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European Heart Journal Advance Access published online on May 8, 2007

European Heart Journal, doi:10.1093/eurheartj/ehm145
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Limitations to the use of virtual histology-intravascular ultrasound to detect vulnerable plaque

Andrew D. Frutkin

Cardiovascular Education Department
Mid America Heart Institute
Saint Luke's Hospital
University of Missouri-Kansas City
4401 Wornall Road
Kansas City
MO 64111
USA

Sameer K. Mehta

Cardiovascular Education Department
Mid America Heart Institute
Saint Luke's Hospital
University of Missouri-Kansas City
4401 Wornall Road
Kansas City
MO 64111
USA

Justin R. McCrary

Cardiovascular Education Department
Mid America Heart Institute
Saint Luke's Hospital
University of Missouri-Kansas City
4401 Wornall Road
Kansas City
MO 64111
USA

Steven P. Marso

Cardiovascular Education Department
Mid America Heart Institute
Saint Luke's Hospital
University of Missouri-Kansas City
4401 Wornall Road
Kansas City
MO 64111
USA
Tel: +1 816 932 5636
Fax: +1 816 932 5613
E-mail address: smarso{at}saint-lukes.org

Surmely et al.1 used virtual histology-intravascular ultrasound (VH-IVUS) to characterize coronary plaque in patients with acute coronary syndrome (ACS) and stable angina. Although VH-IVUS is a promising plaque-imaging platform, we believe that significant methodological issues must be resolved before VH-IVUS is used to detect vulnerable plaque, let alone direct therapy. First, in thrombus-laden arteries, VH-IVUS does not enhance the imprecise detection of plaque borders by grey-scale IVUS. Unfortunately, the authors do not describe their method of thrombus border detection nor their measurement variability in ACS lesions. Inaccurate detection of the borders shared by thrombus, plaque, and lumen may introduce large measurement errors of plaque composition. The site with the minimum lumen diameter may be misidentified. Thrombus may be misclassified as fibrous plaque, proportionally increasing this plaque component at the expense of the others. Thus, errors in border detection may lead to spurious conclusions about culprit plaque composition in ACS. Second, methods to define and measure coronary plaque vary widely, contributing to divergent results and conclusions. Surmely et al. do not define fixed margins for their region of interest. Moreover, they report relative plaque composition as calculated by the VH-IVUS software, a ratio of the absolute area of each plaque component to an estimated plaque area, one that excludes an estimated medial area. It is more appropriate to report relative plaque composition as the ratio of absolute area of each plaque component to the area bound by lumen and the external elastic membrane, as this utilizes direct measurements. Third, VH-IVUS-derived thin cap fibroatheroma (TCFA) is not yet a validated surrogate for plaque prone to thrombosis. VH-IVUS-derived TCFA is loosely based on the histopathological studies of necropsy specimens, which provide at least 100-fold superior spatial resolution to VH-IVUS. Complicating matters, Surmely et al. define TCFA differently from others.2 Larger prospective longitudinal studies, such as PROSPECT, may determine whether any VH-IVUS-derived definition of plaque phenotype has sufficient positive or negative predictive value for coronary thrombosis. Until then, it seems premature to conclude, as does the accompanying editorial, ‘that a plaque with only fibrous content by VH can be considered as stable with minimal risk of causing thrombosis.’3 To advance the invasive detection of vulnerable plaque, the research community should adopt standards to measure thrombus-associated plaque, calculate plaque composition, and define vulnerable plaque. We believe that with such standards investigators will be at lower risk of experimental error.

References

  1. Surmely JF, Nasu K, Fujita H, Terashima M, Matsubara T, Tsuchikane E, Ehara M, Kinoshita Y, Zheng QX, Tanaka N, Katoh O, Suzuki T. Coronary plaque composition of culprit/target lesions according to the clinical presentation: a virtual histology intravascular ultrasound analysis. Eur Heart J (2006) 27:2939–2944.[Abstract/Free Full Text]
  2. Rodriguez-Granillo GA, Garcia-Garcia HM, Mc Fadden EP, Valgimigli M, Aoki J, de Feyter P, Serruys PW. In vivo intravascular ultrasound-derived thin-cap fibroatheroma detection using ultrasound radiofrequency data analysis. J Am Coll Cardiol (2005) 46:2038–2042.[Medline]
  3. Saunamaki KI. Virtual histology and the hunt for the vulnerable plaque. Eur Heart J (2006) 27:2914–2915.[Free Full Text]

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