Myocyte injury along myofibers in left ventricular remodeling after myocardial infarction
Yoichiro Kusakari 1,
Chun-Yang Xiao 1,
Nathan Himes 1,
Stuart D. Kinsella 1,
Masaya Takahashi 1,
Anthony Rosenzweig 1,
Takashi Matsui 1*
1 Beth Israel Deaconess Medical Center, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: tmatsui{at}bidmc.harvard.edu.
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Abstract |
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Left ventricular (LV) remodeling following myocardial infarction (MI) is considered to contribute to cardiac dysfunction. Though myofiber organization is a key component of cardiac structure, functional and anatomical features of injured myofiber during LV remodeling have not been fully defined. We investigated myocyte injury after acute MI in a mouse model. Mice were subjected to surgical coronary occlusion/reperfusion by left anterior descending coronary artery (LAD) ligation and examined at 1 week and 4 weeks post-MI. Magnetic resonance imaging (MRI) analysis demonstrated a significant decrease in systolic regional wall thickening (WT) in the border and remote zones at 4 weeks post-MI compared to that at 1 week post-MI (-86% in border zone, p<0.05, and -77% in the remote zone, p<0.05). Histological assays demonstrated that a broad fibrotic scar extended from the initial infarct zone to the remote zone along mid-circumferential myofibers. Of particular note was the fact that no fibrosis was found in longitudinal myofibers in the epi- and endo-myocardium. This pattern of the scar formation coincided with the helical ventricular myocardial band (HVMB) model, introduced by Torrent-Guasp. MRI analysis demonstrated that the extension of the fibrotic scar along the band might account for the progression in cardiac dysfunction during LV remodeling. Keywords: Muscle fibers; Ventricular function; Ventricular remodeling; Animals
