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Marked QTc Reduction Immediately Following Direct Current Cardioversion of Atrial Fibrillation: Clinical Implications
Arthur Omondi1, Natee Sirinvaravong1, Jenna Spears1
1Lankenau Medical Center and Lankenau Institute for Medical Research, Wynnewood, Pennsylvania, USA.
Background:
The QTc in sinus rhythm (SR) following direct current cardioversion (DCCV) of atrial fibrillation (AF) is commonly used as a baseline QTc for patients who require initiation of antiarrhythmic drugs for rhythm control. Inaccurate baseline QTc may cause drug-induced torsades de pointes.
Objectives:
This study sought to assess time-dependent QTc changes following DCCV.
Methods:
We prospectively assessed QTc changes with Bazett's QTc and Fridericia's QTc formulas in 65 patients following conversion of AF to SR. Among these 65 patients, 48 underwent DCCV and 17 spontaneously converted to SR.
Results:
There was a large and statistically significant decrease in QTc in SR immediately following DCCV in 40 patients, which occurred with an abrupt reduction in heart rate postcardioversion. This finding excluded 8 patients with ventricular-paced QRS. The mean decrease from QTc in AF was 70.7 ± 37.2 milliseconds in the QTc interval for heart rate using Bazett's formula and 33.8 ± 17.9 milliseconds in the QTc interval for heart rate using Fridericia's formula at 1-minute post-DCCV. In 17 patients with spontaneous conversion from AF to SR, the QTc reduction was comparable to those in patients with DCCV. The QTc increased with time and reached a steady state at 5 minutes following conversion. Initiation of Class III drugs based on the "shortened" baseline QTc following DCCV was associated with drug-induced torsades de pointes.
Conclusions:
In patients with AF following conversion, regardless spontaneous or DCCV, the QTc shortened significantly with decreases in heart rate, likely via the mechanism of time-dependent rate adaption of ventricular repolarization. A steady-state QTc at 5-minutes following DCCV should be used as real baseline for guidance of pharmacotherapy in patients with AF.
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