Abstract 11663: T Wave Alternans: A Clue in Plain Sight

Abstract

Introduction: T-wave alternans (TWA) refers to the beat-to-beat variability in T-wave amplitudes or polarity on surface ECGs, and can signify susceptibility to malignant ventricular arrhythmias (VA). Aims: We present a case to emphasize the pathophysiology and clinical significance of this ECG finding. Case description: A 52 year-old female with history of HIV presents with shortness of breath and is treated for heart failure. In the ED, she has witnessed syncope and is found to have VT that progresses to VF. Resuscitation efforts are successful and include amiodarone loading. Figure 1A demonstrates baseline ECG on admission with a QTc of 495 ms. A few days later, an ECG reveals QTc of 696 ms with TWA (figure 1B). Shortly after, she develops polymorphic VT in the setting of long-short sequences and an R on T trigger (figure 1C) that is terminated with cardioversion. Review of pre-admission ECGs reveals that QTc prolongation occurred after initiation of a retroviral regimen that included rilpivirine and worsened with amiodarone. Both medications are discontinued, and she is eventually discharged with a QTc of 450 ms. Early theories for TWA's mechanism hypothesized that dispersion of refractoriness resulted in depolarization through alternating pathways and thus this phenomenon. Recent understanding further suggests that TWA occurs as a result of cellular alternans and variation in action potential duration due to dysregulation of repolarization. If discordant repolarization alternans ensues, whereby neighboring cells repolarize in opposite phases (long-short, short-long), the resultant repolarization gradient and heterogeneity in cellular repolarization serves as the substrate for VA; if a premature beat encounters refractory myocardium and unidirectional block occurs, a re-entrant excitation tachycardia can be initiated. Conclusions: TWA on ECG suggests myocardial electrical instability as a result of cellular repolarization inhomogeneity.