Author + information
- Received June 29, 2010
- Revision received August 12, 2010
- Accepted September 15, 2010
- Published online March 1, 2011.
- Felipe Atienza, MD, PhD⁎,⁎ (, )
- David Calvo, MD⁎,
- Jesús Almendral, MD, PhD⁎,
- Sharon Zlochiver, PhD†,
- Krzysztof R. Grzeda, MD†,
- Nieves Martínez-Alzamora, PhD‡,
- Esteban González-Torrecilla, MD, PhD⁎,
- Ángel Arenal, MD⁎,
- Francisco Fernández-Avilés, MD, PhD⁎ and
- Omer Berenfeld, PhD†,⁎ ()
Objectives The aim of this paper was to study mechanisms of formation of fractionated electrograms on the posterior left atrial wall (PLAW) in human paroxysmal atrial fibrillation (AF).
Background The mechanisms responsible for complex fractionated atrial electrogram formation during AF are poorly understood.
Methods In 24 patients, we induced sustained AF by pacing from a pulmonary vein. We analyzed transitions between organized patterns and changes in electrogram morphology leading to fractionation in relation to interbeat interval duration (systolic interval [SI]) and dominant frequency. Computer simulations of rotors helped in the interpretation of the results.
Results Organized patterns were recorded 31 ± 18% of the time. In 47% of organized patterns, the electrograms and PLAW activation sequence were similar to those of incoming waves during pulmonary vein stimulation that induced AF. Transitions to fractionation were preceded by significant increases in electrogram duration, spike number, and SI shortening (R2 = 0.94). Similarly, adenosine infusion during organized patterns caused significant SI shortening leading to fractionated electrograms formation. Activation maps during organization showed incoming wave patterns, with earliest activation located closest to the highest dominant frequency site. Activation maps during transitions to fragmentation showed areas of slowed conduction and unidirectional block. Simulations predicted that SI abbreviation that heralds fractionated electrograms formation might result from a Doppler effect on wave fronts preceding an approaching rotor or by acceleration of a stationary or meandering, remotely located source.
Conclusions During induced AF, SI shortening after either drift or acceleration of a source results in intermittent fibrillatory conduction and formation of fractionated electrograms at the PLAW.
This work was supported in part by grants from the Spanish Society of Cardiology (to Dr. Calvo); National Heart, Lung, and Blood Institute Grants P01-HL039707, P01-HL87226, and R01-HL060843 (to Dr. Berenfeld); and the Ministerio de Ciencia e Innovación, Red RECAVA (to Drs. Atienza, González-Torrecilla, Arenal, and Fernández-Avilés) and the Centro Nacional de Investigaciones Cardiovasculares (proyecto CNIC-13) (to Drs. Atienza, Almendral, González-Torrecilla, and Berenfeld). Dr. Atienza has served on the advisory board of and received lecture fees from Medtronic; and has received research funding from St. Jude Medical Spain. Dr. Berenfeld has received a research grant from St. Jude Medical. All other authors have reported that they have no relationships to disclose. Drs. Atienza and Calvo contributed equally to this work.
- Received June 29, 2010.
- Revision received August 12, 2010.
- Accepted September 15, 2010.
- American College of Cardiology Foundation