Clinical mapping approach to diagnose electrical rotors and focal impulse sources for human atrial fibrillation

Abstract

Introduction: The perpetuating mechanisms for human atrial fibrillation (AF) remain undefined. Localized rotors and focal beat sources may sustain AF in elegant animal models, but there has been no direct evidence for localized sources in human AF using traditional methods. We developed a clinical computational mapping approach, guided by human atrial tissue physiology, to reveal sources of human AF.

Methods and results: In 49 AF patients referred for ablation (62 ± 9 years; 30 persistent), we defined repolarization dynamics using monophasic action potentials (MAPs) and recorded AF activation from 64-pole basket catheters in left atrium and, in n = 20 patients, in both atria. Careful positioning of basket catheters was required for optimal mapping. AF electrograms at 64-128 electrodes were combined with repolarization and conduction dynamics to construct spatiotemporal AF maps. We observed sustained sources in 47/49 patients, in the form of electrical rotors (n = 57) and focal beats (n = 11) that controlled local atrial activation with peripheral wavebreak (fibrillatory conduction). Patients with persistent AF had more sources than those with paroxysmal AF (2.1 ± 1.0 vs 1.5 ± 0.8, P = 0.02), related to shorter cycle length (163 ± 19 milliseconds vs 187 ± 25 milliseconds, P < 0.001). Approximately one-quarter of sources lay in the right atrium.

Conclusions: Physiologically guided computational mapping revealed sustained electrical rotors and repetitive focal beats during human AF for the first time. These localized sources were present in 96% of AF patients, and controlled AF activity. These results provide novel mechanistic insights into human AF and lay the foundation for mechanistically tailored approaches to AF ablation.

© 2012 Wiley Periodicals, Inc.

Figures

Figure 1. Atrial Basket Positioning for Computational AF Mapping

A. Good catheter placement in both atria (48 mm baskets, anteroposterior fluoroscopy), with MAP catheter at the left superior pulmonary vein antrum. B, C. Intracardiac Echocardiography confirms electrode opposition to walls of B. Left Atrium and C. Right Atrium. D. Good Electrode coverage of left atrium (60 mm Basket, RAO 30° fluoroscopy); E. Spline crowding detracts from otherwise good LA coverage (60 mm Basket, AP fluoroscopy); F. Large Left Atrium, With Poor Electrode Coverage of its Septum, outlined by ablation catheter loop with tip at right superior PV os (60 mm basket, LAO 30° fluoroscopy). G. Poor Coverage of Superior LA, indicated by wide separation of LA basket from the left main bronchus; the RA basket is well-deployed (60 mm baskets, AP fluoroscopy). H. Basket Placement With Pre-existing device leads. The RA basket is well positioned in this AP projection, yet the LA basket poorly covers the inferior LA. This appearance is consistent with basket displacement through the mitral apparatus. I. Anterior displacement of the LA basket through the mitral annulus, with the ablation catheter defining the true posterior border of the LA (same patient as panel H, in 30° RAO fluoroscopy). J. Undersized basket, despite an apparently good deployment, floating freely within the large left atrium that gave very poor signals and was replaced. K. Undersized basket in a patient with heart failure, a cardiac-resynchronization defibrillator and previously diagnosed ‘permanent AF’ now reclassified as longstanding persistent AF and undergoing ablation. L. Underexpanded basket, evident from the elliptical shape due to pinching at the interatrial septum. This was remedied by advancing the basket further into the left atrium with clockwise torque.

Figure 2. Anatomic Reference and Map Nomenclature

A, B. Electrodes Illustrated Within Patient-Specific Atria (NavX system, St Jude Medical, MN) in 30° LAO and 30° RAO projections, showing alternate splines and electrodes for clarity. C. Sinus Rhythm Map on Biatrial Schematic. Activation at basket electrodes, shown as dots, is displayed as a color-coded map from the sinus node to the lateral inferior LA. The RA is opened between its poles with tricuspid annulus opened laterally and medially; the LA is opened along its equator, with mitral annulus opened superiorly and inferiorly. The pulmonary vein ostia are indicated by dashed lines.

Figure 3. Mapping Reveals Spiral Wave during AF in the Human Left Atrium

A. Raw electrograms used to create maps and movies. Unipolar electrograms (locations indicated by circles on grid) are used to construct an isopotential snapshot at any time point T (indicated by vertical green line). Monophasic action potentials (MAP) indicate repolarization and are used to calibrate unipolar electrograms. These isopotential maps are created successively for multiple time points T to create movies (see Supplemental movie). B. Isochronal snapshot of a LA rotor during one cycle of AF, created from activation times determined when each unipolar electrogram crosses a voltage threshold.

Figure 4. Localized Electrical Rotors (Spiral Waves) in Human AF, Revealed by Computational Mapping

A. Solitary Counterclockwise (CCW) Rotor During Persistent AF in the posterior LA; B. CW Rotor in Persistent AF in the anterior LA; C. Two Concurrent Rotors During Paroxysmal AF in the anterior LA (CW) and inferior LA (CCW); D. Right Atrial Rotor (CW) During Paroxysmal AF in the mid-posterior wall, with fibrillatory conduction to the LA. By Contrast, E. Clockwise Rotor of Reverse Typical Atrial Flutter differs from AF, with 1:1 activation throughout the RA that engages Bachmann’s bundle to activate the LA and no fibrillatory conduction. Key: ECG lead I, CS=coronary sinus electrogram.

Figure 5. Repetitive Focal Beats revealed by Computational Mapping

A. Repetitive Focal Beat during Paroxysmal AF (in low septal LA), with activation to remaining LA and fibrillatory conduction to the RA (CL≈100 ms). In contrast, B. Focal Atrial Tachycardia (non-fibrillatory) from the high posterior LA differs from AF by showing 1:1 activation centrifugally to the ipsilateral then contralateral atria (CL 300 ms).