Ayaka Kobashi

Influence of altered loading conditions on left atrial appendage function in vivo

This study sought to examine the influence of heart failure treatment on left atrial (LA) appendage function in 10 patients with left ventricular dysfunction. After treatment of heart failure, LA appendage function markedly improved, less dependent on LA and left ventricular functions, which suggests that with altered loading conditions, LA appendage function changes chiefly through its intrinsic contractile property.

Assessment of left atrial appendage function after cardioversion of atrial fibrillation: Relation to left atrial mechanical function

Although several flow patterns in the left atrial appendage have been described, mechanical determinants of its function have not been elucidated in human beings. We attempted to investigate changes in left atrial appendage function after cardioversion of atrial fibrillation and examine the potential relation between appendage function and left atrial mechanical function. Twenty patients without mitral valvular disease underwent transesophageal and transthoracic echocardiography at 24 hours and 1 week after cardioversion of atrial fibrillation. Left atrial appendage function was assessed by the pulsed Doppler measurements of left atrial appendage emptying and filling velocities corresponding to early and late ventricular diastole, respectively. Left atrial mechanical function was evaluated by the transmitral A-wave velocity, percent atrial contribution of the total left ventricular filling (percent atrial filling), and the pulmonary venous A-wave velocity. Left ventricular function was also estimated with conventional M-mode echocardiography. The late appendage emptying and filling velocities markedly increased during 1 week after cardioversion (p < 0.0001, respectively). This finding was associated with an increase in left atrial mechanical function. Changes in the late emptying and filling velocities significantly correlated with changes in the transmitral A-wave velocity (r = 0.59, p < 0.01), percent atrial filling (r = 0.61, p < 0.005), and the pulmonary venous A-wave velocity (r = 0.56, p < 0.05). In contrast, little change was observed in the early emptying and filling velocities. There was no relation between the indexes of left ventricular function and those of appendage function. In conclusion, unless there was an alteration of the loading conditions, left atrial appendage function improved over several days after cardioversion, and its function was related to left atrial mechanical function.

Reversible Left Atrial Dysfunction Possibly Due to Afterload Mismatch in Patients with Left Ventricular Dysfunction

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.

Ratio of pulmonary venous to mitral A velocity is a useful marker for predicting mean pulmonary capillary wedge pressure in patients with left ventricular systolic dysfunction

In patients with an elevated left ventricular filling pressure, the mitral A wave is diminished while the pulmonary venous A wave is augmented because of decreased left ventricular compliance. We examined whether an increase in the ratio of pulmonary venous to mitral A velocity might be a marker for an elevated mean pulmonary capillary wedge pressure. Forty-one patients who had left ventricular systolic dysfunction underwent transthoracic Doppler echocardiography simultaneously or within 24 hours of right heart catheterization. There were 29 men and 12 women 61 +/- 12 (mean +/- SD) years of age. Underlying heart disease was ischemic cardiomyopathy in 27 and nonischemic cardiomyopathy in 14 patients. The same Doppler-hemodynamic study was performed on 8 patients after optimal management of heart failure. The ratio of pulmonary venous to mitral A velocity correlated strongly with mean pulmonary wedge pressure (r = 0.72, P < .0001). When the cutoff value of the ratio was set at 0.5 or higher, the sensitivity for predicting a pulmonary capillary wedge pressure of 15 mm Hg or more was 88%, and the specificity was 80%. The serial Doppler-hemodynamic study showed that the ratio decreased markedly after treatment of heart failure. The value was 0.84 +/- 0.29 before treatment and 0.36 +/- 0.17 after treatment (P = .001). An increased ratio of pulmonary venous to mitral A velocity is a useful marker for elevated pulmonary capillary wedge pressure among patients with left ventricular systolic dysfunction.