Thorac Cardiovasc Surg 2019; 67(S 02): S101-S128
DOI: 10.1055/s-0039-1679076
Oral Presentations
Monday, February 18, 2019
Grundlagenforschung und Genetik
Georg Thieme Verlag KG Stuttgart · New York

A Noninvasive Way to Calculate Myocardial Infarct Size in Rats after Permanent Coronary Artery Ligation Using 4D High-Resolution Cardiac Magnetic Resonance Imaging In Vivo

M. Alkassar
1   Kinderkardiologie, University of Erlangen, Erlangen, Germany
,
S. Dittrich
1   Kinderkardiologie, University of Erlangen, Erlangen, Germany
,
J. Seufert
1   Kinderkardiologie, University of Erlangen, Erlangen, Germany
› Author Affiliations
Further Information

Publication History

Publication Date:
28 January 2019 (online)

Objectives: Permanent coronary artery ligation is a common surgical procedure to mimic coronary artery ischemia and myocardial infarction (MI). However, the size of MI in rats varies from 4 to 65% of left ventricular volume, which makes ongoing experiments quite difficult regarding quantification. We present a fast and reliable method for MI quantification in vivo using 4D high-resolution cardiac resonance tomography (4D CMRT).

Methods: Sprague-Dawley rats were divided into three groups: control (n = 10), sham (n = 10), and MI (n = 10). MI was induced by permanent ligation of the left anterior descending coronary artery.

Two weeks after MI, hemodynamics was assessed using 4D high-resolution CMRT (7T) in vivo. Hearts were extracted afterward, sliced in 3-µm-thick sections using a microtome, stained in Masson–Goldner and reconstructed as a 3D model using the software “Voloom” (microdimensions). MI infarct size was calculated using the Voloom software.

CMRT data were utilized for 3D reconstruction with the software “3D-Slicer.” The infarcted area was analyzed as STL models. Models from CMRT and histology were compared regarding global and regional cardiac parameters and the infarct size was correlated using Pearson’s correlation and plotted in Altmann. Interobserver variability was evaluated.

Results: MI rats present a wide range of infarct sizes, clearly altered active and passive cardiac properties (reduced, paradox movement) and highly increased stiffness in the ischemic area. No significant differences in the calculation of infarct size between 4D-CMRT and histological methods could be shown (correlation r = 0.92, p < 0.01).

Conclusion: Preliminary results point toward a highly precise comparability of CMRT and histological analysis regarding the quantification of infarct size. This noninvasive method could become a considerable supplement for long-term experiments to already access infarct size in vivo and will simplify analysis of induced infarcts in the rat model.