1. Volume 15, Issue 1, Pages 28-37 (January 2018)
Electrogram signature of specific activation patterns: Analysis of atrial tachycardias at high-density endocardial mapping 
Antonio Frontera, MD, Masateru Takigawa, MD, PhD, Ruairidh Martin, MD, Nathaniel Thompson, MD, Ghassen Cheniti, MD, Grégoire Massoullié, MD, Josselin Duchateau, MD, Jean Yves Wielandts, MD, PhD, Elvis Teijeira, MD, PhD, Takeshi Kitamura, MD, Michael Wolf, MD, Nora Al-Jefairi, MD, Konstantinos Vlachos, MD, Seigo Yamashita, MD, Sana Amraoui, MD, Arnaud Denis, MD, Meleze Hocini, MD, Hubert Cochet, MD, Frederic Sacher, MD, PhD, Pierre Jaïs, MD, Michel Haïssaguerre, MD, Nicolas Derval, MD 
Heart Rhythm 
Volume 15, Issue 1, Pages (January 2018)
DOI: /j.hrthm
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2. Figure 1
Schematic of the electrophysiological mechanisms identified. Timing of conduction is from the patient, representative of each mechanism (in milliseconds).
Heart Rhythm  , 28-37DOI: ( /j.hrthm )
Copyright © 2017 Heart Rhythm Society Terms and Conditions

3. Figure 2
Example of slow conduction occurred along the posterior wall of the left atrium just below the left inferior pulmonary vein. A: The wavefront travels at normal velocity (wide dark-red front) from the anterior wall crossing the ridge between the left appendage and the left upper vein (5, 15, and 27 ms). B: The wavefront is crossing the area of slow conduction evidenced by the narrow dark red front with significant decrease in speed (activation time 75 ms). C: The wavefront regains speed (105 ms).
Heart Rhythm  , 28-37DOI: ( /j.hrthm )
Copyright © 2017 Heart Rhythm Society Terms and Conditions

4. Figure 3
A: Representation of wavefront collision phenomenon. B: Visual depiction of the friction site where the activation of 2 wavefronts occur in opposing directions. C: Description of activation occurring around a pivot point. Bottom left: Craniocaudal activation of the posterior wall with an area of slow conduction starting from the left inferior pulmonary vein causes increasing curvature of the advancing wavefront, which rotates around a pivot point to collide at a line of functional block caused by refractoriness from the initial craniocaudal activation. There is therefore caudocranial activation along the same area of slow conduction.
Heart Rhythm  , 28-37DOI: ( /j.hrthm )
Copyright © 2017 Heart Rhythm Society Terms and Conditions

5. Figure 4
Left anterior oblique projection of the left atrium. A wavefront coming from the anterior wall get arrested at the previous mitral isthmus line (A). A gap allows the passage of the wavefront (B), which finally invades and activates the posterior wall (C).
Heart Rhythm  , 28-37DOI: ( /j.hrthm )
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6. Figure 5
Slow conduction and relative electrograms recorded over the 3 sites of scar, border zone, and boundaries toward healthy tissue (bipolar voltage set from 0.05 to 0.5 mV).
Heart Rhythm  , 28-37DOI: ( /j.hrthm )
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7. Figure 6
A: Inverse relationship between duration and voltage for slow conduction phenomenon: the higher the voltage, the shorter the duration. B: The 3 phenomena (slow conduction, pivot sites, and wavefront collisions) are plotted in different areas of the graph. EGM = electrogram.
Heart Rhythm  , 28-37DOI: ( /j.hrthm )
Copyright © 2017 Heart Rhythm Society Terms and Conditions

8. Figure 7
Schematic of electrogram (EGM) characteristics at pivot sites. EGMs at a pivot point (1) are short in duration and high in amplitude and expressed by multiple deflections. On friction area (2 and 3), EGMs are represented by double potentials, longer in duration and with fractionation.
Heart Rhythm  , 28-37DOI: ( /j.hrthm )
Copyright © 2017 Heart Rhythm Society Terms and Conditions