Abstract
Atrial fibrillation (AF) is common in patients with hyperthyroidism. Although the choice of an antiarrhythmic agent should be based on its electrophysiological effects and the electrophysiological properties of the arrhythmia in question, the atrial electrophysiological features of AF associated with hyperthyroidism are unknown. The purposes of this study are to clarify the atrial electrophysiological abnormalities of AF with hyperthyroidism, and to propose effective therapies for AF in patients with hyperthyroidism. This study included 117 patients who underwent electrophysiological study and were evaluated for thyroid function: 29 patients without AF or hyperthyroidism (Group I), 78 patients with lone paroxysmal AF (Group II), and 10 patients with paroxysmal AF and hyperthyroidism (Group III). The following electrophysiological parameters were assessed and measured quantitatively: (1) the incidence of abnormal right atrial electrograms during sinus rhythm, indicating areas of altered anatomy and conduction where AF is likely to develop; (2) the atrial effective refractory period (ERP); and (3) the atrial conduction delay (CD), which is induced by early atrial premature beats close to the atrial ERP and is thought to facilitate the occurrence of AF. The incidence of abnormal right atrial electrograms during sinus rhythm was significantly higher in Group II (67.1%) than in Group I (20.0%, P < 0.001) and Group III (22.2%, P = 0.009). The atrial ERP was significantly shorter in Group III (187 +/- 7 ms) than in Group I (215 +/- 36 ms, P = 0.019) and Group II (208 +/- 28 ms, P = 0.022). The atrial CD was observed in Group III as well as in Group II. Our data indicate that the electrophysiological features of paroxysmal AF associated with hyperthyroidism are essentially different from those of lone paroxysmal AF. In patients with paroxysmal AF and hyperthyroidism, a shortening of the refractory period in association with a facilitation of the atrial CD could be expected to increase the propensity for AF, and a pre-existent arrhythmogenic substrate might not be essential to the genesis of AF. These findings suggest that the agents that prolong the atrial ERP are effective against AF in patients with hyperthyroidism.
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