Doppler techniques in the detection of valvular regurgitation: their value and limitations

To evaluate the clinical value of various Doppler techniques in detecting valvular regurgitation, we compared the sensitivity, timing and duration of regurgitation, and the peak velocity of regurgitant signals among conventional pulsed Doppler, color Doppler, continuous wave Doppler and HPRF Doppler echocardiography. 1. Sensitivity of Doppler techniques in detecting mitral regurgitation: Among fifty patients with mitral regurgitation confirmed by left ventriculography, mitral regurgitation was detected in 48 (96%) using color Doppler and pulsed Doppler echocardiography; in 41 (82%) by HPRF Doppler; and in 37 (74%) by continuous wave Doppler echocardiography. In 103 consecutive normal volunteers, mitral regurgitant signals were detected in 46 (45%) by color Doppler, in 39 (38%) by pulsed Doppler, in 16 (16%) by HPRF Doppler, and in 8 (8%) by continuous wave Doppler echocardiography. 2. Timing and duration of regurgitant signals: To assess the timing and duration of regurgitant signals, 43 patients with regurgitant signals of short duration during systole or diastole were studied using M-mode color Doppler echocardiography. Using the latter method, regurgitant signals throughout systole and the isovolumic relaxation period could be demonstrated in all but four patients who had regurgitant signals of short duration during systole, but suggesting mitral or tricuspid regurgitation. In all patients with regurgitant signals of short duration during diastole, aortic or pulmonary regurgitant signals throughout diastole could be demonstrated with M-mode color Doppler echocardiography. Thus, this technique is superior to conventional pulsed Doppler echocardiography for detecting accurate timing and duration of valvular regurgitation. 3. Peak velocity of regurgitant flow: To compare the peak velocity of regurgitant flow by continuous wave Doppler and by HPRF Doppler echocardiography, 20 patients with mitral regurgitation and 22 patients with tricuspid regurgitation were examined using the both methods. In patients with severe mitral regurgitation, the peak velocity detected by HPRF Doppler echocardiography correlated well (r = 0.96) with that detected by continuous wave Doppler echocardiography. However, in patients with mild mitral regurgitation, the peak velocity detected by HPRF Doppler echocardiography was higher than that detected by continuous wave Doppler echocardiography. In patients with severe tricuspid regurgitation, the peak velocity had a close correlation (r = 0.99) with the both techniques. In patients with mild tricuspid regurgitation, the peak velocity was higher by HPRF than by continuous wave Doppler echocardiography. In conclusion, color or pulsed Doppler echocardiography should be used for detecting valvular regurgitation. M-mode color Doppler echocardiography is superior to conventional pulsed Doppler echocardiography for detecting timing and duration of valvular regurgitation.(ABSTRACT TRUNCATED AT 400 WORDS)     

Accessory mitral valve associated with aortic and mitral regurgitation and left ventricular outflow tract obstruction in an elderly patient: a case report

A 65-year-old man was admitted to our hospital because of exertional dyspnea. Transthoracic and transesophageal echocardiography showed a parachute-like structure measuring 20 x 16 mm, which projected into the left ventricular outflow tract (LVOT) and passed through the aortic valve in systole, and prolapsed back into the left ventricular cavity in diastole. Moderate aortic and mitral regurgitation were also observed, as well as LVOT obstruction with a peak gradient of 30 mmHg. There were no other congenital cardiac abnormalities. In addition, real-time three-dimensional transthoracic echocardiography showed that the parachute-like structure in the LVOT was attached to the anterior mitral leaflet and left ventricular lateral wall by a chorda tendineae-like structure. The diagnosis of accessory mitral valve was based on the echocardiographic characteristics. Surgical treatment was performed because of the presence of accessory mitral valve, moderate aortic and mitral regurgitation, and LVOT obstruction. The postoperative course was uneventful, and the patient has been asymptomatic during a follow-up period of 24 months. Echocardiographic examination proved to be useful for the detection of accessory mitral valve.     

Evaluation of physiological mitral regurgitant flow using transesophageal Doppler echocardiography

Transesophageal Doppler echocardiography (TEDE) was performed to determine the incidence of physiological mitral regurgitation (MR) and the characteristics of regurgitant blood flow in presumably normal subjects. TEDE included color flow mapping, pulsed Doppler echocardiography and M-mode color flow mapping. Sixty-six surgical patients who had no histories or physical evidence of cardiac abnormalities were studied using TEDE under general anesthesia. MR flow was detected in 94% (62/66) of the patients by transesophageal color flow mapping. Transesophageal color flow mapping clearly differentiated physiological MR flow and signals generated from mitral valve closure. In 40% (25/62) of the patients whose MR flow was detected, transesophageal pulsed Doppler echocardiography (TEPD) revealed regurgitant signals lasting less than half of systole. Only 31% (19/62) had peak MR flow velocities greater than 1 m/sec. TEPD could not detect high velocities reflecting the pressure gradients across the mitral valve. Since the regurgitant volume was very small, TEPD may have been incapable of detecting high velocity components of the MR flow. In conclusion, our data suggested that nearly all normal subjects may have mild mitral regurgitation.     

The influence of atrioventricular asynchronous contraction on left and right ventricular performance]

To investigate the influence of atrioventricular asynchronous contraction on left and right ventricular performance, pulsed Doppler echocardiographic studies were performed in 10 patients who received permanent pacemaker (VVI mode), but without significant heart disease except for complete heart block. After setting the pacing rate at 40 per min, the performance was analyzed during the patient's own slow ventricular rate. Flow velocity patterns at the left (LVOT) and right ventricular outflow tracts (RVOT) were recorded by pulsed Doppler echocardiography, and ejection time (EjT), acceleration time (AcT), peak velocity (PV) and flow velocity integral (FVI), which is proportional to stroke volume, were measured for each outflow tract. When the patient's own atrial contraction occurred during ventricular systole, EjT, AcT, PV and FVI of flow at the LVOT and EjT, AcT and FVI of flow at the RVOT were decreased. Percent change of the FVI of flow at the RVOT (-34.6%) was significantly greater than that of flow at the LVOT (-16.2%, p < 0.01). These results indicate that the loss of right ventricular performance might play a prominent role in the genesis of the hemodynamic deterioration with atrioventricular asynchronous contraction.     

Evaluation of hepatic venous flow patterns using a pulsed Doppler technique

Evaluation of hepatic venous flow patterns was attempted by pulsed Doppler echocardiography. Subjects were 80 patients including those with dilated cardiomyopathy, old myocardial infarction, angina pectoris, pulmonary hypertension, constrictive pericarditis, tricuspid regurgitation (TR), lone atrial fibrillation, and post-cardiac surgery. Eleven normal subjects served as controls. The mean age was 53.0 +/- 12.4 years. Most of the TR patients had atrial fibrillation. Patients with aortic regurgitation and significant mitral regurgitation were excluded. Afterload stress by angiotensin II infusion was performed in 51 subjects, mainly for those with ischemic heart disease, cardiomyopathy and the normal controls. Hepatic venous flow patterns included double-peaked flow signals toward the right atrium, and the relationship between systolic (S) and diastolic flow velocities (D) was expressed as the velocity ratio [S/(S+D)]. A reversed flow during atrial systole was expressed as an "A wave" and that between the S and D waves, as an "O wave". Systolic flow velocity was less than diastolic flow velocity in cases with atrial fibrillation and the post-surgical cases. The velocity ratio was greater than 0.5 in nearly all patients with normal sinus rhythm, and less than 0.5 in cases with atrial fibrillation and the post-surgical cases. In the former, systolic flow velocity was less than diastolic flow velocity after defibrillation, in spite of restoration of normal sinus rhythm. These findings indicate that systolic flow velocity was influenced by atrial relaxation; diastolic flow velocity, by ventricular diastolic function. The A wave was increased in cases with pulmonary hypertension and A wave velocity in the hepatic vein correlated with systolic pulmonary artery pressure. In cases with tricuspid regurgitation, reversed flows were detected during ventricular systole both in normal sinus rhythm and in atrial fibrillation. After infusions of angiotensin II the velocity ratio increased in cases with dilated cardiomyopathy and in normal controls (p less than 0.01). The hepatic venous flow pattern after infusion in the former was characterized by dominant systolic and diminished diastolic flow velocities with a consequent increase in the velocity ratio toward 1.0, while a change in the ratio was less marked in normal controls. In conclusion, analysis of the hepatic venous flow pattern by pulsed Doppler echocardiography is very useful for evaluating cardiac function. A marked increase in the velocity ratio after angiotensin II infusion suggests decreased cardiac function.     

The significance of systolic anterior motion (SAM) on the mitral valve echo pattern in hypertrophic cardiomyopathy

The systolic anterior motion (SAM) of valve structures in the mitral echogram in hypertrophic cardiomyopathy (HCM) has previously been considered to be anterior motion and re-opening of mitral valve leaflets, causing left ventricular outflow tract (LVOT) obstruction and mitral regurgitation. Fifteen patients with HCM underwent cardiac catheterisation and were also examined by M-scan and mechanical real-time B-scan techniques. In all patients SAM was seen during M-scan echocardiography. The mitral valve leaflets were visualised during the entire cardiac cycle during real-time B-scanning without showing any re-opening in systole. Thickened papillary muscles have been observed in 12 patients and prominent chordae tendineae moving in the opposite direction to the anterior mitral valve leaflet in 10 patients. Four patients with SAM did not show mitral regurgitation during left ventricular angiography. In two patients without fixed haemodynamic obstruction, a complete SAM touching the interventricular septum was observed with prolonged apposition in one case. These findings suggest that SAM is due to the motion of chordae tendineae and/or papillary muscles traversing the single dimensional ultrasonic beam in systole, thus producing single linear or multiple spotty echoes within SAM. The mechanism of the upward motion of the subvalvular mitral valve apparatus in systole appears to be due to forceful contraction of the apical left ventricular posterior wall. The observation of SAM in patients without HCM also indicates that its presence during single dimensional echocardiography is neither diagnostic nor specific for HCM, LVOT obstruction or mitral regurgitation, and contradicts the assumption that the anterior mitral valve leaflet plays a significant role in the mechanism of LVOT obstruction. The salient feature of all conditions associated with abnormal mitral subvalvular motion is hyperkinetic contraction of the apical left ventricular posterior wall. Hyperkinetic left ventricular ejection appears to be the main factor in the complex development of an LVOT gradient in hypertrophic cardiomyopathy.     

Impact of left ventricular outflow tract area on systolic outflow velocity in hypertrophic cardiomyopathy: a real-time three-dimensional echocardiographic study.

OBJECTIVES: The aim of this study was to use real-time three-dimensional echocardiography (3DE) to investigate the quantitative relation between minimal left ventricular (LV) outflow tract area (A(LVOT)) and maximal LV outflow tract (LVOT) velocity in patients with hypertrophic obstructive cardiomyopathy (HCM). BACKGROUND: In patients with HCM, LVOT velocity should change inversely with minimal A(LVOT) unless LVOT obstruction reduces the pumping capacity of the ventricle. METHODS: A total of 25 patients with HCM with systolic anterior motion (SAM) of the mitral valve leaflets underwent real-time 3DE. The smallest A(LVOT) during systole was measured using anatomically oriented two-dimensional "C-planes" within the pyramidal 3DE volume. Maximal velocity across LVOT was evaluated by two-dimensional Doppler echocardiography (2DE). For comparison with 3DE A(LVOT), the SAM-septal distance was determined by 2DE. RESULTS: Real-time 3DE provided unique information about the dynamic SAM-septal relation during systole, with A(LVOT) ranging from 0.6 to 5.2 cm(2) (mean: 2.2 +/- 1.4 cm(2)). Maximal velocity (v) correlated inversely with A(LVOT) (v = 496 A(LVOT)(-0.80), r = -0.95, p < 0.001), but the exponent (-0.80) was significantly different from -1.0 (95% confidence interval: -0.67 to -0.92), indicating a significant impact of small A(LVOT) on the peak LVOT flow rate. By comparison, the best correlation between velocity and 2DE SAM-septal distance was significantly (p < 0.01) poorer at -0.83, indicating the superiority of 3DE for assessing A(LVOT). CONCLUSIONS: Three-dimensional echocardiography-measured A(LVOT) provides an assessment of HCM geometry that is superior to 2DE methods. These data indicate that the peak LVOT flow rate appears to be significantly decreased by reduced A(LVOT). Real-time 3DE is a potentially valuable clinical tool for assessing patients with HCM.     

Pulsed and continuous wave Doppler echocardiographic assessment of valvular regurgitation in normal subjects

To assess the prevalence and flow characteristics of valvular regurgitation detected by Doppler echocardiography in normal subjects, pulsed and continuous wave Doppler studies were performed in 100 adult volunteers without evidence of heart disease. Evidence of valvular regurgitation was present in 73% of subjects. There were 46 subjects with regurgitation of one valve, 24 with regurgitation of two valves and 3 with regurgitation of three valves. Right-sided regurgitation was significantly more common than was left-sided regurgitation (81 versus 22 valves, p less than 0.01). Regurgitant flow was never detected farther than 1 cm from the valve by pulsed Doppler study. Tricuspid regurgitation was detected in 50 subjects and was characterized by a holosystolic velocity signal; a complete spectral envelope was recorded in 32 subjects. The peak velocity of the regurgitant jet for this group was 1.7 to 2.3 m/s (mean 2.0 +/- 0.2). Thirty-one subjects were found to have pulmonary regurgitation with a peak velocity of 1.2 to 1.9 m/s (mean 1.5 +/- 0.2); no subject demonstrated regurgitant flow in early diastole. There were 21 subjects with mitral regurgitation; continuous wave Doppler signals were always of low intensity with a poorly defined spectral envelope and an absence of high velocities. Peak velocities ranged from 1.1 to 4.4 m/s (mean 2.3 +/- 0.9) and in 19 subjects were less than 3.5 m/s. The mean age of subjects with mitral regurgitation was significantly higher than that of subjects without mitral regurgitation (p = 0.01). Aortic regurgitation was detected in only one subject. This study provides further evidence that valvular regurgitation is frequently detected by Doppler echocardiography in normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

A new method for estimating left ventricular dP/dt by continuous wave Doppler-echocardiography. Validation studies at cardiac catheterization

In this study, we explored the use of continuous wave Doppler-echocardiography guided by color Doppler flow-mapping as a method for noninvasively calculating the rate of pressure rise (RPR) in the left ventricle. Continuous wave Doppler determination of the velocities in mitral regurgitant jets allows calculation of instantaneous pressure gradients between the left ventricle and the left atrium. Left atrial pressure variations in early systole can be considered negligible; therefore, the rising segment of the mitral regurgitation velocity curve should reflect left ventricular pressure increase. We studied 50 patients (mean age, 51 years; range, 25-66 years) in normal sinus rhythm with color Doppler-proven mitral regurgitation and compared the Doppler-derived left ventricular RPR with peak dP/dt obtained at cardiac catheterization. Doppler studies were performed simultaneously with cardiac catheterization in 11 patients and immediately before in the remaining cases. Two points were arbitrarily selected on the steepest rising segment of the continuous wave mitral regurgitation velocity curve (point A, 1 m/sec, point B, 3 m/sec), and the time interval (t) between them was measured. Following the Bernoulli relation, the pressure rise between points A and B is 32 mm Hg (4vB2-4vA2) and the RPR is 32 mm Hg/t. Results showed a linear correlation between the Doppler RPR and peak dP/dt (r = 0.87, SEE = 316 mm Hg/sec). The RPR in the left ventricle can be derived from the continuous wave Doppler mitral regurgitation velocity curve.     

Pitfalls in the diagnosis of periprosthetic valvular regurgitation by pulsed Doppler echocardiography

Pulsed Doppler echocardiographic diagnosis of periprosthetic valvular insufficiency may be difficult. This report details the pulsed Doppler echocardiographic findings in two patients who developed severe periprosthetic mitral regurgitation after porcine mitral valve replacement. In both patients, mitral regurgitation was difficult to diagnose and left atrial turbulence, when detected, appeared localized, suggesting only mild mitral regurgitation. However, the combination of abnormally high peak transmitral diastolic flow velocity, with a normal pressure half-time, and increased flow velocity in the tricuspid regurgitant jet compatible with severe pulmonary hypertension, in the absence of other apparent left heart disease, suggested the correct diagnosis of severe mitral regurgitation in both cases. Techniques for optimal pulsed Doppler assessment of the mitral anulus region are emphasized, as are the theoretic advantages of continuous wave and color-coded pulsed Doppler echocardiography for detection of periprosthetic regurgitation.     

Diastolic mitral regurgitation in patients with atrioventricular conduction abnormalities: a common finding by Doppler echocardiography

M-mode and Doppler echocardiography were performed in 16 patients with first degree atrioventricular (AV) block, 1 patient with second degree (Wenckebach type) and 3 patients with third degree AV block; 20 individuals with a normal PR interval served as control subjects. The time from the onset of the P wave to the mitral valve closure by M-mode and to the end of mitral flow by Doppler echocardiography were obtained. In 20 normal subjects, the P wave to mitral valve closure interval measured 220 +/- 30 ms by M-mode and to the end of mitral flow 225 +/- 29 ms by Doppler technique (p = NS). In patients with first degree AV block, these intervals measured 242 +/- 41 and 249 +/- 36 ms, respectively (p = NS). Late diastolic (before the onset of the QRS complex) mitral regurgitation was detected by pulsed mode Doppler imaging in 9 (56%) of the 16 patients with first degree AV block but in none with a normal PR interval. In the four patients with advanced AV block, intermittent mid or late diastolic mitral regurgitation was found to depend on the position of the P wave in diastole. With early diastolic P waves, the end of mitral valve flow by Doppler technique occurred 230 to 250 ms after the onset of the P wave and was followed by mild diastolic mitral regurgitation of variable duration. With P waves falling in systole, the mitral valve remained open throughout diastole; during most of diastole, however, there was neither forward mitral flow (diastasis) nor diastolic mitral regurgitation detected by Doppler technique.(ABSTRACT TRUNCATED AT 250 WORDS)     

Continuous wave Doppler echocardiographic evaluations of the severity of mitral regurgitation

To ascertain the usefulness of continuous wave Doppler echocardiography in evaluating the severity of mitral regurgitation (MR), 29 patients with MR and 10 normal subjects were examined. The patients were categorized in three groups according to the angiographic evidence of severity of MR. To analyze the flow velocity patterns of MR, the time to peak velocity index (time from onset of MR signal to peak flow velocity/duration of MR signal), the A/B ratio (the ratio of the first and second half of the systolic MR signal area), systolic peak velocity, and diastolic peak velocity were measured using continuous wave Doppler echocardiograms. The velocity patterns of MR differed significantly among the three groups. With severer MR, the flow velocity pattern showed an earlier appearance of the peak in systole, a steeper decrease in systole and a greater increase in early diastole. The time to peak velocity index was 55 +/- 7% (mean +/- SD) in mild MR, 42 +/- 6% in moderate MR and 35 +/- 5% in severe MR. This index shortened significantly in accord with the severity of MR (mild vs moderate MR: p less than 0.001, moderate vs severe MR: p less than 0.05). The A/B ratio was 1.06 +/- 0.12 in mild MR, 1.23 +/- 0.10 in moderate MR and 1.41 +/- 0.07 in severe MR. This ratio increased significantly with the severity of MR (mild vs moderate MR: p less than 0.01, moderate vs severe MR: p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Progressive restrictive cardiomyopathy--a case report

We present a case of restrictive cardiomyopathy which progressed over a 10 month period. A 69-year-old female was admitted because of acute inferior myocardial infarction; hemodynamically, she was in Forrester subset I. Cardiac catheterization performed 4 weeks post-infarction showed markedly increased left ventricular end-diastolic and pulmonary wedge pressures. Left ventricular ejection fraction was 66% with postero-basal akinesis and minimal mitral regurgitation. The right coronary artery was completely occluded with good collateral circulation from the intact left coronary artery. Doppler echocardiography 4 weeks post-infarction showed pseudo-normalization of the A/E ratio of peak mitral flow velocity in atrial systole (A) to peak mitral flow velocity in early diastole (E). Preload reduction by nitroglycerin increased the A wave. Ten months post-infarction, the patient was re-admitted due to congestive heart failure. The A/E ratio was unchanged, however the A wave no longer increased after the same dose of nitroglycerin. We have hypothesized that dehydration and/or the vigorous use of a nitrate, in the acute phase of myocardial infarction, masked an underlying restrictive cardiomyopathy which progressed in the 10 months post-infarction.     

The relationship between systolic anterior motion of the mitral valve and the left ventricular outflow tract Doppler in hypertrophic cardiomyopathy

In an attempt to investigate the role of left ventricular blood outflow in the generation of systolic anterior motion (SAM) of the mitral valve in patients with hypertrophic cardiomyopathy, we precisely analyzed the temporal relation of SAM and the left ventricular outflow tract (LVOT) systolic Doppler events obtained at the maximal mitral-septal apposition or equivalent area in eight patients with severe SAM, in five patients with mild/moderate SAM, and in seven patients with no SAM, using M-mode and pulsed Doppler echocardiography; the results were compared with those in 10 normal subjects. In all 13 patients with SAM, the timing of SAM generation corresponded to the LVOT Doppler events either between the onset of SAM and the onset of Doppler (r = 0.834, p less than 0.0001) or between the peak of SAM and the peak of Doppler (r = 0.836, p less than 0.0001). The excursion rate of the development of SAM showed a correlation with the LVOT blood outflow acceleration (r = 0.828, p less than 0.0001). The timing of SAM resolution also correlated with the Doppler events, either between the offset of SAM and the offset of Doppler (r = 0.795, p less than 0.001) or the end of SAM and the end of Doppler (r = 0.859, p less than 0.0001). The LVOT blood outflow deceleration showed a correlation with the regression rate of SAM (r = 0.668, p less than 0.013). The LVOT blood outflow acceleration was significantly higher in patients with severe SAM than in patients with mild/moderate SAM or no SAM. This study suggests that the high LVOT blood outflow acceleration in early systole possibly plays an important part in the generation of the Bernoulli pressure drop and results in anterior motion of the mitral valve. At mid-systole, a drag force and/or suction effect of pressure drop produced by continuous outflow blood may sustain the anterior motion of the mitral valve. At late systole, as the blood flow decelerates, the regression of SAM then occurs.     

Relationship between instantaneous trans-mitral blood flow velocity and instantaneous left ventricular volume in normal and hypertrophied hearts.

We examined the relationship between trans-mitral blood flow velocity and left ventricular volume in normal and hypertrophied hearts using cross-sectional Doppler echocardiography. We studied 10 normal subjects and 19 patients with left ventricular hypertrophy, 9 with aortic stenosis and 10 with dilated cardiomyopathy. Trans-mitral Doppler flow velocity signals and cross-sectional echocardiograms of the left ventricular short and long axes were digitized in each patient to obtain instantaneous mitral flow velocity, instantaneous left ventricular volume, left ventricular mass, and left ventricular mass/volume ratio at end-diastole. Peak velocities during rapid filling (E wave) were similar in all three groups. Peak velocities during atrial systole (A wave) were significantly increased in aortic stenosis, (124 +/- 28 cm/sec); but were not different from normal in dilated cardiomyopathy (43 +/- 20 cm/sec versus 32 +/- 9 cm/sec). The peak A/E velocity ratio was elevated in aortic stenosis 1.47 +/- 0.30, but in dilated cardiomyopathy it was similar to normal hearts (0.47 +/- 0.23 versus 0.54 +/- 0.15). The percentages of left ventricular filling achieved at the time of the peak E wave, the end of rapid filling, and at the time of the peak A wave were similar in all three patient groups. There was no correlation between blood flow velocities at peak E wave, peak A wave or the A/E velocity ratio and left ventricular volume or mass. There was a significant correlation between peak A velocities and left ventricular muscle/cavity areas (r = 0.81; P less than 0.001). There was a similarly close correlation between the peak A/E velocity ratios and left ventricular muscle/cavity areas (r = 0.80; P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

彩色多普勒超声心动图评价扩张型心肌病左心室舒张功能

目的　用彩色多普勒超声探讨扩张型心肌病患者左心室舒张功能的改变。方法　利用彩色多普勒超声心动图将 37例扩张型心肌病患者分为合并二尖瓣反流组及无二尖瓣反流组 ,观察其二尖瓣及肺静脉血流频谱并与正常人对照。结果　扩张型心肌病无二尖瓣反流组中仅有 41.2 %患者二尖瓣血流频谱 E/ A小于 1,其余均表现为 E/A大于 1,甚至 E/ A大于 2。扩张型心肌病合并二尖瓣反流组 E/ A均大于 2。而扩张型心肌病患者肺静脉血流频谱 ,与正常人组比较有明显差异 ,S峰均明显降低 ,D峰 >S峰 ,结论　扩张型心肌病在收缩功能减退同时有舒张功能异常 ,二尖瓣血流频谱可出现“假性正常化”,掩盖其左心室舒张功能的异常 ,应用肺静脉血流频谱有助于识别二尖瓣血流频谱“假性正常化”,但在评价扩张型心肌病合并二尖瓣反流患者左心室舒张功能时有其局限性     

Valvular regurgitation in patients with complete heart block by color Doppler echocardiography

We studied valvular regurgitation (pulmonary, aortic, tricuspid and mitral regurgitation) in 30 patients with complete heart block by color Doppler echocardiography, pulse Doppler and continuous wave Doppler echocardiography. The prevalence rate of multivalvular regurgitation of these subjects was 83.3%. Regurgitation involving all four valves appeared in 30.0% of these patients. The prevalence rate of pulmonary, aortic, tricuspid and mitral regurgitation was 56.7%, 33.3%, 100%, and 76.7% respectively. Pulmonary regurgitation (PR) was observed in patients with complete heart block without pulmonary hypertension. PR velocity was slow and interrupted by atrial contraction. It might be possible to evaluate atrial pressure from the interruption of PR. Tricuspid regurgitation (TR) during systole was often present in patients with right ventricular endocardial pacing. Systolic TR was influenced by atrial contraction. When atrial contraction occurred during systole, TR was interrupted, or shortened. Diastolic TR and MR were easily detected by M mode color Doppler echocardiography. The diastolic TR and MR were of slow velocity and appeared 240-290 msec after P wave. These atypical valvular regurgitation in patients with complete heart block reflect of the inverse atrial-ventricular pressure gradient across the atrio-ventricular valve.     

Doppler evaluation of severity of mitral regurgitation: Relation to pulmonary venous blood flow patterns in an animal study

Objectives. This study examined the influence of regurgitant volume on pulmonary venous blood flow patterns in an animal model with quantifiable mitral regurgitation.Background. Systolic pulmonary venous blood flow is influenced by atrial filling and compliance and ventricular output and by the presence of mitral regurgitation. The quantitative severity of the regurgitant volume itself is difficult to judge in clinical examinations.Methods. Six sheep with chronic mitral regurgitation produced by previous operation to create chordal damage were examined. At reoperation the heart was exposed and epicardial echocardiography performed. Pulmonary venous blood flow waveforms were recorded by pulsed Doppler under color flow Doppler guidance using a Vingmed 750 scanner. The pulmonary venous systolic inflow to the left atrium was expressed as a fraction of the total inflow velocity time integral. Flows across the aortic and mitral valves were recorded by electromagnetic flowmeters balanced against each other. Pressures in the left ventricle and left atrium were measured directly with high fidelity manometer-tipped catheters. Preload and afterload were systematically manipulated, resulting in 24 stable hemodynamic states.Results. Simple logarithmic correlation between the regurgitant volume and size of a positive or negative pulmonary venous inflow velocity time integral during systole was good (r = −0.841). By stepwise linear regression analysis with pulmonary venous negative systolic velocity time integral as a dependent variable compared with the regurgitant volume, fractional shortening, left atrial νwave size, systemic vascular resistance and left ventricular systolic pressure, only contributions from νwave size and regurgitant volume (r = 0.80) reached statistical significance in determining pulmonary venous negative systolic flow.Conclusions. Evaluation of systolic pulmonary venous blood flow velocity time integral can give valuable information helpful for estimating the regurgitant volume secondary to mitral regurgitation.     

Effect of mitral regurgitation on pulmonary venous velocities derived from transesophageal echocardiography color-guided pulsed Doppler imaging

The effect of mitral regurgitation on pulmonary venous flow velocity was studied in 66 patients undergoing transesophageal echocardiography. Nine patients were studied intraoperatively before and after surgery, so that 75 pulmonary venous flow tracings were analyzed. Fifty-four patients had no significant (0 to 1+) mitral regurgitation and 21 had significant (2 to 3+) mitral regurgitation. Comparison of both groups revealed significant differences in the pulmonary venous flow pattern. In patients with no significant mitral regurgitation, the peak systolic velocity was higher (55 +/- 16 vs. -4 +/- 16 cm/s; p less than 0.0001) and the peak diastolic velocity was lower (43 +/- 13 vs. 59 +/- 17 cm/s; p less than 0.01) when compared with values in patients with significant mitral regurgitation. Consequently, the peak systolic/diastolic velocity ratio was significantly higher in the patients without significant mitral regurgitation (1.4 +/- 0.5 vs. 0.4 +/- 1.3; p less than 0.0001). The same trend was noted with respect to the systolic and diastolic velocity integrals. As the degree of mitral regurgitation increased, the peak diastolic velocity and diastolic velocity integral increased, whereas the peak systolic velocity and systolic velocity integral decreased. In patients with severe mitral regurgitation, the systolic flow became reversed (retrograde). The sensitivity of reversed systolic flow for severe mitral regurgitation was 90% (9 of 10), the specificity was 100% (65 of 65), the positive predictive value was 100% (9 of 9), the negative predictive value was 98% (65 of 66) and the predictive accuracy was 99% (74 of 75).(ABSTRACT TRUNCATED AT 250 WORDS)     

Phase differences between left ventricular wall motion and transmitral flow in man: evidence for involvement of ventricular restoring forces in normal rapid filling

To assess the possible role of restoring forces underlying left ventricular wall motion during rapid filling, the time relations between left ventricular dimensions and filling velocity were studied by digitised M-mode and Doppler echocardiography in 23 normal children and 43 patients: 11 with mild and 17 with severe mitral regurgitation, and 15 with left ventricular hypertrophy due to aortic stenosis. In normal children, peak mitral flow velocity characteristically lagged peak rate of dimension increase by 50 +/- 15 msec, and peak rate of posterior wall thinning by 35 +/- 15 msec, (P less than 0.01 for both). Towards the apex, and along the long axis of the ventricle, these phase differences between dimension and flow velocity were not apparent. The characteristic time relations between flow velocity and transverse dimension were also present in patients with left ventricular hypertrophy or mild mitral regurgitation, but when mitral regurgitation was severe they were lost and there was no significant difference in timing between peak flow velocity and peak rate of dimension change (-2 +/- 30 msec) or wall thinning (-4 +/- 25 msec). We conclude that phase differences between left ventricular wall motion and mitral inflow velocity are present in the normal ventricles of children. They cannot be explained on the basis of simple shape changes or passive filling of the relaxing ventricle, but strongly suggest the additional presence of ventricular restoring forces. They persist in patients with left ventricular hypertrophy or mild mitral regurgitation, but are lost when the regurgitation is severe, the filling pattern reverting to that predicted for passive distension of the ventricular cavity by a high left atrial pressure.