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There is a need for animal models of plaque rupture. We previously reported that elastin fragmentation, due to a mutation (C1039G^+/−) in the fibrillin-1 (Fbn1) gene, promotes atherogenesis and a highly unstable plaque phenotype in apolipoprotein E deficient (ApoE^−/−) mice on a Western-type diet (WD). Here, we investigated whether plaque rupture occurred in ApoE^−/−Fbn1^C1039G+/− mice and was associated with myocardial infarction, stroke, and sudden death.

Female ApoE^−/−Fbn1^C1039G+/− and ApoE^−/− mice were fed a WD for up to 35 weeks. Compared to ApoE^−/− mice, plaques of ApoE^−/−Fbn1^C1039G+/− mice showed a threefold increase in necrotic core size, augmented T-cell infiltration, a decreased collagen I content (70 ± 10%), extensive neovascularization, intraplaque haemorrhage, and a significant increase in matrix …