Author + information
- Received February 8, 2016
- Accepted February 18, 2016
- Published online October 1, 2016.
- aDepartment of Internal Medicine, Geisinger Medical Center, Danville, Pennsylvania
- bDepartment of Cardiology, Geisinger Medical Center, Danville, Pennsylvania
- ↵∗Reprint requests and correspondence:
Dr. Saquib A. Siddiqi, Department of Internal Medicine, Geisinger Medical Center, 102 North Academy Avenue, Danville, Pennsylvania 17822.
A 62-year-old male with history of atrial fibrillation and coronary artery disease experienced a sudden collapse at home. Emergency medical services arrived in 5 min and cardiopulmonary resuscitation was initiated. His initial rhythm was ventricular fibrillation, and he was defibrillated to normal sinus rhythm. He was brought to the emergency room where an electrocardiogram revealed no acute injury with a QT interval corrected for heart rate of 500 ms. Therapeutic hypothermia was initiated, and no evidence of an acute infarction was detected by biomarkers or angiography. Fourteen hours after his arrival, his electrocardiogram revealed T-wave alternans (TWA) and a QT interval corrected for heart rate of 690 ms. After reaching a minimal temperature of 34.8°C, patient rewarming was started. While his temperature remained 35.0°C, and 23 h after initial documentation of TWA, he experienced his first of 2 polymorphic ventricular tachycardia arrests, requiring cardioversion.
TWA is the beat-to-beat variability in the timing or morphology of T waves on electrocardiogram, best seen in Figure 1, in leads V2 to V6, as T waves alternating between positive and negative delections. TWA can be associated with rapid changes in heart rate or prolongation of the QT interval, and in the latter case, is a precursor to torsades de pointes. It reflects dispersion of ventricular repolarization, which is an important mechanism for reentrant arrhythmias. Although TWA has not been previously described during therapeutic hypothermia, heterogeneity of repolarization has been demonstrated in a cellular model of severe hypothermia. The mechanism that has been proposed is via temperature-dependent sarcolemma ion channels (1).
Hypothermia has a potential for ventricular pro-arrhythmia, but the mechanism is unclear. This patient with post-arrest QT prolongation developed TWA during therapeutic hypothermia, which was followed by torsades de pointes. The finding of TWA is an ominous predictor of ventricular arrhythmias in this setting.
All authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received February 8, 2016.
- Accepted February 18, 2016.
- American College of Cardiology Foundation