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Coronary Plaque Characterization by T₁-Weighted Cardiac Magnetic Resonance^_*

King's College London British Heart Foundation Centre of Research Excellence, Imaging Sciences Division, The Rayne Institute, St. Thomas' Hospital, London, United Kingdom

Key Words: CMR • atherosclerosis • cardiac magnetic resonance • coronary artery disease

Noninvasive techniques for imaging subclinical and advanced atherosclerosis currently include cardiac magnetic resonance (CMR) (4–6), multislice computed tomography (MSCT) (7), positron emission tomography/computed tomography (8,9), and ultrasound (10). Among these modalities, CMR offers several different methods to assess and characterize atherosclerotic plaque burden and activity. These methods, which include noncontrast (4–6) and contrast-enhanced (11) vessel wall imaging, have shown great promise to assess morphologic as well as biological characteristics of potentially vulnerable plaques, such as inflammatory activity (12), necrotic core size (6), neovascularization (13), intraplaque hemorrhage (6), and positive vessel wall remodeling (14).

In this issue of iJACC, Kawasaki et al. (15) report the observation of hyperintense coronary plaques (HIP) with noncontrast enhanced T₁-weighted (T1W) coronary CMR (16) and investigate their relationship with MSCT, intravascular ultrasound (IVUS), and coronary flow by X-ray angiography. HIP were more likely to demonstrate positive remodeling, ultrasound attenuation, lower Hounsfield units, and transient slow flow after percutaneous coronary intervention. All these features have been associated with unstable plaques (7,17). These findings are in good agreement with those from earlier studies using T1W magnetic resonance for carotid plaque characterization using histology as the gold standard. In those studies, HIP correlated with complicated plaque, lipid-rich core, intraplaque hemorrhage, and recent ischemic cerebrovascular events (18). Similarly, positive remodeling by MSCT has been found to correlate with lower Hounsfield units and with a higher frequency of lipid-rich plaque. A positive remodeling by MSCT was also found to correlate with increased values of high-sensitivity C-reactive protein (hs-CRP), an emerging marker for adverse outcome in patients with CAD (19). Positive remodeling by IVUS has been observed primarily in patients with unstable CAD; negative remodeling was more common in patients with stable CAD (7,17). In a study using optical coherence tomography, positive remodeling in patients with CAD (vs. no remodeling vs. negative remodeling) was associated with a higher frequency of lipid-rich plaque (100% vs. 60% vs. 47.4%, p = 0.01) and thin cap fibroatheromas (80% vs. 38.5% vs. 5.6%, p < 0.001) and a thinner fibrous cap (median 40.2 µm vs. 51.6 µm vs. 87 µm, p = 0.003) (20).

A recent IVUS study (21) demonstrated a higher frequency of positive remodeling, no reflow, and fibro-fatty and necrotic plaque material in patients with ACS compared to stable CAD, similar to the findings in the study by Kawasaki et al. (15) in this issue. Given the relatively high diagnostic accuracy of T1W magnetic resonance for the detection of complicated plaques in the carotid arteries (sensitivity and specificity of 84%, negative predictive value of 70%, and positive predictive value of 93%) and the strong association of HIP with other markers for plaque vulnerability, noncontrast T1W coronary plaque imaging may have the potential for identification of complex coronary lesions in patients with suspected unstable CAD. A limitation of the study by Kawasaki et al. (15) is that no reproducibility data are provided and that no follow-up imaging and correlation with clinical endpoints were performed. In conclusion, noncontrast enhanced T1W coronary CMR appears to be a promising technique for visualization of complex coronary lesions, but studies in larger patient cohorts with clinical endpoints such as myocardial infarction and stroke are now warranted to demonstrate the clinical applicability and prognostic value of this technique.

	Footnotes

 
^_* Editorials published in JACC: Cardiovascular Imaging reflect the views of the authors and do not necessarily represent the views of JACC: Cardiovascular Imaging or the American College of Cardiology.

^_* Reprint requests and correspondence: Dr. René M. Botnar, Imaging Sciences Division, King's College London, The Rayne Institute, 4th Floor, Lambeth Wing, St. Thomas' Hospital, London, SE1 7EH, United Kingdom (Email: rene.botnar{at}kcl.ac.uk).

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