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Reversible left atrial dysfunction possibly due to afterload mismatch in patients with left ventricular dysfunction.

作者信息

Ito T, Suwa M, Kobashi A, Yagi H, Hirota Y, Kawamura K

机构信息

Department of Internal Medicine, Osaka Medical College, Takatsuki.

出版信息

J Am Soc Echocardiogr. 1998 Mar;11(3):274-9. doi: 10.1016/s0894-7317(98)70089-6.

Abstract

Limited data are available concerning the influence of altered loading conditions on left atrial (LA) function. In addition, the underlying mechanism of the augmentation of atrial filling (A) velocity (assessed by transmitral Doppler measurement) after treatment of heart failure has been less studied. Therefore, we examined various indexes of LA function during the depression of left ventricular (LV) filling pressure resulting from treatment of heart failure. Twelve patients with LV dysfunction (ejection fraction < 50%) underwent right heart catheterization and transthoracic echocardiography before and after optimal treatment of heart failure. LV/LA volume and ejection fraction and mitral and pulmonary venous flow velocities were measured. LV stiffness (substitute for LA afterload) was assessed by the ratio of LV filling pressure to LV end-diastolic volume. After treatment of heart failure, the mitral A velocity significantly increased (38 +/- 9 to 58 +/- 16 cm/sec, p < 0.005) and there was a distinct attenuation of the difference of the pulmonary venous and mitral A-wave duration (43 +/- 29 to -8 +/- 31 msec, p < 0.005). These findings were associated with a marked decrease in LV stiffness (0.12 +/- 0.04 to 0.05 +/- 0.02 mm Hg/ml, p = 0.0001) and an increase in LA ejection fraction (27% +/- 7% to 38% +/- 8%, p < 0.005). There was a significant curvilinear relation between LA ejection fraction and LV stiffness (r = 0.63, p < 0.01). The mitral A velocity correlated positively with LA ejection fraction (r = 0.77, p < 0.0001) and inversely with LV stiffness (r = -0.52, p < 0.01). The reversible LA dysfunction suggests that the initial LA dysfunction is due to LA afterload mismatch rather than intrinsic LA disease, which also contributes to the augmentation of the mitral A velocity after heart failure treatment.

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