Heart failure (HF) is a leading cause of morbidity and mortality, particularly in older adults and patients with multiple metabolic comorbidities. Heart failure with preserved ejection fraction (HFpEF) is a clinical syndrome with multisystem organ dysfunction. Patients with this condition develop HF symptoms as a result of high left ventricular (LV) diastolic pressure in the context of normal or near normal LV ejection fraction (LVEF; ≥50 percent). The challenges in creating and reproducing a robust rodent phenotype that recapitulates the disease's multiple comorbidities explain the presence of various animal models that fail to meet all the HFpEF criteria. Despite numerous animal models showing cardiac hypertrophy and fibrosis, an "ideal" HFpEF mouse model should demonstrate exercise intolerance, cardiac fibrosis, hypertrophy, capillary rarefaction, diastolic dysfunction, and alteration in lung physiology. Several experimental endeavors have focused on the development of myocardial fibrosis (one of the major features of HFpEF) and its treatment aspects. However, other clinical criteria of the HFpEF phenotype have not been investigated or met. Standard animal models lack some of the clinically significant common comorbidities associated with, and could trigger, human HFpEF. In addition to developing the HFpEF model, it is essential to establish and validate noninvasive methods such as echocardiography to accurately demonstrate diastolic dysfunction (a major clinical component of HFpEF). In our characterization of AngII/PE-treated mice, we demonstrate the utility of echocardiographic analysis in displaying diastolic dysfunction and associated LA pathology.