
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Act Local, Act Global*

Inflammation and the Multiplicity of "Vulnerable" Coronary Plaques

Peter Libby, MD, FACC*

Donald W. Reynolds Cardiovascular Clinical Research Center, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts



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  		Figure 1 Prevalence of multiple coronary artery plaque ruptures detected by intravascular ultrasonography (IVUS) in five studies. Interrogation of coronary arteries of patients with acute coronary syndromes by IVUS reveals coincident ruptures of nonculprit lesions in 13% to 79% of cases. The differences in the prevalence of multiple plaque ruptures among studies may depend on technical issues (e.g., use of contrast), patient selection, timing of the investigation with relation to the index event, and other variables (8–12).

 


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  		Figure 2 Mechanisms by which inflammation can promote plaque disruption and the acute coronary syndromes. The pathophysiology of the acute coronary syndromes depends on plaque disruption and the thrombotic/fibrinolytic balance of the plaque’s "solid state" and the blood’s "fluid phase." Inflammation regulates two major mechanisms of plaque disruption: a frank fracture of the fibrous cap and superficial erosion of the intimal surface. Inflammatory mediators also influence the thrombotic/fibrinolytic balance of both the plaque and the blood.

 




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Copyright © 2005 by the American College of Cardiology Foundation.