Dallas, TX

November 8-11, 1998

Background: Microvolt T wave alternans (TWA) is a risk marker for ventricular tachyarrhythmias. The exact electrophysiologic mechanism is unknown, specifically whether macroscopically visual TWA and microvolt TWA share the same mechanism. Methods: In 12 isolated rabbit hearts electrical alternans was induced by incremental pacing together with global ischemia (A, n = 7) or d-sotalol and hypothermia (B, n = 5). Simultaneously, 8 epicardial and 4 endocardial monophasic action potentials (MAP, contact electrode method) as well as a 15-channel volume conducted ECG was recorded. The ECG was divided into 128 beat segments and submitted to the clinically utilized spectral analysis method (CHI) using identical criteria to evaluate TWA as positive or negative (alternans voltage > 1.9 mcV, alternans ratio > 3). Alternans voltage and ratio in each of the 12 limb and precordial leads were correlated with the occurrence of alternans in the MAPs. The ECG lead and MAP with maximal alternans amplitudes were identified. Results: In all experiments, at least microvolt-TWA was induced. Macrovolt-TWA was induced in 4 of the sotalol experiments and was always preceded by microvolt-TWA. Increases in alternans amplitude both in the ECG and the MAP were usually gradual with a continuous change between microvolt and macrovolt alternans. The time of onset of detectable alternans was identical in ECG and MAPs. When comparing alternating segments vs. non-alternating segments, APD90 (243 ± 32 vs. 400 ± 107 msec, p > 0.001) and the diastolic interval were shortened (78 ± 13 vs. 213 ± 75 msec, p < 0.0001) while dispersion of MAPs (max-min_ did not differ (87 ± 45 vs. 80 ± 32 msec, p = ns). Maximal amplitude of alternans was found in the free wall of the left ventricle. Conclusion: Microvolt and macrovolt alternans reflect quantitatively different expressions of the same electrophysiologic phenomenon.