Role of conduit volume as a compensatory mechanism to left atrial dysfunction in severe aortic stenosis

Abstract

Abstract Background Left atrial (LA) function has a central role in maintaining optimal cardiac output despite impaired left ventricular (LV) diastolic function through atrial reservoir, conduit and contractile functions. In normal subjects, the contribution of LA volume (conduit and contractile) to LV filling volume is approximately 60–70% and the rest is completed by the conduit volume (CV) defined as the blood flow from pulmonary veins to LV during passive emptying that does not produce change in atrial volume. As LV filling pressures progressively increase, the limits of preload reserve are reached and LA serves predominantly as a conduit with increase in CV. Severe aortic stenosis is characterized by diastolic dysfunction (DD) in early stages of the disease and LA dysfunction in more advanced stages. Purpose The aim of the study was to analyze the role of CV as a compensatory mechanism to complete LV filling volume in presence of atrial dysfunction. Methods 210 patients (p) (age 69±11 years, 48% female) with severe aortic stenosis (aortic valve area index 0.37±0.12 cm2/m2) were studied with Doppler echocardiography. LA function were evaluated by LA (total) emptying fraction (LAEF) as the difference between maximum (Mx) (include conduit and contractile phases) and minimum (Mn) volumes/Mx volume x 100 and peak LA strain. The contribution of CV to SV was estimated as a percentage of SV (CV%): SV − (LA Mx − Mn volume)/SV x 100. LA volumes, SV and left ventricular ejection fraction (LVEF) were calculated by Simpson method. Grade of DD was classified according to ASE/EACVI recommendation and p were divided in 3 groups: DD grade I (98 p), DD grade II (74 p) and DD grade III (38 p). Results CV% were negatively related to LAEF (r=−0.57, p<0.0001) and peak LA strain (r=−0.38, p<0.001) and directly to the grade of DD (r=0.35, p<0.001). LVEF correlated with LAEF (r=0.57, p<0.0001) and CV% (r=−033, p<0.001). In group DD grade III SV was maintained by increase in CV% despite significant decrease in LAEF and peak LA strain. Conclusion LA dysfunction expressed as a decreased in LAEF and LA strain correlated with an increase in contribution of CV to SV (CV%). In patients with AS, as the DD progress, SV is maintained by increase in CV as a compensatory mechanism to LA dysfunction. Funding Acknowledgement Type of funding sources: None. Table