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

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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 (VO₂) 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 VO₂ 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 VO₂ with the multiple regression analysis was : VO₂=-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. (Circ J 2002; 66: 937 - 942)