Myocyte injury along myofibers in left ventricular remodeling after myocardial infarction.

Abstract

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 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.