Pulmonary vein properties in lone atrial fibrillation

ADELAIDE, AUSTRALIA. In April 2009 Professor Prash Sanders and colleagues at the Royal Adelaide Hospital published a landmark study concerning the electroanatomic properties of the left atrium in patients with lone atrial fibrillation (LAF). Before getting into details of their study it is, however, necessary to ensure that the reader has a basic understanding of the parameters governing normal as well as abnormal heart rhythms (arrhythmias). See HEART RHYTHM 101.

As a result of this study, we now know that lone, paroxysmal afibbers have an abnormal atrial substrate, and that this abnormality is what promotes the progression of AF. In a follow-up to the 2009 study, the Adelaide team now reports the results of a study designed to elucidate the electroanatomic properties of the pulmonary veins (PVs) which, as discovered by Professor Michel Haissaguerre in 1998, are the prime source of the “misfirings” initiating the vast majority of AF episodes.

The electrophysiology study (carried out as part of a scheduled ablation) involved 21 patients with paroxysmal AF, 18 with persistent AF, and 15 age-matched controls with supraventricular tachycardia (left-sided accessory pathways). The average age of the participants was 58 years and 78% were male. The researchers made the following observations.

  • The local voltage in the PVs (defined as the amplitude of the peak positive to peak negative deflections of the local electrograms) during constant pacing at 100 bpm (600 ms cycle length) was significantly lower in AF patients than in controls, and the percentage of low voltage readings was significantly higher in afibbers than in controls, with the highest percentage found in persistent afibbers. This finding is consistent with the presence of fibrosis within the PVs.

  • The PV muscle sleeves (an extension of the left atrial tissue into the PVs) were shorter among AF patients than among controls.

  • Conduction velocity was significantly slower among persistent afibbers than among paroxysmal ones and, in both cases, slower than that observed for controls. This finding is also consistent with the presence of fibrosis in the PVs.

  • In the group of paroxysmal afibbers, the ERPs in the left and right superior PVs were significantly shorter than the ERPs measured in the posterior left atrium, the left atrial appendage and the distal coronary sinus (CSd), and also shorter than in the control group.

  • In the group of persistent afibbers, the ERPs measured in the left and right superior PVs were significantly shorter than the ERPs measured in the CSd and also shorter than the average ERP in the control group.

  • In contrast to the findings for the PVs, the ERPs in the posterior left atrium and left atrial appendage were prolonged in paroxysmal afibbers compared with controls, while persistent afibbers had shorter ERPs than both the control group and the paroxysmal group.

  • Complex signals (defined as those with 3 or more deflections of more than 50 ms duration, or those with 2 separate deflections separated by more than 30 ms) were significantly more prevalent among persistent afibbers than among paroxysmal, and both had a higher percentage of these signals than did the control group.

The authors of the study conclude that paroxysmal and persistent afibbers demonstrate electrical and electroanatomic remodelling of the PVs compared to controls without prior AF. Some of the changes were more marked in patients with persistent AF.
Teh, AW, et al. Electroanatomic properties of the pulmonary veins: slowed conduction, low voltage and altered refractoriness in AF patients. Journal of Cardiovascular Electrophysiology, Vol. 22, October 2011, pp. 1083-91

Editor’s comment: This study adds valuable information to our knowledge of the mechanism underlying atrial fibrillation and explains the major role played by the pulmonary veins in the initiation of AF episodes. It also explains why electrical isolation of the pulmonary veins through catheter ablation is an effective means of eliminating AF, especially in the case of paroxysmal AF.