CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Hiroshi Ashikaga, MD, PhD*,
Elliot R. McVeigh, PhD and
Jeffrey H. Omens, PhD
* Laboratory of Cardiac Energetics, National Heart, Lung, and Blood Institute, 10 Center Drive, Building 10/B1D416, Bethesda, Maryland 20892 (Email: ha8000{at}gmail.com).
Our recent article (1) reported a new observation that there is discrepancy between cardiac electrical and mechanical behaviors by detecting relatively large mechanical dispersion with little electrical dispersion during both activation and relaxation in the canine mid-anterior left ventricle (LV). In his letter, Dr. Karagueuzian logically and correctly points out the potential contribution of transmural difference in intracellular calcium handling (2) to the transmural mechanical gradients that we had described in the article. Given a slower decay of intracellular calcium to diastolic levels at the endocardium, due in part to significantly lower levels of sarcoplasmic reticulum Ca2+ ATPase (SERCA2a) expression in endocardial cells than epicardial cells, the transmural differences in calcium handling likely contribute to the transmural dispersion of myofiber relaxation and should be added to the list of potential contributing factors, such as transmural dispersion of electrical repolarization, even if it is small at physiological heart rates, and tissue tethering. However, this does not seem to be the case with the transmural dispersion of myofiber shortening. Transmural differences in intracellular calcium during activation, where endocardial cells have a slower time to peak than epicardial cells, result in an earlier onset of myofiber shortening in the epicardium than in the endocardium by approximately 20 ms (3). This delay is close to the transmural conduction delay in the canine LV (1,4), thus allowing the impulse to traverse the LV wall to synchronize contraction across the ventricular myocardium; that is, the transmural differences in calcium handling do not contribute to but rather "negate" the transmural dispersion of myofiber shortening due to the delay in action potential propagation across the wall. Therefore, the transmural dispersion of myofiber shortening should be accounted for by other factors, including tethering.
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References
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- 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]
- 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]
- Cordeiro JM, Greene L, Heilmann C, Antzelevitch D, Antzelevitch C. Transmural heterogeneity of calcium activity and mechanical function in the canine left ventricle Am J Physiol Heart Circ Physiol 2004;286:H1471-H1479.[Abstract/Free Full Text]
- Yan GX, Shimizu W, Antzelevitch C. Characteristics and distribution of M cells in arterially perfused canine left ventricular wedge preparations Circulation 1998;98:1921-1927.[Abstract/Free Full Text]
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