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This Article Full Text Full Text (PDF) All Versions of this Article: 294/1/H330    most recent 01109.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hankiewicz, J. H. Articles by Lewandowski, E. D. Search for Related Content PubMed PubMed Citation Articles by Hankiewicz, J. H. Articles by Lewandowski, E. D.

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

¹Program in Integrative Cardiac Metabolism and ²Center for Cardiovascular Research, University of Illinois at Chicago College of Medicine, Chicago, Illinois

Submitted 24 September 2007 ; accepted in final form 20 October 2007

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- (PKC-) 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- TG provided a model of pure dilated cardiomyopathy without evidence of hypertrophy (PKC- TG, n = 6). Ejection fraction, wall thickness, and principal strains were determined at 1-mo intervals in hearts of PKC- TG vs. age-matched, nontransgenic mice (NTG, n = 5) from age 6 to 13 mo. Through the study, PKC- TG displayed lower ejection fraction than NTG. At 7 mo, average principal strain E1 in PKC- TG hearts was lower compared with NTG (PKC- 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- TG mice (P < 0.01 vs. 8 mo) to 21% below values in NTG (P < 0.001). Average E1 strain diverged between PKC- 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.

protein kinase C; magnetic resonance imaging; ventricular function