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Background: Although cardiac resynchronization therapy (CRT) provided functional and clinical improvement in patients with heart failure (HF) and electrical intraventricular conduction disturbances, some patients had re-worsening left ventricular (LV) function after a favorable CRT response. We analyzed the clinical variables and cardiac outcomes associated with this re-worsening LV function after CRT., Methods: In this study, 71 patients with CRT response who received CRT between 2006 and 2017 were included. CRT response was defined as a "≥ 10% improvement in LV ejection fraction (LVEF) on follow-up." Patients were classified into two groups: (i) persistent: (n = 48, 68%), defined as those with a CRT response and (ii) re-worsening: (n = 23, 32%), consisting of those who fell out of the definition of a CRT response after an initial CRT response., Results: Half of the patients in the re-worsening group failed to maintain a CRT response from two years upwards. A longer duration from HF diagnosis to CRT implantation, nonspecific intraventricular conduction delay (NIVCD) on electrocardiogram at CRT implantation, and a lower increased LVEF at initial CRT response were independent predictors for the re-worsening group. Patients in the re-worsening group had a higher incidence rate for HF hospitalization and cardiac deaths, compared with those in the persistent group., Conclusion: One-third of CRT responders experienced re-worsening LVEF, which was associated with poor outcomes. CRT responders with NIVCD, longer HF duration, and a lower increased LVEF at initial CRT response should be monitored with caution., (Copyright © 2021. Published by Elsevier Ltd.)

Background: Patients with non-ischemic dilated cardiomyopathy (DCM) often show ischemia-like electrocardiographic findings. We aimed to elucidate the clinical impact of ischemia-like electrocardiographic findings in DCM, focusing on left ventricular reverse remodeling (LVRR)., Methods: We evaluated 195 patients hospitalized with heart failure (HF) and diagnosed with DCM. All patients underwent twelve-lead electrocardiography (ECG) and echocardiography during hospitalization and at the 2-year follow-up., Results: During hospitalization, 152 (78%) patients experienced ischemia-like ECG findings (Minnesota codes I3, IV1-3, V1-3, or VII1); 43 patients (22%, non-ischemia-like group) did not experience these findings. Ischemia-like ECG findings were normalized during hospitalization in 64 patients (33%, transient-ischemia-like group) but were unchanged in 88 patients (45%, persistent-ischemia-like group). The highest rates of LVRR, defined as an increase in LV ejection fraction from ≥10% to a final value of ≥35%, along with decreased LV end-diastolic dimension of ≥10% during 2 years of follow-up, were shown in the transient-ischemia-like group (transient-ischemia-like group, 91%; persistent-ischemia-like group, 40%; non-ischemia-like-group, 51%; p < 0.001). The transient-ischemia-like group had lowest composite event rates, including readmission for HF, the detection of major ventricular arrhythmia, and sudden cardiac death., Conclusions: Normalization of ischemia-like ECG findings during the first HF treatments was associated with a higher occurrence of mid-term LVRR and favorable long-term outcome in patients with DCM., (Copyright © 2021. Published by Elsevier Ltd.)

Background: Various measures of aortic stiffness have been proposed as cardiovascular risk markers, but interest has now shifted to more direct and easier evaluation of aortic function. The present study was conducted to determine the feasibility of measuring aortic stiffness (β) with two-dimensional (2D) strain echocardiography and the impact of age and gender on preclinical atherosclerosis., Methods and Results: The peak circumferential strain of the abdominal aorta was measured using 2D strain echocardiography, and β was determined in 54 clinically normal individuals and 104 patients with cardiovascular risk factors and no evidence of cardiovascular disease. The β correlated significantly with age in all 158 patients. However, the relationship was nonlinear, and β was markedly greater in patients ≥ 50 years. In 54 clinically normal individuals, the relationship was comparatively linear. The systolic blood pressure and pulse pressure were significantly greater in patients ≥ 50 years. There were no significant differences in β and blood pressure parameters between genders., Conclusions: The β increased dramatically with advanced age (≥ 50 years), regardless of gender, in clinically healthy and community-based patients with cardiovascular risk factors. The aortic circumferential strain was measured with 2D strain echocardiography which is a new tool that can be used to directly and easily evaluate aortic stiffness., (Copyright © 2011 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

Background: Left ventricular (LV) untwisting is commonly seen during left atrial (LA) contraction. The purpose of this study was to test the hypothesis that this characteristic motion is associated with chronic LV diastolic dysfunction., Methods and Results: Ninety-two patients with cardiovascular risk factors and 36 age-matched normal individuals were included in the present study, and were examined by echocardiography, including conventional, tissue Doppler, and two-dimensional speckle tracking methods, to clarify the predictors related to late diastolic untwisting rate (LDUTR). There was no significant difference in LV ejection fraction between patient and control groups. The ratio of peak early diastolic transmitral flow velocity to peak early diastolic mitral annular motion velocity (E/e') and LA volume index in the patient group were significantly greater compared to the ratio of peak early to late diastolic transmitral flow velocity (E/A) ≥1 group of the controls. The LDUTR in the E/A <1 group of the controls was significantly greater compared to the E/A ≥1 group of the controls and patient group. The LDUTR correlated with end-diastolic LV diameter, LA volume index, peak A velocity, E/e', relative LV wall thickness, and mean peak systolic LV radial strain. Multivariate regression analysis indicated that LA volume index is defined as a strong predictor related to LDUTR., Conclusions: Late diastolic LV untwisting reduces with a gradual increase in the LA size in patients with cardiovascular risk factors, and may reflect the disease history of chronic LV diastolic dysfunction., (Copyright © 2010 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

Background: We hypothesized that deterioration of systolic left ventricular (LV) myocardial deformation exists as an early sign of "isolated" diastolic heart failure in patients with hypertension (HT) and LV hypertrophy (LVH)., Methods and Results: Two-dimensional strain echocardiography was performed in 98 patients with HT and 22 age-matched normal controls. The LV mass index and relative wall thickness were used to assign patients into 3 groups with normal geometry (N-LV, n=31), concentric hypertrophy (C-LVH, n=25), and eccentric hypertrophy (E-LVH, n=42). The LV ejection fraction was preserved (> or =50%) in the 3 HT groups. The mean peak systolic longitudinal, circumferential, and radial strains in the C-LVH group were lower compared to the control and other 2 HT groups. The mean peak systolic strain rates in the 3 directions in the C-LVH group and those in the longitudinal and radial directions in the E-LVH and N-LV groups were lower compared to the control group. In addition, the mean peak systolic circumferential strain rate was lower in the C-LVH group than in the other 2 HT groups. There were no differences in the LV torsion and torsional rate between the control and 3 HT groups. The mean peak systolic circumferential strain was an independent predictor related to LV ejection fraction in all patients., Conclusions: C-LVH caused deterioration of the systolic longitudinal, circumferential, and radial myocardial deformation in patients with HT. LV torsion and circumferential shortening were considered to be compensatory mechanisms for maintaining LV pump function., (2009 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

Mitral valve prolapse (MVP) is closely related to myocardial sympathetic nerve function. This study evaluated the presence of impaired myocardial sympathetic nerve function by Iodine-123-metaiodobenzylguanidine (MIBG) scintigraphy in nine patients with MVP. For comparison, 15 healthy subjects without heart disease were investigated (control group). Single photon emission computed tomography (SPECT) and anterior planar myocardial scintigraphy were performed 15 min (initial images) and 3 hours (delayed images) after injection of MIBG (111 MBq). The location and degrees of reduced tracer uptake were evaluated. Myocardial MIBG uptake was quantified by uptake ratio of the heart (H) to upper mediastinum (M) on the anterior planar images (H/M). Percentage washout of MIBG in nine sectors of all oblique slices along the short-axis was calculated. The washout rates were higher at the inferoposterior and septal segments in patients with anterior leaflet prolapse, and at inferoposterior and lateral segments in patients with posterior leaflet prolapse. The bull's eye map showed increased washout rate in the apical and posteroseptal basal segments. There was no significant difference in the H/M ratio between MVP patients and the control group. These results indicate that MIBG can be used to evaluate localized myocardial sympathetic nerve function in MVP.

Transesophageal echocardiography was performed to elucidate the mechanisms of mitral regurgitation (MR) in 40 patients with hypertrophic cardiomyopathy with asymmetric septal hypertrophy, 15 obstructive and 25 nonobstructive, and the organic changes of the mitral leaflet were compared to those of 30 patients with sigmoid interventricular septum. Thirty subjects without cardiac diseases served as the control group. Transthoracic and transesophageal echocardiography were performed in all subjects to measure the following: left ventricular dimension, interventricular septal thickness and peak velocity at the left ventricular outflow tract by transthoracic echocardiography; the lengths and the thicknesses of the rough zone of the anterior and posterior mitral leaflets at mid-diastole and the distance between the tip of the posterior papillary muscle and the anterior mitral annulus by transesophageal echocardiography. The presence of systolic anterior motion of the mitral complex, contact between the anterior mitral leaflet and the interventricular septum during diastole, and the occurrence of mitral valve prolapse (MVP) were also investigated. The maximum area and timing of MR during systole was measured by M-mode color Doppler technique. The following results were obtained. 1. MR was observed in 35 (88%) of the 40 patients with hypertrophic cardiomyopathy. The maximum regurgitant area in the obstructive group was significantly greater than in the other groups, and the regurgitation was frequently pansystolic. 2. The lengths of both mitral leaflets at mid-diastole were significantly greater in both groups with hypertrophic cardiomyopathy than in the other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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 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.

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)

Pulmonary venous flow (PVF) patterns in left heart failure were evaluated using transesophageal pulsed Doppler echocardiography in 30 patients with dilated hearts (DH) and 30 normal subjects. Eighteen patients had myocardial infarction and 12 patients had dilated cardiomyopathy. The diagnostic criteria by using M-mode echocardiography were left ventricular end-diastolic dimensions (LVDd) of 5.5 cm or more and % LV fractional shortening (%FS) of less than 30%. Peak velocities of the first systolic (PVS1) and second systolic (PVS2) forward waves of PVF, %FS and total amplitude of mitral annular motion in the patient group were significantly decreased compared with the normal group. However, there were no differences in these parameters between the 22 patients (DH-1 group) with a mean pulmonary capillary wedge pressure (PCWP) of less than 18 mmHg and 8 patients (DH-2 group) with a PCWP of 18 mmHg or greater. Peak velocities of the diastolic forward wave of PVF and the early diastolic wave (D) of the LV inflow velocity in the DH-1 group were significantly decreased, and the peak velocity of the atrial contraction wave (A) of the LV inflow velocity was increased compared with those of the normal group. D of the LV inflow velocity, peak velocity of the diastolic forward wave, and peak velocity of the atrial systolic backward wave of the PVF in the DH-2 group were significantly increased compared with those of the DH-1 group. Significant positive correlations were observed between peak velocity of the diastolic forward wave and D or PCWP in the patient group, but the latter relationship was not linear. The A/D ratio of the LV inflow velocity was significantly decreased, and the ratio of the amplitudes of atrial contraction wave to total vertical deflection on the apexcardiogram of the DH-2 group were significantly increased compared with those of the DH-1 group. A patient with extensive myocardial infarction associated with development of severe LV dysfunction (PCWP = 23 mmHg) and a "pseudonormalization" pattern of LV inflow velocity demonstrated markedly increased peak velocities of the diastolic and atrial systolic forward wave, and decreased PVS2. However, the peak velocities of the diastolic and atrial systolic forward wave were decreased, and that of PVS2 was increased with fair improvement of LV dysfunction (PCWP = 10 mmHg) and with compensatory augmentation of the atrial contraction wave A of LV inflow velocity.(ABSTRACT TRUNCATED AT 400 WORDS)

To clarify the characteristics of the jugular venous pulse and its genesis in Ebstein's anomaly, 6 patients with Ebstein's anomaly whose mean age was 45 +/- 9 years, and 10 normal subjects with a mean age of 27 +/- 6 years were studied by phono-mechanocardiography and echocardiography. The parameters included the relative height of the jugular "c" wave, the relative timing of the upstroke (Q-Cu interval) and the peak of the jugular "c" wave (Q-Cpeak interval), the relative timing of the upstroke of the carotid artery pulse, the relative timing of tricuspid valve closure (Q-Tc interval), the excursion of the closing motion of the anterior tricuspid leaflet (TV excursion), the distance between the anterior mitral annulus and the septal tricuspid annulus (M-T distance), the area of atrialized right ventricle (ARV area) and the maximum area of the tricuspid regurgitant signal. Among 6 patients with Ebstein's anomaly, tricuspid regurgitation was predominant in 4 and mild in the remaining 2. The results were as follows: 1. A large jugular "c" wave was observed in 4 of the 6 patients. Two patients with large ARV area had giant "c" wave. 2. The interval of the upstroke of the carotid artery pulse and that of the jugular "c" wave was about 39.2 msec. 3. The Q-Tc interval was significantly longer and the TV excursion was significantly greater in the patients than in the normal controls. 4. There was only a weak positive correlation between the Q-Cpeak interval and the Q-Tc interval. No significant correlation was observed between the relative height of the jugular "c" wave and the TV excursion. 5. There was a positive correlation between the relative height of the jugular "c" wave, the ARV area and M-T distance. 6. No obvious correlation was observed between the grade of tricuspid regurgitation and the relative height of the jugular "c" wave. These results suggest that augmentation of the "c" wave of the jugular venous pulse is characteristic of Ebstein's anomaly and that it correlates closely with the severity of displacement of the tricuspid valve and the size of the atrialized right ventricle.

To evaluate the relationships between regurgitant flow dynamics of tricuspid regurgitation (TR) and cardiac physical signs, and to clarify the role of atrial function on central venous flow, we investigated physical signs by cardiac auscultation and palpation of the liver. In addition, phonocardiography, jugular venous and hepatic pulse tracings and Doppler echocardiographic recordings were performed. The subjects, 109 patients with Doppler-detected TR, were categorized as an SR group of 42 with sinus rhythm, an Af group of 63 with atrial fibrillation and four with sinus arrest. Thirty-five patients underwent open heart surgery before six months or more. Results were as follows: 1. In the Af group, the maximum systolic flow velocity data in the superior vena cava (SVC) and hepatic vein (HV) correlated well with the maximum tricuspid regurgitant signal area on the color Doppler echocardiogram, and systolic backward flow from the heart was more evident in the HV than in the SVC. In the SR group, however, no correlation was observed between the maximum systolic flow velocity and the TR signal area, and systolic backward flow was not evident even in cases with severe TR. 2. After open heart surgery, systolic flow velocities in the SVC and HV were significantly decreased in the SR group compared to the Af group. 3. There was close correlation between the presence of hepatomegaly and systolic backward flow towards the liver. Hepatomegaly was more marked in the Af group than in the SR group. 4. Jugular venous and hepatic pulse data correlated well with the flow velocity data in the SVC and HV and with the TR signal area. 5. Intensity of the tricuspid regurgitant murmur as estimated by the Levine's classification correlated relatively well with the systolic pressure gradient between the right ventricle and right atrium as calculated by the modified Bernoulli equation, but did not correlate with the TR signal area. From these results, we conclude that the intensity of the tricuspid regurgitant murmur and the jugular venous or hepatic pulse patterns are useful for evaluating tricuspid regurgitant dynamics, when they are applied clinically with precise recognition of their significance and limitations, and that sinus rhythm or atrial fibrillation is also an important factor.

The genesis and clinical significance of an apical diastolic rumble after replacement with mitral Björk-Shiley prosthesis were studied in 20 patients by left ventricular (LV) inflow dynamics using Doppler echocardiography. 1. The rumble was audible in 17 of the 20 patients (85%). In all but one patient, its intensity was less than Levine 2/6. Duration of the rumble ranged from 248 to 544 (mean 377) msec. There was no case of prosthetic valve dysfunction. Duration of the slow filling wave (SF interval) of the apexcardiogram in 19 cases ranged from 150 to 541 (mean 317) msec, and it correlated significantly with the duration of the rumble (r = 0.95) in 15 cases. 2. In 20 patients, peak velocity of the LV inflow obtained from continuous wave Doppler echocardiograms ranged from 1.17 to 1.89 (mean 1.56) m/sec, and pressure half time (PHT) ranged from 82 to 233 (mean 134) msec. In 19 patients, the SF interval correlated significantly with PHT (r = 0.87), but not with peak inflow velocity. 3. Peak inflow velocity was significantly slower in cases without a rumble than in cases with a rumble. PHT and the SF interval tended to be shorter in the former than in the latter. 4. There was no significant difference in the SF interval, peak inflow velocity and PHT between eight patients with smaller valve sizes (less than or equal to 25 mm) and 12 with larger valve sizes (greater than or equal to 27 mm). 5. There was no obvious relation between the direction of the main LV inflow jet as assessed by Doppler color flow mapping and the presence of the rumble in 19 patients. 6. In 19 patients, the SF interval correlated significantly with left atrial dimension (r = 0.47), but it did not correlate with LV end-diastolic dimension, fractional shortening of the LV, and the peak lengthening rate of LV internal dimension. 7. Three patients with both the rumble and SF lasting 500 msec had prolonged PHT longer than 190 msec. One of these three had congestive heart failure and suspected prosthetic mitral valve stenosis. From these results, we concluded that an apical diastolic rumble after replacement with mitral Björk-Shiley valve is mainly due to the increase in resistance and velocity of the LV inflow, and that both durations of the rumble and the SF intervals as well as PHT of the Doppler echocardiogram are useful in detecting stenosis of prosthetic mitral valves.

The genesis of a musical systolic murmur produced by systolic anterior motion (SAM) of the mitral apparatus was investigated in four patients using phonocardiography and echocardiography. Two patients (Case 1 and 3) had hypertrophic cardiomyopathy (one, the obstructive type; the other, the nonobstructive type) and the remaining two (Case 2 and 4) had redundant chordae tendineae. 1. In every patient, regular oscillation of the SAM was observed, coinciding in time with the musical systolic murmur, which was simultaneously recorded. The fundamental frequency of the musical systolic murmur was recorded as integrally multiplied numbers of the SAM. Such regular oscillation was not observed in the echograms of other cardiac structures. In a patient with hypertrophic obstructive cardiomyopathy (Case 1), both the amplitude and oscillation of the SAM were increased by amyl nitrite inhalation, and were decreased by angiotensin II infusion. Correspondingly, the intensity of the musical murmur showed similar reaction. No findings suggestive of mitral valve prolapse or mitral regurgitation were found in any patients. Therefore, the oscillation of the SAM produced by blood ejected from the left ventricle was considered the source of the musical systolic murmur in these patients. 2. Two patients with redundant chordae tendineae had no clinical abnormalities except for chordal redundancy; therefore, the musical murmur in these cases was considered to be functional. Particularly, one of them was compatible in character with the so-called Still's murmur. In conclusion, the regular oscillation of the SAM may be the source of the musical systolic murmur, and they must be taken into consideration as part of the genesis of Still's murmur.

To clarify the genesis of a high-pitched diastolic rumble in mitral stenosis, 51 patients with mitral stenosis were studied. They were subdivided into two groups based on the pitch of a rumble; six patients with a high-pitched rumble and 45 patients with an ordinary low-pitched rumble. Phonocardiography, and M-mode and two-dimensional (2-D) echocardiography were performed in all patients. Color and continuous wave Doppler echocardiography were performed in four patients with a high-pitched rumble and in 13 with a low-pitched rumble. Results obtained were as follows: 1. Points of the maximum intensity of a rumble: A low-pitched rumble was best heard at the apex in all patients. A high-pitched rumble was best heard at the mesoapical area, except in one patient who had an oval mitral orifice by 2-D echocardiography. 2. Correlation between the pitch of rumble and the shape of the mitral orifice: In five of the six patients with a high-pitched rumble, the mitral orifice had a tadpole-shaped deformity, in which commissural fusion and valvular thickening were more marked anterolaterally than posteromedially. Among 45 patients with oval, slit or pinhole-like valve orifices, only one had a high-pitched rumble. 3. Direction of the left ventricular (LV) inflow jet as observed by color Doppler echocardiography: On the short-axis view at the level of the papillary muscles, the inflow jet was directed toward the medial portion of the LV cavity in the patients with a high-pitched rumble. However, it was directed towards the central portion of the LV cavity in all patients with a low-pitched rumble. On the apical long-axis view, no distinct difference was detected in the direction of the LV inflow jet between the two groups. 4. Other findings: There were no significant differences between the two groups in the mitral orifice area, the peak velocity of LV inflow, fractional shortening of the LV, dimension of the left atrium, Wells' index and the degree of organic change in the subvalvular structures. These results suggest that the deformity of the mitral valve and resultant changes in the direction of the LV inflow jet may play an important role in the mechanism of producing a high-pitched diastolic rumble in mitral stenosis.

The genesis and clinical significance of the aortic ejection sound with a low-frequency predominance and delayed appearance were studied. This is recorded on the phonocardiogram in some patients with left ventricular dysfunction. Subjects studied consisted of 10 patients with a low-pitched ejection sound and seven patients with an ordinary high-pitched aortic ejection sound. No patients had echocardiographic findings suggestive of organic lesions of the aortic valve. Time relationships among the ejection sounds, aortic valve echograms and carotid artery pulses, and then movements of the aortic valve cusps and non-invasively estimated left ventricular systolic function were compared between the two groups. Results were as follows: 1. The low-pitched ejection sound: 1) The beginning of the sound was nearly coincident with the onset of the upstroke of the carotid artery pulse and the initial full opening of the aortic valve cusps. 2) The beginning of the ejection systolic murmur followed immediately after the ejection sound. 3) The amplitude of the sound was closely related to the height of the carotid artery pulse in a case of atrial fibrillation. 2. The low-pitched ejection sound vs the high-pitched ejection sound: 1) The onset of the low-pitched ejection sound was significantly delayed. 2) The amplitude and the velocity of the initial opening of the aortic valve cusps were significantly decreased. 3) The preejection period (PEP) was significantly prolonged; the ejection time (ET) was significantly shortened; and the PEP/ET ratio was significantly increased.(ABSTRACT TRUNCATED AT 250 WORDS)

In the present study, the ballooning pattern of the anterior mitral valve (AMV) in mitral valve prolapse (MVP) was investigated, and new diagnostic criteria for MVP were established using two-dimensional and Doppler echocardiography. The study population consisted of 164 patients with prolapse of the AMV alone, including 86 patients with idiopathic MVP, 52 associated with atrial septal defect (ASD), 17 having chordal rupture and nine associated with connective tissue disorders. There were 60 normal controls. The results were as follows: 1. The AMV was divided into two zones, clear and rough (CZ and RZ), according to the point of insertion of the strut chordae based on two-dimensional long-axis echocardiograms of the left ventricle. The severity of AMV prolapse was determined by an angle between the posterior aortic wall (PAO)-CZ and the CZ-RZ. a) Type A: Apparently there was a transitional point between CZ and RZ, despite normal PAO-CZ and CZ-RZ angles. The RZ showed mild ballooning or prolapse into the left atrium. b) Type B: Although the PAO-CZ angle was normal, the CZ-RZ angle was markedly narrowed. Therefore, prolapse of the RZ was more severe compared with that of type A. c) Type C: An overall zone of the AMV showed ballooning or prolapse into the left atrium due to a narrowed PAO-CZ angle. 2. Type B prolapse was frequently observed in idiopathic MVP (58%), the ASD group (71%) and the chordal rupture group (71%), and type C prolapse in MVP of connective tissue disorders (89%). 3. All of 18 patients (100%) with type A, 48 of 99 (48%) with type B, and 10 of 47 (21%) with type C could not be diagnosed as MVP using Gilbert's criterion. 4. Doppler mitral regurgitation (MR) was detected in 40 of the 47 patients (85%) with type C in 56 of the 99 (59%) with type B, and in seven of the 18 (39%) with type A. These results suggested that classification of the two-dimensional echocardiography of the AMV into two zones, clear and rough (CZ and RZ), could contribute to determining not only the severity of AMV prolapse, but also to the extent of myxomatous changes of the AMV and to evaluating the correlations between the degree of MVP and the incidence of MR.

To evaluate the relationship between the motion pattern and degree of organic change of the anterior mitral leaflet (AML) and the features of the mitral component of the first heart sound (M1) or the opening snap (OS), 37 patients with mitral stenosis (MS) were studied by auscultation, phonocardiography and echocardiography. Based on the features of M1 and OS according to auscultation and phonocardiography, the patients were categorized as group I, 18 patients with loud and snappy M1 and OS; group II, 12 patients with snappy M1 but small and dull OS; and group III, seven patients with small and dull M1 and OS. Intensities of M1 and OS were calculated by the ratios of their amplitudes to the aortic component of the second heart sound on the high frequency phonocardiograms recorded at points of the maximum intensities, respectively. Echocardiographic parameters related to productions of M1 and OS were obtained from M-mode and two-dimensional echograms of the AML; they were amplitudes and velocities on closing and opening, M1 area defined as that between end-diastolic and systolic echoes, OS area between systolic and early diastolic echoes, the doming area between the trailing edge of an early diastolic echo and a line projected from the anterior annulus to the tip of the leaflet, and the degree of systolic ballooning. Results were as follows: 1. Significant differences in the area of the mitral valve orifice were found among three groups. The area was maximum in group II, minimum in group III and intermediate in group I. 2. In group I, the body of the AML was pliable, resulting in a ballooning into the left atrium in systole and a marked doming toward the left ventricle in early diastole. Various parameters related to the production of M1 and OS in group I were significantly increased as compared with those of the other two groups. 3. In group II, the body of the AML was not pliable in spite of mild organic changes in the valve. The degree of early diastolic doming was mild. Compared to group III, the intensity of M1 in group II was significantly larger, but no significant difference was observed in the parameters related to the production of M1 between the two groups.(ABSTRACT TRUNCATED AT 400 WORDS)

To assess right ventricular (RV) filling dynamics, RV inflow velocity patterns of pulsed Doppler echocardiograms and jugular pulse tracings were analyzed in 59 patients with various types of RV overloads and in 20 normal subjects. The patients were classified as (1) RV volume overload group (RVVO) consisting of 25 patients with atrial septal defect (ASD) without pulmonary hypertension (PH), (2) RV pressure overload group consisting of 26 patients including 12 with primary pulmonary hypertension (PPH), eight with mitral stenosis, three with pulmonary stenosis and three with cor pulmonale, and (3) RV volume and pressure overload group consisting of eight patients with ASD and PH. The acceleration time (AT), deceleration time (DT) and the A/D ratio were measured from the RV inflow velocity patterns, and v-y interval and the y/H ratio were measured from jugular pulse tracings. The results were as follows: 1. AT was significantly prolonged in groups with pressure overload as well as pressure and volume overload compared with that of the normal controls. 2. DT was significantly prolonged in all overload groups compared with that of the normal controls except for PPH, and was particularly prolonged in the group with pressure overload. 3. The A/D ratio was significantly increased in all overload groups, particularly in the groups with pressure overload. 4. In patients with volume overloads, the v-y interval was longer and the y/H ratio was higher than in the normal controls. RVVO shifted to the right and superiorly. The reverse was true in the pressure overload group, and the high ratios were observed in the remainder. 5. In 12 patients with ASD evaluated pre- and postoperatively, AT, DT and the A/D ratio were restored to normal after surgery. These findings suggest that RV volume overload was characterized not only by increased inflow velocity during the rapid filling period, but prolongation of this period and compensatory increase of atrial inflow velocity. However, the pressure overload group had disturbed rapid filling and a decrease in end-diastolic RV compliance. The group with both pressure and volume overloads was between the two. In conclusion, the mode of RV filling in patients with RV overload showed various patterns depending on the type of overload. The RV inflow velocity pattern recorded by pulsed Doppler echocardiography is of use in discriminating these varieties.

To clarify the mechanisms and time course of mitral regurgitation (MR) in mitral valve prolapse (MVP), the relationship between the timing of MR flow patterns on pulsed Doppler echocardiography and phase of mitral valve prolapse on two-dimensional echocardiography was investigated. 1. Thirty-seven patients with MVP were followed by pulsed Doppler echocardiography for one to six years with an average of 2.5 years. At the initial examination, the patients were classified in five subsets on the basis of the presence or timing of MR: 10 without MR, five with early systolic MR, one with mid-systolic MR, 15 with late systolic MR and six with pansystolic MR. During the follow-up period, the timing of MR did not change in 21 patients (three with no MR, five with early systolic MR, seven with late systolic MR and six with pansystolic MR). Various changes were observed in 16 patients, i.e., developments of late systolic MR from no MR in four, of pansystolic from no MR in three, from late systolic MR in five and from mid-systolic MR in one, and disappearing late systolic MR in three. 2. Mitral annular diameter and the prolapsing phase of 118 patients with MVP (44 without MR, eight with early systolic MR, 30 with late systolic MR and 36 with pansystolic MR) were examined by long-axis two-dimensional echocardiography. The mitral annular diameter in patients with early systolic MR was significantly less than that of other MR groups, and the diameter in patients with pansystolic MR was markedly increased. The timing of MR was determined according to the prolapsing phase and the grade of the prolapse and the systolic size of the mitral annulus. Six of the eight patients with early systolic MR first had early systolic prolapse of either mitral leaflet, and then the regurgitant gap of the mitral valve orifice was plugged by the prolapsing leaflet and/or the narrowed mitral annulus during mid-to-late systole. In 18 of the 30 patients with late systolic MR, the grade of prolapse of the mitral valve during mid-to-late systole was more severe, compared with that of early systole. The results of the present study indicated that the occurrence of MR in MVP is various in timing (early, mid-, late or pansystole) and shows various changes the during follow-up study, and that pulsed Doppler echocardiography allows phase analysis of MR in MVP.

A hitherto unrecognized case of van der Hoeve's syndrome complicated by Ebstein's anomaly, and prolapse of the mitral and aortic valves was reported. A 46-year-old woman presented with blue sclera, osteogenesis imperfecta and a hearing loss, which are typical symptoms of this syndrome. The electrocardiogram showed a type B WPW syndrome. The phonocardiogram showed a loud and widely split first heart sound, an accentuated protodiastolic extrasound, a decrescendo regurgitant systolic murmur, and a presystolic murmur. The x descent of the jugular phlebogram was obliterated by a markedly increased c wave. Based on M-mode and two-dimensional echocardiograms, 1) the interventricular septal motion was paradoxical and the closure of the tricuspid valve was delayed, 2) the septal tricuspid leaflet was displaced toward the apex from its normal annular insertion on the apical four-chamber view, 3) the three leaflets of the tricuspid valve were abnormally elongated, 4) the anterior mitral leaflet and the non-coronary cusp of the aortic valve were elongated and prolapsed. Doppler echocardiography detected severe tricuspid and mild mitral regurgitations. We suggest that the development of Ebstein's anomaly is possibly related to that of osteogenesis imperfecta genetically and that not only Ebstein's anomaly but a connective tissue disorder contributes to the elongated and prolapsed leaflets.