[Show abstract][Hide abstract] ABSTRACT: A 64-year-old male was admitted to hospital because of repeated episodes of syncope and palpitation. Ambulatory monitoring revealed paroxysmal atrial fibrillation (AF) as the cause of palpitation; he did not have structural heart disease. The induction of AF by rapid pacing (50 Hz for 1 s) in an upright position provoked syncope with a vasodepressor response. Atropine sulfate blocked the induction of syncope. The possible etiology was neurally mediated syncope that manifested only during AF, which suggests that the abnormal vagal activity during AF in this case exaggerated the vasodepessor response while upright.
No preview · Article · Oct 2002 · Circulation Journal
[Show abstract][Hide abstract] ABSTRACT: A 69-year-old woman was admitted to our hospital for the examination of syncope. When she ate solid food, she had dizziness or loss of consciousness. The ambulatory ECG suggested sino-atrial block during swallowing with a maximum sinus pause of 6 seconds. An electrophysiologic study revealed pre-existing sinus node dysfunction, which was exaggerated by the balloon inflation in the esophagus. Atropine counteracted the slowing of the basal sinus rate induced by esophageal pressure, but it did not block the effect on the maximum sinus node recovery time. This observation suggested that the syncope was mediated partly by a non-vagal mechanism.
No preview · Article · Apr 2002 · Internal Medicine
[Show abstract][Hide abstract] ABSTRACT: INOUE, K., et al.: Clinical Significance of the Atrial Fibrillation Threshold in Patients with Paroxysmal Atrial Fibrillation. AF threshold and the other electrophysiological parameters were measured to quantify atrial vulnerability in patients with paroxysmal atrial fibrillation (PAF, n = 47), and those without AF (non-PAF, n = 25). Stimulations were delivered at the right atrial appendage with a basic cycle length of 500 ms. The PAF group had a significantly larger percentage of maximum atrial fragmentation (%MAF, non-PAF: mean ± SD = 149 ± 19%, PAF: 166 ± 26%, P = 0.009), fragmented atrial activity zone (FAZ, non-PAF: median 0 ms, interquartile range 0–20 ms, PAF: 20 ms, 10–40 ms, P = 0.008). Atrial fibrillation threshold (AF threshold, non-PAF: median 11 mA, interquartile range 6–21 mA, PAF: 5 mA, 3–6 mA, P < 0.001) was smaller in the PAF group than in the non-PAF group. Sensitivity, specificity, and positive predictive value of electrophysiological parameters were as follows, respectively: %MAF (cut off at 150%, 78%, 52%, 76%), FAZ (cut off at 20 ms, 47%, 84%, 85%), AF threshold (cut off at 10 mA, 94%, 60%, 81%). There were no statistically significant differences between the non-PAF and PAF groups in the other parameters (effective refractory period, interatrial conduction time, maximum conduction delay, conduction delay zone, repetitive atrial firing zone, wavelength index), that were not specific for PAF. In conclusion, the AF threshold could be a useful indicator to evaluate atrial vulnerability in patients with AF.
No preview · Article · Apr 2001 · Pacing and Clinical Electrophysiology
[Show abstract][Hide abstract] ABSTRACT: SD3212 is a new antiarrhythmic drug which has class I, III, and IV effects. The purpose of this study was to elucidate the electrophysiological effects of this compound on a rabbit atrial fibrillation model, and to test a hypothesis that atrial fibrillation threshold is a quantitative indicator of atrial vulnerability. Whole hearts were excised from rabbits, and the aortas cannulated to perfuse the coronary arteries. Atrial fibrillation was induced with a burst stimulation of 50 Hz for 1 s while 3 microM acetylcholine (ACh) was perfused. When the right atrial appendage was paced at 200-ms intervals, SD3212 prolonged interatrial conduction time: control 30 +/- 1.2 ms, ACh 33 +/- 1.4 ms, ACh + SD 1 microM 37 +/- 2.4 ms, ACh + SD 3 microM 52 +/- 8.1 ms. The drug also prolonged the effective refractory period: control 80 +/-3.0 ms, ACh 48 +/- 3.8 ms, ACh + SD 1 microM 65 +/- 4.7 ms, ACh + SD 3 microM 98 +/- 15 ms. The rate of induction of atrial fibrillation by rapid pacing was 26% in Tyrode's solution, 85% in the presence of ACh, and 38% in the presence of ACh + SD 1 microM. The atrial fibrillation threshold decreased from 8.6 +/- 0.8mA (control) to 2.5 +/- 0.7 mA in the presence of ACh. It increased again to 7.8 +/- 1.0 mA in the presence of SD3212 (1 microM). SD3212 prolonged both the conduction time and refractory period. A reversed use-dependency was not prominent. These features caused antifibrillatory effects. Thus, the atrial fibrillation threshold seems to be a good quantitative indicator of atrial vulnerability.
No preview · Article · Feb 1999 · Heart and Vessels