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European Heart Journal Advance Access originally published online on January 31, 2006
European Heart Journal 2006 27(14):1670; doi:10.1093/eurheartj/ehi766
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Atrial pathology in cardiac amyloidosis: evidence from ECG and cardiovascular magnetic resonance

C. Paul Leeson1,*, Saul G. Myerson2, Genevieve B. Walls1, Stefan Neubauer2 and Oliver J. Ormerod1

1 Department of Cardiology, John Radcliffe Hospital, Headley Way, Oxford, OX3 9DU, UK
2 University of Oxford Centre for Clinical Magnetic Resonance Research, John Radcliffe Hospital, Oxford, UK

* Corresponding author. Tel: +44 1865 741166; fax: +44 1865 221734. E-mail address: paul.leeson{at}cardiov.ox.ac.uk

A 59-year-old man presented with chest pain and single-vessel coronary disease on angiography. Left ventricular function was normal with mild hypertrophy. He was treated for coronary disease but represented 18 months later with biventricular heart failure. There had been a striking ECG evolution: ST-segment change; reduced QRS amplitude; increased P-wave width and amplitude; and progressive increase in PR interval (196–276 ms) (Panel A). Echocardiography now demonstrated a grossly hypertrophied, ‘sparkling’, left ventricle (Panel B) and Doppler evidence of restrictive cardiomyopathy. Cardiac magnetic resonance imaging (Panel C) revealed widespread, diffuse enhancement with contrast on inversion recovery sequences, including both atria, in keeping with an infiltrative cardiomyopathy such as amyloid. Left ventricular function was poor (ejection fraction 23%), with severe hypertrophy (septal thickness 19 mm; mass index 134 g/m2) and small left ventricular volumes (EDV 69 mL, ESV 51 mL). Urine electrophoresis revealed lambda light chain proteinuria and bone marrow biopsy a plasma cell dyscrasia. Progressive reduction in QRS amplitude with progressive increase in left ventricular thickness is classical for cardiac amyloid. P-wave morphology demonstrated additional significant atrial involvement. Restrictive cardiomyopathy leads to bi-atrial enlargement and increased P-wave amplitude and width. Furthermore, atrial amyloid deposition delays atrial conduction and thereby increases the PR interval and broadens the P-wave. Both atrial pathologies were clearly demonstrated by cardiovascular magnetic resonance imaging, with bi-atrial enlargement and marked wall enhancement consistent with atrial amyloid deposition. Cardiovascular magnetic resonance imaging is a powerful tool to aid diagnosis and assess severity in infiltrative cardiomyopathies.

Panel A. Repeat electrocardiograms in the same patient over 18 months. There has been a marked increase in P-wave width and amplitude, lengthening of the PR interval, and a reduction in amplitude of the QRS voltage.

Panel B. Echocardiogram showing gross increase in size of left ventricle with sparkling appearance suggestive of amyloid.

Panel C. Cardiovascular magnetic resonance image showing extensive enhancement (white) of the ventricular myocardium, and also of both atria, with gadolinium contrast using a late inversion-recovery technique.

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This Article
Right arrow FREE Full Text (PDF) Freely available
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27/14/1670    most recent
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