Problems of porcelain fused to metal crowns (III).
Explore the source record for details and available documents.
Color↗
Biomedical subjects
T Tabata
Publications and source records attributed to T Tabata.
[Phonocardiographic and Doppler echocardiographic study on the mechanism of the presystolic murmur in mitral stenosis, especially the relationship to mitral inflow dynamics].
The cause of the "presystolic murmur" in mitral stenosis was investigated by phonocardiography and continuous wave Doppler echocardiography in 31 patients with mitral stenosis and sinus rhythm classified into two groups: 18 patients with and 13 without "presystolic murmur". 1. The "presystolic murmur" group demonstrated high frequency vibrations preceding the first heart sound coinciding with the initial low frequency component of the first heart sound recorded at the apex in both groups. 2. There were two types of "presystolic murmur": The first type observed in three of the 18 patients occurred during the accelerated phase of the atrial (A) wave of mitral inflow signals and lasted until the first heart sound. The A wave velocity in mitral inflow signals was high at the onset and peak, and rapidly decreased after the peak. The second type observed in 15 patients occurred during the decelerated phase of the A wave and lasted until the first heart sound. The A wave velocity in mitral inflow signals was low at the onset, but high at the peak and rapidly decreased after the peak. 3. The mitral orifice area tended to be smaller in all patients with "presystolic murmur". The peak flow velocity, deceleration rate of the A wave, and maximal pressure gradient across the mitral valve during atrial contraction were significantly increased in all patients with "presystolic murmur". 4. Five patients with newly developed "presystolic murmur" after amyl nitrite inhalation had an increased initial low frequency component of the first heart sound coinciding with the latter half of "presystolic murmur". The rate of increase in the peak flow velocity and the deceleration rate of the A wave were significantly larger and the maximal atrioventricular pressure gradient during atrial contraction tended to be larger in these five patients than those in five who did not develop "presystolic murmur". 5. The peak flow velocity, deceleration rate of the A wave and the maximal atrioventricular pressure gradient during atrial contraction had increased 1 year later compared with those immediately after cardioversion of atrial fibrillation, and newly developed "presystolic murmur" appeared according to the recovery of left atrial mechanical function. These results suggest that the latter half of "presystolic murmur" originates from augmentation and prolongation of the initial low frequency component of the first heart sound up to the audible range caused by the sudden deceleration of mitral inflow velocity due to left ventricular contraction, and that the early half of "presystolic murmur" is the atriosystolic murmur produced by the increase in mitral inflow velocity during atrial contraction.
Blood Flow Velocity↗
[Changes in left ventricular inflow and pulmonary venous flow patterns during preload alteration in dilated heart].
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)
Adult↗
[Detection of right-to-left shunt flow in atrial septal defect using transesophageal color and pulsed Doppler echocardiography].
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.
Adolescent↗