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Technology Insight: in vivo coronary plaque classification by intravascular ultrasonography radiofrequency analysis

Nature Clinical Practice Cardiovascular Medicine volume 5, pages 219–229 (2008)Cite this article

Abstract

Acute coronary syndromes or sudden coronary death are often the first manifestations of coronary artery disease. In the majority of patients, acute coronary syndrome events are caused by plaque rupture in flow-limiting and non-flow-limiting angiographically intermediate stenoses. Histopathologic analyses have shown that plaque composition is related to the occurrence of acute clinical events and, therefore, to the vulnerability of the plaque. The emerging importance of adaptive coronary remodeling processes, such as the compensatory enlargement of the coronary artery in response to initial lesion development, has focused our interest on the nonstenotic lesions of the coronary tree. In vivo intravascular ultrasonography can demonstrate the discrepancies between the actual extent of coronary atherosclerosis and that seen by angiographic imaging. The spectral analysis of intravascular ultrasonography derived radiofrequency data enables more precise analysis of plaque composition and type than grayscale intravascular ultrasonography.

Key Points

  • Histopathologic analyses have shown that plaque composition is related to acute clinical events and, therefore, to the vulnerability of coronary plaques

  • The spectral analysis of intravascular ultrasonography-derived radiofrequency data enables more precise analysis of plaque composition and type

  • Intravascular ultrasonography derived virtual histology provides the most comprehensive imaging method for detailed assessment of plaque components in both cross-sectional and longitudinal views of the coronary artery

  • The present system for plaque classification by intravascular ultrasonography derived virtual histology represents the current translation of histopathological knowledge into in vivo intracoronary diagnosis

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Figure 1: Real-time intravascular-ultrasonography-derived virtual histology images in (A) tomographic and (B) longitudinal views.
Figure 2: Intravascular ultrasonographic images of an eccentric plaque.
Figure 3: Intravascular ultrasonographic images and histologic specimen of the same thin-cap fibroatheroma.
Figure 4: Current coronary plaque classification according to virtual histology intravascular ultrasonography.
Figure 5: Current classification for plaque type.
Figure 6: A new vulnerability index currently under development for improved classification and stratification of thin-cap fibroatheroma.
Figure 7: The relation between the site of plaque rupture and the site of the MLD of the interrogated lesion, as suggested by post-mortem studies.

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Acknowledgements

Désirée Lie, University of California, Irvine, CA, is the author of and is solely responsible for the content of the learning objectives, questions and answers of the Medscape-accredited continuing medical education activity associated with this article.

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Authors and Affiliations

  1. A König is Cardiologist and V Klauss is Head of the Department of Cardiology at the Medizinische Poliklinik—Campus Innenstadt, Ludwig-Maximilians-Universität, Munich, Germany,

    Andreas König & Volker Klauss

  2. MP Margolis is Medical Director of Volcano Corporation, Rancho Cordova, CA,

    M Pauliina Margolis

  3. R Virmani is Medical Director of the CVPath Institute, Gaithersburg, MD,

    Renu Virmani

  4. D Holmes is Professor of Medicine at the Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, Rochester, MN, USA.,

    David Holmes

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  1. Andreas König
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  5. Volker Klauss
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Corresponding author

Correspondence to Andreas König.

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Competing interests

MP Margolis is Medical Director of Volcano Corporation.

R Virmani is a Consultant to Volcano Corporation.

The other authors declared no competing interests.

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König, A., Margolis, M., Virmani, R. et al. Technology Insight: in vivo coronary plaque classification by intravascular ultrasonography radiofrequency analysis. Nat Rev Cardiol 5, 219–229 (2008). https://doi.org/10.1038/ncpcardio1123

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