Circulation. 2007;115:e10
doi: 10.1161/CIRCULATIONAHA.106.661447
(Circulation. 2007;115:e10.)
© 2007 American Heart Association, Inc.
Response to Letter Regarding Article, "Upsurge in T-Wave Alternans and Nonalternating Repolarization Instability Precedes Spontaneous Initiation of Ventricular Tachyarrhythmias in Humans"
Vladimir Shusterman, MD, PhD;
Anna Goldberg, BSc;
Barry London, MD, PhD
Cardiovascular Institute, University of Pittsburgh, Pittsburgh, Pa
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Introduction
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We thank Drs Selvaraj and Chauhan for their interest in our
work
1 and discussion of the possible impact of white noise and
respiration. We do not feel that white noise is a significant
problem, although respiration (along with other physiological
factors) may play a role, as emphasized in our report.
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Impact of Noise
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We used the "surrogate" analysis (ie, test of baseline stability)
to control for white noise, respiration, movement, and other
sources of artifacts. In addition, we removed noisy segments
of data and used sectional (T-wave) averaging to reduce the
level of white noise. Each data segment was carefully reviewed
at high magnification at each processing step. The residual
white noise was small (<3 µV), was relatively constant
over time, and could not explain the dynamics of T-wave alternans
(TWA) or other frequency components. The level of TWA was at
least 2 times greater than all sources of noise combined. In
addition, the assumption that changes in TWA could be a mere
result of noise caused by elevated heart rate and sympathetic
activity contradicts the observation that the magnitude of TWA
before the arrhythmia was higher than at similar or faster heart
rates during arrhythmia-free periods. Therefore, changes in
repolarization before the onset of the arrhythmia cannot be
explained by an increase in noise at faster heart rates or elevated
sympathetic drive.
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Impact of Respiration
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We explicitly defined the "respiratory" range and emphasized
that the greatest increase occurred in that range. Thus, the
connection to respiration is clear. However, because the data
on respiratory patterns were not available, we avoided speculations
about the exact impact of respiration. Furthermore, changes
in heart rate in the studied group were relatively small (8%),
which does not support the assumption of major respiratory changes.
It is well known that spectral estimates of TWA in real-life recordings are affected by respiration. The magnitude of this effect, which is different for spectral and nonspectral techniques because of the different filtering properties of modified moving average and intrabeat average, needs to be estimated. Therefore, we have provided an explicit estimate of the possible impact of respiratory oscillations on TWA. This estimate shows that the increase in TWA could not be completely explained by this factor. Adding white noise would not change the relationship between spectral components.
Thus, we believe that our presentation of the results is appropriate. Our goal was to describe (not "interpret") the high-risk periods before the onset of tachyarrhythmias. Although respiration may play some role, the exact role of each contributor requires further study.
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Acknowledgments
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Disclosures
Dr Shusterman has ownership interest in PinMed, Inc. A. Goldberg and Dr London report no conflicts of interest.
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References
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- Shusterman V, Goldberg A, London B. Upsurge in T-wave alternans and nonalternating repolarization instability precedes spontaneous initiation of ventricular tachyarrhythmias in humans. Circulation. 2006; 113: 28802887.[Abstract/Free Full Text]