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European Heart Journal Advance Access originally published online on May 2, 2008
European Heart Journal 2008 29(13):1696-1697; doi:10.1093/eurheartj/ehn190
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

The role of endomyocardial biopsy in the management of cardiovascular disease: a Scientific Statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology: reply

Elena Ladich

Armed Forces Institute of Pathology
CVPath Institute, Inc.
19 Firstfield Road
Gaithersburg, MD 20878
USA

Renu Virmani

Armed Forces Institute of Pathology
CVPath Institute, Inc.
19 Firstfield Road
Gaithersburg, MD 20878
USA
Tel/fax: +1 202 782 9021
Email:rvirmani{at}cvpath.org

We thank Dr Anderson for pointing out that in patients with iron overload in the heart irrespective of the underlying aetiology, e.g. thalassemia, sickle cell anaemia, chronic transfusion therapy, or hereditary haemochromatosis, there is no need for endomyocardial biopsy. Magnetic resonance imaging (MRI) is now an accepted method for the evaluation of myocardial iron overload, and the method has been validated in multiple laboratories.1 It has been shown that serum ferritin measurements are a reasonable surrogate of liver iron, but are poorly correlated with cardiac iron stores. Recently, a new method using the cardiovascular magnetic resonance (CMR) T2* technique has been used for the measurement of tissue iron in the liver, but what has not yet been shown is calibration of myocardial T2* against absolute myocardial iron levels in humans.2,3 In the clinical setting, T2* measurements have been used to assess cardiac iron loading and the studies suggest a useful correlation between myocardial T2* and cardiac function thereby allowing early diagnosis and treatment. Although there is no disputing the clinical merits of CMR-measured myocardial T2* in the evaluation of cardiac function, there may be additional value in knowing the relationship between myocardial T2* and directly measured myocardial iron levels. Validation of myocardial T2* and myocardial tissue iron may not be feasible in humans and may not be required since cardiac iron estimates by MRI in animal models has been validated.4

References

  1. Wood JC, Ghugre N. Magnetic resonance imaging assessment of excess iron in thalassemia, sickle cell disease and other iron overload diseases. Hemoglobin (2008) 32:85–96.[CrossRef][Web of Science][Medline]
  2. Anderson LJ, Holden S, Davis B, Prescott E, Charrier CC, Bunce NH, Firmin DN, Wonke B, Porter J, Walker JM, Pennell DJ. Cardiovascular T2-star (T2*) magnetic resonance for the early diagnosis of myocardial iron overload. Eur Heart J (2001) 22:2171–2179.[Abstract/Free Full Text]
  3. Cohen AR, Galanello R, Pennell DJ, Cunningham MJ, Vichinsky E. Thalassemia. Hematol Am Soc Hematol Educ Program (2004) 14–34.
  4. Wood JC, Otto-Duesse M, Aguilar M, et al. Cardiac iron determines cardiac T2*, T2, and T1 in the Gerbil model of iron cardiomyopathy. Circulation (2005) 112:535–543.[Abstract/Free Full Text]

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This Article
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29/13/1696-a    most recent
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