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. 2004 Apr;90(4):400-5.
doi: 10.1136/hrt.2003.015347.

Fibrosis in left atrial tissue of patients with atrial fibrillation with and without underlying mitral valve disease

A Boldt  1 , U Wetzel, J Lauschke, J Weigl, J Gummert, G Hindricks, H Kottkamp, S Dhein
Affiliations

Fibrosis in left atrial tissue of patients with atrial fibrillation with and without underlying mitral valve disease

A Boldt et al. Heart. 2004 Apr.

Abstract

Objective: To examine the hypothesis that major extracellular matrix (ECM) proteins are expressed differently in the left atrial tissue of patients in sinus rhythm (SR), lone atrial fibrillation (AF), and AF with underlying mitral valve disease (MVD).

Design: Case-control study.

Patients: 118 patients with lone AF, MVD+AF, and SR.

Main outcome measures: Collagen I, collagen III, and fibronectin protein expression measured by quantitative western blotting techniques and immunohistochemical methods.

Results: Protein concentrations increased in patients with AF (all forms) compared with those in SR (all forms): collagen I (1.15 (0.11) v 0.45 (0.28), respectively; p = 0.002), collagen III (0.74 (0.05) v 0.46 (0.11); p = 0.002, and fibronectin (0.88 (0.06) v 0.62 (0.13); p = 0.08). Especially, collagen I was similarly enhanced in both lone AF (1.49 (0.15) and MVD+AF (1.53 (0.16) compared with SR (0.56 (0.28); both p = 0.01). Collagen III was not significantly increased in lone AF but was significantly increased in AF combined with MVD (0.84 (0.07) both compared with SR (0.46 (0.11); p = 0.01). The concentration of fibronectin was not significantly increased in lone AF and MVD+AF (both compared with SR). Furthermore, there was a similar degree of enhanced collagen expression in paroxysmal AF and chronic AF.

Conclusions: AF is associated with fibrosis. Forms of AF differ from each other in collagen III expression. However, there was no systematic difference in ECM expression between paroxysmal AF and chronic AF. Enhanced concentrations of ECM proteins may have a role in structural remodelling and the pathogenesis of AF as a result of separation of the cells by fibrotic depositions.

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Figures

Figure 1
Figure 1
Sirius red staining of left atrial tissue for connective tissue (red staining) from patients (A) in sinus rhythm (SR) and (B) with chronic atrial fibrillation (lone CAF). Immunohistological results in left atrial tissue from (left) patients in SR and (right) patients with lone CAF for (C, D) collagen type I, (E, F) collagen type III, and (G, H) fibronectin. Original magnification ×400.
Figure 2
Figure 2
(A) Collagen I, collagen III, and fibronectin expression in atrial tissue of (left columns) patients in SR (left columns) and (right columns) patients with atrial fibrillation. (B) Comparison of all patients in the study either (left columns) with underlying mitral valve disease (MVD) or (right columns) without MVD.
Figure 3
Figure 3
(A) Collagen I, (B) collagen III, and (C) fibronectin expression in left atrial tissue of patients in SR, with lone AF, and with AF with underlying MVD (MVD+AF).
Figure 4
Figure 4
Quantitative analysis of (A) collagen I, (B) collagen III, and (C) fibronectin expression in human atrial tissue of the SR, paroxysmal atrial fibrillation (PAF), and CAF subgroups of lone AF and MVD+AF.
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