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The time course of recovery of left atrial mechanical function after electrocardioversion of atrial fibrillation was examined in 25 patients with atrial fibrillation by recording pulmonary venous and transmitral flow velocities and interatrial septal motion during atrial systole within a day (16 +/- 5 hours) and ten days after cardioversion of atrial fibrillation by transesophageal and transthoracic Doppler and M-mode echocardiography. There were 6 patients with hypertension, 4 with ischemic heart disease, 2 with alcoholic heart, 5 with dilated cardiomyopathy, and 8 without underlying heart disease. The peak velocities of the atrial systolic waves of the transmitral and pulmonary venous flow velocities (A and PVA, respectively) and first systolic wave (PVS1) of pulmonary venous flow, durations of both atrial systolic waves, and amplitude of interatrial septal motion during atrial systole increased significantly ten days after cardioversion compared with those measured within a day of cardioversion in all patients except the 5 patients with dilated cardiomyopathy. Peak velocity of the second systolic wave (PVS2) of pulmonary venous flow increased, and that of the early diastolic and diastolic waves (E and PVD, respectively) of transmitral and pulmonary venous flow decreased ten days after cardioversion compared with those within a day of cardioversion. These results suggested that active atrial systolic (A and PVA) and relaxant (PVS1) parameters obtained from transmitral and pulmonary venous flow velocities are good indicators of left atrial mechanical function after cardioversion of atrial fibrillation.

The clinical significance of right-to-left (R-L) shunt flow dynamics in atrial septal defects (ASD) were investigated using transesophageal color and pulsed Doppler echocardiography in 30 patients with ASD of the ostium secundum type, including 20 with systolic pulmonary artery pressures (sPA) less than 40 mmHg, 4 with sPA of 40 to 60 mmHg, 3 with sPA of 90 mmHg or greater, 2 with pulmonic stenosis and 1 with Ebstein's anomaly. R-L shunting was detected by a shunt flow signal across the defect during a cardiac cycle. The timing of the R-L shunt was compared with various parameters obtained by echocardiography or cardiac catheterization. R-L shunt flow at the onset of ventricular contraction or closing phase of the tricuspid valve was detected in five patients with isolated ASD associated with increased mean right atrial pressure, but no severe pulmonary hypertension. R-L shunt flow during systole was detected in five of 26 patients with isolated ASD and tricuspid regurgitation and in one patient with Ebstein's anomaly. The tricuspid regurgitation signals in three of the five patients were directed toward the defect, while the other two had massive tricuspid regurgitation. R-L shunt flow during mid-diastole was detected in three patients without pulmonary hypertension. Massive left-to-right shunt flows occurred during the phase from end-systole to early diastole. R-L shunt flow during atrial systole was detected in three patients with severe pulmonary hypertension and two with pulmonic stenosis. The severe pulmonary hypertension patients, in particular, showed the aliasing signal as a high speed shunt flow, and in two of these, R-L shunt flow continued from atrial systole to early ventricular systole, and was also observed in early diastole. R-L shunt flow was detected in ASD patients with and without pulmonary hypertension, and was influenced by right atrial pressure at the phase of tricuspid valve closing, volume or direction of tricuspid regurgitation, rebound flow due to massive left-to-right shunt flow, grade of right ventricular distensibility or pulmonary hypertension, and other cardiac complications.

Changes in left ventricular inflow (LVIF) and pulmonary venous flow (PVF) patterns during preload alteration were assessed in 30 patients with dilated heart, including 10 patients with dilated cardiomyopathy and 20 with old myocardial infarction. Transesophageal Doppler echocardiography was performed during lower body negative (LBNP, -40 mmHg) and positive pressure (LBPP, +40 mmHg) in all 30 patients and 20 normal controls. Eight of the 30 patients showed the "pseudonormalization (PN)" pattern, and 22 showed the "decreased early diastolic wave (E) and compensatorily increased atrial contraction wave (A) (N-PN)" pattern of LVIF in the control state. The diastolic wave (PVD) of the PVF and E of the LVIF were significantly higher, and the second systolic wave (PVS2) of the PVF and A of the LVIF were lower in the PN group than in the N-PN group. The amplitude of the atrial contraction wave (PVA) of the PVF in both groups of dilated heart patients was larger than in the normal group. The ratio of the amplitude of the atrial contraction wave to the total vertical deflection (A/H) of the apexcardiogram and mean pulmonary capillary wedge pressure (PCWP) in the PN group were greater than those in the N-PN group in the control state. LVIF in six of the 22 N-PN patients changed to the PN pattern during LBPP, and in three of eight PN patients changed to the N-PN pattern during LBNP. The six patients demonstrating the change from the N-PN to PN pattern showed a significant increase in PVD and PVA during LBPP compared with the control state, and a significant increase in PCWP in the control state compared with the 14 patients without a change in LVIF. Peak velocity of E in each group was decreased during LBNP and increased during LBPP, but peak velocity of A did not change during preload alteration. Peak velocity of PVS2 in the normal group was significantly decreased, and those of the PN and N-PN groups were decreased but not significantly during LBNP. The peak velocity of PVD was decreased during LBNP in the PN and N-PN groups, and the decrease was significantly higher in the former than in the latter.(ABSTRACT TRUNCATED AT 400 WORDS)