[Evaluation of cardiac function by pulsed and continuous Doppler echocardiography and tissue Doppler imaging].
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Biomedical subjects
Publications and source records attributed to A Iuchi.
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We investigated temporary changes in left atrial appendage (LAA) flow velocity patterns in patients undergoing electrical cardioversion for chronic isolated atrial fibrillation, and evaluated the role of active LAA contraction in directing blood flow to the left atrial main chamber and left ventricle. The study consisted of 26 patients with chronic isolated atrial fibrillation treated with electrical cardioversion and 20 normal controls in sinus rhythm. Using transthoracic and transesophageal Doppler echocardiography, we recorded transmitral, pulmonary venous, and LAA flow velocity patterns before, 24 hours, and 1 week after cardioversion in all subjects. In the 15 patients who underwent successful cardioversion, the maximal LAA area 24 hours after cardioversion was smaller than the area before cardioversion, whereas LAA ejection fraction during atrial systole and peak atrial systolic emptying velocity of the LAA flow were lower 24 hours after cardioversion than those in the control group. One week after cardioversion, maximal LAA area and LAA peak atrial systolic emptying velocity were restored to levels approximately equivalent to those in the control group, although LAA ejection fraction was lower than in the control group. Maximal LAA area and LAA peak atrial systolic emptying velocity correlated negatively and positively with LAA ejection fraction, respectively, 24 hours and 1 week after cardioversion. These results suggest that LAA and the left atrial main chamber show stunning 24 hours after cardioversion, and the atrial systolic emptying wave of LAA flow is generated by active LAA contraction.
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.
BACKGROUND: It has become evident that mitral regurgitation (MR) is not uncommon in healthy subjects, and Doppler color flow mapping is a technique that imparts important information relevant to its detection. HYPOTHESIS: Using transthoracic echocardiography, this study evaluated the mechanism of physiologic MR in young normal subjects using transthoracic echocardiography. METHODS: The study population consisted of 48 young normal subjects (mean 21 +/- 5 years) with MR (physiologic MR group), 40 age-matched young normal subjects (mean 20 +/- 5 years) without MR (control group), 45 patients (mean 41 +/- 15 years) with mitral valve prolapse with MR (MVP group), and 27 patients (mean 59 +/- 13 years) with ruptured chordae tendineae (rupture group). RESULTS: Men were predominant in the rupture group, whereas there were no significant gender differences in the other three groups. Left ventricular end-diastolic dimension and left atrial systolic dimension were slightly smaller in the physiologic MR group than in the control group, but were significantly smaller than those in the MVP and rupture groups. The ratio of the maximum anteroposterior diameter to the maximum transverse diameter on chest radiography and the ratio of the short- to long-axis diameter of the left ventricular cavity at end diastole, determined from two-dimensional short-axis echocardiogram, were significantly lower in the physiologic MR group than in the other three groups. Mitral regurgitation occurred more frequently at the posteromedial commissural site in the physiologic MR and MVP groups, whereas there was no preference for location in the rupture group. Early systolic MR was often observed in the physiologic MR group, whereas pansystolic MR was common in the MVP and rupture groups. CONCLUSION: As a causal mechanism for physiologic MR detected in young normal subjects, "flattening" of the thorax during growth may cause morphologic abnormalities of the left atrial and ventricular cavities, resulting in spatial imbalance of the mitral complex and resulting in malcoaptation of the valve.
OBJECTIVE: To investigate the influence of the absence of the pericardium on the left ventricular wall, particularly on interventricular septal motion, using M mode and cross sectional short axis echocardiography in patients with congenital total absence of the left pericardium. METHODS: 21 patients with, congenital total absence of the left pericardium were divided into three groups according to the interventricular septal motion; systolic type (n = 6) with paradoxical motion during systole, diastolic type (n = 11) with abnormal posterior motion during mid to late diastole, and mixed type (n = 4) with paradoxical motion during systole and abnormal posterior motion during diastole. RESULTS: On cross sectional short axis echocardiograms of the left ventricle, in the diastolic type the degree of angular displacement of the papillary muscles during end diastole to end systole showed excessive anticlockwise rotation about the long axis of the left ventricle without marked anteroposterior displacement. In the systolic type, there was shift of the left ventricle towards the anteromedial portion in systole and towards the posterolateral portion in diastole without significant rotation. There was a significantly positive correlation between the degree of angular displacement and the amplitude of diastolic interventricular septal motion during mid to late diastole in all patients. CONCLUSIONS: There was abnormal interventricular septal motion during systole and diastole in patients with total absence of the left pericardium. Abnormal systolic motion was induced by anteroposterior displacement of the left ventricle, and abnormal diastolic motion by left ventricular rotation about the long axis of the heart during the cardiac cycle. Analysis using cross sectional echocardiography was useful for elucidating the mechanisms of abnormal interventricular septal motion.
We report a patient in whom hypertrophic cardiomyopathy, with both left ventricular hypertrophy and diastolic dysfunction, was masked by acute severe aortic regurgitation and marked left ventricular dilation. Upon admission, 1) two-dimensional echocardiogram of the left ventricle revealed a dynamic and flail vegetation on the aortic right coronary cusp and marked left ventricular dilation, 2) a massive aortic regurgitant signal was recorded by color Doppler flow imaging, and 3) transmitral flow velocity by pulsed Doppler echocardiogram revealed a pseudonormalization. However, symmetric hypertrophy of the left ventricular wall, a decrease in early diastolic wave and a compensatory increase in atrial systolic wave of the transmitral flow velocity appeared after successful aortic valve replacement.
Left atrial appendage (LAA) flow velocities prior to electrical cardioversion were recorded using transesophageal pulsed Doppler echocardiography to predict initially successful cardioversion of isolated atrial fibrillation (AF). Patients with AF were placed into either a success group (19 patients) in which sinus rhythm was maintained for at least 2 days or a failure group (12 patients). The duration of AF was shorter in the success group. The maximum left atrial diameter was the same for the two groups. The maximum LAA area was smaller in the success group. The maximum forward and backward LAA velocities were greater in the success group, as were the mean forward and backward LAA velocities. In the patients with mean LAA flow velocities greater than 19 cm/sec, the success of cardioversion could be predicted with high sensitivity (80%) and specificity (88%). We conclude that the duration of AF, the maximum LAA area, and LAA flow velocities prior to cardioversion predict the initial recovery of sinus rhythm for isolated AF.
BACKGROUND AND AIMS OF THE STUDY: Changes in tricuspid inflow and regurgitant flow dynamics were evaluated in patients with functional tricuspid regurgitation (TR) who underwent mitral valve replacement (MVR) with and without tricuspid annuloplasty (TAP). METHODS: In a group of 30 patients, all with atrial fibrillation, 15 underwent TAP performed according to the modified De Vega technique; the remaining 15 did not undergo TAP. Patients were studied before and serially after surgery, using pulsed and color Doppler echocardiography. The mean follow up was 4.7 years in the TAP group and 5.1 years in the non-TAP group. RESULTS: In the TAP group, immediately after surgery, the area of the TR jet decreased markedly, and the deceleration time of the tricuspid inflow velocity wave was significantly prolonged compared with that before surgery. By contrast, in the non-TAP group, both the area of the TR jet and deceleration time of tricuspid inflow velocity were virtually unchanged. The area of the TR jet remained small for a long period in the TAP group, but in non-TAP patients was increased in four cases over seven years, with two patients developing right-sided heart failure. Recent data showed the area of the TR jet to be significantly smaller, with maximum tricuspid inflow velocity significantly increased, and deceleration time of the tricuspid inflow velocity wave significantly prolonged in the TAP group compared with the non-TAP group. CONCLUSIONS: In patients with functional tricuspid regurgitation undergoing MVR, concomitant TAP may cause mild tricuspid stenosis, but produces sustained preventive effects against TR. Careful follow up is needed in patients who have not undergone TAP, as TR is not markedly decreased and may even be exacerbated. Aggressive TAP is recommended in patients showing dilatation of the tricuspid annulus, even if TR is mild.
We describe a patient with Ebstein's anomaly in whom Doppler echocardiography was used to clarify the mechanism responsible for 'sail sound' and tricuspid regurgitation associated with this condition. Phonocardiography revealed an additional early systolic heart sound, consisting of a first low-amplitude component (T1) and a second high-amplitude component (T2, 'sail sound'). In simultaneous recordings of the tricuspid valve motion using M mode echocardiography and phonocardiography, the closing of the tricuspid valve occurred with T1 which originated at the tip of the tricuspid leaflets, while T2 originated from the body of the tricuspid leaflets. Using color Doppler imaging, the tricuspid regurgitant signal was detected during pansystole, indicating a blue signal during the phase corresponding to T1 and a mosaic signal during the phase corresponding to T2 at end-systole. Thus, 'sail sound' in patients with Ebstein's anomaly is not simply a closing sound of the tricuspid valve, but a complex closing sound which includes a sudden stopping sound after the anterior and/or other tricuspid leaflets balloon out at systole.
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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.
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.
HYPOTHESIS: This study was undertaken to clarify the mechanisms of mitral regurgitation (MR) in dilated hearts. METHODS: In all, 68 patients with dilated heart and MR, including 26 patients with dilated cardiomyopathy (DCM), 24 with prior anterior myocardial infarction (A-MI), and 18 with prior posteroinferior myocardial infarction (I-MI), as well as 25 normal subjects were examined by transesophageal two-dimensional and color Doppler echocardiography. RESULTS: The maximum area of the MR signal in the DCM group correlated positively with the anteroposterior diameter of the mitral annulus at late systole. Although the coaptation edge length of the anterior and posterior mitral leaflets appeared shorter in dilated hearts than in the hearts of controls, a significant difference did not exist. The length of the coaptation edge correlated negatively with the maximum area of the MR signal in all dilated hearts, and characteristic systolic displacement of the coaptation point of both mitral leaflets occurred. The MI groups demonstrated anterior and posterior displacement in the direction of the short axis of the left ventricle in the A-MI and I-MI groups, respectively. However, the DCM group demonstrated inferior displacement toward the long axis of the left ventricle; its magnitude correlated positively with the maximum area of the MR signal. CONCLUSION: A major cause of MR in dilated hearts is mitral malcoaptation due to displacement of the coaptation point of the mitral leaflets along the long or short axis of the left ventricle. This is caused by left ventricular enlargement and/or asynergy of the left ventricular wall, rather than by a decrease in mitral coaptation edge length due to mitral annular dilation.
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.
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.
OBJECTIVE: To investigate the relationship between the angiotensin converting enzyme (ACE) gene polymorphism and the effects of the ACE inhibitor enalapril on left ventricular hypertrophy and impaired diastolic filling. DESIGN AND METHODS: Enalapril (5-10 mg/day) was administered for 12 months to 60 previously untreated patients with essential hypertension. M-mode and pulsed Doppler echocardiography were performed before and after treatment, and changes in various parameters after treatment with enalapril were examined. ACE gene polymorphism was examined by the polymerase chain reaction method and the patients were classified as having the 190 bp deletion homozygous (DD) genotype, the 490 bp insertion homozygous (II) genotype or the 490 bp insertion 190 bp deletion heterozygous (ID) genotype. RESULTS: The DD genotype was observed in 10 patients (17%), the ID genotype in 24 patients (40%) and the II genotype in 26 patients (43%). Plasma ACE activity before treatment with enalapril was significantly higher in seven patients with DD genotype than it was in 18 patients with ID genotype and in 14 patients with II genotype. In all of the 60 patients, the left ventricular mass index, the peak atrial systolic velocity:early diastolic velocity ratio and the deceleration time from the peak of the early diastolic wave to the baseline in transmitral flow velocity were decreased significantly after treatment with enalapril. The changes in left ventricular mass index and atrial systolic velocity:early diastolic velocity ratio after enalapril administration were significantly greater in the DD genotype group than they were in the other two genotype groups. CONCLUSION: Enalapril-induced regression of left ventricular hypertrophy and improvement in left ventricular impaired diastolic filling were significantly greater in the DD genotype group than they were in the ID and II genotype groups, suggesting that the circulating and tissue renin-angiotensin systems, particularly the former system, are most active in hypertensive patients with the DD genotype.
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.
A rare case of annulo-aortic ectasia is reported in a 65-year-old man who had aortic and mitral regurgitation during systole and diastole. He was hospitalized for further examination of the heart due to cardiomegaly and heart murmurs. Aortography revealed severe aortic regurgitation. On color Doppler flow imaging, we could detect red aortic regurgitant signals in the left ventricular cavity during diastole, and mosaic and blue mitral regurgitant signals in the left atrial cavity during systole and diastole associated with a relatively long R-R interval, respectively. The unique observation of diastolic mitral regurgitation is discussed.