(Circulation. 2005;112:e52.)
© 2005 American Heart Association, Inc.
Correspondence |
Mount Sinai School of Medicine, New York University, New York, NY, Division of Cardiology, Elmhurst Hospital Center, Elmhurst, NY
I read with great interest the contribution of Shvilkin et al.1 The issue they tackled is of utmost importance because of the high prevalence of both the postpacing T-wave inversion, cardiac memoryrelated changes (CM), and the ischemia-associated but similar-appearing T-wave alterations (ISC). The authors have been delving into the mechanisms of the CM ECG phenomenon from the basic science vintage for some time,25 and are now venturing into the clinical applications of the concept. All interested in materia electrocardiographica are now eager to put to the test of practice the authors contentions. I would like to offer some thoughts and direct to the authors some questions regarding their hypothesis and their methods.
Considering the diverse topography of the ischemic territories, which depends on the particulars of each case, why do they feel that there will be no ischemic T-wave vectors that could be similar in direction and magnitude to the ones generated by right apical pacing and subsequent CM development? For example, some of the patients with right coronary artery occlusion/stenosis and right ventricular involvement could generate a T-wave vector with the characteristics described in the article.
I wonder why more ECGs were not recorded in the 13 patients with pacemakers after reprogramming the device to AAI; it would have been interesting to know whether the T wave of CM is stable in its direction, as it dissipates. The exclusion of patients undergoing multivessel percutaneous coronary intervention in the ISC group could be questioned. Multivessel coronary artery disease is frequently encountered, and thus to exclude such patients is the equivalent of shying away from reality. Besides, this particular group with its diverse myocardial topography and sometimes perpetually changing in magnitude and direction resultant T-wave vector would have been expected to provide the greater challenge to the hypothesis that there is a way to differentiate CM from ISC.
Why were not more ECGs (if available) from each patient of the ISC group put to the test? Is it implied that the ISC T-wave vector is stable in magnitude and direction? Clinical practice attests to the opposite, particularly in patients with unstable acute cononary syndrome. It is conceivable that some of the repeat ECGs could have shown T-wave vectorial characteristics of CM, thus making the differential diagnostic boundary of CM and ISC fuzzier. This carefully thought out and implemented work will be incorporated in the "toolbox" of the electrocardiographer and the generalizability of the authors conclusions will be easy to test.
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Beth Israel Deaconess Medical Center, Boston, Mass
Center for Molecular Therapeutics, Columbia University, New York, NY
We1 derived our criteria to differentiate ischemic and postpacing T-wave inversion (TWI) from retrospective cohorts of ischemic (ISC) and cardiac memory (CM) patients that can be viewed as derivation cohorts. A larger validation study needs to be performed to confirm the clinical utility of our criteria.
Dr Madiass concern is most relevant to the small subset of ISC patients with right coronary artery lesions that demonstrated precordial TWI with frontal plane direction similar to CM. Comparison of tracings of 9 such patients with >40 CM patients, including some chronically atrioventricular paced, continues to support our criterion of TWIprecordial > TWIIII in discriminating CM from ISC. We believe that CM TWI results from changes in 2 noncontiguous areas of myocardium (sites with the earliest and latest activation), and therefore its spatial characteristics cannot be duplicated by ischemia in any single territory.
We recorded serial ECGs in CM patients documenting its evolution. During the first 7 days, we typically observed counterclockwise frontal plane T vector rotation similar to that described in the dog model.2 The time course of CM development and dissipation in humans has been recently re-addressed, demonstrating a steady-state CM after 1 week of AV pacing.3
The reason to exclude patients with multivessel percutaneous coronary intervention from the ISC group was not to "shy away from reality" but to assess the culprit vesselrelated characteristics of ISC TWI in the "cleanest" derivation sample. We agree that multivessel ischemia may present a differential diagnostic challenge, which we plan to address in a future study.
We collected a series of ECGs on the ISC patients. We chose the first-available ECG from the index admission for our analysis because it was the one on which the clinical decision was made. We observed significant variations in TWI amplitude but few directional changes on subsequent recordings.
In conclusion, we feel that the application of vector concepts to T-wave analysis (via tools that can be simply added to present electrocardiographic methods) can significantly improve ECG interpretation.
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