Aberrant electrical activity

Normal heart beats depend on co-ordinated electrical activity that spreads from the sinoatrial node through the walls of the atria causing contraction (Figure 5).

Normal electrical control in the heart

Figure 5. Normal electrical control in the heart.

Many atrial fibrillation (AF) cases arise when cardiomyocytes develop ‘pacemaker-like activity’ that over-rides control from the sinoatrial node.11 These focal AF triggers cause spontaneous premature atrial depolarisations, re-entry circuits or both.11 

Re-entry circuits

Re-entry, an electrical impulse that repeatedly travels around an abnormal circuit, can arise from anatomical factors or from functional differences in the electrophysiological properties of neighbouring tissues. Anatomical and functional re-entry circuits seem to give rise to atrial flutter and AF respectively.29 

AF may arise from numerous wavelets of functional re-entry that travel through the atria, where they collide, combine or divide. This creates daughter wavelets that perpetuate AF. Conditions that increase atrial size, decrease conduction velocity or shorten the refractory period permit multiple wavelets and promote AF.29 For instance, focal AF triggers usually arise from atrial myocytes in muscles running from the left atrium to the pulmonary veins. Transient ectopic tachycardia in the pulmonary veins decrease electrical refractoriness in the atria, which triggers AF.6 

Foci can, however, arise in several other areas including the walls of the right and left atria, the interatrial septum, the coronary sinus and the superior vena cava.11 A few high-energy and rapidly firing re-entrant circuits, usually in the left atrium, can generate the abnormal electrical activity that overcome regular atrial pluses, thereby producing the disorganised rhythm associated with AF.11

Triggered activity may underlie more than 80% of cases of paroxysmal AF. Following AF onset, the arrhythmia may persist possible due to the effect of multiple independent re-entrant wavelets, focal activity in the ganglionic plexi in the atrium or small spiral re-entrant drivers (rotors). Over time, the repeated firing and remodelling of the atria results in self-sustaining AF.6

Atrial remodelling is discussed in the next section


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