Alterations in transmural strains adjacent to ischemic myocardium during acute midcircumflex occlusion.
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.
Rodriguez
Filiberto
F
Department of Cardiothoracic Surgery, Stanford University School of Medcine, Stanford, CA 94305-5247, USA.
Langer
Frank
F
Harrington
Katherine B
KB
Cheng
Allen
A
Daughters
George T
GT
Criscione
John C
JC
Ingels
Neil B
NB
Miller
D Craig
DC
D000818:Animals; D001696:Biomechanical Phenomena; D002933:Cineradiography; D004699:Endocardium / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology*; D021621:Imaging, Three-Dimensional; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000502:physiology; D017202:Myocardial Ischemia / Q000503:physiopathology*; D009206:Myocardium / Q000166:cytology; D009210:Myofibrils / Q000502:physiology; D010496:Pericardium / Q000503:physiopathology; D012756:Sheep; D013314:Stress, Mechanical; D013599:Systole / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology; D017725:Ventricular Pressure / Q000502:physiology