Low-Dose Ibutilide Combined with Catheter Ablation of Persistent Atrial Fibrillation: Procedural Impact and Clinical Outcome

Figures

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  Figure 1. The ablation protocol used in this study. PsAF = persistent atrial fibrillation; SR = sinus rhythm; AT = atrial tachycardia; LA = left atrial; CV = cardioversion.

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  Figure 2. Examples of ablation targets. (a) Surface ECG lead V1, intracardiac recordings from an ablation catheter (abl), and a mapping catheter within the coronary sinus (CS). Note that, after circumferential pulmonary vein isolation (CPVI) and ibutilide, the atrial activity with CS had become very organized; however, an area on the anterior wall of the left atrium (LA) still presented with continuous, low-voltage (0.134 mV), and fractionated atrial electrograms. (b) Surface ECG lead V1 and intracardiac recording from an ablation catheter and CS 3-4 electrodes. After CPVI and ibutilide, the local atrial fibrillation cycle length (AFCL) was 107 ms on the lower part of the posterior wall of the LA, whereas the AFCL recorded by the adjacent CS catheter was more rapid (151 ms) (top). After ablation, the local AFCLs at the ablation site and CS were prolonged to 155 and 167 ms, respectively (bottom).

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  Figure 3. An example of persistent atrial fibrillation (AF) ablation with this low-dose ibutilide-guided approach. (a) The AF cycle length (AFCL) within the left atrial appendage (LAA) at baseline, after circumferential pulmonary vein isolation (CPVI), and 5 and 15 minutes after administration of 0.25 mg ibutilide. (b) Three electroanatomic maps showing the sites where low-amplitude complex fractionated atrial electrograms (CFAEs) were recorded on the anterior wall of the left atrium (LA). The pink, yellow, and white points represent CFAEs recorded before CPVI, after CPVI, and after administration of 0.25 mg ibutilide, respectively. The CFAE areas were minimized after CPVI plus ibutilide. (c) Ablation targeting these areas converted AF to atrial tachycardia (AT). (d) The 3D electroanatomic mapping of LA suggested that the mechanism of this AT was perimitral reentrant tachycardia (left upper), and ablation (alone) at the mitral isthmus terminated this AT.

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  Figure 4. Ablation of the site with the most rapid atrial fibrillation cycle length (AFCL) uncovered by low-dose ibutilide administration terminated persistent AF. The middle figure is the 3D electroanatomic map of the left atrium (LA) in this patient. The red points represent the lesions surrounding the PV antrum. After administration of 0.25 mg ibutilide, the LA activity became organized, and the AFCL could be measured at most of the sites in the LA. From top to bottom on the right panel are the intracardiac recordings (abl) from the LA roof, septum, and bottom. The activity at these sites and in the LA appendage (left upper) was longer than that in the coronary sinus. However, the AFCL at the posterolateral aspect of the LA (left middle, yellow point) was significantly shorter than that in the CS (194 vs 245 ms), suggesting that this area was harboring an AF driver. During regional ablation of this small region, AF converted to atrial tachycardia (AT, green point).

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  Figure 5. Kaplan–Meier plots depicting atrial tachyarrhythmia-free survival at 2 years after the first procedure. Persistent atrial fibrillation (AF) was terminated by circumferential pulmonary vein isolation (CPVI) alone (blue line), CPVI combined with left atrial modification guided by low-dose ibutilide (red line), and cardioversion (CV) (green line).