The mystery of diastolic heart failure (DHF), described by authorities as a "puzzle" and a "clinical paradox," stems from the following misperception: (1) that the normal ejection fraction implies normal cardiac output (CO), (2) that therefore low CO is not operative (it is rarely mentioned in relation to the pathophysiology of DHF), and (3) the congestive phenomena are due to the stiff left ventricle. In fact, a normal ejection fraction is not a reliable indicator of normal CO; low CO is the fundamental pathophysiologic abnormality of all heart failure (HF), whether systolic and/or diastolic (or, indeed, "high output"); and increased ventricular stiffness is not the principal cause of congestion in DHF. Pathophysiologic explorations supporting these understandings further reveal the following: (1) the premise that a clinical event as dramatic as acute pulmonary edema (systolic and/or diastolic) would be contingent on similarly dramatic acute hypertensive or ischemic ventricular dysfunction, while intuitive, is unsubstantiated, and there is an alternate explanation satisfying both theoretical and clinical observations; (2) contrary to general perception, DHF is no more vulnerable to diuretic-induced hypotension than systolic HF; (3) heart rate reduction should not yet be considered an established therapeutic goal in DHF; (4) since HF is HF whether systolic and/or diastolic, studies are likely to show that therapeutic similarities outweigh differences except as the various agents might modify the underlying structural and/or functional pathology; (5) although long evident that HF occurs by only two mechanisms (systolic dysfunction and/or diastolic dysfunction), it has only recently been acknowledged that the mere exclusion of one is diagnostic of the other; and (6) the definition of HF currently in widespread use is unnecessarily confounded by neglect of the fundamental distinction between ventricular dysfunction and failure.