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Infarct rupture and cardiac remodeling after myocardial infarction in 5 different mouse strains
Author(s) -
Janssen Ben,
Borne Susanne,
BrounsStrzelecka Agnieszka,
Hermans Rob,
Blankesteijn Matthijs
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.793.15
Subject(s) - myocardial infarction , medicine , cardiology , cardiac rupture , myofibroblast , cardiac function curve , infarction , heart failure , ejection fraction , fibrosis
Background Transgenic mouse models are used extensively to study the process of infarct healing. However, genetic background may affect the outcome of such studies. Methods We compared in 5 different mouse strains (BalbC, C57Bl6, FVB, 129S6 and Swiss) the process of infarct healing after myocardial infarction (MI). Cardiac dimensions were monitored by echocardiography and histology. Cardiac function was determined by intraventricular pressure measurements. Results The area at risk was not different between mouse strains. Infarct rupture, which occurred 3‐6 days post‐MI, was most frequent in 129S6 (62%), followed by C57Bl6 (31%), FVB (24%), Swiss (15%) and FVB (3%). This frequency correlated strongly with systolic pressures at 3 days post‐MI, number of inflammatory cells and MMP‐9 activity. Acute heart failure was observed in 25% of FVB mice in the first week after MI, but was rare in other groups. Cardiac dilatation was most marked in Swiss mice and least prominent in surviving 129S6. The dilatation correlated positively with dP/dt values at 14 and 28 days post‐MI. Secondary thinning of the infarct area between 14 and 28 days post‐MI was marked in BalbC (385±55 to 262±26 μm), FVB (480±128 to 300±49 μm) and Swiss (498±135 to 333±72 μm, all P<0.05), but absent in C57Bl6 (409±55 to 402±32 μm) and 129S6 (517±103 to 484±47 µm). This was paralleled by the highest amounts of alpha‐smooth muscle actin positive fibroblasts, so‐called myofibroblasts, in the latter two groups. Conclusions Infarct healing in mice strongly depends on genetic background. For studies on the prevention of infarct rupture, 129S6 is the background of choice, whereas BalbC, FVB and Swiss are best suited to study infarct dilatation. The amount of myofibroblasts at 14 days post‐MI predicts the secondary dilatation of the infarct.