Background After cardioversion of sustained atrial fibrillation (AF),
the electrical and contractile functions of the atria are impaired, an
d recurrences of AF frequently occur. Whether remodeling of the struct
ure of atrial myocardium is the basis for this problem is not known. M
ethods and Results Sustained AF was induced by electrical pacing in 13
goats instrumented long-term. The goats were killed after 9 to 23 wee
ks, and the atrial myocardium was examined by light and electron micro
scopy. The changes were quantified in left and right atrial free walls
, appendages, trabeculae, the interatrial septum, and the bundle of Ba
chmann. A substantial proportion of the atrial myocytes (up to 92%) re
vealed marked changes in their cellular substructures, such as loss of
myofibrils, accumulation of glycogen, changes in mitochondrial shape
and size, fragmentation of sarcoplasmic reticulum, and dispersion of n
uclear chromatin. These changes were accompanied by an increase in siz
e of the myocytes (up to 195%). There were virtually no signs of cellu
lar degeneration, and the interstitial space remained unaltered. The d
uration of sustained AF did not significantly affect the degree of myo
lytic cell changes. Conclusions Sustained AF in goats leads to predomi
nantly structural changes in the atrial myocytes similar to those seen
in ventricular myocytes from chronic hibernating myocardium. These st
ructural changes may explain the depressed contractile function of atr
ial myocardium after cardioversion. This goat model of AF offers a new
approach to study the cascade of events leading to sustained AF and i
ts maintenance.