Mouse model of post-infarct ventricular rupture: time course, strain- and gender-dependency, tensile strength, and histopathology.
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.


CONCLUSIONS
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.
Gao
Xiao-Ming
XM
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.
Xu
Qi
Q
Kiriazis
Helen
H
Dart
Anthony M
AM
Du
Xiao-Jun
XJ
D000818:Animals; D005260:Female; D005783:Gender Identity; D006342:Heart Rupture, Post-Infarction / Q000473:pathology*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D023421:Models, Animal; D009203:Myocardial Infarction / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D013045:Species Specificity; D013718:Tensile Strength