Advances in Cardiovascular Imaging Established and Novel Clinical Applications of Diastolic Function Assessment by Echocardiography

A cardiac cycle consists of systolic (contraction) and diastolic (relaxation and filling) phases that are linked closely together for optimal function of the heart. Normal diastolic function allows adequate filling of the heart without an excessive increase in diastolic filling pressure both in the resting state and with stress or exertion.1 The diastolic phase is remarkably well designed to ensure that the ventricle is optimally filled for a given clinical condition.2 Basically, at the end of systole, left ventricular (LV) relaxation begins as an initial diastolic process, and LV pressure falls rapidly as the LV expands. This relaxation phase is accompanied by active movement of the mitral annulus away from the apex. The velocity of LV dilatation and mitral annular movement during early diastole correlates well with how fast the LV fills and relaxes, respectively.3,4 Myocardial relaxation continues during early diastole to reach the minimal LV diastolic pressure, which helps with “sucking” or “pulling” the blood actively into the LV (Figure 1, online-only Data Supplement Video 1A). The minimal LV diastolic pressure or completion of relaxation normally occurs by 3.5 times the value of tau—the time constant of relaxation (normal 45 ms)—after the mitral opening.5 LV pressure then rises to be equilibrated with left atrial (LA) pressure, at which time the early diastolic filling decelerates to close the mitral valve until the time of atrial contraction when LA pressure increases to initiate the late filling to complete diastole (Figure 1, online-only Data Supplement Video 1B). In the healthy young heart, early diastole is responsible for the majority of ventricular filling, providing a good diastolic reserve. As myocardial relaxation becomes less active with aging or abnormally delayed due to a disease process, the rate of LV pressure decline during the early diastole is reduced, and it takes a longer time to reach the minimal LV diastolic pressure. The rate of LV dilatation during early diastole is reduced, and both elongation of the LV and mitral annular motion are reduced (Figure 1), resulting in reduced diastolic filling and a longer time to reach equilibration of LV-LA pressure. Under this circumstance, atrial contraction is responsible for a substantial proportion of diastolic filling. As long as all the necessary filling can be completed through this mechanism with intact atrial contraction and an adequate diastolic filling period, the mean LA pressure remains normal, although it may be increased at the end of diastole if LA compliance is decreased. A major problem with delayed relaxation, however, is a reduced diastolic reserve. Healthy individuals with normal relaxation are able to increase the rate of myocardial relaxation when there is a need for increased diastolic filling. Faster relaxation allows the achievement of a lower minimal LV diastolic pressure at a shorter time interval than in the resting state. Hence, increased LV filling can occur even with a shortened diastolic filling time. When myocardial relaxation is reduced in the resting state, it cannot be increased as much as necessary to meet the demands of exertion or stress. In this situation with abnormal myocardial relaxation, a reduced diastolic filling period and a lack of atrial contraction compromise LV filling substantially, causing the increase in LA and LV diastolic pressures (hence, decreased diastolic reserve). As LA pressure increases, the early diastolic filling becomes more dominant despite the impaired myocardial relaxation. Early filling is initiated by the increased LA pressure (by “pushing” as illustrated in Figure 1), and myocardial relaxation actually starts after the opening of the mitral valve.2 After initial filling, which increases LV diastolic pressure, delayed myocardial relaxation may lower LV pressure during mid-diastole causing the mid-diastolic filling (L wave) followed by late filling with atrial contraction6,7 (Figure 2). Although the L wave can occur in healthy, well-conditioned individuals with bradycardia, its peak velocity usually is 20 cm/s in that setting. As diastolic function worsens, LA pressure is elevated and myocardial relaxation is impaired at rest, clinically manifesting as heart failure. In this stage, most of the diastolic filling that occurs during early diastole and LA contraction may not be able to contribute substantially to LV filling because of the increased LV diastolic pressure. In these patients, LA contraction pushes blood back into the pulmonary veins, especially if pulmonary venous diastolic forward flow is already completed at the time of atrial contraction. Various patterns of diastolic dysfunction can occur with normal as well as abnormal ejection fractions. It has been