Assessing atrial mechanical remodeling and its consequences.

The principal function of the left atrium is to modulate left ventricular (LV) filling and cardiovascular performance through reservoir, conduit, and booster pump functions; the latter is often (mistakenly) regarded synonymously with atrial function, and in contrast to the reservoir and conduit phases, has been studied extensively. Typically, the importance of atrial contraction has been estimated by measurements of cardiac output and end-diastolic volumes both with and without effective atrial systole, by relative LV filling using Doppler transmitral velocimetry (E/A ratios) or radionuclide angiography, or by atrial shortening using 2D echocardiography, angiography, and sonomicrometry. Despite considerable investigation, the magnitude and relative importance of the atrial contribution to LV filling and cardiac output remain controversial and provide motivation for a more complete evaluation of the atrial cycle. In this regard, nearly half of the LV stroke volume and its associated energy is stored in the left atrium during ventricular systole, which acts as a ventricular restoring force during the ensuing ventricular diastole.1 This reservoir function of the left atrium is governed by atrial compliance, which is most rigorously measured by mathematically fitting atrial pressure and volume data during ventricular systole. A number of studies have shown, however, that the proportion of left atrial inflow during ventricular systole with Doppler pulmonary venous flow (ie, S/D ratios) can estimate relative reservoir function. Thus, we showed that an isolated change in left atrial compliance alters predictably reservoir function and the pattern of pulmonary venous flow.2 Decreased atrial compliance is associated with greater phasic atrial pressures but a lower mean level of atrial pressure during ventricular filling, and as a result, a smaller end-diastolic volume and decreased venous return.3 In contrast, increased atrial compliance increases early LV filling and atrial systolic shortening.4