Contraction-excitation feedback in human atrial fibrillation

Contraction-excitation feedback, that is, electrophysiologic changes that are caused or preceded by mechanical changes of the myocardium, has been extensively studied in the ventricles. The role of contraction-excitation feedback in the atria, and more particularly in the genesis and maintenance of atrial fibrillation, has been less adequately investigated.

The aim of the present study was to determine whether increased right atrial pressure (RAP) facilitates the induction of atrial fibrillation (AF) in patients with a history of lone AF.

Sixteen patients with a history of paroxysmal AF but without structural heart disease were included in the study. All patients underwent electrophysiologic study at both a lower (3.1 +/- 2.0 mmHg) and (in 13 cases) a higher (6.4 +/- 2.5 mmHg) RAP. "Higher" was considered the pressure following rapid (in about 30 min) intravenous administration of normal saline or before the administration of a diuretic.

Rapid atrial pacing induced AF in 19 of 29 attempts. At a lower pressure, rapid pacing induced brief (3 s to 3 min) AF in 3 of 16 patients, long-lasting (> 3 min) AF in 3 of 16 patients, and no AF in 10 of 16 patients. At a higher pressure, brief AF was induced in 3 of 10 patients in whom no AF could be induced at a lower pressure, and long-lasting AF in 10 patients in whom either brief AF (3 cases) or no AF (7 cases) was induced at a lower pressure. In 11 patients, in whom Wenckebach periodicity was determined at both higher and lower pressure, the critical cycle length at which atrioventricular block appeared was significantly (p < 0.001, paired t-test) longer (349.1 +/- 44.4 ms, i.e., +15.5 +/- 11.3 ms) at higher than at lower atrial pressure (333.6 +/- 41.0 ms). In nine patients, in whom Wenckebach periodicity was determined and two rhythms occurred at different pressures, the critical cycle length was 332.2 +/- 45.8 ms when associated with sinus rhythm, and significantly (p < 0.01) longer (344.4 +/- 48.0 ms, i.e., +12.2 +/- 8.3 ms) when associated with induction of AF.

In patients with lone atrial fibrillation, modest increases in atrial pressure may facilitate the induction of atrial fibrillation.