Pathophysiology of Diastole and Left Ventricular Filling in Humans: Noninvasive Evaluation

Abstract

The relationship between cardiac output and filling volume was first recognized by Starling at the beginning of this century and called“the law of heart”(47). According to this law and to the ventricular pressure-volume curve, the functional evaluation of myocardial performance in the clinical setting was initially based on the assessment of left ventricular (LV) filling pressure alone. A higher-than-normal filling pressure was considered an index of LV dilatation and systolic failure. In 1963 Braunwald and Ross (3) highlighted the limitation of using LV filling pressure as index of systolic dysfunction and reflected on the possible role of an impaired diastolic function as a cause of higher than normal LV diastolic pressure. However, until the 1970s, LV diastolic pressure was used as a surrogate for volume in evaluating systolic function (17). In the following years, it was learned from studies in patients that many factors can affect LV relaxation and filling and that diastolic abnormalities appear early in the course of many cardiac diseases independent of systolic function. Left ventricular pressure-volume loops of diastolic and systolic dysfunction were then well characterized and the pathophysiologic differences highlighted. During the past 10 years, experimental research on left ventricular myocardial function and the increasing possibility of its noninvasive evaluation in clinical setting have lead to a remarkable advance in the understanding of LV diastolic function, filling, and failure in man (8,27,53,54).