Xiao-Ming Gao1, Qi Xu, Helen Kiriazis, Anthony M Dart, Xiao-Jun Du. 1. Experimental Cardiology Laboratory, Wynn Domain, Baker Medical Heart Research Institute and Alfred Heart Centre, Alfred Hospital, Commercial Road, P.O. Box 6492, Melbourne, Victoria 3004, Australia.
Abstract
OBJECTIVE: Recent studies on mice with surgically induced acute myocardial infarction (AMI) have documented the frequent occurrence of ventricular rupture, an event not previously reported in other laboratory species. We have examined the natural history, histopathology and myocardial mechanical strength in mice with AMI. METHODS: AMI was induced by coronary artery occlusion and animals were monitored for fatal events. Gross and histological examinations were undertaken. RESULTS: Rupture occurred in the left ventricular free wall at 2-6 days after AMI. Incidence of rupture in male mice varied among three strains studied (3% for FVB/N, 27% for C57B/6J, and 59% for 129sv, P<0.05) and was lower in female than male mice (23% vs. 59%, P<0.05). Histologically, ruptured hearts had rapid-occurring and severe infarct expansion, multifocal intramural hemorrhage and leucoyte infiltration at the border zone and infarcted zone. In vitro, infarcted left ventricles demonstrated a 50-60% reduction in muscle tensile strength. This reduction preceded the onset of rupture and was related to the time-window of rupture and to infarct size. CONCLUSION: LV wall rupture in the mouse occurs within a narrow time-window after AMI and is strain- and gender-dependent. Infarct expansion, regional hemorrhage with formation of hematoma and leuocyte accumulation are important pathological changes leading to reduced myocardial tensile strength.
OBJECTIVE: Recent studies on mice with surgically induced acute myocardial infarction (AMI) have documented the frequent occurrence of ventricular rupture, an event not previously reported in other laboratory species. We have examined the natural history, histopathology and myocardial mechanical strength in mice with AMI. METHODS: AMI was induced by coronary artery occlusion and animals were monitored for fatal events. Gross and histological examinations were undertaken. RESULTS:Rupture occurred in the left ventricular free wall at 2-6 days after AMI. Incidence of rupture in male mice varied among three strains studied (3% for FVB/N, 27% for C57B/6J, and 59% for 129sv, P<0.05) and was lower in female than male mice (23% vs. 59%, P<0.05). Histologically, ruptured hearts had rapid-occurring and severe infarct expansion, multifocal intramural hemorrhage and leucoyte infiltration at the border zone and infarcted zone. In vitro, infarcted left ventricles demonstrated a 50-60% reduction in muscle tensile strength. This reduction preceded the onset of rupture and was related to the time-window of rupture and to infarct size. CONCLUSION: LV wall rupture in the mouse occurs within a narrow time-window after AMI and is strain- and gender-dependent. Infarct expansion, regional hemorrhage with formation of hematoma and leuocyte accumulation are important pathological changes leading to reduced myocardial tensile strength.
Authors: David A White; Yidan Su; Peter Kanellakis; Helen Kiriazis; Eric F Morand; Richard Bucala; Anthony M Dart; Xiao-Ming Gao; Xiao-Jun Du Journal: J Mol Cell Cardiol Date: 2014-02-05 Impact factor: 5.000
Authors: Melissa A Wasilewski; Laurel A Grisanti; Jianliang Song; Rhonda L Carter; Ashley A Repas; Valerie D Myers; Erhe Gao; Walter J Koch; Joseph Y Cheung; Arthur M Feldman; Douglas G Tilley Journal: Clin Sci (Lond) Date: 2016-09-02 Impact factor: 6.124
Authors: Mark W M Schellings; Davy Vanhoutte; Melissa Swinnen; Jack P Cleutjens; Jacques Debets; Rick E W van Leeuwen; Jan d'Hooge; Frans Van de Werf; Peter Carmeliet; Yigal M Pinto; E Helene Sage; Stephane Heymans Journal: J Exp Med Date: 2008-12-22 Impact factor: 14.307