QTc prolongation following CV
In our study, during prolonged monitoring using 7-day Holter, we were
able to demonstrate a significant number of patients with new
significant QTc prolongation following CV. In 32 patients (35%), the
median QTc reached new values ≥500 msec, and in 14 patients (16%) it
even reached QTc ≥550 msec (baseline QTc was < 480 msec). Our
observations are in line with previous case series and small
studies.11,12 Houltz and colleagues had previously
reported QTc prolongation up to a mean of 672 ± 26 ms in patients that,
in fact, developed Torsade de pointes.13 In another
study Choy and colleagues reported that QTc was prolonged from 405 ± 55
to 470 ± 67 ms following CV.3 These reports, however,
included a relatively small number of patients (less than 10 patients in
average) or included patients who were treated with new antiarrhythmic
drug, such as Sotalol or Dofetilide. Notably, in our study, neither
initiation of a new antiarrhythmic medication nor an increase in dose
occurred.
The exact mechanisms of QTc prolongation following CV remains unclear.
Possible causes include: 1) bradycardia - several studies demonstrated
that lower heart rates following CV may prolong the QTc
interval14, 2) increased drug toxicity - changes in
the neuro-hormonal status, such as change in sympathetic nervous
activity and ANP were reported following CV15, and can
potentially modulate the sensitivity to antiarrhythmic
drugs, 3) abrupt slowing of heart rates, following
termination of fast ventricular rates, that may lead to QTc
prolongation16, 4) ventricular repolarization
remodeling during atrial fibrillation - QTc during SR following CV was
reported to be significantly and transiently prolonged (although of
limited magnitude, the prolongation was substantial (approximately 15%)
in some individuals5), and 5) ion channels
modification - in several previous studies17 an
alterations in ion channels and several gene expressions in the atria
and ventricle of patients with persistent AF were reported as leading to
change in the QTc interval; In particular, the inward rectifier I(K1)
channel, affecting the inward rectifier potassium current which
regulates the terminal portion of phase 3 of the
repolarization.18 Of note, in our study, we found that
the magnitude of QTc prolongation was similar regardless of CV method,
Midazolam use and regardless of the need to additional use/reloading of
antiarrhythmic medication peri-cardioversion.