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Three-dimensional alignment of the aggregated myocytes in the normal and hypertrophic murine heart


Schmitt, B; Fedarava, K; Falkenberg, J; Rothaus, K; Bodhey, N K; Reischauer, C; Kozerke, S; Schnackenburg, B; Westermann, D; Lunkenheimer, P P; Anderson, R H; Berger, F; Kuehne, T (2009). Three-dimensional alignment of the aggregated myocytes in the normal and hypertrophic murine heart. Journal of Applied Physiology, 107(3):921-927.

Abstract

Several observations suggest that the transmission of myocardial
forces is influenced in part by the spatial arrangement of the myocytes
aggregated together within ventricular mass. Our aim was to assess,
using diffusion tensor magnetic resonance imaging (DT-MRI), any
differences in the three-dimensional arrangement of these myocytes in
the normal heart compared with the hypertrophic murine myocardium.
We induced ventricular hypertrophy in seven mice by infusion of
angiotensin II through a subcutaneous pump, with seven other mice
serving as controls. DT-MRI of explanted hearts was performed at 3.0
Tesla. We used the primary eigenvector in each voxel to determine the
three-dimensional orientation of aggregated myocytes in respect to
their helical angles and their transmural courses (intruding angles).
Compared with controls, the hypertrophic hearts showed significant
increases in myocardial mass and the outer radius of the left ventricular
chamber (P < 0.05). In both groups, a significant change was
noted from positive intruding angles at the base to negative angles at
the ventricular apex (P < 0.01). Compared with controls, the hypertrophied
hearts had significantly larger intruding angles of the aggregated
myocytes, notably in the apical and basal slices (P < 0.001). In
both groups, the helical angles were greatest in midventricular sections,
albeit with significantly smaller angles in the mice with hypertrophied
myocardium (P < 0.01). The use of DT-MRI revealed
significant differences in helix and intruding angles of the myocytes in
the mice with hypertrophied myocardium.

Several observations suggest that the transmission of myocardial
forces is influenced in part by the spatial arrangement of the myocytes
aggregated together within ventricular mass. Our aim was to assess,
using diffusion tensor magnetic resonance imaging (DT-MRI), any
differences in the three-dimensional arrangement of these myocytes in
the normal heart compared with the hypertrophic murine myocardium.
We induced ventricular hypertrophy in seven mice by infusion of
angiotensin II through a subcutaneous pump, with seven other mice
serving as controls. DT-MRI of explanted hearts was performed at 3.0
Tesla. We used the primary eigenvector in each voxel to determine the
three-dimensional orientation of aggregated myocytes in respect to
their helical angles and their transmural courses (intruding angles).
Compared with controls, the hypertrophic hearts showed significant
increases in myocardial mass and the outer radius of the left ventricular
chamber (P < 0.05). In both groups, a significant change was
noted from positive intruding angles at the base to negative angles at
the ventricular apex (P < 0.01). Compared with controls, the hypertrophied
hearts had significantly larger intruding angles of the aggregated
myocytes, notably in the apical and basal slices (P < 0.001). In
both groups, the helical angles were greatest in midventricular sections,
albeit with significantly smaller angles in the mice with hypertrophied
myocardium (P < 0.01). The use of DT-MRI revealed
significant differences in helix and intruding angles of the myocytes in
the mice with hypertrophied myocardium.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Biomedical Engineering
Dewey Decimal Classification:170 Ethics
610 Medicine & health
Language:English
Date:2009
Deposited On:02 Dec 2009 15:36
Last Modified:05 Apr 2016 13:33
Publisher:American Physiological Society
ISSN:0161-7567
Additional Information:Inhalt ist nach 12 Monaten frei über HighWire Press
Publisher DOI:10.1152/japplphysiol.00275.2009
Permanent URL: http://doi.org/10.5167/uzh-24036

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