Myocyte injury along myofibers in left ventricular remodeling after myocardial infarction.
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.
Kusakari
Yoichiro
Y
Cardiovascular Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Xiao
Chun-Yang
CY
Himes
Nathan
N
Kinsella
Stuart D
SD
Takahashi
Masaya
M
Rosenzweig
Anthony
A
Matsui
Takashi
T
D000818:Animals; D004195:Disease Models, Animal; D005355:Fibrosis; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology; D019028:Magnetic Resonance Imaging, Cine; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000473:pathology*; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D020257:Ventricular Remodeling