13th International Congress
THE "NEW FRONTIERS"
OF ARRHYTHMIAS 1998

January 24-31, 1998
Marilleva, Trento, Italy

RT-170

T-wave alternans: will it revolutionize risk stratification for sudden cardiac death?

Hans D. Esperer, Helmut U. Klein, Richard J. Cohen*.
Dept. of Internal Medicine, Division of Cardiology, Otto-von-Guericke, Magdeburg University, Germany, *Harvard University, MIT Division of Health Sciences and Technology, Cambridge, MA, USA

Electrophysiologic basis

Many observations, under a variety of conditions, support the concept that prolongation of repolarization is pro-reentry rather than anti-reentry when the prolongation is heterogeneous and dispersion of refractoriness is significantly enhanced². Finite-element models simulating myocardial conduction display alternation in synthesized ECG waveforms as these models are rendered increasingly unstable^4,5. In these models, subpopulations of areas with prolonged refractory periods may respond to every other stimulation, leading to alternate patterns of excitation and recovery in successive beats, thus giving rise to observable electrical alternans. The subpopulations exhibiting prolonged recovery provide evanescent barriers to conduction, which facilitate wavefront fractionation and reentry. This constitutes the elctrophysiologic link between the mechanisms of formation of electrical alternans and reentrant arrhythmogenesis. That TWA in fact results from enhanced dispersion of refractoriness has subsequently been shown in animal experiments mainly in dogs or pigs whose ventricles were made electrical unstable either through coronary artery occlusion or systemic hypothermia^3,4. These experiments demonstrated that a relative increase in the amount of TWA detected was accompanied by a relative decrease in the measured VF threshold. However, it became also clear from these studies that TWA in vivo may be to subtle as to be visually detectable⁴. Therefore, a signal averaging technique using fast Fourier spectral analysis was developed enabling reliable detection of TWA at the microvolt level⁵.

Recently, it has been hypothesized that, in addition to solely providing a marker of myocardial vulnerability to ventricular tachyarrhythmias, TWA per se may also be causally linked to arrhythmogenesis⁶. Thus, action potential alternans may generate excitatory current of sufficient magnitude to initiate spontaneous electrical activity. Especially in the border zones of a myocardial infarct where discordant TWA can occur, with adjoining regions showing opposite polarities, the phenomenon may be a contributing mechanism of arrhythmia generation⁷.