Background:

The left atrium (LA) plays a key role in maintaining stroke volume (SV) in the presence of left ventricular (LV) diastolic dysfunction (DD) through its reservoir, conduit and booster pump function. In normal subjects, the contribution of atrial volume (conduit and booster pump function) to the SV is approximately 60-70%, and the rest is completed by the conduit volume (CV), defined as the blood volume that flows from the pulmonary veins to the LV during passive filling, without producing changes in the atrial volume. In LVDD, when ventricular filling pressures increase and the limits of preload reserve are reached, the LA behaves predominantly as a conduit with reduction of the reservoir, conduit, and booster pump function, resulting in increased CV. Severe aortic stenosis (AS) is characterized by DD in the early stages and LA dysfunction in more advanced stages.

Objective:

The aim of the present study was to analyze the role of CV as a compensating mechanism for LA dysfunction to complete LV filling in severe AS.

Methods:

A total of 210 patients (pts.), aged 69 ± 11 years, with 48% if women, with severe AS (aorta aortic valve area index 0.37 ± 0.12 cm2/m2) were assessed using Doppler echocardiography. Left atrial function was assessed though LA emptying fraction (LAEF) as the difference between maximum LA volume (maxLAV), which includes conduction and contraction phases, and minimum LA volume (minLAV)/maxLAV ×100, and peak LA strain. The contribution of CV to stroke volume (SV) was estimated as percentage of SV (CV%): SV - (maxLAV - minLAV) /SV × 100. Left atrial volume, SV and LV ejection fraction (LVEF) were calculated using the Simpson's method. Diastolic dysfunction was staged according to the ASE/EACVI recommendations, and the pts. were divided into 3 groups: DD grade 1 I (98 pts.), DD grade 2 II (74 pts.) and DD grade 3 III (38 pts.).

Results:

The CV% had a negative correlation with LAEF (r = -0.57, p < 0.0001) and peak LA strain (r = - 0.38, p < 0.001), and a positive correlation with DD grade (r = 0.35, p < 0.001). LVEF correlated with LAEF (r = 0.45, p < 0.01) and CV% (r = - 0.33, p < 0.001). In the DD grade III group, the SV was maintained by the increased CV% despite the significant reduction of LAEF and peak LA strain.

Conclusions:

Left atrial dysfunction, expressed as decreased LAEF and peak LA strain, correlates with greater contribution of the CV to the SV (CV%). In patients with severe AS, as DD progresses, the SV is preserved due to increased CV as a compensating mechanism for LA dysfunction.