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Am J Physiol Heart Circ Physiol. 2008 Jan;294(1):H330-6. Epub 2007 Oct 26.

Principal strain changes precede ventricular wall thinning during transition to heart failure in a mouse model of dilated cardiomyopathy.

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  • 1Department of Physiology and Biophysics, University of Illinois at Chicago College of Medicine, 835 South Wolcott Ave., Chicago, IL 60612, USA.


This study was performed to elucidate the relation between in vivo measurements of two-dimensional principal strains and the progression of left ventricle (LV) wall thinning during development of dilated cardiomyopathy in the protein kinase C-epsilon (PKC-epsilon) transgenic (TG) overexpressing mouse heart. Principal two-dimensional strains, E1 and E2, were determined in the LV wall of the anesthetized mouse using cardiac MRI tagging at 14.1 T. PKC-epsilon TG provided a model of pure dilated cardiomyopathy without evidence of hypertrophy (PKC-epsilon TG, n = 6). Ejection fraction, wall thickness, and principal strains were determined at 1-mo intervals in hearts of PKC-epsilon TG vs. age-matched, nontransgenic mice (NTG, n = 5) from age 6 to 13 mo. Through the study, PKC-epsilon TG displayed lower ejection fraction than NTG. At 7 mo, average principal strain E1 in PKC-epsilon TG hearts was lower compared with NTG (PKC-epsilon TG = 0.14 +/- 0.03, NTG = 0.19 +/- 0.03, P < 0.05). The greatest reductions in regional E1 occurred in the lateral segments. The principal strain E2 did not change significantly in either group. At 9 mo, LV wall thinning occurred in PKC-epsilon TG mice (P < 0.01 vs. 8 mo) to 21% below values in NTG (P < 0.001). Average E1 strain diverged between PKC-epsilon TG and NTG hearts by 25-43%. These E1 changes preceded LV wall thinning and predated the eventual transition from a compensated circumstance to the dilated phenotype. The findings indicate a near step function in E1 depression that precedes the onset of LV wall thinning and suggest E1 as a prognostic indicator of dilated cardiomyopathy.

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