Heart failure with preserved ejection fraction (HFpEF) is emerging as a metabolic disease. HFpEF initiation and progression is associated with the pro-inflammatory state found in conditions such as hypertension, obesity and diabetes. Although the role of dietary fat in the genesis of metabolic disorders and tissue inflammation has been characterised, dietary fat induced cardiac pathology and inflammation in the context of pressure-overload is less well defined. In this study, we reveal the cardioprotective effects of saturated fat intake on cardiac phenotype and cardiac inflammation in an established rat model of hypertension. Ten week old male normotensive Wistar (WKY), control rats (n=10), and matched SHR (n=20), were split into low-10%kcal and high-45%kcal fat chow. After 16 wks of diet intake, bodyweight profiles were similar among all groups (p=NS). Unconscious tail-cuff plethysmography confirmed elevated arterial pressure (>140mmHg) in both SHR dietary groups, (SBP in 45%kcal; 154.4 ± 21.7 mmHg, p<0.05 and 10%kcal; 151.4 ± 31.5 mmHg, p<NS). Endpoint echocardiography revealed increased LVMi (normalised: tibia length) in 10%kcal, which was ameliorated in 45%kcal (respectively; 24.7 ± 2.2 mg/mm vs. WKY, p<0.05 and 22.5 ± 1.3 mg/mm, vs. WKY, p=NS). Furthermore, anterior wall thickness in both systole and diastole was greater in 10%kcal fed animals (p<0.01 vs. WKY). Left ventricular remodelling was exaggerated in 10%kcal vs. 45%kcal, with significant increases in cardiomyocyte cross-sectional area and collagen deposition (vs. WKY control). In SHR groups, cardiac CD68 + macrophage infiltration was increased (10%kcal; 122.5 cells/mm 2 , & 45%kcal; 151.1 cells/mm 2 , p<0.05 vs. WKY). Alterations in markers of metabolic dysfunction was evident with increased total cholesterol (10%kcal, 21.7 ± 0.52 mg/dL, p<0.01 vs. WKY and 45%kcal; 22.01 ± 0.83 mg/dL, p<0.001 vs. WKY), and glycated hemoglobin (HbA1c) in high-fat fed rats vs. 10%kcal control (p<0.05). In summary, dietary fat intake may prevent heart failure development, despite cardiac inflammation and dysfunctional metabolism. Collectively, our data show long-term saturated fat intake attenuates pathological cardiac fibrosis and hypertrophy in a rat model of chronic pressure-overload.