The subjects were symptomatic patients undergoing ablations for atypical, non-right atrial isthmus-dependent flutter at Sequoia Hospital, Redwood City, CA, from October 4, 2013 to October 21, 2014. All signed the written informed consent. Data analysis was retrospective and approved by the Western Institutional Review Board.
Our ablation protocol has been described previously . Antiarrhythmic drugs were stopped at least five half-lives and amiodarone at least 3 months before ablation. General anesthesia was used in all, and venous access was from the right groin only. A 9F Boston Scientific (Natick, MA) Ultra Ice™ catheter guided the transseptal puncture, done using a 71-cm Baylis (Montreal, QC) NRG™ needle. The mapping and ablation catheters were both placed in the left atrium across a single transseptal puncture. All ablations were done using a Safire™ BLU™ (St Jude Medical, St. Paul, MN) open irrigated tip ablation catheter at 50 W. Patients had a femoral or radial arterial line. Our peri-procedural anticoagulation protocols have also been previously described .
3D geometry and mapping were done using the St. Jude EnSite Velocity system with Precision Mapping Module. A 7F 20 electrode catheter (St. Jude Livewire™, 2-10-2 mm electrode spacing catheter) was placed around the tricuspid valve annulus with the distal poles in the coronary sinus. Following access to the left atrium, a 3D geometry was created. Patients who were in their clinical atrial arrhythmia at the start of the case had activation mapping simultaneous with geometry creation. A stable atrial bipolar electrogram, preferably from an electrode pair inside the coronary sinus, was chosen as an activation mapping reference and a reference detection algorithm was chosen to ensure consistent detection and timing of the reference electrogram. A surface ECG with a visible atrial flutter wave was added to the mapping window to confirm stability of the reference electrogram relative to the atrial flutter wave. The left edge of the mapping window was set at 60 ms ahead of the onset of the most prominent atrial flutter wave on the surface ECG, and the right edge of the mapping window was set so that at least 95% of the tachycardia cycle length was encompassed within the mapping window. Timing within the arrhythmia cycle length was divided into eight equal parts, each tagged with a different color to create an isochronal color map. These color maps are similar to traditional isochronal maps where lines are drawn to reflect zones of similar activation times. The only difference was that there are no lines drawn between the various colors. Slower conduction is indicated by a narrowing of the width of the individual color zones or a compression of the colors. A circular mapping catheter (St. Jude Reflexion Spiral™) with 20 electrodes, and a 15–25 mm variable loop was used as a roving mapping catheter. The bipolar electrograms were recorded from 1 mm electrodes (except for the tip which is 2 mm) separated by 1 mm. Up to 10 simultaneously collected bipolar electrograms were obtained at each anatomical position of the roving catheter. The detection setting was configured to automatically detect the largest amplitude bipolar peak, and the sensitivity was set to the maximum of 10 mV. This combination allowed the computer to detect and annotate the largest amplitude bipolar peak in the mapping window regardless of the voltage. In the case of double potentials or fractioned electrograms within an area of interest, the user could manually override the automatic detection to annotate the timing of the said point to the peak of the sharpest near-field component of the signal. Using this method of collecting a high density of points with a multipolar mapping catheter, the need for this manual annotation is generally minimal. However, when delineating activation in areas of dense scar and mapping locations was prone to high amplitude far-field signals, such as the anterior left superior pulmonary vein which often also has right atrial signals or the AV groove which often also has ventricular signals, manual editing may still be necessary.
The low voltage identification level was set to 0.1 mV initially to allow low voltage zones to be collected and displayed as gray colored low voltage zones on the map. This helped to prevent inaccurate timing measurements when sampling from regions of scarred or non-conductive tissue.
Following the appropriate setting of all map values, the first set of activation mapping points were collected from the coronary sinus reference catheter to store the map settings as well as the reference catheter activation sequence for the atrial arrhythmia. This allowed a set of waveform shadows to be visualized behind the live coronary sinus catheter electrograms. If a change occurred in the intracardiac activation sequence, these shadows helped the user identify that a rhythm change had taken place or that the reference catheter had moved. When either no anatomical surface model had been created or the mapping catheter was in a new area of the chamber that had not previously had geometry created, anatomical static shell points and activation mapping points were collected simultaneously. While the roving circular catheter was being moved throughout the chamber, the mapping system rapidly acquired 10 activation points at a time. During rapid acquisition, the operator monitored the signals to eliminate collection of points with noise or ventricular signal. When the full chamber was mapped, field scaling was applied, the geometry was edited and completed, and the activation map was projected onto the geometry surface to evaluate the arrhythmia circuit. Mapping points not in close proximity to the static model geometry surface were excluded from the analysis. This eliminated any far-field electrograms collected inside the chamber from being used to create the activation map of the atrial arrhythmias. Both color isochronal and propagation maps were generated. If any areas of interest in the chamber were determined to be under-sampled, additional points were added to the activation map as deemed necessary. This was most often needed in the areas of slowest conduction. In a highly diseased atrial chamber, or to determine the activation sequence through the areas of slow conduction, the low voltage level was adjusted to as low as 0.03 mV for visualization of low-amplitude signals within the areas of scar. The circuit of each macroreentrant atrial flutter was measured by tracing the leading edge of each color isochronal zone. Although we used eight color isochrones during the clinical studies, during post hoc evaluation of the circuit, we sometimes used 15 and 22 isochrones to more accurately define the atrial flutter circuit. This allowed measurement of the total length of the atrial flutter circuit. The area of slowest conduction was determined for each atrial flutter, and the length of the slow zone and time of conduction through this zone were determined. Microreentrant atrial flutter or focal atrial tachycardia was defined as an arrhythmia where the origin of the arrhythmia occurred in a very small area (<1 cm) and radiated outward from that site. At the end of each ablation, all pulmonary veins were checked to make certain that they were isolated with both entrance and exit block and any which were still connected were re-ablated to complete PV isolation. Arrhythmia induction with and without isoproterenol was undertaken until all inducible organized atrial arrhythmias had been mapped an ablated.
Data collection and analysis
For each patient, we recorded age, gender, duration of AF or atrial flutter, prior antiarrhythmic drug therapy, CHADS2 and CHA2DS2-VASC score, cardioversions, body mass index, left atrial (LA) size, prior strokes/TIA’s, and the presence of hypertension, coronary artery disease, and dilated cardiomyopathy. A successful ablation was defined as no AF, atrial flutter, or tachycardia lasting more than 30 s off of all antiarrhythmic drugs after a 3-month blanking period.
Some patients were treated with antiarrhythmic drugs and/or cardioverted during the 3 months following the ablation. Patients sent daily transtelephonic ECG strips for 1–3 months after ablation and were seen at 3 and 12 months, at which time 7–14 days of continuous monitoring using a ZIO patch (iRhythm Technologies, Inc., San Francisco, CA) was done. Thereafter, patients were seen directly or contacted by phone at least annually and arrhythmia records were obtained from the hospitals and referring physicians. ECG recorders were reissued for any arrhythmia symptoms. Pacemaker AF data were utilized when available.
Continuous data were described as mean ± standard deviation and counts and percent if categorical. Kaplan-Meier curves were generated for freedom from all atrial arrhythmias and for freedom from atrial tachycardia and atrial flutter after the ablation using XLStat, 2015 (Paris, France).