Author + information
- Received March 18, 2011
- Revision received May 9, 2011
- Accepted May 24, 2011
- Published online November 15, 2011.
- Pyotr G. Platonov, MD, PhD⁎,⁎ (, )
- Lubov B. Mitrofanova, MD, PhD†,
- Victoria Orshanskaya, MD† and
- Siew Yen Ho, PhD‡
- ↵⁎Reprint requests and correspondence:
Dr. Pyotr Platonov, Department of Cardiology, Lund University, Lund 221 85, Sweden
Objectives The purpose of this study was to assess the association between structural changes in human atria, age, and history of atrial fibrillation (AF).
Background Development of fibrosis in atrial walls is associated with deterioration of atrial conduction and predisposes to AF in experiment. Human data, however, are scarce, and whether fibrosis is a cause or consequence of AF is not known.
Methods Medical records for consecutive autopsies were checked for AF history and duration. Atrial specimens from 30 patients (ages 64 ± 12 years) were collected in 3 equal age-matched groups as patients without AF history, with paroxysmal AF, or with permanent AF. Tissue samples were obtained at the level of superior pulmonary veins, inferior pulmonary veins, center of posterior left atrial wall, terminal crest, and Bachmann's bundle. Histology sections were assessed for extent of fibrosis, fatty tissues, and inflammatory infiltration at each location.
Results No correlation was observed between age and fibrosis at any location. Fibrosis extent and fatty infiltration were twofold to threefold higher at all locations in patients with history of AF and correlated with lymphomononuclear infiltration. Patients with permanent AF had greater fibrosis extent than did patients with paroxysmal AF.
Conclusions In post-mortem material, structural changes in the atria were not associated with age, but were significantly correlated with presence of AF and its severity. Our findings suggest that age-related changes per se are unlikely to be the sole cause of advanced fibrosis underlying AF.
This work has received government funding of clinical research within the Swedish National Health Service, and research grants from Lund University Hospital, Lund, Sweden, and the Swedish Heart-Lung Foundation. The authors have reported they have no relationships relevant to the contents of this paper to disclose.
- Received March 18, 2011.
- Revision received May 9, 2011.
- Accepted May 24, 2011.
- American College of Cardiology Foundation