Prolonged fractionation of paced right atrial electrograms in patients with atrial flutter and fibrillation
Ching-Tai Tai, MD*,
Shih-Ann Chen, MD*,
Jyh-Woei Tzeng, PhD ,
Benjamin I. Kuo, MD, PhD*,
Yu-An Ding, MD, PhD,
Mau-Song Chang, MD* and
Liang-Yu Shyu, PhD
* Division of Cardiology, Department of Medicine, National Yang-Ming University School of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
Institute of Biomedical Engineering, Chung-Yuan Christian University, Chung-Li, Taiwan
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Figure 1 The principle of the method. (A) The right atrium is paced at one site and recordings are made from five other sites. The electrogram in response to an extrastimulus is processed to emphasize small potentials, and then (B) the delay of each fractionated potential is measured for every electrogram recorded during the pacing sequence. (C) The delay of each potential is plotted against the S1S2 interval to form five conduction curves that characterize myocardial conduction between the pacing and recording electrodes. Point I is the S1S2 interval at which delay starts to increase. Each site is paced in turn with recordings made from the remaining electrodes, and 30 conduction curves are obtained. (D) The mean increase in electrogram duration and S1S2 interval at which delay increases is plotted on a scattergram. CSO = coronary sinus ostium; HARA = high anterior right atrium; HPRA = high posterior right atrium; IVC = inferior vena cava; LARA = low anterior right atrium; LPRA = low posterior right atrium; RAP = right atrial appendage; SRA = septal right atrium; SVC = superior vena cava.
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Figure 2 Two sets of electrograms obtained from the high posterior right atrium while the high anterior wall was paced. The left-hand set was obtained from a control patient and the right-hand set was obtained from a patient with atrial fibrillation (AF). The electrograms in each pair were recorded in response to the same stimulus-coupling interval during the pacing protocol. The electrograms from the patient with AF demonstrate that with increasing stimulus prematurity, there is increasing fragmentation in the electrogram and increasing latency of its individual potentials.
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Figure 3 (A) A conduction curve from a control patient. Each data point represents the delay of a fractionated potential at a particular S1S2 coupling interval. There is a slight fluctuation in the delay with premature stimulation until it increases rapidly at S1S2 intervals below 220 ms. (B) A conduction curve from a patient with atrial flutter. There is a rapid increase in delay and a gradual increase in electrogram duration at S1S2 intervals below 260 ms. (C) A conduction curve from a patient with atrial fibrillation. There is a gradual increase in delay and electrogram duration at S1S2 intervals below 310 ms.
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Figure 4 Scatterplot of change in electrogram duration versus S1S2 interval at which delay starts to increase. Each point is the mean of all the observations in a particular patient. The discriminant line (A) separates the atrial flutter patients from the control patients, and the other line (B) separates the atrial fibrillation patients from the atrial flutter patients. AF = atrial fibrillation; AFL = atrial flutter.
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