INTRODUCTION
Atrial fibrillation (AF) is the most common cardiac tachyarrhythmia..
Its pathophysiology is complex1 and can be described
with: 1) triggers for the initiation of the arrhythmia (pulmonary and
non-pulmonary foci); 2) a fibrotic substrate for the maintenance of AF;
and 3) various modulators acting by multiple potential mechanisms
(hypertension, obesity, obstructive sleep apnea, inflammation, endurance
sports…).
Atrial remodeling and fibrosis development are associated with a variety
of electric disturbances, such as heterogeneities in atrial action
potential duration, effective refractory period, and conduction
velocity2. These phenomena can promote and sustain AF.
Left atrial (LA) scarring can be detected by late enhancement MRI
(MRI-DE) and can be correlated well with reduced electrogram amplitudes
as recorded by endocardial voltage maps3. However, MRI
to assess atrial fibrosis is not available in all centers due to its
complex evaluation.
Electroanatomic mapping (EAM) can provide information regarding local
voltage abnormalities that may be used as a surrogate marker for
fibrosis. Specific voltage cut-off values have been reproducibly shown
to accurately identify scar and/or fibrosis in the
ventricles,4,5. EAM voltage cut-off values to identify
myocardial scars in the atrial tissue are not as well defined as in the
ventricle. Voltage-guided AF substrate modification targeting low
voltage areas (LVA) has been carried out in some studies to improve
long-term AF ablation efficacy 6-11. In most of them
mapping has been performed using voltage cut-offs during sinus rhythm
(SR), and in one study mapping was performed during
AF11. However, a recent study has documented that the
correlation between low-voltage and posterior LA MRI-DE is significantly
improved when acquired during AF vs. sinus rhythm12.
The aim of our study was to evaluate the LVA extent and location in
patients with persistent AF undergoing pulmonary veins isolation, and
compare the findings on maps obtained in SR and AF in each patient.