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Focal automaticity manifesting as incessant right atrial tachycardia
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Focal automaticity manifesting as incessant right atrial tachycardia Radoslaw Marek Kiedrowicz, MD, PhD,* Steven Podd, MD,* Mark O’Neill, MD, PhD, FHRS, FRCP*† From the *Cardiology Department, Guy’s and St Thomas’ NHS Foundation Trust, King’s College London, Rayne Institute, St. Thomas’ Hospital, London, United Kingdom, and †Division of Imaging Sciences and Biomedical Engineering, King’s College London, Rayne Institute, St. Thomas’ Hospital, London, United Kingdom.
A 75-year-old woman without structural heart disease presented with incessant regular monomorphic atrial tachycardia (AT). Spontaneous arrhythmia termination was repeatedly followed by a single sinus beat before reinitiation. Variations in tachycardia cycle length (CL) between 200 and 400 ms were frequently observed. The P-wave morphology was consistent with a focal origin from the crista terminalis; however, electroanatomic mapping (CARTO 3 system, Biosense Webster Inc., Diamond Bar, CA) demonstrated centrifugal activation of the right atrium originating from the atrial septal wall near the fossa ovalis. Further mapping at the site of the earliest atrial activation during AT revealed a rapid, regularly discharging focus (Figure 1, blue dot) at fixed 100-ms CL represented by the low-amplitude (0.17 mV) spike electrograms (↓) with an isoelectric interval between successive spikes. The accompanying local atrial potential (▼) during firing was clearly sharper, higher (0.75 mV), and well separated from the preceding spike at fixed 30-ms conduction delay but of lower amplitude (0.95 mV) than that during sinus beats (*). The recorded abnormal activity could not be detected when the catheter tip was moved a few millimeters. The initiation and termination of firing at the site of interest were recorded during catheter
manipulation. The onset of AT on the surface electrocardiogram did not always coincide with the initiation of local, high-frequency activity but did terminate immediately with cessation of local firing. The first tachycardia P wave and subsequent discernible P waves were identical. Alterations in the degree of atrial capture by the focal activity (from 2:1 to 4:1) explain why the AT CLs were variable. A single radiofrequency application limited to the superior aspect of the initiating focus converted AT to permanent sinus rhythm. Following this application, the electrograms at the ablation site revealed persisting rapid local activity with far-field atrial potential but without atrial capture while sinus rhythm continued in the surrounding atrial tissue. The rapid focal discharge was eliminated with further discrete applications (red dots). Although impossible to ascertain categorically the tachycardia mechanism, these observations support abnormal automaticity creating a high-frequency atrial focal source as a driver of atrial arrhythmia. Lack of multicomponent fractionated electrograms at the successful AT ablation site, markers of the requisite nonuniformly anisotropic substrate that favors the development of microreentry by creating regions of slow conduction, support an automatic
KEYWORDS Atrial tachycardia; Automaticity; Extrasystolic activity; Arrhythmogenic focus; Catheter ablation (Heart Rhythm 2015;0:0–2) Address reprint requests and correspondence: Dr Radoslaw Marek Kiedrowicz, Cardiology Department, Guy’s and St Thomas’ NHS Foundation Trust, St Thomas’ Hospital, 6th Floor E Wing, Westminster Bridge Rd, London SE1 7EH, United Kingdom. E-mail address: [email protected].
1547-5271/$-see front matter B 2015 Heart Rhythm Society. All rights reserved.
http://dx.doi.org/10.1016/j.hrthm.2015.12.014
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Heart Rhythm, Vol 0, No 0, Month 2015
Figure 1
mechanism. The absence of conduction to the atrium during the first 700 ms of the tachycardia may be explained by slow conduction over the exit pathway(s) along with a relatively long effective refractory period of the surrounding atrial tissue. An alternative explanation is the presence of a low electrotonic load in the vicinity of the discharging focus that
would require a longer train of stimuli to capture the atrium. This hypothesis is supported by focal ablation increasing the mass of electrically inexcitable tissue in the region of the focus, thereby decreasing further the local electrotonic load and preventing atrial capture during ongoing focal discharges.
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IMAGE
Focal automaticity manifesting as incessant right atrial tachycardia Radoslaw Marek Kiedrowicz, MD, PhD,* Steven Podd, MD,* Mark O’Neill, MD, PhD, FHRS, FRCP*† From the *Cardiology Department, Guy’s and St Thomas’ NHS Foundation Trust, King’s College London, Rayne Institute, St. Thomas’ Hospital, London, United Kingdom, and †Division of Imaging Sciences and Biomedical Engineering, King’s College London, Rayne Institute, St. Thomas’ Hospital, London, United Kingdom.
A 75-year-old woman without structural heart disease presented with incessant regular monomorphic atrial tachycardia (AT). Spontaneous arrhythmia termination was repeatedly followed by a single sinus beat before reinitiation. Variations in tachycardia cycle length (CL) between 200 and 400 ms were frequently observed. The P-wave morphology was consistent with a focal origin from the crista terminalis; however, electroanatomic mapping (CARTO 3 system, Biosense Webster Inc., Diamond Bar, CA) demonstrated centrifugal activation of the right atrium originating from the atrial septal wall near the fossa ovalis. Further mapping at the site of the earliest atrial activation during AT revealed a rapid, regularly discharging focus (Figure 1, blue dot) at fixed 100-ms CL represented by the low-amplitude (0.17 mV) spike electrograms (↓) with an isoelectric interval between successive spikes. The accompanying local atrial potential (▼) during firing was clearly sharper, higher (0.75 mV), and well separated from the preceding spike at fixed 30-ms conduction delay but of lower amplitude (0.95 mV) than that during sinus beats (*). The recorded abnormal activity could not be detected when the catheter tip was moved a few millimeters. The initiation and termination of firing at the site of interest were recorded during catheter
manipulation. The onset of AT on the surface electrocardiogram did not always coincide with the initiation of local, high-frequency activity but did terminate immediately with cessation of local firing. The first tachycardia P wave and subsequent discernible P waves were identical. Alterations in the degree of atrial capture by the focal activity (from 2:1 to 4:1) explain why the AT CLs were variable. A single radiofrequency application limited to the superior aspect of the initiating focus converted AT to permanent sinus rhythm. Following this application, the electrograms at the ablation site revealed persisting rapid local activity with far-field atrial potential but without atrial capture while sinus rhythm continued in the surrounding atrial tissue. The rapid focal discharge was eliminated with further discrete applications (red dots). Although impossible to ascertain categorically the tachycardia mechanism, these observations support abnormal automaticity creating a high-frequency atrial focal source as a driver of atrial arrhythmia. Lack of multicomponent fractionated electrograms at the successful AT ablation site, markers of the requisite nonuniformly anisotropic substrate that favors the development of microreentry by creating regions of slow conduction, support an automatic
KEYWORDS Atrial tachycardia; Automaticity; Extrasystolic activity; Arrhythmogenic focus; Catheter ablation (Heart Rhythm 2015;0:0–2) Address reprint requests and correspondence: Dr Radoslaw Marek Kiedrowicz, Cardiology Department, Guy’s and St Thomas’ NHS Foundation Trust, St Thomas’ Hospital, 6th Floor E Wing, Westminster Bridge Rd, London SE1 7EH, United Kingdom. E-mail address: [email protected].
1547-5271/$-see front matter B 2015 Heart Rhythm Society. All rights reserved.
http://dx.doi.org/10.1016/j.hrthm.2015.12.014
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P R I N T & W E B 4 C / F P O
Heart Rhythm, Vol 0, No 0, Month 2015
Figure 1
mechanism. The absence of conduction to the atrium during the first 700 ms of the tachycardia may be explained by slow conduction over the exit pathway(s) along with a relatively long effective refractory period of the surrounding atrial tissue. An alternative explanation is the presence of a low electrotonic load in the vicinity of the discharging focus that
would require a longer train of stimuli to capture the atrium. This hypothesis is supported by focal ablation increasing the mass of electrically inexcitable tissue in the region of the focus, thereby decreasing further the local electrotonic load and preventing atrial capture during ongoing focal discharges.
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