Premature atrial complexes initiating sustained atrial arrhythmia

ECG: On this ECG, there is an initial atrial sinus activity with 2 premature atrial complexes (sharply modifying the T wave pattern); the QRS complexes following the premature beats are slightly altered with a right bundle branch block-type conduction aberration of varying degree; an apparently identical premature atrial complex (characteristic P-on-T pattern) initiates an atrial arrhythmia episode corresponding to an atrial fibrillation (very rapid, disorganized atrial activity);

Comments: This tracing shows an example of the triggering of an atrial arrhythmia by a premature atrial complex (occurring at the peak of the T wave) suggesting a focal origin. The determinants of the genesis and maintenance of atrial arrhythmias are complex, multiple and often linked. The occurrence of premature atrial complexes has long been considered a benign consequence of excessive caffeine intake. This tracing, however, illustrates the central role of atrial fibrillation episodes in the initiation and maintenance of a particular type of premature atrial complexes recognizable by their characteristic P-on-T electrocardiographic pattern. The paroxysmal focal AF presented by this patient is the consequence of the expression of very rapid automatic foci mostly located at the anastomosis of the pulmonary veins. These foci, which bombard the atria and completely disrupt the activation, originate mainly from the ostium of the pulmonary veins but can also originate from the superior or inferior vena cava, Marshall’s ligament, the crista terminalis, the coronary sinus or the posterior aspect of the left atrium. The prematurity of these atrial complexes may be difficult to identify, based on the presence of a limited deformation of the T wave. The axis and morphology of the P wave can help determine its anatomical origin (pulmonary veins or other foci, differentiation between right or left, inferior or superior pulmonary veins). The reason for which the anastomosis of the pulmonary veins is the predominant source of the extrasystolic foci initiating the arrhythmia resides in the presence of striated myocardial fibers in the wall of the pulmonary veins (especially the superior veins) and originating from the roof of the left atrium. The refractory periods of these cells are shorter than those of the left atrium, which may partly explain their arrhythmogenic nature. The complex entanglement of myocardial infiltrates in the venous wall also favors conduction anisotropy as well as the occurrence of localized micro-reentries.

The key role of these arrhythmogenic sites justifies that the pulmonary veins have become the target of ablative techniques. The principle of atrial fibrillation ablation is to eliminate the arrhythmia trigger (electrical isolation of the pulmonary veins) and to modify the atrial arrhythmogenic substrate.

Take-home message: A particular type of premature atrial complexes (recognizable by their P-on-T pattern) plays a central role in the initiation and maintenance of atrial fibrillation episodes. This characteristic electrocardiographic pattern most often corresponds to foci localized in the ostium of the pulmonary veins.