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J Thorac Cardiovasc Surg 2005;129:791-803
© 2005 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Alterations in transmural strains adjacent to ischemic myocardium during acute midcircumflex occlusion

^a Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, Calif
^b Laboratory of Cardiovascular Physiology and Biophysics, Palo Alto Medical Foundation Research Institute, Palo Alto, Calif
^c Department of Biomedical Engineering, Texas A&M University, College Station, Tex

Read at the Eighty-fourth Annual Meeting of The American Association for Thoracic Surgery, Toronto, Ontario, Canada, April 25–28, 2004.

Received for publication May 11, 2004; revisions received September 29, 2004; accepted for publication November 12, 2004.

^_* Address for reprints: D. Craig Miller, MD, Department of Cardiothoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247 (E-mail: dcm{at}stanford.edu).

OBJECTIVE: Helically oriented left ventricular fibers assemble into transmural sheets, which are important for wall-thickening mechanics: 15% fiber shortening results in 40% cross-fiber left ventricular wall thickening and a 60% ejection fraction through sheet extension, thickening, and shear. Normal cardiac microstructure and strains are optimized; deviations could result in apoptosis and deleterious matrix remodeling, which degenerates into global cardiomyopathy. We studied alterations in transmural strains adjacent to ischemic myocardium during acute midcircumflex occlusion.

METHODS: Nine sheep had radiopaque markers implanted to measure left ventricular systolic fractional area shortening; 3 transmural bead columns were inserted into the midlateral wall for strain analysis. Three-dimensional marker coordinates were obtained with biplane videofluoroscopy before and during 70 seconds of ischemia. Systolic strains were quantified along circumferential, longitudinal, and radial axes (n = 9) and were transformed into fiber-sheet coordinates by using quantitative microstructural measurements (n = 5).

RESULTS: A functional border was defined in the midlateral left ventricle; ischemia decreased posterolateral fractional area shortening, and anterolateral fractional area shortening increased. In this demarcation junction, subepicardial end-systolic radial wall thickening decreased (0.16 ± 0.08 vs 0.11 ± 0.06) and sheet-normal shear was abolished (0.08 ± 0.04 vs –0.01 ± 0.03). Longitudinal shortening decreased in the subepicardium and midwall (–0.05 ± 0.04 vs ± –0.01 ± 0.06), but circumferential-radial shear increased at these depths (0.04 ± 0.04 vs 0.11 ± 0.05). Subendocardial fiber stretch occurred during early systole (–0.01 ± 0.03 vs 0.02 ± 0.03), and end-systolic fiber-sheet shear increased (0.07 ± 0.01 vs 0.11 ± 0.04, all P < .05).

CONCLUSIONS: Increased circumferential-radial shear and altered fiber-sheet strains reflect mechanical interactions between ischemic and nonischemic myocardium, which might be important in triggering remodeling processes that evolve into global ischemic cardiomyopathy.

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