Abstract 3534: Occurrence of Atrial Fibrillation in Advanced Heart Failure Reflects Increased Atrial Wall Stress Rather Than Fibrosis
Introduction: Structural atrial remodeling and fibrosis are considered as the main mechanism for development of atrial fibrillation (AF). In advanced heart failure (HF), the independent role of fibrosis for development of AF is less equivocal, because HF itself leads to atrial scarring. The aim of the study was to identify tissue and clinical characteristics discriminating HF patients with or without AF.
Methods: Myocardial samples from anterior wall of the right atrium were obtained during heart transplantation from the explanted hearts of 21 male patients (age 51.6±8.9 y) with advanced HF. Permanent AF was present in 10 patients, remaining 11 patients served as sinus rhythm (SR) controls. Echocardiographic and hemodynamic measurements, type I collagen volume fraction (CVF-I), transforming growth factor-beta (TGF-beta), and connective tissue growth factor (CTGF) were analyzed.
Results: The groups were well matched according to age and co-morbidities. The AF group presented with significantly higher pressure in the right atrium (13.6±7.7 vs. 6.0±5.0 mmHg; p=0.02), larger left atrium diameter (56.1±7.7 vs. 50±5.1 mm; p=0.04), left atrium wall stress (254.8±81.3 vs. 169.9±75.7 kdynes/m2; p=0.03), and longer time period of HF (2.0±1.6 vs. 5.0±2.9y; p=0.008). There were no significant differences in CVF-I (13.9±5.4% vs. 12.0±6.2%; p=0.4), and in CTGF expression (119.6±10.6 vs. 122.0±11.9; p=0.6) between two groups. TGF-beta was detected in only very low level in both groups.
Conclusions: In advanced HF, atrial extracellular matrix remodeling is invariably present. However, development of AF is associated with other mechanisms, namely with increased atrial wall stress.