CORRESPONDENCE: LETTER TO THE EDITOR
On the Mechanisms of Transmural Dispersion of Myocardial Mechanics
Hrayr S. Karagueuzian, PhD, FACC*
* Division of Cardiology, Cedars-Sinai Medical Center, David Geffen School of Medicine at UCLA, Los Angeles, California 90048-1804 (Email: karagueuzian{at}cshs.org).
The study by Ashikaga et al. (1) in the February 27, 2007, issue of the Journal demonstrates left ventricular (LV) transmural gradient near the left anterior descending coronary artery (LAD) at the onset of shortening and relaxation of myocardial fibers with transmural bead markers under biplane cineradiography. These anesthetized open-chest dog studies provide novel insight and help for a fuller understanding of what constitutes a normal cardiac electro-mechanical function. Such an understanding could be instrumental in developing optimal goals for therapy (i.e., cardiac resynchronization therapy) after a disease disrupts stability (i.e., heart failure). Of note in this study was the observation that transmural gradients in contraction and relaxation developed in the virtual absence of transmural gradient in electrical repolarization (shown by T-wave analysis of nearby transmural plunge bipolar electrodes). The authors suggest that the depth-dependent (transmural) differences in myocardial mechanics result solely from the complex interactions of myofiber mechanics within and between the layers due to myocardial cell architecture in the bundles ("tissue tethering") (1). Although tethering might influence regional mechanics and cause regional differences in the onset of contraction-relaxation of the LV, the potential role of transmural differences in intracellular calcium ion (Cai
2+) handling in the observed in vivo gradients of mechanics was dismissed (2). It is known that Cai
2+ elevation is associated with the onset of contraction (shortening) and the uptake of Cai
2+ by the sarcoplasmic reticulum (SR) with the onset of relaxation. For example, it has been shown in isolated canine LV wedge preparations near the LAD (same species and same site as in the in vivo studies of Ashikaga et al.) that whereas the onset of the epicardial and endocardial Cai
2+ transients are almost synchronous, the epicardial decline of the Cai
2+ transient (onset of relaxation) precedes the endocardial decline (3). Furthermore, the rate of Cai
2+ uptake by the SR is faster in the epicardium compared with endocardium (3). These effects mimic the in vivo canine observations made by Ashikaga et al. (1). Because the dynamics of Cai
2+ mirror that of contractility, changes in Cai
2+ are considered to be surrogate of myocardial contractility (4). Consequently, we think that the combined tissue tethering and transmural cellular differences in Cai
2+ handling need to be considered simultaneously as possible mechanisms for the in vivo observation of depth-dependent differences in myocardial mechanics in the canine mid-anterior LV.
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References
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1. Ashikaga H, Coppola BA, Hopenfeld B, Leifer ES, McVeigh ER, Omens JH. Transmural dispersion of myofiber mechanics: implications for electrical heterogeneity in vivo J Am Coll Cardiol 2007;49:909-916.[Abstract/Free Full Text]2. Laurita KR, Katra R, Wible B, Wan X, Koo MH. Transmural heterogeneity of calcium handling in canine Circ Res 2003;92:668-675.[Abstract/Free Full Text] 3. Laurita K, Katra R. Delayed after depolarization-mediated triggered activity associated with slow calcium sequestration near the endocardium J Cardiovasc Electrophysiol 2005;16:418-424.[Web of Science][Medline] 4. Eisner DA, Diaz ME, Li Y, O’Neill SC, Trafford AW. Stability and instability of regulation of intracellular calcium Exp Physiol 2005;90:3-12.[Abstract/Free Full Text]
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