Table 1.

Echocardiographic and hemodynamic changes in animal models of aortic valve sclerosis and stenosis.

Species/Strain	DietREF	Histopathological changes in aortic valve	Hemodynamically significant stenosis?
Mice
C57BL/6	HF16	Lipid deposition Modest calcification	No
ApoE−/−	Chow15	Lipid deposition Calcification Monocyte/Inflammatory cell infiltration	<2%
	HF/HC19, 33	Lipid deposition Fibrosis19, 33 Calcification19, 33 Monocyte/Inflammatory cell infiltration19, 33	<2%
Ldlr−/−	HF/HC16, 223	Lipid deposition Calcification Monocyte/Inflammatory cell infiltration	No
Ldlr−/−/apoB100/100	Chow14	Lipid deposition Calcification Monocyte/Inflammatory cell infiltration Myofibroblast activation	Yes, ~30% of mice
	HF/HC12, 13	Lipid deposition Calcification Fibrosis Monocyte/Inflammatory cell infiltration Myofibroblast activation	Yes, >50% of mice
EGFRWa2/Wa2	Chow11	Fibrosis Calcification Inflammatory cell infiltration	Yes, but background strain dependent
eNOS−/−	Chow224	Bicuspid aortic valves in ~40% of mice	Not known
Notch1+/−	HF/HC125, 126	Calcification	No
Periostin−/−	Chow225	Calcification Fibrosis	Not known
	HF/HC226	Reduced valve thickening and fibrosis	No
MGP−/−	Chow122	Calcification	Not known
Chm1−/−	Chow227	Neoangiogenesis Lipid deposition Calcification	Not known
Rabbits
New Zealand	HF/HC49, 79, 89, 209, 228–238	Lipid deposition	<10%
White		Calcification Inflammatory cell infiltration	Mostly moderate sclerosis
	Chow +	Fibrosis	<10%
	HTN229	Inflammation
Watanabe	HF/HC49	Lipid deposition Fibrosis Calcification Inflammatory cell infiltration	No
Pigs
Yorkshire Landrace	HF/HC83, 239	Lipid deposition	No