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Tracking cardiac electrical instability by computing interlead heterogeneity of T-wave morphology

Cardiology Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215

Submitted 17 June 2003 ; accepted in final form 28 July 2003

Oscillations in T-wave morphology, particularly T-wave alternans (TWA), have been fundamentally linked to increased susceptibility to ventricular fibrillation (VF). We investigated whether the escalation in complexity of T-wave oscillations before VF is attributable to increased spatial heterogeneity of repolarization. Peak interlead T-wave heterogeneity (TWH) was measured by second central moment analysis of T-wave morphology in epicardial electrograms in dogs during left anterior descending coronary artery occlusion. TWH differentiated cases in which myocardial ischemia provoked VF from those without VF (563 ± 56 vs. 139 ± 36 µV, P < 0.01). In the former group, progressive, significant increases in TWH above preocclusion baseline (70 ± 8 µV) began at 2.25 min after the start of occlusion and were associated successively with TWA (at 155 ± 19 µV), T-wave multupling (at 386 ± 100 µV), complex oscillatory T-wave forms (at 560 ± 76 µV), discordant TWA (at 572 ± 98 µV), and VF at 4.36 ± 0.14 min. TWH in precordial ECGs in 12 pigs during angioplasty-balloon-induced myocardial ischemia also discriminated animals that experienced VF (from 90 ± 14 at baseline to 382 ± 39 µV, P < 0.05) from those without VF (from 96 ± 17 at baseline to 199 ± 61 µV, NS). Ischemia-induced changes in ST segment and T-wave amplitude did not predict VF. Heightened spatial heterogeneity of repolarization, as assessed by second central moment analysis of TWH, underlies TWA and increased risk for ischemia-induced VF. Monitoring spatial TWH from precordial leads could prove useful in stratifying risk for life-threatening arrhythmias.

sudden cardiac death; ventricular fibrillation; heterogeneity of repolarization

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