Septal-lateral annnular cinching perturbs basal left ventricular transmural strains

Tom C. Nguyen, Allen Cheng, Frederick (Fred) Tibayan, David Liang, George T. Daughters, Neil B. Ingels, David Craig Miller

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

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 (Xf, Xs, Xn) oriented along the fiber (f), sheet (s), and sheet-normal (n) axes using fiber (α) and sheet (β) 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.

Original languageEnglish (US)
Pages (from-to)423-429
Number of pages7
JournalEuropean Journal of Cardio-thoracic Surgery
Volume31
Issue number3
DOIs
StatePublished - Mar 2007
Externally publishedYes

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Diastole
Mitral Valve Insufficiency
Systole
Pericardium
Sheep
Thorax
Therapeutics

Keywords

  • Ischemic mitral regurgitation
  • Mitral annuloplasty
  • Mitral regurgitation
  • Myocardial ischemia
  • Myocardial strain
  • Surgery

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Septal-lateral annnular cinching perturbs basal left ventricular transmural strains. / Nguyen, Tom C.; Cheng, Allen; Tibayan, Frederick (Fred); Liang, David; Daughters, George T.; Ingels, Neil B.; Miller, David Craig.

In: European Journal of Cardio-thoracic Surgery, Vol. 31, No. 3, 03.2007, p. 423-429.

Research output: Contribution to journalArticle

Nguyen, Tom C. ; Cheng, Allen ; Tibayan, Frederick (Fred) ; Liang, David ; Daughters, George T. ; Ingels, Neil B. ; Miller, David Craig. / Septal-lateral annnular cinching perturbs basal left ventricular transmural strains. In: European Journal of Cardio-thoracic Surgery. 2007 ; Vol. 31, No. 3. pp. 423-429.
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title = "Septal-lateral annnular cinching perturbs basal left ventricular transmural strains",
abstract = "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{\circledR}, 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 (Xf, Xs, Xn) oriented along the fiber (f), sheet (s), and sheet-normal (n) axes using fiber (α) and sheet (β) 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.",
keywords = "Ischemic mitral regurgitation, Mitral annuloplasty, Mitral regurgitation, Myocardial ischemia, Myocardial strain, Surgery",
author = "Nguyen, {Tom C.} and Allen Cheng and Tibayan, {Frederick (Fred)} and David Liang and Daughters, {George T.} and Ingels, {Neil B.} and Miller, {David Craig}",
year = "2007",
month = "3",
doi = "10.1016/j.ejcts.2006.12.019",
language = "English (US)",
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pages = "423--429",
journal = "European Journal of Cardio-thoracic Surgery",
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TY - JOUR

T1 - Septal-lateral annnular cinching perturbs basal left ventricular transmural strains

AU - Nguyen, Tom C.

AU - Cheng, Allen

AU - Tibayan, Frederick (Fred)

AU - Liang, David

AU - Daughters, George T.

AU - Ingels, Neil B.

AU - Miller, David Craig

PY - 2007/3

Y1 - 2007/3

N2 - 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 (Xf, Xs, Xn) oriented along the fiber (f), sheet (s), and sheet-normal (n) axes using fiber (α) and sheet (β) 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.

AB - 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 (Xf, Xs, Xn) oriented along the fiber (f), sheet (s), and sheet-normal (n) axes using fiber (α) and sheet (β) 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.

KW - Ischemic mitral regurgitation

KW - Mitral annuloplasty

KW - Mitral regurgitation

KW - Myocardial ischemia

KW - Myocardial strain

KW - Surgery

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