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Letters to the Editor |
University of Milan School of Medicine, Department of Medical and Surgical Sciences, Radiology Unit, IRCCS, Policlinico San Donato, Via Morandi 30, 20097 San Donato Milanese, Milan, Italy
e-mail: f.sardanelli{at}grupposandonato.it
We read with great interest the article by Dr Schlosser and colleagues (1) in the September 2005 issue of Radiology. The authors report a prospective comparison of gadobenate dimeglumine and gadopentetate dimeglumine for delayed enhancement of chronic myocardial infarction by using a double dose (0.2 mmol per kilogram body weight) of each contrast agent. This study clearly confirmed the higher T1 relaxivity of gadobenate (2,3), demonstrating that the T1 values of infarcted and noninfarcted myocardium were significantly lower with gadobenate compared with gadopentetate at all time points (1, 3, 5, 10, and 20 minutes) after contrast agent injection. Similar findings were obtained for the T1 values of the blood in the left ventricular cavity except for the first postinjection time point (1 minute), when a slight difference in favor of gadobenate was not significant. Reduced T1 values produced higher signal intensity on strongly T1-weighted magnetic resonance (MR) images, as is to be expected for an inversion-recovery gradient-echo sequence with optimized inversion time. As a consequence, at 15 minutes after contrast agent injection, the combination of high signal intensity of both infarcted myocardium and left ventricular cavity resulted in a reduced contrast-to-noise ratio of subendocardial infarcts for gadobenate compared with gadopentetate. The authors suggest that "late-enhancement studies with gadobenate might benefit from a longer delay after contrast agent injection."
This phenomenon (higher signal intensities resulting in a lower contrast-to-noise ratio) is a paradoxical effect of the higher T1 relaxivity of gadobenate owing to its transient weak interaction with serum proteins—that is, of its superior performance as a paramagnetic contrast agent. Numerous previous direct comparisons of gadobenate and gadopentetate for MR imaging of the central nervous system, breast, liver, and vasculature have demonstrated an increased contrast effect of gadobenate when these two agents are administered at an equivalent single dose of 0.1 mmol per kilogram of body weight (4–6) or a comparable or better effect when a 0.05 or a 0.1 mmol/kg dose of gadobenate is compared directly with a 0.1 or a 0.2 mmol/kg dose of gadopentetate, respectively (7–10).
It is plainly obvious that contrast agent dose is one of the most important factors for optimizing the contrast-to-noise ratio of myocardial delayed enhancement. On the basis of the published literature and our own personal clinical experience, the study by Dr Schlosser and colleagues is inherently limited in that a double dose of gadobenate dimeglumine was used (1). In our opinion, a double dose of gadobenate dimeglumine is probably too much for delayed enhancement of infarcted myocardium.
In our experience, the most practical approach to avoiding the paradoxical effect of a lower detectability of delayed enhancement of subendocardial infarction with gadobenate dimeglumine is to use no more than a single dose (0.1 mmol/kg) and to obtain optimized images at about 10 minutes after contrast agent injection. This approach, reported for both research trials (11) and daily clinical practice (12), allows saving both time and money.
From a clinical perspective, it should also be pointed out that perfusion imaging is typically performed before any evaluation of delayed enhancement. In most cases, perfusion imaging (at rest or under pharmacologic stress) is performed with 0.05 mmol/kg of contrast agent, prior to the injection of a second 0.05 mmol/kg dose to complete the perfusion study or to obtain the final 0.1 mmol/kg dose required for delayed enhancement.
Specifically designed intraindividual dose-finding studies are needed for gadobenate-enhanced delayed enhancement of acute, subacute, and chronic myocardial infarct, to compare doses from 0.05 to 0.2 mmol/kg by using both single bolus or fractionated administration regimens.
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Department of Diagnostic and Interventional Radiology and Neuroradiology, University Hospital Essen, Hufelandstrasse 55, Essen 45122, Germany
e-mail: thomas.schlosser{at}uni-essen.de
While we appreciate the interest of Drs Sardanelli and Quarenghi in our work, we must take issue with the content of their letter.
The authors state that gadobenate dimeglumine has a superior performance as a paramagnetic contrast agent because of its transient weak interaction with serum proteins. Whereas this seems to be true for MR angiography (1), there are no data available that support this general statement for cardiac MR imaging. Independent of the contrast agent dose, the mild protein binding of gadobenate results in an increased signal intensity of blood for several minutes after injection compared with contrast agents without protein binding. This phenomenon can be used to explain the potential advantages of gadobenate for MR angiography, but it may be a disadvantage for late-enhancement imaging as shown in our study, because it can decrease the contrast-to-noise ratio between blood and infarcted tissue.
Drs Sardanelli and Quarenghi imply that our study is inherently limited in that a double dose of gadobenate dimeglumine was used. However, most preclinical and clinical studies on late-enhancement imaging have been performed by using a double dose of 0.5 mol/L contrast agents (2–6). The recommendation to use a single dose of gadobenate dimeglumine is based only on the authors' personal experiences, because the citied literature does not supply clinical data to support this suggestion. The first article, by Huber et al (7), only focuses on different pulse sequences for late-enhancement imaging and the second, by Schneider et al (8), is a collection of case reports.
Additionally, the statement that a single dose of gadobenate dimeglumine allows saving money has to be taken with caution. At least in Germany, gadobenate dimeglumine is quite expensive, and the price for a single dose is at least as high as that for a double dose of a standard extracellular contrast agent.
However, we agree that specifically designed intraindividual dose finding studies are desirable, and we hope that the results of our initial study encourages others to support us in this effort.
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