The Electrophysiology of Atrial Fibrillation: From Basic Mechanisms to Catheter Ablation

Abstract

The electrophysiology of atrial fibrillation (AF) has always been a deep mystery in understanding this complex arrhythmia. The pathophysiological mechanisms of AF are complex and often remain unclear despite extensive research. Therefore, the implementation of basic science knowledge to clinical practice is challenging. After more than 20 years, pulmonary vein isolation (PVI) remains the cornerstone ablation strategy for maintaining the sinus rhythm (SR). However, there is no doubt that, in many cases, especially in persistent and long-standing persistent AF, PVI is not enough, and eventually, the restoration of SR occurs after additional intervention in the rest of the atrial myocardium. Substrate mapping is a modern challenge as it can reveal focal sources or rotational activities that may be responsible for maintaining AF. Whether these areas are actually the cause of the AF maintenance is unknown. If this really happens, then the targeted ablation may be the solution; otherwise, more rough techniques such as atrial compartmentalization may prove to be more effective. In this article, we attempt a broad review of the known pathophysiological mechanisms of AF, and we present the recent efforts of advanced technology initially to reveal the electrical impulse during AF and then to intervene effectively with ablation.

Figure 1

(a) Leading circle reentry. The impulse spreads to the inside of the circuit continuously, making it permanently unexcitable. (b) Typical reentrant circuit around an anatomical barrier. (c) Reentrant circuit with the excitation gap. (d) Reentrant circuit without the excitation gap. (e) Unsustainable reentrant circuit as its frontal part collides with its nonexcitable terminal part.

Figure 2

(a) The arrhythmic firing from the left inferior PV propagates normally to the atrial myocardium. (b, c) Special conditions such as conduction anisotropy or anatomical obstacle at the central point of the wavefront can create two waves with rotational propagation, capable of maintaining AF.

Figure 3

The deflectable 20-polar catheter is placed in the tricuspid annulus in order to perform a linear lesion in the cavotricuspid isthmus. Atrial extrasystoles produced with each movement of the catheters in the right atrium trigger AF.

Figure 4

An example of the extrapulmonary trigger. In a patient with long-standing persistent AF, after PVI and the electrical cardioversion to SR, a repeated onset of AF (a, b) is observed with firing from the same point mapped and ablated in the area between left superior PV and LAA (ligament of Marshall). (c) The firing fails to induce AF. Ablation of this area resulted in the long-term SR maintenance for >18 months.

Figure 5

Schematic representation of a rotor. The front of the depolarization wave (red line) propagates at a higher speed in the periphery (point 1) than in the center (point 3). The green line represents the repolarized edge. The wavelength, the refractoriness, and the conduction velocity differ from the periphery to the center; however, the depolarization frequency in a stable rotor is the same (see text for details).

Figure 6

Doppler-type effect with an increase and decrease in the depolarization frequency when the rotor is moving [28]. (a) Stable rotor. (b) Moving rotor.

Figure 7

Focal automatic firing (cycle length: 100 ms) from LSPV enters the LA either by 2 : 1 conduction or by fibrillatory conduction.

Figure 8

The hypothetical mechanism of the occurrence of fibrillatory conduction in macrocircuits, studied by the technique of selective activation remapping. (a) Clockwise perimitral flutter with 205 ms CL and constant 1 : 1 conduction throughout the atria (regular atrial tachycardia). (b) Acceleration of the CL to 187 ms with fibrillatory conduction (unstable atrial tachycardia) (from Ioannidis et al. [29]).

Figure 9

FIRM mapping. (a) The 64-pole basket catheter in the left atrium. (b) ECG (blue) and unipolar intracardiac signals (black) from the 64-pole basket catheter. (c) Isochronal activation map reconstructed from the corresponding electrograms, illustrating a left atrial rotational activity (from Baykaner et al. [51]).

Figure 10

Noninvasive body surface mapping. (a) The vest of 252 electrodes and the three-dimensional reconstruction of cardiac chambers with the computed tomography. The voltage at each point of the torso, taken from the 252 electrodes of the vest, is depicted with virtual electrograms on the surface of the atria. (b) Isochronous maps showing the rotational activity near the antrum of the right inferior PV.

Figure 11

Organization and termination of persistent AF with ablation of CFAEs. (a) Recording of fragmented potentials at the base of the LAA at the onset of ablation. (b) Organization of arrhythmia shortly before termination. (c) Termination of the arrhythmia during ablation in the same area.

Figure 12

AcQMap noncontact mapping system (Acutus Medical, CA, USA). (a) The multipolar spherical AcQMap catheter with a diameter of 25 mm (deployed), which consists of 6 splines, each of which contains 8 electrodes and 8 ultrasound transducers (total 48). (b) The three-dimensional model of the LA is constructed by emitting ultrasonic waves reflecting them to the cardiac wall. (c) The system displays on the three-dimensional model the propagation of the impulse, calculated by measuring the dipole density.

Figure 13

Possible ablation techniques, beyond PVI, after revealing an AF driver. (a) Direct targeting of the rotor path. (b) Standard linear lesions (box lesion and mitral isthmus block). (c) Linear isolation of the rotor path.