When QTc Shrinks After Rhythm Conversion

Abstract

Case Summary

An 83-year-old man with a history of atrial fibrillation on amiodarone therapy was admitted for direct-current cardioversion because of recurrent atrial fibrillation with a ventricular rate of approximately 105 beats per minute. Cardioversion successfully restored sinus rhythm. Postcardioversion 12-lead electrocardiography revealed an unexpectedly short QTc of 344 ms despite chronic treatment with a QT-prolonging agent. This finding was attributed to QT hysteresis, reflecting delayed adaptation of ventricular repolarization to the abrupt reduction in heart rate after rhythm conversion.

Take-Home Message

QT hysteresis can result in transient QTc shortening and has important implications for interpretation of QT intervals during antiarrhythmic therapy.

Graphical Abstract

An 83-year-old man with symptomatic atrial fibrillation (AF) on amiodarone therapy (200 mg daily) and uninterrupted anticoagulation was admitted for direct-current cardioversion for recurrent AF with a ventricular rate of 105 beats/min (Figure 1A). Cardioversion successfully restored sinus rhythm. Postcardioversion 12-lead electrocardiography (ECG) demonstrated an unexpectedly short corrected QT interval (QTc) interval of 344 ms calculated using Bazett's formula (Figure 1B) despite current treatment with the QT-prolonging agent amiodarone.

Figure 1.

Immediate Post-Cardioversion Apparent QTc Shortening

(A) Admission 12-lead electrocardiogram demonstrating AF with a ventricular rate of approximately 105 beats/min in an 83-year-old man prior to elective direct-current cardioversion (DCCV). (B) Postcardioversion 12-lead ECG demonstrating restoration of sinus rhythm with an unexpectedly short QTc-B of 344 ms and QTc-F of 354 ms. AF = atrial fibrillation; ECG = electrocardiography; QTc-B = QT corrected by Bazett; QTc-F = QT corrected by Fridericia.

Question

What is the most likely underlying mechanism for the short QTc interval observed after direct-current cardioversion (DCCV)?

• A.DCCV itself accelerates ventricular repolarization
• B.QTc during sinus bradycardia is underestimated by Bazett's formula
• C.The 12-lead ECG was obtained too soon after DCCV
• D.The patient has congenital short QT syndrome

The correct answer is C.

The ECG obtained approximately 1 minute after DCCV demonstrated sinus bradycardia at 51 beats/min. Although DCCV is known to cause transient bundle branch block and ST-segment elevation without elevation in cardiac enzymes,¹ the electrical current itself has minimal effect on the QT interval.² Therefore, accelerated ventricular repolarization (Choice A) does not explain the shortened QTc.

Bazett's formula may underestimate the QTc during bradycardia.³ However, QTc calculated using Fridericia's formula remains abnormally short at 354 ms, arguing against bradycardia-dependent undercorrection (Choice B).

With abrupt changes in heart rate or pacing rate, ventricular repolarization requires time to reach a new steady state which manifests on the ECG as QT hysteresis.^4,5 Here, the ventricular rate during AF was 105 beats/min and abruptly slowed to 51 beats/min after DCCV. Because the ECG was obtained too soon (approximately 1 minute) after DCCV, the abrupt drop in heart rate produced an apparent QTc shortening (Choice C). The QT interval can take up to 5 minutes to reach a new steady state after a large heart rate change.² As shown in Supplemental Figure 1, the QTc was within the normal range on the ECG recorded 3 hours later despite an even slower heart rate of 50 beats/min (QT 440 ms; QTc 402 ms by Bazett's formula; QTc 414 ms by Fridericia's formula), further arguing against Choice B.²

Patients with congenital short QT syndrome are predisposed to AF, but this is unlikely in an elderly patient. QTc during AF, calculated using Fridericia's formula (reliable in AF),² was 410 ms, ruling out short QT syndrome (Choice D).

QT/RR hysteresis is described in exercise–recovery and other dynamic ECG settings, where QT at a given RR differs during accelerating vs. decelerating heart rates. Therefore, QTc measurements before a new steady state can be misleading.⁵ A transiently shortened QTc from QT hysteresis is common yet often overlooked in clinical practice despite its important implications for patients with AF requiring rhythm control with class III antiarrhythmics. For example, during in-hospital dofetilide initiation, QTc is reassessed 2 to 3 hours after each dose to guide dose adjustment and discontinuation thresholds. If post-DCCV QT is measured before repolarization re-equilibrates, a misleadingly short QTc may mask QT prolongation and contribute to unsafe dosing of class III agents (including dofetilide and amiodarone), which may lead to the development of torsades de pointes.²

Funding Support and Author Disclosures

Dr Yan was supported by the Sharpe-Strumia Research Foundation. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Appendix

Supplemental Figure 1

Delayed ECG Demonstrating QTc Normalization 3 Hours After Cardioversion