Septal-lateral annnular cinching perturbs basal left ventricular transmural strains.
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 (alpha) and sheet (beta) angle measurements.


RESULTS
SLAC markedly reduced (approximately 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.
Nguyen
Tom C
TC
Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305-5247, United States.
Cheng
Allen
A
Tibayan
Frederick A
FA
Liang
David
D
Daughters
George T
GT
Ingels
Neil B
NB
Miller
David Craig
DC
D000818:Animals; D001696:Biomechanical Phenomena; D005471:Fluoroscopy; D006339:Heart Rate / Q000502:physiology; D008944:Mitral Valve Insufficiency / Q000503:physiopathology / Q000601:surgery*; D017202:Myocardial Ischemia / Q000503:physiopathology; D011183:Postoperative Complications / Q000503:physiopathology*; D012756:Sheep; D013314:Stress, Mechanical; D013318:Stroke Volume / Q000502:physiology; D013536:Suture Techniques; D018487:Ventricular Dysfunction, Left / Q000209:etiology* / Q000503:physiopathology; D020257:Ventricular Remodeling