Enhanced Conduit Flow Compensates for the Reduction in Left Atrial Passive and Booster Functions in Advanced Diastolic Dysfunction

Abstract

AbstractBackgroundQuantification of left atrial (LA) conduit function and its contribution to left ventricular (LV) filling is challenging because it requires simultaneous measurements of both LA and LV volumes. The functional relationship between LA conduit function and the severity diastolic dysfunction remains controversial. We studied the role of LA conduit function in maintaining LV filling in advanced diastolic dysfunction.MethodsWe performed volumetric and flow analyses of LA function across the spectrum of LV diastolic dysfunction, derived from a set of consecutive patients undergoing multiphasic cardiac CT scanning (n=489). From LA and LV time-volume curves we calculated 3 volumetric components: 1) early “passive” emptying volume; 2) late “active” (booster) volume; and 3) conduit volume. Results were prospectively validated on a group of patients with severe aortic stenosis (n=110).ResultsThe early passive filling progressively decreased with worsening diastolic function (P<0.0001). The atrial booster contribution to stroke volume (SV) modestly increases in impaired relaxation (P<0.05) and declined with more advanced diastolic function (P<0.001), thus failing to compensate for the reduction in early filling. The conduit volume increased progressively (P<0.0001), accounting for 75% of SV (IQR 63–81%) with restrictive filling pattern, compensating for the reduction in both early and booster functions. Similar results were obtained in patients with severe aortic stenosis. The pulmonary artery systolic pressure increased in a near-linear fashion when the conduit contribution to SV increased above 60%. Maximal conduit flow rate strongly correlated with mitral E-wave velocity (r=0.71,P<0.0001), indicating that the increase in mitral E-wave in diastolic dysfunction represents the increased conduit flow.ConclusionAn increase in conduit volume contribution to SV represents a compensatory mechanism to maintain LV filling in advanced diastolic dysfunction. The increase in conduit volume despite increasing LV diastolic pressures is accomplished by an increase in pulmonary venous pressure.