Data associated with: AHA grant 20SRG35490443 Cardiac Sarcomere Dysfunction in HFpEF.

Heart failure with preserved ejection fraction (HFpEF) has few effective therapies yet exacts substantial mortality. Its multi-system nature has made animal modeling difficult, but recent efforts combining diet-induced obesity and hemodynamic stress are popular: mouse - L-NAME/high-fat diet (HFD), the ZSF1 rat which combines leptin deficiency with genetic-based diabetes, hypertensive and heart failure phenotypes, and an obese/hypertensive Göttingen minipig. We have reported that human HFpEF myocytes particular from patients who are obese display a profound reduction in systolic Ca2+-activated tension, that is negatively correlated with body mass index (Circulation. 2021;143:965–967). Here we tested whether such deficits are found in these three HFpEF animal models. Of the three models, we only find a change in systolic level calcium activated tension in the Göttingen minipig. The mouse and rat models show results that are superimposable with their respective controls. The data are from permeabilized myocytes obtained from the heart tissue for each model and respective controls. The data file provides the raw data for myocyte cross section area, measured force at fixed sarcomere length (2.1 µ), and then the different calcium concentrations used. (2024-03)