4.2. Typical electrophysiologic remodeling in AF and SSS
Typical electrophysiologic remodeling in AF includes down-regulation of
L-type Ca2+ channel (ICa,L), down-regulation ofI to, and upregulation ofI KACh andI K1.17,
18 The remodeling of ionic current could
reduce the slope of phase 0, hyperpolarize membrane voltage, and reduce
heart rate. Funny current down-regulation might contribute to the
association between SAN dysfunction and supraventricular
tachyarrhythmias.19Compared with the normal SANs, those of patients or animals with AF did
not exhibit spontaneous late diastolic Ca2+ elevation
or cranial shifting of the earliest atrial activation sites upon
isoproterenol infusion, suggesting impaired spontaneous sarcoplasmic
reticulum Ca2+release.5,
20
Patients with conditions associated with atrial remodeling, ischemia,
and atrial stretch (e.g., congestive heart failure) manifest altered SAN
function.21,
22 Therefore, we excluded heart failure
and myocardial ischemia cases but without affecting the final results.
Moreover, there is evidence to indicate that antiarrhythmic drugs used
for the treatment of AF can cause SAN
dysfunction.23 In this
study, antiarrhythmic drug was a factor associated with SSS in patients
with AF.
SSS might also be accompanied by intra-atrial conduction delay, AV nodal
conduction disturbances, and paroxysmal atrial tachycardia as part of
the tachycardia-bradycardia syndrome. Damage to SAN is an important
factor for the formation of AF. When sinus impulse formation is
depressed in the presence of SSS, during the slow atrial cycle, an
atrial extrasystole may occur. Moreover, SAN may also facilitate
re-entry. Thus, ischemic damage to the SAN alone, without atrial wall
disturbances, such as fibrosis, stretch, or muscle loss, may result in
chronic AF.