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LETTER TO THE EDITOR
Accordingly, we additionally analyzed T-wave area and peak amplitude from the surface ECG for each dog in our volume overload study at baseline, midinfusion, peak infusion, and in the postdiuresis phase. Both T-wave indexes were computed semi-automatically from digital ECG data using custom software written in Labview (National Instruments, Austin, TX; Ref. 5). T-wave area was integrated using the trapezoid method from the ECG J-point to the T-wave offset, defined by visual return of the T-wave to the TP baseline. When T-waves were inverted or biphasic, absolute areas were summated. T-wave peak amplitude was defined as the absolute maximum voltage deviation from the TP segment.
We observed a weak linear relationship between T-wave area and TWA amplitude, measured as voltage of alternation (Valt, mV), with a correlation coefficient R = 0.40 (P = 0.08), and between T-wave peak voltage and Valt (correlation R = 0.42; P = 0.06). Actual T-wave areas did not differ with volume overload and, normalized to baseline values for each dog, were 1.21 ± 0.44 (midinfusion), 1.06 ± 0.25 (peak infusion), and 1.06 ± 0.30 [postdiuresis; P = not significant (NS)]. Similarly, T-wave peak amplitudes did not alter significantly with volume challenge and, normalized to baseline, were 0.90 ± 0.24 (midinfusion), 1.08 ± 0.33 (peak infusion), and 0.87 ± 0.85 (postdiuresis; P = NS).
Thus, although TWA magnitude in our study (Valt) may reflect T-wave amplitude, elevated TWA magnitude with volume overload did not relate to T-wave amplitude per se. This may reflect our small series. However, these results agree with preliminary clinical data from our laboratory that TWA is sensitive to T-wave magnitude, although the extent to which T-wave magnitude fluctuates according to the Brodie effect (1) remains unclear. Further clinical studies are needed to examine how ventricular dilatation alters T-wave magnitude, shape and beat-to-beat dynamics, and their potential arrhythmic consequences in patients with structural heart disease and volume overload.
GRANTS
This work was supported by a grant from the National Institutes of Health (SBIR-1R43HL-80815-1) and from the American Heart Association, Western Regional Affiliate to S. M. Narayan (0265120Y).
FOOTNOTES
Address for reprint requests and other correspondence: S. M. Narayan, Electrophysiology Service, VA San Diego, Univ. of California San Diego, Box 111A, 3350 La Jolla Village Dr., San Diego, CA 92161 (e-mail: snarayan{at}ucsd.edu)
REFERENCES
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