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Karlon, William J., Andrew D. McCulloch, James W. Covell, John J. Hunter, and Jeffrey H. Omens. Regional dysfunction correlates with myofiber disarray in transgenic mice with ventricular expression of ras. Am. J. Physiol. Heart Circ. Physiol. 278: H898-H906, 2000.--A hallmark of certain cardiac diseases such as familial hypertrophic cardiomyopathy is focal myofiber disarray. Regional ventricular dysfunction occurs in human subjects with hypertrophic cardiomyopathy; however, no direct evidence exists to correlate regional dysfunction with myofiber disarray. We used a transgenic mouse, which exhibits regional myofiber disarray via ventricular expression of the human oncogene ras, to investigate the relationship between myofiber disarray and septal surface strain. An isolated ejecting mouse heart preparation was used to record deformation of markers on the septal surface and to determine nonhomogeneous septal surface strain maps. Myofiber disarray made in histological tissue sections was correlated with gradients in surface systolic shortening. Significantly smaller maximum principal shortening was associated with disarray located near the right ventricle (RV) septal surface. There was also significantly smaller surface shear strain associated with disarray located either near the RV surface or at the midwall. Because surface shear is a local indicator of torsion, we conclude that myofiber disarray is associated with reduced septal torsion and reduced surface shortening. hypertrophic cardiomyopathy; fiber angle; surface strain; ventricular torsion

Zimmerman, Scott D., William J. Karlon, Jeffrey W. Holmes, Jeffrey H. Omens, and James W. Covell. Structural and mechanical factors influencing infarct scar collagen organization. Am. J. Physiol. Heart Circ. Physiol. 278: H194-H200, 2000.--Although large collagen fibers in myocardial infarct scar are highly organized, little is known about mechanisms controlling this organization. The preexisting extracellular matrix may act as a scaffold along which fibroblasts migrate. Conversely, deformation within the ischemic area could guide fibroblasts so new collagen is oriented to counteract the stretch. To investigate these potential mechanisms, we infarcted three groups of pigs. Group 1 served as infarct controls. Group 2 had the endocardium slit longitudinally to alter local systolic deformation. Group 3 had a plug sectioned from ischemic tissue and rotated 90 [degrees]. The slit altered systolic deformation in the infarcted tissue, changing circumferential strain from expansion to compression and increasing radial strain and shears and the variability of collagen fiber angles but not the mean angle. In the plug pigs, when deformation, matrix orientation, and continuity are altered in the infarct area, the result is complete disarray in the organization of collagen within the infarct scar. cardiac strain; infarct healing; myocardial infarction; collagen fiber angles

Identifies the structural and mechanical factors that controls the organization of collagen fibers in myocardial infarct scar. Fibroblasts in deformed ischemic area; Alterations of systolic deformation in the infarcted issue; Increase in radial strain and shears; Facts about fibroblasts.