LETTER TO THE EDITOR
A paradigm shift in myocardial stunning
Marc Ovadia, MD
Laboratory of Cellular Electrophysiology, Fellowship Program in Pacing and Electrophysiology, Departments of Medicine and Pediatrics, University of Illinois College of Medicine, Hope Children’s HospitalAdvocate Christ Medical Center840 S. Wood Street, M/C 856, Chicago, Illinois 60612, USA
The study by Burnes et al. (1) in a recent issue of JACC was presented to show the close correlation of reconstructed and measured electrograms in and out of ventricular tachycardia, in a chronic (four-day-old) infarction model. The investigators make the additional observation that a large amount of living myocardium may underlie an epicardial region that manifests a pure Q- wave, that is, a pure QS complex.
The investigators suggest that the existence of "regions of noninfarcted tissue below recording sites that show no local electrophysiologic activity" (p. 2073) may imply "the presence of stunned or hibernating myocardium" (p. 2073). In characterizing the electrograms observed in these areas further, Burnes et al. (1) describe "electrograms... which showed pure Q-wave morphologies during RA pacing" and which "have a subthreshold –dV/dtmax indicating no local activation" (p. 2074, emphasis added). Later, adding further description, they state that "the presence of pure Q-wave epicardial electrograms over a large portion of the infarcted myocardium... provides evidence for transmural myocardial damage and the absence of an excitable epicardial border zone. ... [P]ure Q-wave electrograms, indicating lack of local activation, are reconstructed (and directly measured with both epicardial sock electrodes and rod-tip electrodes) over regions of tissue that appear viable in the TTC-stained slices. A possible explanation for these observations is that the apparently viable stained myocardium was not activated because of stunning caused by... [and there follows a list of causes of stunning]" (p. 2074, emphasis added).
This correspondent desires to make two points. First, the recording technique, relying as it does on ordinary metal electrodes placed epicardially and on the reconstruction of local electrograms from similarly recorded distant electrograms, may be insensitive to signal of lower frequency content, as these recording techniques record through a metal-electrolyte interface, which is a high-pass filter (2,3) and therefore fails to reproduce signal components of low-frequency content faithfully. Whereas the coordinated activation front of a hundred thousand heart cells depolarized simultaneously via the action potential Na channel is expected to have a high-frequency content, the uncoordinated depolarization perhaps also characterized cellularly by less sharp up(down)strokes may escape detection by this technique. Perhaps this latter scenario is familiar from the case of concealed conduction into atrioventricular (AV) node tissues, which cannot be recorded by these techniques either. The former, less familiar scenario has been presented by various researchers, including Delmar et al. (4). This first comment, even if accurate, does not detract from the accuracy of the interpretation offered by the investigators (1) for their data. This comment would merely support the possibility of local activation not detected by the presented techniques. That such may occur is in any case implicit in their discussion of the path of the ventricular tachycardia impulse.
The second point has to do with the use of the term "stunning" in the text that is quoted above. When the term stunning is used, most investigators do not conceptualize viable myocardium with no local activation subjacent to a QS complex four days after the occurrence of acute myocardial infarction. Without questioning the interpretation or the propriety of use of the term stunning by the investigators (1), this correspondent merely wishes to point to the novelty of this use of the term. (Furthermore, there can be no question about the accuracy of localization of the QS complexes in relation to the viable myocardium in this carefully performed work, where quadruply redundant verification existed—electrogram by sock, electrogram by rod, distant electrogram and reconstructed local electrogram.)
If the usage is accurate, then a paradigm shift has been introduced surreptitiously—the idea that what is termed stunning may include myocardium that is viable, and perhaps even healthy, yet which is not activated electrically. If this were a tiny speck of muscle in a scar-encircled island, the paradigm shift would be, at most, of trivial significance. But being a large piece of viable muscle situated at a border zone of infarction (where it might have corresponded to clinical stunning or to clinical infarction) this third possibility—that is, stunned myocardium which is neither infarcted nor stunned in the ordinary fashion—is a significant extension of the meaning of the term stunning.
Concepts exist in the literature to account for this behavior as a new category of stunning, although the category has existed only theoretically prior to these observations of Burnes et al. (1). While in the relatively recent review of Bolli and Marban (5) of molecular and cellular mechanisms of stunning, no mechanistic concept was presented that could encompass this category of stunning, the more recent channels biophysics-based review (6) suggested that disruption of intercellular communication (i.e., gap junction uncoupling) could emulate clinical stunning, with precisely these characteristics of viable but not locally activated myocardium. Not emphasized in that review was the obvious implication that such viable tissue would underlie a region of QS complex, identical to what has been shown to exist by Burnes and colleagues.
Also significant is the fact that, of all the categories of stunning, this one is likely to be the most arrhythmogenic.
Finally, irrespective of whether these comments find their way into print, this correspondent appreciates the opportunity to comment to this great team of investigators who have taught electrocardiographic–electrophysiologic correlation to an entire generation of researchers.
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References
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1. Burnes JE, Taccardi B, Ershler PR, Rudy Y. Noninvasive electrocardiographic imaging of substrate and intramural ventricular tachycardia in infarcted hearts. J Am Coll Cardiol. 2001;38:2071–2078[Abstract/Free Full Text]
2. Ovadia M, Chou HA, Zavitz DH. Theoretical limiting transfer function for electrodes in biological tissue. Comput Cardiol. 2000;26:579–582
3. Chou HA, Ovadia M, Moskowitz M, Zavitz DH. In vivo potentiostatic studies at the electrode-tissue interface: filter properties of the monophasic action potential (Ag/AgCl) electrode in living rat heart. Pacing Clin Electrophysiol. 2000;23:386–394[CrossRef][Medline]
4. Delmar M, Michaels DC, Johnson T, Jalife J. Effects of increasing intercellular resistance on transverse and longitudinal propagation in sheep epicardial muscle. Circ Res. 1987;60:780–785[Abstract/Free Full Text]
5. Bolli R, Marban E. Molecular and cellular mechanisms of myocardial stunning. Physiol Rev. 1999;79:609–634[Abstract/Free Full Text]
6. Ovadia M, Brink PR. Channels, ischemia and stunning: cellular electrophysiology and intercellular communication. Dilsizian V. Myocardial Viability: A Clinical and Scientific Treatise. Mt. Kisco, NY: Futura; 2000. p. 115–179
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