Abstract 13794: Fibrosis in Atrial Walls is Associated with the Presence and Severity of Atrial Fibrillation but not with Age
Background: Development of fibrosis in atrial walls is associated with deterioration of atrial conduction and predisposes to atrial fibrillation (AF) in experiment. Human data, however, are scarce and whether fibrosis is the cause or consequence of AF in humans is not known. Aim of our study was to assess the association between the extent of fibrosis in human atria, age and history of AF.
Methods: Human atria collected from autopsies in 21 pts (61±12 y., range 39–82, 9 females) died from myocardial infarction (n=15), stroke (n=1) and pulmonary embolism (n=5) were studied. According to medical records, 5 pts had no AF history (65±13 y.), 9 pts had paroxysmal AF (63±10 y.) and 7 pts had permanent AF (55±12 y.). Tissue samples were obtained from 3 locations in the left atrium: between superior pulmonary veins (SPV), in the center of the posterior LA wall (CPV) and between inferior pulmonary veins (IPV); and 2 locations in the right atrium: crista terminalis (CT) and Bachmann's bundle (BB). Histological sections were stained with Masson's trichrome and analysed using automatic image analyser for assessment of fibrosis extent (FE) in % of specimen area at each location.
Results: In the total population, there was no difference in FE concerning either gender or age. No correlation between FE and age was observed at any of the studied locations. FE was associated with history of AF being two- to threefold higher at all locations in patients with AF history. Pts with permanent AF had greater FE compared with paroxysmal AF pts that reached significance for BB, CPV and SPV locations (see Table).
Conclusion: In post-mortem material of pts died from cardiovascular causes, the extent of fibrosis in the atria was not associated with age but significantly correlated with the presence of AF and its severity. The reasons for fibrosis development in pts with AF are not fully understood but our findings suggest that age-related changes per se are unlikely to be the sole cause of advanced fibrosis underlying AF.
- © 2010 by American Heart Association, Inc.