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Eur J Cardiothorac Surg 2007;31:423-429. doi:10.1016/j.ejcts.2006.12.019
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

Septal-lateral annnular cinching perturbs basal left ventricular transmural strains

^a Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA, United States
^b Division of Cardiovascular Medicine, Stanford, CA, United States
^c Research Institute of the Palo Alto Medical Foundation, Palo Alto, CA, United States

Received 21 September 2006; received in revised form 4 December 2006; accepted 14 December 2006.

^_* Corresponding author. Address: Department of Cardiothoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247, United States. Tel.: +1 650 725 3826; fax: +1 650 725 3846. (Email: dcm{at}stanford.edu).

Objective: Septal-lateral annular cinching (‘SLAC’) corrects both acute and chronic ischemic mitral regurgitation in animal experiments, which has led to the development of therapeutic surgical and interventional strategies incorporating this concept (e.g., Edwards GeoForm ring, Myocor Coapsys^®, Ample Medical PS³). Changes in left ventricular (LV) transmural cardiac and fiber-sheet strains after SLAC, however, remain unknown. Methods: Eight normal sheep hearts had two triads of transmural radiopaque bead columns inserted adjacent to (anterobasal) and remote from (midlateral equatorial) the mitral annulus. Under acute, open chest conditions, 4D bead coordinates were obtained using videofluoroscopy before and after SLAC. Transmural systolic strains were calculated from bead displacements relative to local circumferential, longitudinal, and radial cardiac axes. Transmural cardiac strains were transformed into fiber-sheet coordinates (X _f, X _s, X _n) oriented along the fiber (f), sheet (s), and sheet-normal (n) axes using fiber () and sheet (ß) angle measurements. Results: SLAC markedly reduced (60%) septal-lateral annular diameter at both end-diastole (ED) (2.5 ± 0.3 to 1.0 ± 0.3 cm, p = 0.001) and end-systole (ES) (2.4 ± 0.4 to 1.0 ± 0.3 cm, p = 0.001). In the LV wall remote from the mitral annulus, transmural systolic strains did not change. In the anterobasal region adjacent to the mitral annulus, ED wall thickness increased (p = 0.01) and systolic wall thickening was less in the epicardial (0.28 ± 0.12 vs 0.20 ± 0.06, p = 0.05) and midwall (0.36 ± 0.24 vs 0.19 ± 0.11, p = 0.04) LV layers. This impaired wall thickening was due to decreased systolic sheet thickening (0.20 ± 0.8 to 0.12 ± 0.07, p = 0.01) and sheet shear (–0.15 ± 0.07 to –0.11 ± 0.04, p = 0.02) in the epicardium and sheet extension (0.21 ± 0.11 to 0.10 ± 0.04, p = 0.03) in the midwall. Transmural systolic and remodeling strains in the lateral midwall (remote from the annulus) were unaffected. Conclusions: Although SLAC is an alluring concept to correct ischemic mitral regurgitation, these data suggest that extreme SLAC adversely effects systolic wall thickening adjacent to the mitral annulus by inhibiting systolic sheet thickening, sheet shear, and sheet extension. Such alterations in LV strains could result in unanticipated deleterious remodeling and warrant further investigation.

Key Words: Mitral regurgitation • Ischemic mitral regurgitation • Mitral annuloplasty • Myocardial ischemia • Surgery • Myocardial strain

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