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J Am Coll Cardiol, 2008; 51:2444-2445, doi:10.1016/j.jacc.2008.02.074
© 2008 by the American College of Cardiology Foundation
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CORRESPONDENCE: LETTER TO THE EDITOR

Local Amyloidosis as a Possible Component of the Atrial Remodeling Accompanying Trial

Ornella Leone, MD*, Giuseppe Boriani, MD, PhD, Giuseppe Marinelli, MD and Claudio Rapezzi, MD

* Department of Pathology, Policlinico S. Orsola-Malpighi, via Massarenti 9, 40138 Bologna, Italy (Email: ornella.leone{at}aosp.bo.it).

In their extensive state-of-the-art paper on the clinical implications for atrial fibrillation of structural and functional remodeling of the left atrium, Casaclang-Verzosa et al. (1) do not mention an important structural aspect of the process, namely, intra-atrial amyloid deposition accompanying long-term atrial fibrillation (AF). In the last few years, 2 separate research groups have provided evidence that, in humans, longstanding AF is associated with intra-atrial deposition of amyloid, particularly in women with valvular atrial fibrillation (2,3). Amyloid deposits appear to occur preferentially in the left atrium (3). An immunohistochemical study showed that similar deposits were invariably immunoreactive for atrial natriuretic peptide (ANP) (2). These observations have prompted the hypothesis that AF-related overproduction of ANP leads to localized amyloidogenesis and deposition, which in turn augments conduction heterogeneity, helping to perpetuate AF (and thereby stimulating further ANP production in a paracrine loop) (4). In this view, atrial amyloid deposition could be considered to be a further negative consequence of the neurohormonal disturbances elegantly discussed by the authors of the article. In any case, we believe amyloid deposition deserves serious consideration as a potential player in the complex interplay between anatomical and electrical left atrial remodeling, together with the other pathophysiological changes (stressors) discussed by the authors, such as interstitial fibrosis, myocyte hypertrophy, ion channel alterations, inflammatory reactions, and so on. Although no pharmacological treatment is currently available to remove the amyloid deposits, much research is being carried out in this field (5).


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  1. Casaclang-Verzosa G, Gersh BJ, Tsang TSM. Structural and functional remodeling of the left atrium: clinical and therapeutic implications for atrial fibrillation J Am Coll Cardiol 2008;51:1-11.[Abstract/Free Full Text]
  2. Rocken C, Peters B, Juenemann G, et al. Atrial amyloidosis: an arrhythmogenic substrate for persistent atrial fibrillation Circulation 2002;106:2091-2097.[Abstract/Free Full Text]
  3. Leone O, Boriani G, Chiappini B, et al. Amyloid deposition as a cause of atrial remodelling in persistent valvular atrial fibrillation Eur Heart J 2004;25:1237-1241.[Abstract/Free Full Text]
  4. Goette A, Röcken C. Atrial amyloidosis and atrial fibrillation: a gender-dependent "arrhythmogenic substrate"? Eur Heart J 2004;14:1185-1186.
  5. Selvanayagam JB, Hawkins PN, Biju P, Myerson SG, Neubauer S. Evaluation and management of the cardiac amyloidosis J Am Coll Cardiol 2007;50:2101-2110.[Abstract/Free Full Text]

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Grace Casaclang-Verzosa, Marion E. Barnes, and Teresa S.M. Tsang
J. Am. Coll. Cardiol. 2008 51: 2445. [Full Text] [PDF]




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