Diastolic heart failure (DHF) is an important entity, the significance of which is increasingly recognized. This report examines the available evidence regarding the role, significance, and mechanisms of DHF. Epidemiologic studies have documented the rising burden of DHF, and experimental data are revealing the unique mechanisms distinguishing it from systolic heart failure. Despite controversies on the definition of DHF, or heart failure with preserved ejection fraction, standardized clinical criteria with supplementary imaging and structural data have identified DHF as a distinct pathophysiological entity. The mechanisms underlying DHF include abnormal matrix dynamics, altered myocyte cytoskeleton, and impaired active relaxation. The commonly held belief that survival of patients with DHF is better than that of patients with systolic heart failure has been challenged by updated data. The heterogeneous etiologies or risk factors for the condition include aging, diabetes, hypertension, and ischemia, making a common diagnostic or treatment pathway difficult. Novel therapeutic targets that address the pathophysiology of this disease are under consideration, although there are no proven therapies for DHF to date. Exacerbating factors include volume and sodium indiscretion, arrhythmias, ischemia, and comorbidities. Strategies to ameliorate or to obviate these precipitating factors are most effective in preventing DHF and its exacerbations. Meanwhile, prevention of DHF through appropriate and aggressive risk factor identification and management must remain the cornerstone of clinical intervention.