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. Author manuscript; available in PMC: 2022 Jun 1.
Published in final edited form as: Nat Rev Cardiol. 2021 Jan 11;18(6):400–423. doi: 10.1038/s41569-020-00480-6

Table 1 ∣.

Animal models of HFpEF

Animal Model LVH HTN Obesity
T2DM
Diastolic
Dysfunction
Skeletal
Muscle
Abnl and/or
Exercise
Intolerance
Fluid
overload
>Lung wt
Improved
by
ACE/ARB
Dahl-salt sensitive rats ++ ++ ++ + Not pre-HF +/+
Spontaneously hypertensive rats ++ ++ + + Not pre-HF +/+
ZSF-1 rat + + + + + +
Aortic constriction (mouse, rat) + +/− ND mild +/+
Aldosterone Infusion (mouse, rat) + + ++ ND mild +
Ageing models (e.g. SAM-WD) mouse Mild +/− + + +
L-Name + HFD, mouse + ++ + + + + Not tested
db/db or ob/ob mice + + + + + ND +
Aged dogs subjected to peri-nephritis-induced hypertension + + + ND Not tested
Aortic Banded Cat + ++ ++ ND + +
DOCA and salt loaded pigs on HFD + + + + + ND Not tested

Animal models that focus solely on LV pressure/volume overload such as the Dahl-salt sensitive or spontaneously hypertensive rat, aortic banded cat, or aldosterone infusion – generate principally cardiac disease such as hypertrophy, diastolic dysfunction, and fibrosis. Pure obesity models, such as the leptin or leptin receptor deficient models (db/db or ob/ob) generate marked obseity and some cardiac disease. Other models such as L-NAME+high fat diet (HFD) in mice, or the DOCA-HFD pig model, or the senescence accelerated mouse on western diet (SAM-WD) attempt to integrate both components. The latter two do not develop significant heart failure however, reflected by less increase in diastolic pressure and fluid accumulation in the lungs.