Left atrial function preserves pulmonary circulatory pressure during pacing-tachycardia and contributes to exercise capacity in patients with idiopathic dilated cardiomyopathy in sinus rhythm, whose exercise is limited by dyspnea

The aim of this study was to determine whether left atrial (LA) function contributes to pulmonary circulatory pressure during pacing-tachycardia and exercise capacity in patients with idiopathic dilated cardiomyopathy (DCM). Thirty-two patients with DCM and in sinus rhythm had limited exercise capacity because of dyspnea. The correlation between peak oxygen consumption (<(V)over dot>O-2) and the variables of cardiac function by cardiac catheterization and 2-dimensional, Doppler echocardiography, and plasma neurohumoral factor levels was tested, as was the correlation between non-invasive LA functional parameters and pulmonary circulatory pressure during pacing-tachycardia. A significant correlation was observed between <(V)over dot>O-2 and LA dimension (r=-0.45, p<0.01), the peak velocities of LA appendage empty flow during atrial systole (r=0.63, p<0.0001) and the pulmonary venous forward flow in early ventricular systole (PVS1; r=0.74, p<0.0001), as well as plasma brain natriuretic peptide (BNP) concentrations. The predictable equation to <(V)over dot>O-2 with the multiple regression analysis was : <(V)over dot>O-2=-0.01 BNP+0.21 PVS1+15.4 (r=0.81, p<0.0001). Furthermore, LA functional variables derived from pulmonary venous flow, especially PVS1, but not plasma BNP concentration, were useful for predicting the degree of the increase in pulmonary circulatory pressure during pacing-tachycardia. Therefore, it is suggested that LA function contributes to exercise capacity through its influence on pulmonary hemodynamic reserve in patients with DCM with sinus rhythm whose exercise is limited by dyspnea.