Epidemiological and experimental studies have documented both the rising burden of diastolic heart failure (DHF) and several mechanisms that distinguish this disease from systolic heart failure (SHF). Controversies continue to surround the term 'DHF' as well as its existence as a pathophysiological entity distinct from SHF. Approximately half of all patients who present with heart failure have near-normal systolic function and predominately abnormal diastolic function. Recent reports counter the commonly held belief that survival of patients with DHF is better than that of patients with SHF. The challenges associated with managing the DHF phenotype arise from the heterogeneous etiologies of the condition that include aging, diabetes mellitus, hypertension and ischemia. Lack of diastolic distensibility in DHF has been attributed primarily to hypertrophy and fibrosis. Extracellular matrix and cytoskeletal components including matrix metalloproteinases, titin isoforms, and the quality and quantity of collagen are implicated in DHF development. Impaired active relaxation of the contractile apparatus also contributes to DHF. Novel therapeutic targets that address the pathophysiology of this disease are being actively explored, although as yet there are no proven therapies for DHF. New epidemiologic and mechanistic data regarding DHF highlight the urgency with which the scientific community must address this important public health problem.