慢性心房顫動病人的竇房結功能及心房電生理:心房加速驅動與抗心律不整藥物的角色

Chronic persistent atrial fibrillation is at risk of multiple cerebral and peripheral
embolization and causes great socio-economic burden. For the purpose of
investigation of the atrial electro-pathophysiology and relevant sinus node functional
reserve, we studied 36 consecutive patients of chronic persistent atrial fibrillation by
sequential clinical assessment, cardiac echocardiography and invasive cardiac
electrophysiology study with bi-atrial basket electrodes. The underlying clinical-pathophysiological
property of chronic persistent atrial fibrillation is correlated with
the efficacy of electrical cardioversion and the subsequent maintenance of stable
sinus rhythm and adequate sinus node function.
Global atrial mapping of the chronic atrial fibrillation revealed a significantly
shorter local A-A intervals in the left atrium than that in the right atrium (160±14 ms
vs 170±15 ms, P<0.01). The electrophysiological gradient of reentrant wavelets was
not changed under the use of sotalol and propafenone. However, the energy
requirement for electrical cardioversion could be lessened by sotalol, but not
propafenone, although both drugs help facilitate the success rate of direct current
shocks. Meanwhile, the vulnerable atrial ectopies appearing after successful electrical
cardioversion were located mostly at the pulmonary vein convergence area of the left
atrium, the left atrial appendage and the sinus node and crista terminalis area of the
right atrium. Nevertheless, the ectopies from the remaining areas of the atria were not
uncommon. Sotalol and propafenone could decrease the number, but not the
distribution of the vulnerable atrial foci. Apparently, in patients with chronic atrial
fibrillation, the abnormalities in atrial pathology and electrophysiology are wide-spread
and inter-relevant, which may disturb the restoration of stable sinus node
activity after successful conversion.
Despite of the deepened atrial pathophysiology, the sinus node function was
generally acceptable, with only mild prolongation of post-suppression sinus node
recovery time or intrinsic heart rate in half of the patients evaluated 3 months after
conversion of chronic atrial fibrillation. None of these patients has had
bradyarrhythmia-relevant symptoms, nor needing the implantation of a permanent
pacemaker.
Chronic persistent atrial fibrillation in humans deteriorated the structrual,
functional and electrophysiological properties of the atria, which may not always be
reversible. Fortunately, the underlying sinus node function remained competent after
the conversion of long-term atrial fibrillation.