EDITORIAL COMMENT
Contrast-Enhanced Magnetic Resonance Imaging as the Newest Tool to Detect Transplant Coronary Artery Disease*
Pascal J. Goldschmidt-Clermont, MD, FACC* and
Chunming Dong, MD, FACC
Department of Medicine, The Leonard M. Miller School of Medicine, University of Miami, Miami, Florida
* Reprint requests and correspondence: Dr. Pascal J. Goldschmidt-Clermont, Leonard M. Miler School of Medicine, 1600 NW 10th Avenue, RMSB 1140 (R-699), Miami, Florida 33136 (Email: pgoldschmidt{at}med.miami.edu).
Key Words: CE-MRI • transplant coronary artery disease
The development of obstructive transplant coronary artery disease (TCAD) is the major factor limiting long-term survival after cardiac transplantation (1). TCAD is characterized as accelerated arteriosclerosis affecting the entire coronary tree with distal obliteration (2). A major problem is the lack of a valid "gold standard" technology for the early detection of the diffuse and concentric narrowing. Coronary angiography often underestimates the disease severity (3), because of the diffuse and concentric characteristic of the lesions. Intravascular ultrasonography (IVUS) has the potential to delineate the vessel wall morphology (4), but it is invasive and limited to large epicardial vessels. Owing to its diffuse character, TCAD has a tendency to occlude smaller arteries first. Furthermore, because the cardiac allografts are denervated, the clinical manifestations of acute coronary syndromes in the transplant recipients are usually silent or atypical as opposed to the angina (5) associated with garden-variety atherosclerosis. Thus, a noninvasive and sensitive imaging modality is needed to identify patients at risk for TCAD.
The team of Raymond Kim and Robert Judd has provided evidence that contrast-enhanced lesions of the infarcted myocardium overlap quite accurately with lesions detected on pathological slides (6). The presence of such contrast-enhanced lesions indicates an irreversible scar of the affected territory. Recovery of function after revascularization (bypass surgery) is inversely proportional to the extent of contrast-enhanced myocardium observed by magnetic resonance imaging (MRI) before the revascularization procedure. Other conditions can be enriched with dispersed contrast-enhanced lesions, such as myocarditis, hypertrophic cardiomyopathy, and sarcoidosis—hence, the idea that contrast-enhanced lesions could be found in the natural history of TCAD.
In this issue of the Journal, Steen et al. (7) present results that suggest the feasibility of gadolinium-enhanced MRI to detect chronic TCAD-related myocardial infarctions (MIs), even in patients with angiographically mild coronary narrowing. The authors found that infarct-typical contrast-enhanced magnetic resonance imaging (CE-MRI) was present in approximately one-fourth of patients with mild TCAD, one-third with manifest TCAD, and 84% of patients with severe TCAD, as detected by coronary angiography. The distribution of the infarct-typical segments is consistent with the angiographic appearance of TCAD lesions. Remarkably, the presence of infarct-typical CE-MRI was associated with a significantly worse left ventricular function and higher end-diastolic and -systolic volumes. Furthermore, infarct-atypical CE-MRI suggesting fibrosis was detected in approximately 50% of all cases, evenly distributed across all TCAD stages. The authors concluded that CE-MRI could be helpful to establish an earlier diagnosis of TCAD, in particular, microvascular dysfunction that might be missed by conventional coronary angiography, so that all available prevention treatments could be provided in a timely fashion. Although there is little doubt that CE-MRI is a very promising technique, the data should be interpreted with caution.
First, although the presence of infarct-typical CE-MRI was associated with worsening left ventricular function, it is still uncertain whether CE-MRI findings are predictive of clinical outcome. Thus, prospective studies are warranted to establish the clinical significance of infarct-typical CE-MRI findings in cardiac transplant recipients.
Second, although CE-MRI is noninvasive, it is not an established and validated method for the detection of MI and TCAD in cardiac transplant patients. The current study used coronary angiography—a technique notoriously known to underestimate TCAD (8)—to correlate with CE-MRI findings. More vigorous studies using IVUS as the standard need to be carried out to validate the CE-MRI findings. It is still conceivable that some contrast-enhanced lesions could result from the rejection process rather than TCAD. Also, IVUS measurements of TCAD are impressively reproducible (9), whereas there are no data yet supporting the reproducibility of CE-MRI in detecting MI and correlating with TCAD. Similarly, targeted biopsy needs to be performed to determine the clinical significance and pathological basis for the infarct-atypical CE-MRI patterns. These studies will help determine whether CE-MRI could serve as a "virtual biopsy" for transplant patients, which will undoubtedly reduce the discomfort and risks associated with the rather frequent biopsy procedures in post-transplant patients.
Third, the 20% to 30% failure rate associated with CE-MRI studies is unequivocally high. Further improvements in the MRI technology and the operators' techniques are imperative to render this approach practical in its clinical applications.
Despite these limitations, the findings presented in this report are clearly important, in that they provide proof of concept for the feasibility of CE-MRI in differentiating tissue ischemia, MI, and fibrosis. Further research aiming to correlate CE-MRI findings with IVUS and targeted biopsy and to improve the MRI technology will almost certainly lead to the acceptance of MRI-based methods that will vastly improve the care of cardiac transplant patients.
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Footnotes
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* Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. 
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References
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1. Clague JR, Cox ID, Murday AJ, Charokopos N, Madden BP. Low clinical utility of routine angiographic surveillance in the detection and management of cardiac allograft vasculopathy in transplant recipients Clin Cardiol 2001;24:459-462.[Web of Science][Medline]2. Hirohata A, Nakamura M, Waseda K, et al. Changes in coronary anatomy and physiology after heart transplantation Am J Cardiol 2007;99:1603-1607.[CrossRef][Web of Science][Medline] 3. Konig A, Kilian E, Rieber J, et al. Assessment of early atherosclerosis in de novo heart transplant recipients: analysis with intravascular ultrasound-derived radiofrequency analysis J Heart Lung Transplant 2008;27:26-30.[CrossRef][Web of Science][Medline] 4. Konig A, Kilian E, Sohn HY, et al. Assessment and characterization of time-related differences in plaque composition by intravascular ultrasound-derived radiofrequency analysis in heart transplant recipients J Heart Lung Transplant 2008;27:302-309.[CrossRef][Web of Science][Medline] 5. Mitchell RN. Allograft arteriopathy: pathogenesis update Cardiovasc Pathol 2004;13:33-40.[Web of Science][Medline] 6. Kim RJ, Wu E, Rafael A, et al. The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction N Engl J Med 2000;343:1445-1453.[CrossRef][Web of Science][Medline] 7. Steen H, Merten C, Refle S, et al. Prevalence of different gadolinium enhancement patterns in patients after heart transplantation J Am Coll Cardiol 2008;52:1160-1167.[Abstract/Free Full Text] 8. Ramzy D, Rao V, Brahm J, Miriuka S, Delgado D, Ross HJ. Cardiac allograft vasculopathy: a review Can J Surg 2005;48:319-327.[Web of Science][Medline] 9. Schmauss D, Weis M. Cardiac allograft vasculopathy: recent developments Circulation 2008;117:2131-2141.[Abstract/Free Full Text]
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