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The purpose of the present study was to examine the mechanisms of improvement in left ventricular (LV) diastolic function in hypertensive patients treated with cilnidipine, a new and unique calcium antagonist that has both L-type and N-type voltage-dependent calcium channel blocking actions, using pulsed Doppler echocardiography and pulsed tissue Doppler imaging. The study comprised 35 untreated patients with essential hypertension (19 men and 16 women; mean age 65+/-10 years). The peak early diastolic and atrial systolic transmitral flow velocities (E and A, respectively) and their ratio (E/A), and the peak early diastolic and atrial systolic motion velocities (Ew and Aw, respectively) of the LV posterior wall and their ratio (Ew/Aw) were determined in all patients before and after 1, 3 and 6 months on cilnidipine (10 mg/day). One month: Systolic and diastolic blood pressures were significantly decreased. E and E/A were significantly increased, whereas there were no significant changes in Ew and Ew/Aw. Three months: Ew and Ew/Aw were significantly increased compared to those before and 1 month after cilnidipine. Six months: E and E/A were significantly increased compared with before and 3 months after cilnidipine, and Ew and Ew/Aw were significantly increased compared with before cilnidipine. Moreover, the LV mass index was significantly decreased compared to that before cilnidipine. In summary, changes in LV diastolic performance in patients with essential hypertension following cilnidipine treatment were biphasic with an initial increase in early diastolic transmitral flow velocity and a later increase in early diastolic LV wall motion velocity. The initial and later changes can be related to an acute change in afterload and a later improvement in LV relaxation.

Our objective was to evaluate the influence of aging on left ventricular (LV) regional systolic function along the long and short axes in clinically normal patients. We recorded LV wall motion velocity patterns at the mid-wall portion of the middle of the LV posterior wall in the parasternal long-axis view (short-axis direction) and at the endocardial portion of the middle of the LV posterior wall in the apical long-axis view (long-axis direction) with pulsed tissue Doppler imaging in 80 normal patients (age range 15 to 78 years). In all patients the LV pressure curve and its first derivative (dP/dt) were recorded. The systolic wave of the LV posterior wall motion velocity pattern exhibited 2 peaks, the first (Sw(1)) and second (Sw(2)) systolic waves. No significant changes were seen with aging in the percent LV fractional shortening determined by M-mode echocardiography, LV ejection fraction determined by left ventriculography, the peak Sw(1) and Sw(2) along the short axis, the peak Sw(2) along the long axis, and the peak dP/dt. The peak Sw(1) along the long axis correlated inversely with age (P <.0001) but did not correlate significantly with the peak dP/dt. These results suggest that shortening of the longitudinal fibers in early systole is impaired with increased age in healthy individuals. This impairment results in insufficient spherical change in the LV cavity, although global LV pump function and myocardial contractility are maintained.

We recorded left ventricular inflow (LVIF) and pulmonary venous flow (PVF) velocities by transesophageal pulsed Doppler echocardiography in 25 patients with a ratio of peak atrial systolic to early diastolic LVIF velocity of <1 and a left ventricular end-diastolic pressure (LVEDP) of 15 mmHg or greater, as well as in 30 normal subjects. The group consisted of 14 patients with prior myocardial infarction, 7 with dilated cardiomyopathy, and 4 with cardiac amyloidosis, and were divided into: (1) group A (n = 7): peak atrial systolic LVIF velocity of 40 cm/sec or greater; (2) group B (n = 7): peak atrial systolic LVIF velocity of <40 cm/sec and peak atrial systolic PVF velocity of 30 cm/sec or greater; and (3) group C (n = 11): peak atrial systolic LVIF velocity of <40 cm/sec and peak atrial systolic PVF velocity of <30 cm/sec. Although LVEDPs in groups B and C were significantly greater than in group A, there was no difference between groups B and C. The mean pulmonary capillary wedge pressure (mPCWP) in group C was significantly greater than in groups A and B, but there was no difference between groups A and B. The difference between LVEDP and mPCWP (LVEDP - mPCWP) in group B was significantly higher than in groups A and C. Dilatation of the left atrium (LA) was seen in all three groups, particularly in groups B and C. There were no differences in peak atrial systolic LVIF velocity and LA volume change during atrial contraction between group A and the control group, and there were no differences in LA volume change and peak second systolic PVF velocity between groups A and B. LA volume change and peak second systolic PVF velocity were significantly less in group C than in groups A and B. Among the four patients whose courses could be observed after medical treatment with diuretic and vasodilator, one changed from group B to A, one from group B to C, one from group C to A, and one remained in group C. Thus, recording of peak atrial systolic LVIF and PVF by transesophageal pulsed Doppler echocardiography permits detailed evaluation of LA systolic performance in the presence of elevated LVEDP. These two variables provide important information for less invasive differentiation of LA afterload mismatch from LA myocardial failure.

Background: Hypertrophic cardiomyopathy (HC) is characterized by impaired left ventricular (LV) diastolic function due to an increase in LV wall thickness. The severity of this disease varies depending on the localization and extent of the hypertrophied myocardium and the presence and extent of myocardial disarray or fibrosis., Hypothesis: The purpose of this study was to examine the background of hemodynamic abnormalities between the left atrium and the left ventricle during atrial systole in patients with HC using pulsed Doppler echocardiography., Methods: Hemodynamic abnormalities between the left atrium and left ventricle during atrial systole were evaluated in patients with HC using transmitral flow (TMF) and pulmonary venous flow (PVF) velocities obtained by transesophageal pulsed Doppler echocardiography. The study population included 50 patients with HC, including 39 with asymmetric septal hypertrophy and 11 with apical hypertrophy, and showing fractional shortening of the left ventricle > or = 30%. They were classified into three groups: (1) Group A (n = 11): the ratio of the late to early TMF velocity < 1, and peak atrial systolic PVF velocity (PVA) < 25 mm/s; (2) Group B (n = 13): their ratio < 1, and PVA > or = 25 mm/s; and (3) Group C (n = 26): their ratio > or = 1. The mean age of patients in Group A was lower than that in Groups B and C., Results: Left atrial dimension in Group B was significantly greater than that in the other HC groups and the control group. Furthermore, left atrial volume changes during atrial systole in Group B were significantly smaller than those in the other HC groups and the control group. Peak atrial systolic PVF velocity in Group B was significantly higher than that in the control group and in Group C. The duration of the atrial systolic waves of the TMF and PVF in Group B was significantly shorter and longer, respectively, than that in Group A. Left ventricular end-diastolic pressure (LVEDP) decreased in descending order with Group B > Group C > Group A. In all patients there was a significant positive correlation between the LVEDP and peak atrial systolic PVF velocity or the difference in duration between the atrial systolic waves of PVF and TMF. Plots of these values shifted toward the left and inferiorly in Group A, and toward the right and superiorly in Group B., Conclusion: Peak velocity and duration of TMF and PVF during atrial systole by transesophageal pulsed Doppler echocardiography are useful indices of hemodynamic abnormalities between the left atrium and the left ventricle during atrial systole, particularly a forceful atrial contraction mismatched to the left atrial afterload and severity of LV diastolic dysfunction, in HC.

To examine changes in left atrial appendage flow velocity patterns in relation to left atrial pressures during sinus rhythm, transesophageal echocardiography and cardiac catheterization were performed in 31 patients with myocardial diseases in sinus rhythm and 20 control subjects without cardiovascular disease. The 31 patients were divided into two groups according to mean pulmonary capillary wedge pressure: the group with high wedge pressure (19.9 +/- 5.8 mmHg) and the group with low wedge pressure (8.6 +/- 2.9 mmHg). The left atrial appendage peak early emptying velocity was decreased significantly in the groups with both high and low wedge pressure compared with the control group. The left atrial appendage peak late emptying velocity was significantly greater in the group with low wedge pressure compared with the control group, whereas it was decreased significantly in the group, with high wedge pressure compared with the control group. The left atrial appendage peak late emptying velocity had a significant negative correlation with wedge pressure. The maximum left atrial appendage area at end systole in the group with high wedge pressure was significantly greater than that in both the group with low wedge pressure and the control group. There was a significant positive correlation between the maximum left atrial appendage area and the wedge pressure, as well as a significant negative correlation between the left atrial appendage ejection fraction during atrial contraction and the wedge pressure. In the group with high wedge pressure, one patient had evidence of left atrial appendage thrombi and two had spontaneous echo contrast. These results suggest that even in patients in sinus rhythm, a marked elevation in the left atrial pressure is likely to reduce the left atrial appendage peak early and late emptying velocities. These changes may be accompanied by an increased incidence of thrombus formation in the left atrial appendage compared with individuals with normal or only slightly elevated left atrial pressures.

A patient of cardiac amyloidosis was found to have mid- to late diastolic retrograde flow from the left atrium (LA) to the pulmonary vein. Congo-red staining was positive for amyloid in the rectal tissue. M-mode and two-dimensional echocardiograms revealed symmetric hypertrophy and typical speckled pattern of the left ventricle (LV). The LV pressure curve showed a dip and plateau configuration during diastole, and end-diastolic pressure was 28 mmHg. In addition, the LV pressure was high at mid-diastole, surpassing the pulmonary capillary wedge pressure from mid- to late diastole. The transmitral flow velocity revealed "restrictive" pattern, and the pulmonary venous flow velocity showed retrograde flow from the LA to the pulmonary vein during mid-diastole and atrial systole. It is suggested that recording of the pulmonary venous flow velocity by transesophageal pulsed Doppler echocardiography is useful for understanding the mechanism of the development of pulmonary congestion or edema. (ECHOCARDIOGRAPHY, Volume 13, November 1996)

Background: A large V wave in a pulmonary capillary wedge pressure (PCWP) tracing is characteristic of mitral regurgitation. However, the V wave is often increased in patients without or with no significant mitral regurgitation., Methods and Results: The V wave was in the PCWP tracing investigated in 65 patients using transmitral flow (TMF) and pulmonary venous flow (PVF) velocity patterns obtained by transesophageal pulsed Doppler echocardiography. A large V wave was defined if the peak V wave minus the mean PCWP (V-mPCWP) was greater than 7 mmHg. Three study groups were formed: 15 patients with large V waves and significant mitral regurgitation, 15 patients with large V waves with no significant mitral regurgitation, and 35 patients with small V waves. The mPCWP and left ventricular end-diastolic pressure were greatest in the group with large V waves and no significant mitral regurgitation. Peak early diastolic TMF and PVF velocities were significantly greater in the two groups with large V waves. The peak second systolic PVF velocity was lowest in the group with large V waves and significant mitral regurgitation, followed by the group with large V waves and no significant mitral regurgitation. The V-mPCWP was positively correlated with the peak early diastolic TMF and PVF velocities and negatively correlated with the peak second systolic PVF velocities. Additionally, mitral regurgitation severity in patients with large V waves and significant mitral regurgitation was positively correlated with the peak early diastolic TMF and PVF velocities and negatively correlated with the peak second systolic PVF velocity., Conclusions: These results suggest that large V waves in PCWP tracings appear not only in severe mitral regurgitation, but also in any condition with markedly elevated left ventricular end-diastolic pressure. Combined analysis of the TMF and PVF velocity patterns is helpful in determining the etiology of these hemodynamic abnormalities.

Transesophageal pulsed Doppler echocardiography was performed to examine changes with age in the left atrial appendage flow velocity patterns in 50 normal subjects (15 to 80 years) in sinus rhythm. There was a significant negative correlation between the peak early diastolic forward and backward left atrial appendage flow velocities and age, as well as a significant positive correlation between the peak early diastolic forward left atrial appendage flow velocity and the peak early diastolic transmitral and pulmonary venous flow velocities. Although there was a significant positive correlation between the peak atrial systolic transmitral flow velocity and age, there was a negative correlation between the peak atrial systolic forward and backward left atrial appendage flow velocities and age. There was a positive correlation between both the maximum left atrial diameter and the amplitude of the interatrial septal motion during atrial systole and age. There was a significant negative correlation between the left atrial appendage ejection fraction during atrial systole and age. Left atrial appendage thrombi and spontaneous echo contrast were detected in two subjects with low peak early diastolic and atrial systolic left atrial appendage flow velocities. In conclusion, both peak early diastolic and atrial systolic left atrial appendage flow velocities decreased with age. A decrease in the peak atrial systolic flow velocity appeared to be an important sign of left atrial appendage thrombus formation even in normal elderly subjects in sinus rhythm.

To determine whether transmitral and pulmonary venous flow velocity patterns can be used to evaluate left atrial pressure and volume changes during atrial systole, we performed transesophageal pulsed Doppler echocardiography and right heart catheterization in 85 patients (20 with hypertrophic cardiomyopathy, 20 with dilated cardiomyopathy, 30 with prior myocardial infarction, and 15 with mitral regurgitation), and 35 normal subjects. Pulsed Doppler variables from transmitral and pulmonary venous flow velocities during atrial systole were compared with mean pulmonary capillary wedge pressure (mean PCWP), pressure rise during atrial systole (PCWP-A), and left atrial volume change during atrial systole (delta LAV). The mean PCWP correlated significantly with the peak atrial systolic transmitral flow (r = -0.38, p < 0.05) and pulmonary venous flow (r = 0.40, p < 0.05) velocities in all patients. The PCWP-A correlated significantly with the peak atrial systolic transmitral flow (r = -0.39, p < 0.05) and pulmonary venous flow (r = 0.68, p < 0.0001) velocities in all patients. There was a particularly close correlation between the PCWP-A and the peak atrial systolic pulmonary venous flow velocities. The sum of the time-velocity integral of the atrial systolic transmitral and pulmonary venous flow velocities (TAI) correlated closely with the delta LAV (r = 0.70, p < 0.0001) in all patients. Thus, the peak atrial systolic pulmonary venous flow velocity correlated well with left atrial pressure changes during atrial systole. Furthermore, the sum of the time-velocity integral of the atrial systolic transmitral and pulmonary venous flow velocities correlated well with left atrial volume changes during atrial systole. Therefore, transesophageal echocardiographic measurements of atrial systolic transmitral and pulmonary venous flow velocities are reasonable indicators of left atrial pressure and volume changes during atrial systole.

For evaluation of pulmonary venous flow (PVF) in mitral stenosis, transthoracic and transesophageal echocardiography were performed in 33 patients with mitral stenosis and 20 normal controls. The peak systolic flow velocity of the PVF was significantly lower in patients with mitral stenosis and atrial fibrillation. The peak diastolic flow velocity of the PVF was significantly lower in the patients with mitral stenosis than in normal controls. The diastolic wave recorded as laminar flow in the mitral stenosis group showed a peak in the rapid filling phase with a gradually descending slope of velocity during mid to late diastole. There was a significant negative correlation between the peak diastolic flow velocity of the PVF and the pressure half time from transmitral flow obtained by continuous wave Doppler in the mitral stenosis group. These results demonstrate that evaluation of the PVF is helpful in understanding hemodynamic events between the left atrium and left ventricle in patients with mitral stenosis.

To examine the recovery time of left atrial mechanical function after electrical cardioversion of atrial fibrillation, we recorded transmitral flow, pulmonary venous flow velocities, and interatrial septal motion during atrial systole within 24 hours (16 +/- 5 hours) and 10 days after cardioversion in 25 patients with atrial fibrillation, including 6 patients with hypertension, 4 with ischemic heart disease, 2 with alcoholic heart disease, 5 with dilated cardiomyopathy, and 8 with no evidence of underlying heart disease. With the exception of the five patients with dilated cardiomyopathy, the peak atrial systolic transmitral and pulmonary venous flow velocities, peak first systolic velocity of pulmonary venous flow, duration of both atrial systolic waves, and amplitude of the interatrial septal motion during atrial systole decreased markedly within 24 hours after cardioversion and increased 10 days after cardioversion. These results suggest that active atrial systolic and relaxant variables obtained from transmitral and pulmonary venous flow velocities may reflect left atrial mechanical function after cardioversion of atrial fibrillation.

Systolic ejection murmurs of the left heart usually have their peak during early to mid-systole. Few reports have addressed ejection murmurs with their peak at late systole. We evaluated the clinical significance of an apical systolic ejection murmur with a peak intensity during late systole using Doppler and two-dimensional (2-D) echocardiography and phonocardiography. The apical late systolic ejection murmur was observed in 9 of 13 consecutive patients with mid-left ventricular obstruction. We investigated the ejection flow velocity and the timing of maximum velocity at the three different sites of the left ventricle, the left ventricular cavity shape, and the timing of the peak murmur intensity in these nine patients (late-murmur group). The same parameters were also examined in 8 consecutive patients with mid-systolic ejection murmurs (mid-murmur group), 10 with early systolic ejection murmurs (early-murmur group), and 7 controls without murmurs. Patients with aortic stenosis were excluded. The mid-ventricular ejection flow velocity was significantly higher in the late-murmur group than in the other three groups; that of the outflow tract was markedly higher in the mid-murmur group. The ejection flow velocity at the aortic orifice of patients in the early-murmur group was significantly high compared with that of the controls. The timing of the peak murmur intensity in each group correlated with that of the peak flow signal at the corresponding site with maximum velocity. In all patients in the late-murmur group, 2-D echocardiography revealed a systolic narrowing of the cavity at the mid-ventricle. Amyl nitrite inhalation induced a marked increase in the intensity of the murmur without evidence of appearing or increasing mitral regurgitation. It was concluded that the apical ejection murmur with a late systolic peak intensity is a new phonocardiographic sign indicative of dynamic, mid-left ventricular obstruction. This murmur should be differentiated from the mitral regurgitant murmur.

The aim of the present study was to assess the changes of left ventricular inflow (LVIF) and pulmonary venous flow (PVF) velocities during preload alteration in 30 patients with dilated heart (LV end-diastolic dimension > or = 6.0 cm) and impaired LV systolic function (% fractional shortening of the LV < or = 25%). We performed transesophageal pulsed Doppler echocardiography during lower body negative (LBNP, -40 mmHg) and positive pressure (LBPP, +40 mmHg) in 10 patients with dilated cardiomyopathy, in 20 with old myocardial infarction, and in 22 healthy controls. Eight of the patients showed a pseudonormalization (compliance failure) pattern, and 22 showed a decreased early diastolic wave and compensatorily increased atrial systolic wave (relaxation failure) pattern of LVIF in the control state. Mean pulmonary capillary wedge pressure (PCWP) was greater in the compliance failure group than in the relaxation failure group in the control state. LVIF in 6 of the 22 patients with the relaxation failure pattern changed to the compliance failure pattern during LBPP, and that in 3 of 8 patients in the compliance failure group changed to the relaxation failure pattern during LBNP. The 6 patients with a change from the relaxation failure to the compliance failure pattern showed significantly higher peak diastolic and atrial systolic PVFs during LBPP than in the control state, and significantly higher PCWPs in the control state than the 16 patients with no change in LVIF. These findings suggest that the compliance failure and relaxation failure patterns of LVIF are readily interchangeable in various hemodynamic conditions, and that pattern analysis of LVIF and PVF during preload alteration is useful for understanding the hemodynamic severity and for evaluating preload reduction therapy in the dilated heart.

We evaluated the characteristics of left ventricular diastolic hemodynamics in hypertrophic cardiomyopathy (HCM) by measuring left ventricular inflow (LVIF) and pulmonary venous flow (PVF) velocities in 62 patients with asymmetric septal hypertrophy and 34 normal controls. The patients were divided into four groups according to the LVIF pattern and left ventricular end-diastolic pressure (LVEDP): 1) the pseudonormalization group; 13 patients with the ratio of peak atrial systolic (A) to early diastolic (E) LVIF velocity (A/E) < or = 1 and LVEDP > or = 15 mm Hg, 2) the normal pattern group; 10 patients with the A/E < or = 1 and LVEDP < 15 mm Hg, 3) the relaxation failure group; 25 patients with the A/E > 1, and 4) the mid-diastolic wave group; 14 patients with a mid-diastolic wave. The peak early diastolic LVIF velocities in the pseudonormalization, relaxation failure and mid-diastolic wave groups were significantly smaller than in the control group. The deceleration time from the peak of the E wave and the isovolumic relaxation time were significantly prolonged in the relaxation failure and mid-diastolic wave groups. The peak diastolic PVF velocity in the relaxation failure and mid-diastolic wave groups was significantly decreased, and was significantly increased in the pseudonormalization group. The peak atrial systolic PVF velocity was significantly increased in all patients with HCM, particularly in the pseudonormalization group. LVEDP was the highest in the pseudonormalization group, followed by the mid-diastolic wave, relaxation failure and normal pattern groups, in that order. In conclusion, combined analysis of the LVIF and PVF provides useful information regarding various abnormalities of left ventricular diastolic hemodynamics in patients with HCM.

We evaluated the distribution of the nerves in valve tissue of humans to clarify the relationship between mitral valve prolapse and autonomic nerve dysfunction. We studied 15 autopsy specimens of normal mitral valve, 10 prolapsed mitral valves, five each of normal tricuspid, aortic, and pulmonary valves, and three prolapsed mitral valves obtained at cardiac surgery. Immunohistochemical studies utilized the avidinbiotin peroxidase complex (ABC) method and several nerve-related antigens: 1) S-100 protein, glial fibrillary acidic protein (GFAP), and neurofilament protein (NFP) as markers of glial and Schwann cells of the nervous system; 2) choline acetyltransferase (ChAT) to identify cholinergic nerve endings; 3) neuropeptide Y (NPY), a neuropeptide that is distributed in accordance with sympathetic nerves; and 4) calcitonin gene-related peptide (CGRP), a neuropeptide that is distributed in accordance with afferent nerves. Distribution of adrenergic nerve fibers was also examined by fluorescence method. Morphology of nerve endings of the normal mitral valve was studied by electron microscopy. In normal valves, distributions of S-100 protein, GFAP, and NFP immunoreactivities were clearly visible along the subendocardial site on the coaptation aspect of the base-to-body portion of each valve, regardless of the kind of valve. In contrast, there was only a scanty distribution of these reactivities on the physiologic coaptation area of the tip. In prolapsed mitral valves, there was no distribution of S-100-positive protein or other nerve-related antigens in areas of the valve with myxomatous degeneration. Distribution of CGRP, ChAT, and NPY immunoreactivities, and adrenergic fluorescence, were the same as those of the nerve-related antigens in both normal and prolapsed mitral valves. Electron microscopic study of the atrial aspect of normal mitral valves revealed numerous small axons with aggregations of small clear vesicles, indicating cholinergic features. The results suggest that the subendocardial site on the atrial aspect at the middle portion of the mitral valve is rich in nerve endings, including the afferent nerves, and that mechanical stimuli from this area caused by abnormal coaptation in mitral valve prolapse may produce an improper circuit in autonomic nerve function between the central and mitral valve nervous systems.

To elucidate predisposing factors for severe mitral regurgitation (MR) in idiopathic mitral valve prolapse (MVP), 124 MVP patients were classified into the following categories: 55 with isolated clicks (click group), 35 with a late-systolic murmur (late-SM group), and 34 with a holosystolic murmur (holo-SM group). Their clinical and echocardiographic findings were compared with those of 26 patients with spontaneous chordal rupture (rupture group). In 22 patients in the click group, 24 in the late-SM group, and 22 in the holo-SM group, follow-up studies were performed for a mean of 4.5 years (range 1 to 13.5). The mean age was youngest in the click group and oldest in the rupture group. The click and late-SM groups showed a female predominance, but the holo-SM and rupture groups showed a male predominance. There was no difference in the incidence of systemic hypertension among the 4 groups. Most patients in the click and late-SM groups had anterior leaflet prolapse. In the holo-SM and rupture groups, however, the incidence of posterior leaflet involvement was significantly increased. The incidence of thickened mitral valve increased in order of the click (8%), late-SM (21%), holo-SM (38%), and rupture (50%) groups. Six patients in the holo-SM group developed chordal rupture with severe MR during the follow-up period. In the click and late-SM groups, however, there were no complications and no development into a holo-SM. Thus, aging, male sex, posterior leaflet prolapse, thickened mitral valve, and holo-SM were found to be important predisposing factors for severe MR in idiopathic MVP.

In conclusion, alterations in venous return are more marked in the right side of the heart than in the left side of the heart in patients with complete absence of the left pericardium.

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.

To investigate the clinical significance and problems of right-to-left (R-L) shunt flow dynamics in atrial septal defects, we performed transesophageal color and pulsed Doppler echocardiography in 30 patients with atrial septal defects of the ostium secundum type. The 30 patients consisted of 20 with a pulmonary artery systolic pressure of less than 40 mm Hg, four with a pressure of 40 to 60 mm Hg, three with a pressure of 90 mm Hg or more, two patients with pulmonic stenosis, and one patient with Ebstein's anomaly. R-L shunting was determined by the presence of a shunt flow signal across the defect during each cardiac cycle. The time of R-L shunt flow was compared with the various parameters obtained by echocardiography and cardiac catheterization. R-L shunt flow signals were detected at the following times: (1) at the onset of ventricular contraction or the closing phase of the tricuspid valve in five patients with isolated atrial septal defect. These patients showed an increase of mean right atrial pressure but had no severe pulmonary hypertension; (2) during ventricular systole in five of 26 patients with tricuspid regurgitation and one patient with Ebstein's anomaly. The tricuspid regurgitant signal was directed toward the ostium of the defect in three patients and was massive in the other patients; (3) during middiastole in three patients without pulmonary hypertension. These patients showed massive left-to-right shunt flow from end systole to early diastole; and (4) during atrial systole in three patients with severe pulmonary hypertension and two patients with pulmonic stenosis. The former, in particular, showed the aliasing signal as a high-speed shunt flow. In two of the three patients with severe pulmonary hypertension, R-L shunting continued from atrial systole to early ventricular systole and was also observed in early diastole. R-L shunt flow was detected in patients with atrial septal defects not only with pulmonary hypertension but also without pulmonary hypertension and was influenced by the right atrial pressure in the phase of tricuspid valve closing, the volume or direction of tricuspid regurgitation, rebound flow caused by massive left-to-right shunt flow, the grade of right ventricular distensibility or the complication of pulmonary hypertension, and complications with other cardiac anomalies. Thus R-L shunt flow in patients with atrial septal defects was detected easily by transesophageal color and pulsed Doppler echocardiography because of the high efficiency of this method for its detection.

Although data from cardiac catheterization and in vivo studies are available, phonocardiographic and ultrasonic characteristics of the Medtronic Hall valve in the mitral position have not been adequately established. Phonomechanocardiographic, echocardiographic and Doppler echocardiographic examinations were performed in 15 patients (Medtronic Hall group) with a Medtronic Hall mitral valve prosthesis to elucidate the phonocardiographic and ultrasonic characteristics of the normally functioning Medtronic Hall valve in the mitral position. These findings were compared with those obtained from 20 patients (Björk-Shiley group) with a normally functioning Björk-Shiley 60 degrees mitral valve prosthesis. Simultaneous recordings of the phonocardiogram and M-mode echocardiogram of the prosthetic valve in patients in the Medtronic Hall group revealed three opening clicks relating to disc motion. The timing of the three opening clicks correlated with the onset of disc opening, the completion of disc opening, and a notch which appeared about 30 msec after the completion of disc opening. Similar recordings performed in patients in the Björk-Shiley group revealed that the third opening click was detected in only half of the patients and that its timing was nearly twice as early as that noted in the Medtronic Hall group. The Medtronic Hall group had significantly shorter durations of the apical diastolic rumble and the slow filling wave on the apexcardiogram, as well as significantly reduced peak mitral inflow velocity during early diastole and shortened pressure half-time on the mitral inflow velocity curve. Transesophageal Doppler echocardiography demonstrated slight mitral regurgitation in all patients in both the Medtronic Hall and the Björk-Shiley groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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)

To investigate the predisposing factors and the clinical significance of the musical aortic component of the second heart sound (musical S2), 18 patients with musical S2 (musical group) among the consecutive 2,000 patients with phonocardiographic examination were noninvasively studied by analyzing underlying diseases, phonocardiographic findings, organic changes of the aortic valve, severity of aortic regurgitation and left ventricular dysfunction. Organic changes of the aortic valve were assessed by two-dimensional echocardiography, and aortic regurgitation was assessed by color Doppler flow imaging. Twenty-two normal subjects (normal group) and 17 patients with essential hypertension (hypertensive group) served as controls. Mean ages were matched among the three groups. 1. Left ventricular dilatation (seven patients) and hypertension (six patients) were the dominant part of underlying disease in the musical group. 2. Musical S2 was classified in the following two types based on the phonocardiographic characteristics; musical vibrations followed immediately after the accentuated S2, and the S2 which was replaced by regular vibratory waves. 3. Frequency of the musical vibrations ranged from 120 to 200 Hz, and its duration ranged from 60 to 120 msec. Amplitude of the musical vibrations decreased by inhalation of amyl nitrite, but increased by infusion of methoxamine. In a case with mild rheumatic valve disease, methoxamine induced marked intensification of the amplitude and prolongation of the duration of the musical vibrations, finally giving a typical cooing murmur. 4. Echo intensity of the aortic valve tended to be higher in the musical group than in the other two groups. 5. Echocardiographically, aortic regurgitation appeared more frequently in the musical group (88%) than in the normal (36%) and hypertensive (41%) groups. Area of the aortic regurgitant signal was significantly larger in the musical group (4.1 +/- 1.4 cm2) than in the normal (1.2 +/- 0.8 cm2) and hypertensive (2.3 +/- 1.2 cm2) groups. 6. Left ventricular end-diastolic dimension was significantly larger in the musical group (5.8 +/- 0.6 cm) than in the normal (4.7 +/- 0.5 cm) and hypertensive (4.8 +/- 0.7 cm) groups. Fractional shortening of the left ventricle was significantly smaller in the musical group (26 +/- 10%) than in the normal (37 +/- 5%) and hypertensive (37 +/- 8%) groups. In a case of the musical group, musical vibrations following the S2, which was large in amplitude at the state of heart failure, decreased markedly after the recovery from heart failure.(ABSTRACT TRUNCATED AT 400 WORDS)

To determine the clinical significance and effect of cycle length on systolic backward (C) and forward (S) flow patterns of the pulmonary vein, we performed transesophageal and transthoracic echocardiography in patients with atrial fibrillation (Af). Study population consisted of 10 patients with mitral stenosis and sinus rhythm (MS-SR), 15 with MS and Af (MS-Af), 15 with mitral valve replacement and Af (MVR-Af), 10 with Af without organic heart disease (lone-Af) and 15 normal subjects. Various parameters, including peak velocities of C and S waves, closing amplitude of anterior mitral valve echogram during end-diastole, amplitude of the mitral annulus and interatrial septal motion during systole and left atrial pressure during the mitral closing period or end-diastole, were measured in each group. Results were as follows: 1. C wave was observed in all Af groups and six of 10 patients with MS-SR. Particularly, peak velocity of the C wave in MS-Af group was increased significantly compared with those of every other group. 2. Peak velocity of S wave in all Af groups, particularly in MS- and MVR-Af groups, decreased significantly compared with that of the normal group. 3. There were significant negative correlations between preceding R-R interval and peak velocity of the C wave or closing amplitude of anterior mitral valve echogram or left atrial pressure during end-diastole in MS-Af group. 4. There were significant positive correlations between preceding R-R interval and peak velocity of the S wave or amplitude of the mitral annulus or interatrial septal motion during systole in MS-Af group. 5. Peak velocities of the C and S waves had no correlations to preceding R-R interval in lone-Af group. We concluded that the C and S waves of pulmonary venous flow velocity pattern in MS-Af are affected by cycle length, and that the former is influenced by left atrial pressure and/or pliability of the mitral valve during the mitral closing period, and the latter by the grade of left atrial dilatation and/or preceding left atrial emptying.