Reply to “Intracardiac T-wave alternans, ischemia, and arrhythmias, in a canine model”

LETTER TO THE EDITOR Reply to ‘‘Intracardiac T-wave alternans, ischemia, and arrhythmias, in a canine model’’ We appreciate the interest in the article on T-wave alternans (TWA) and arrhythmia. The issues of interest that were raised in the initial letter to the editor are addressed in the following paragraphs. As noted in the initial letter, an increase in amplitude of R-waves and T-waves is observed in the hyperacute phase of myocardial ischemia (MI); indeed we noted similar results with R-waves under our experimental conditions as well but in less than 2% of cases. As indicated in Reference 23 in the article of interest, the reduction in electrogram voltage is tightly correlated with blood flow measurements documenting ischemia; this is our routine measurement in all past studies in this model. With regard to the ST/T-wave changes with the emergence of myocardial infarction, the ST segment was not always well defined on intracardiac bipolar electrograms (IBEs; see Fig 1, EN1 and EP3); it was therefore difficult to characterize reliably/reproducibly ST changes in the context of ST-T alternans. With regard to changes in T-wave polarity with the emergence of MI (ie, in the first minutes of coronary occlusion), we could not specifically address this question because we collected data only with ventricular tachycardia (VT) and after 20 minutes of coronary occlusion.

With respect to the effect of increasing the QRS duration in diagnosing and measuring TWA changes, we consider the electrogram QRS prolongation and T-wave changes after ischemia as manifestation of the sum of subcellular changes including perturbation in Na, K, and Ca transport, which together result in a conduction delay and repolarization change. Additionally, we defined and analyzed TWA as beat-to-beat variation in T-waves without a beat-to-beat change in QRS. The QRS widening by itself is therefore less likely to account for opposing effects in T-waves from beat to beat that result in the increases in TWA magnitude observed after MI. More importantly, we also observe that the TWA magnitude increases after MI on IBEs where QRS widening is not observed. Conversely, we observe no change in TWA magnitude in some cases of QRS prolongation. In short, although we cannot rule out the secondary effects of QRS on TWA changes post-MI, our data do not clearly support such a phenomenon either. Michael A. Kwofie James B. Martins Division of Cardiovascular Diseases Department of Internal Medicine University of Iowa College of Medicine, and Veterans Administration Medical Center Iowa City, Iowa

Translational Research 2012;159:507. 1931-5244/$ - see front matter Ó 2012 Mosby, Inc. All rights reserved. doi:10.1016/j.trsl.2011.11.004

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