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European Heart Journal Advance Access originally published online on February 7, 2006
European Heart Journal 2006 27(6):756; doi:10.1093/eurheartj/ehi771
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Left atrial volume predicts cardiovascular events in patients originally diagnosed with lone atrial fibrillation: three-decade follow-up: reply

Martin Osranek

Division of Cardiovascular Diseases
Mayo Clinic
Mayo Foundation
Rochester
MN
USA

James B. Seward

Division of Cardiovascular Diseases
Mayo Clinic
Mayo Foundation
Rochester
MN
USA

We appreciate the interest of Rienstra M and Van Gelder IC in our study.1 They correctly note that patients with clinically diagnosed ‘lone atrial fibrillation (AF)’ may physiologically be represented by two different diseases. This notion is validated by animal models of AF:

Disease 1. True lone AF can be replicated by atrial tachypacing following AV node ablation or intermittent burst atrial tachypacing without inducing heart failure (HF).2,3 Tachypacing without HF effectively underloads the atrial myocyte, which metabolically downregulates (dedifferentiates) to a foetal isoform. In the absence of elevated filling pressure there is no atrial enlargement, cell death, or fibrosis.4 The loss of gap junctions, connecting the cytoplasms of neighbouring cardiomyoctes, causes electrical heterogeneity and ultimately AF.3

Disease 2. HF–AF is induced by sustained tachypacing, which induces HF and atrial pressure overload.4,5 Pressure-induced stretch of the atrial and pulmonary vein myocyte causes atrial enlargement, angiotensin-II mediated cell death, and fibrosis.3 Interstitial collagen deposition causes myocyte–myocyte disconnection, reduced transfer of electrical current from one cardiomyocyte to another, ultimately causing AF.

Atrial enlargement most commonly represents chronic elevation of filling pressure and is more useful than the clinical diagnosis alone to distinguish the two types of AF. Patients with enlarged atria at the onset of AF should not any longer be called lone AF, even in the absence of other overt cardiovascular disease or risk factors. Furthermore, our study validates that the development of HF as reflected in atrial enlargement explains the evolution of benign true lone AF in younger patients into HF–AF associated with adverse events.

We agree that the correct diagnosis of lone AF should incorporate cardiac physiology. On the basis of the literature and our data, we are however confident that left atrial enlargement is a valid surrogate measure of the chronic elevation of left ventricular filling pressures.

References

  1. Osranek M, Bursi F, Bailey KR, Grossardt BR, Brown RD Jr, Kopecky SL, Tsang TS, Seward JB. Left atrial volume predicts cardiovascular events in patients originally diagnosed with lone atrial fibrillation: three-decade follow-up. Eur Heart J 2005;26:2556–2561.[Abstract/Free Full Text]
  2. Ausma J, Litjens N, Lenders MH, Duimel H, Mast F, Wouters L, Ramaekers F, Allessie M, Borgers M. Time course of atrial fibrillation-induced cellular structural remodeling in atria of the goat. J Mol Cell Cardiol 2001;33:2083–2094.[CrossRef][Web of Science][Medline]
  3. Ausma J, Wijffels M, Thone F, Wouters L, Allessie M, Borgers M. Structural changes of atrial myocardium due to sustained atrial fibrillation in the goat. Circulation 1997;96:3157–3163.[Abstract/Free Full Text]
  4. Li D, Fareh S, Leung TK, Nattel S. Promotion of atrial fibrillation by heart failure in dogs: atrial remodeling of a different sort. Circulation 1999;100:87–95.[Abstract/Free Full Text]
  5. van der Velden HM, Ausma J, Rook MB, Hellemons AJ, van Veen TA, Allessie MA, Jongsma HJ. Gap junctional remodeling in relation to stabilization of atrial fibrillation in the goat. Cardiovasc Res 2000;46:476–486.[Abstract/Free Full Text]

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This Article
Right arrow FREE Full Text (PDF) Freely available
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27/6/756-a    most recent
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