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Volume 47, Issue 8, Pages 1655-1662 (18 April 2006)


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Noninvasive Assessment of Plaque Morphology and Composition in Culprit and Stable Lesions in Acute Coronary Syndrome and Stable Lesions in Stable Angina by Multidetector Computed Tomography

Udo Hoffmann, MDCorresponding Author Informationemail address, Fabian Moselewski, BS, Koen Nieman, MD, Ik-Kyung Jang, MD, PhD, Maros Ferencik, MD, PhD, Ayaz M. Rahman, MD, Ricardo C. Cury, MD, Suhny Abbara, MD, Hamid Joneidi-Jafari, BS, Stephan Achenbach, MD, Thomas J. Brady, MD

Received 13 June 2005; received in revised form 25 September 2005; accepted 9 November 2005. published online 24 March 2006.

Noninvasive Assessment of Plaque Morphology and Composition in Culprit and Stable Lesions in Acute Coronary Syndrome and Stable Lesions in Stable Angina by Multidetector Computed Tomography

Udo Hoffmann, Fabian Moselewski, Koen Nieman, Ik-Kyung Jang, Maros Ferencik, Ayaz M. Rahman, Ricardo C. Cury, Suhny Abbara, Hamid Joneidi-Jafari, Stephan Achenbach, Thomas J. Brady

With contrast-enhanced submillimeter 16-slice multidetector computed tomography (MDCT), we noninvasively assessed morphology and composition of 40 culprit and stable coronary lesions. Culprit lesions in patients with acute coronary syndrome (ACS) had significantly greater plaque area and a higher remodeling index than stable lesions both in patients with ACS and in patients with stable angina (p = 0.02 and p = 0.04; respectively). Lesion composition was also different between the three groups. This study introduces the concept of noninvasive detection and characterization of coronary atherosclerotic lesions in patients with ACS, emphasizing the potential of MDCT to improve noninvasive risk stratification in patients with acute chest pain.

Objectives

The purpose of this study was to assess morphology and composition of culprit and stable coronary lesions by multidetector computed tomography (MDCT).

Background

Noninvasive identification of culprit lesions has the potential to improve noninvasive risk stratification in patients with acute chest pain.

Methods

Thirty-seven patients with acute coronary syndrome (ACS) or stable angina underwent coronary 16-slice MDCT and invasive selective angiography. In all significant coronary lesions two observers measured the degree of stenosis, plaque area at stenosis, and remodeling index and assessed plaque composition. Differences between culprit lesions in patients with ACS and stable lesions in patients with ACS or stable angina were determined.

Results

We analyzed 40 lesions with excellent image quality in 14 patients with ACS and 9 patients with stable angina. Culprit lesions in patients with ACS (n = 14) had significantly greater plaque area and a higher remodeling index than both stable lesions in patients with ACS (n = 13) and in patients with stable angina (n = 13) (17.5 ± 5.9 mm2 vs. 9.1 ± 4.8 mm2 vs. 13.5 ± 10.7 mm2, p = 0.02; and 1.4 ± 0.3 vs. 1.0 ± 0.4 vs. 1.2 ± 0.3, p = 0.04, respectively). The prevalence of non-calcified plaque was 100%, 62%, and 77%, respectively, and the prevalence of calcified plaque was 71%, 92%, and 85%, respectively, in culprit lesions in patients with ACS and in stable lesions in patients with ACS or stable angina.

Conclusions

We introduce the concept of noninvasive detection and characterization of coronary atherosclerotic lesions in patients with ACS by MDCT. We identified differences in lesion morphology and plaque composition between culprit lesions in ACS and stable lesions in ACS or stable angina, consistent with previous intravascular ultrasound studies.

 Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts

 Division of Cardiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts

 Department of Internal Medicine II, University of Erlangen, Erlangen, Germany

Corresponding Author InformationReprint requests and correspondence: Dr. Udo Hoffmann, Department of Radiology, Massachusetts General Hospital, 165 Charles River Plaza, Suite 400, Boston, Massachusetts 02114.

 This work was supported in part by New York Cardiac Center, New York and Siemens Medical Solutions. Dr. Nieman was supported by the Interuniversity Cardiology Institute of the Netherlands. Dr. Ferencik was supported in part by National Institutes of Health Grant 1 T32 HL076136-02.

PII: S0735-1097(06)00179-3

doi:10.1016/j.jacc.2006.01.041


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