BACKGROUND Recent studies with the implantable atrial cardioverter have shown that atrial fibrillation (AF) recurs almost immediately after successful cardioversion in about 27% of cases. In the present study, we determined the electrophysiologic properties of the caprine atrium immediately after spontaneous termination of AF both before and after 48 hours of AF-induced electrical remodeling. RESULTS In eight goats, atrial effective refractory period (AERP), intra-atrial conduction velocity, and atrial wavelength were measured during sinus rhythm both before (t = 0) and after 48 hours (t = 48) of electrically maintained AF (baseline). After baseline, a 5-minute paroxysm of AF was induced, during which the refractory period (RPAF) was determined. AERP, conduction velocity, and atrial wavelength also were measured immediately after spontaneous restoration of sinus rhythm (post-AF values). Both in normal and remodeled atria, immediately after AF, AERP and conduction velocity were markedly decreased compared with baseline (P < 0.01). In normal atria, post-AF AERP (107+/-14 msec) gradually prolonged from its AF value (114+/-17 msec) to its baseline value (138+/-13 msec). Conduction velocity decreased from 130+/-9 cm/sec to 117+/-9 cm/sec. After 48 hours of AF, AERP had shortened to 74+/-8 msec. RPAF was 89+/-9 msec. Surprisingly, immediately after termination of AF, AERP shortened further to 58+/-6 msec (P < 0.01). Post-AF conduction velocity decreased from 136+/-11 cm/sec to 122+/-10 cm/sec (P < 0.01). As a result, the post-AF atrial wavelength became as short as 7.1+/-1 cm. These changes were transient, and all parameters gradually returned to baseline within 1 to 2 minutes after conversion of AF. CONCLUSIONS Due to a combined decrease in AERP and conduction velocity, marked shortening of the atrial wavelength occurs during the first minutes after conversion of AF. In electrically remodeled atria, this results in a transient ultrashort value of AERP (<60 msec) and atrial wavelength (7.1 cm). These observations imply a highly vulnerable substrate for reentry immediately after termination of AF. During this supervulnerable phase, both early and later premature beats reinitiated immediate recurrences of AF.