Alterations in left ventricular filling in hypertensive patients with left ventricular hypertrophy as assessed by Doppler echocardiography.
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Regional denervation of adrenergic nerves has been clinically demonstrated in patients with myocardial infarction using I-123 metaiodobenzylguanidine (MIBG) scintigraphy. However, it is not clarified whether adrenergic denervation can be induced by prolonged myocardial ischemia as well as by myocardial infarction. This case with effort angina had 99% stenosis of right coronary artery and showed perfusion defects at inferior myocardial regions in the exercise thallium-201 study. However, inferior wall motion estimated by echocardiography and left ventriculography was normal indicating the absence of myocardial infarction. After percutaneous transluminal coronary angioplasty for the stenosis, I-123 metaiodobenzylguanidine (MIBG) and thallium-201 (Tl-201) myocardial scintigraphies were done to estimate the therapeutic effect of PTCA. Although the Tl-201 study during exercise showed normal findings indicating the success of PTCA, marked defects was detected at inferior myocardial regions in the I-123 MIBG studies just after and 4 hours after an intravenous injection of I-123 MIBG. These results suggest that adrenergic derangement may be induced by prolonged myocardial ischemia and may persist for periods even though myocardial perfusion is normalized.
To assess atrial contribution to left ventricular (LV) filling in hypertension, we studied, using pulsed Doppler echocardiography, 22 hypertensive patients without apparent LV hypertrophy (LVH), 12 hypertensive patients with LVH, and 24 age-matched normal subjects. From mitral flow velocity waveform, we determined peak velocity of early diastolic filling flow (peak E), peak velocity of late diastolic filling flow (peak A), and the peak A/peak E ratio (peak A/peak E). Peak E decreased in hypertensives without apparent LVH and showed a further decrease in hypertensives with LVH compared with normal subjects (57 +/- 8 [mean +/- SD]; P less than 0.001, 46 +/- 7; P less than 0.0001, vs 65 +/- 10 cm/s). On the other hand, peak A/peak E increased in hypertensives without apparent LVH, and greatly increased in hypertensives with LVH (1.06 +/- 0.14; P less than 0.001, 1.40 +/- 0.29; P less than 0.0001, vs 0.79 +/- 0.21). However, increased peak A was not significantly different between the hypertensive groups (60 +/- 8 vs 64 +/- 8; NS, both; P less than 0.001 vs 50 +/- 10 cm/s for normal subjects). In hypertensives, we found no significant correlation between peak A and the wall thickness index (WTI, determined as mean LV wall thickness normalized by LV diastolic dimension), whereas peak E was significantly correlated with WTI (r = -0.65; P less than 0.001). Our findings indicate that atrial contraction can not fully compensate the decrease in early diastolic filling caused by advanced LVH. We conclude that atrial compensation for reduced early diastolic filling is limited in hypertensive patients with advanced left ventricular hypertrophy.
To elucidate the clinical features of mitral valve prolapse in apparently healthy young population, two-dimensional echocardiography was performed in the students (18-22 years) without documented organic heart diseases. Focusing on the systolic dislocation and configuration of the anterior mitral leaflet, a following two-dimensional echocardiographic criterion for grading prolapse was used: Grade I: subjects only with slight slip of the tip of the anterior mitral leaflet (AML) toward the left atrium, Grade II: those with considerable slip of the AML but keeping a normal convex shape in the leaflet body toward the left atrium, and Grade III: those with severe slip of the AML with its ballooning toward the left atrium. Among 2016 students examined, 1507 subjects (74.8%) were judged to be normal, 343 (17.0%) to be Grade I, 141 (7.0%) to be Grade II, and 25 (1.2%) to be Grade III. Of the 25 subjects in Grade III, 20 subjects underwent further examination including a questionnaire about the subjective complaints, physical examination, electrocardiograms at rest and during exercise, Doppler echocardiography and postural tests. Concerning the subjective symptoms, eight subjects had some complaints including chest pain, shortness of breath, dizziness, palpitation, fatigability and synocope, and four of the eight had more than three complaints. Mid-systolic click and a late systolic murmur were audible in four and funnel chest was observed in one. No specific findings were found by electrocardiograms. Mild mitral and tricuspid regurgitations were observed by Doppler echocardiography in four and nine subjects, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
In the noninvasive evaluation of aortic regurgitation by Doppler echocardiography, flow mapping of the aortic regurgitant jet using the long-axis approach is of limited value in cases of combined mitral stenotic lesions. This is because the transmitral flow yields flow disturbances in the left ventricle, making it difficult to identify the extent of the aortic regurgitant jet. To overcome these limitations, the severity of aortic regurgitation was evaluated using the cross-sectional area of the aortic regurgitant jet at the level of the aortic valve as visualized by color flow imaging technique. The study population consisted of 16 patients with aortic regurgitation (10 with pure aortic regurgitation, five with superimposed mitral stenosis, and one with mitral valve replacement). Three normal subjects served as controls. The cross-section of the aortic regurgitant jet was visualized as a mosaic of yellow and blue in all patients with aortic regurgitation, but not in any of the controls. Planimetric measurements of the cross-sectional area of the regurgitant jet (J) and the aortic annulus area (Ao) were performed, and the Doppler parameter, J/Ao, was calculated. As a reference, the aortic regurgitant fraction (RF) was calculated from Doppler measurements of systolic aortic and pulmonary flows (AF and PF); RF (%) = (AF - RF)/AF x 100. The Doppler parameter, J/Ao, correlated well with the Doppler measurement of RF (r = 0.82, p less than 0.005), irrespective of the presence of associated mitral lesions. Thus, the cross-sectional area of the aortic regurgitant jet determined by color flow imaging technique would be a useful estimate of the severity of aortic regurgitation, even in the presence of associated mitral stenotic changes.
The aortic regurgitant fraction was estimated noninvasively in 20 patients with aortic regurgitation from systolic aortic and pulmonary volume flow determined by duplex Doppler echocardiography. By assuming that an excess of the aortic volume flow (AF) compared with the pulmonary volume flow (PF) is due to aortic regurgitant flow, the aortic regurgitant fraction (RF) was calculated as follows: RF(%) = (AF - PF)/AF X 100. The aortic and pulmonary volume flows were determined as products of systolic integrals of ejection flow velocities and cross-sectional areas of the left and right ventricular outflow tracts, respectively. The Doppler estimate of the regurgitant fraction was compared by semiquantitative grading (1+ to 4+) by cineaortography and with the measurement of regurgitant fraction by catheter technique. The mean Doppler-determined aortic regurgitant fraction was 2.4% for normal subjects, 28.0% for the patients with 1+, 32.6% for the patients with 2+, 53.3% for the patients with 3+, and 62.4% for the patients with 4+. A fair correlation was found between Doppler estimates of regurgitant fraction and semiquantitative cineaortographic grades (r = .80, p less than .01). In the patients without associated mitral regurgitation, a close correlation was observed between Doppler and catheter estimates of regurgitant fraction (r = .96, p less than .01; y = 1.0x - 0.08). In the patients with associated mild mitral regurgitation, however, Doppler estimates of regurgitant fraction substantially underestimated those determined by the conventional catheter technique, which cannot separately quantitate the aortic regurgitant fraction in the presence of mitral regurgitation. These observations indicate that the proposed Doppler technique provides a useful method to evaluate the aortic regurgitant fraction specifically regardless of the presence of associated mitral lesions.
Intracardiac flow dynamic alterations in patients (pts) with prosthetic mitral valve (PMV) were studied to assess prosthetic valve functions using pulsed Doppler technique and two-dimensional echocardiography. The study population consisted of 23 pts who underwent mitral valve replacement (11 with the Starr-Edwards disc valve, nine with the Björk-Shiley tilting disc valve, two with the Hancock porcine valve, and one with the homograft valve), 20 pts with mitral stenosis, and 17 control subjects (15 healthy persons and two with lone atrial fibrillation). All pts had a normal functioning PMV by clinical evaluation except for one patient with a dysfunctioning homograft valve, which was angiographically documented. Flow velocity patterns were obtained at various sites in the left ventricle (LV) and the left atrium (LA). Flow dynamic alterations in pts with PMV were evaluated from the half time of transmitral flow velocity descent in diastole, as an index of the atrioventricular pressure gradient, the extent of dispersion of Doppler frequency spectrum of intraventricular flow as an index of the degree of flow disturbances and the Doppler signals with broadening spectra indicating transvalvular regurgitant flow into the LA. The results were as follows: In pts with PMV, the velocity of transmitral flow decreased slowly and linearly throughout diastole. The half time was significantly prolonged for pts with PMV as compared with that for control subjects (272 + 94 ms [mean + SD] vs 79 + 15 ms, p less than .001), though it was shorter than that in pts with mitral stenosis (457 + 145 ms, p less than .001). In pts with PMV, the half time for pts with the Björk-Shiley valve was relatively short as compared with that for pts with other valve. Marked prolongation of the half time (483 ms) was observed in a patient with a dysfunctioning homograft valve. These findings indicate that any PMV is obstructive, even with normal valve function, as compared with healthy mitral valves and that the Björk-Shiley valve is superior to the other PMVs studied in regard to the pressure gradient across PMV. Diastolic flow velocity patterns in the LV were highly dependent on the type of PMV. Apparently, the flow characteristics in the LV were disturbed in every patient with PMV regardless of the type of PMV. The high pressure gradient across the PMV suggested by the prolonged half time in pts with PMV, may be partially caused by flow disturbances produced by PMV.(ABSTRACT TRUNCATED AT 400 WORDS)
The ratio of pulmonary to systemic flow (Qp/Qs) was noninvasively evaluated by duplex Doppler echocardiography in 22 patients with atrial septal defects (ASDs). Right and left ventricular stroke volumes (RSV, LSV) were determined from the recordings of ejection blood flow velocity and diameter at the level of the pulmonary and aortic orifices in each ventricular outflow tract. The ratio RSV/LSV, determined by the duplex Doppler echocardiography, was compared with Qp/Qs by oximetry. The RSV/LSV for 10 normal subjects was 0.99 +/- 0.05 (mean +/- SD), whereas the RSV/LSV for patients with ASD, 2.26 +/- 0.63, was significantly higher than that for normal subjects (p less than .01). In patients with ASD, a fairly good correlation was found between RSV/LSV and Qp/Qs (r = .92, p less than .01; y = 1.11x - 0.30), and this high correlation was found even in patients with complications such as pulmonary hypertension, mitral and tricuspid regurgitation, Eisenmenger complex, and ventricular septal defect. We also found that semilunar valve regurgitation modified the value of RSV/LSV in accordance with the degree of regurgitation. These findings indicate that, with a few limitations, the Doppler index RSV/LSV is clinically useful in the estimation of the magnitude of the shunt flow in patients with ASD and that the limitations could be overcome by additional Doppler examination.
We attempted to estimate transmitral pressure gradient and mitral valve area (MVA) noninvasively in mitral stenosis (MS) by a bi-directional pulsed Doppler flowmeter combined with an electronic two-dimensional echocardiograph. Eleven patients with MS in sinus rhythm were studied by cardiac catheterization. Fifteen healthy subjects (H) served as normal control. The pulsed Doppler flowmeter operated with a carrier frequency of 2.5 MHz, a pulse repetition rate of either 5 KHz or 10 KHz and a sample volume of 1 X 3 X 3 mm. The velocity of transmitral central flow was measured by this system, monitoring audible Doppler sounds and cardiac images which depict the anatomic location of the sampling site. The Doppler signal was analyzed by a sound spectrograph. In estimating the transmitral pressure gradient and MVA, we employed a Doppler parameter (half time) defined as the time for instantaneous maximal blood flow velocity to reduce to one-half from its rapid inflow peak, which is independent of the angle between the ultrasonic beam and blood flow. Transmitral pressure gradient (delta P100) was measured as the pressure gradient between either left atrial or pulmonary capillary pressure and left ventricular pressure at the point after 100 msec from the nadir of left ventricular early diastolic pressure [( LA or PC--LVDP]100). MVA was obtained using a Gorlin's formula. The transmitral blood flow velocity in both MS and healthy groups revealed a narrow frequency band pattern with two peaks, R and A, in diastole. The former peak occurred during rapid inflow phase and the latter following atrial contraction. In the healthy group, the descent rate of R wave was increased than that in the MS group. The square root of the pressure gradient also reduced linearly with transmitral flow velocity in the MS group. Thus in the MS group, the transmitral velocity was directly proportional to the square root of the pressure gradient as described by a Bernoulli theorem, and the half time was proportional to the transmitral velocity. The square of the half time (delta t2) was highly correlated with delta P100 (r = 0.97), and the inverse of the half time (delta t-1) was correlated with MVA (r = 0.76). There was no significant correlation between delta P100 and diastolic descent rate of anterior mitral leaflet (DDR). The present study indicates that the half time is useful in estimating transmitral pressure gradient and MVA in mitral stenosis.
Hemodynamic studies were performed in a case of Shy-Drager syndrome with severe orthostatic hypotension. Marked depression of blood pressure was recognized immediately after the tilt-up, wherein decrease in cardiac output was detected (65 leads to 35 ml; stroke volume) during measurements by echocardiography. In association with the depression of blood pressure and decrease in cardiac output, Doppler sonograms showed the overall blood flow reduction in the brain-supplying arteries, suggesting some breakdown of autoregulation of the cerebral blood flow. Medication with indomethacin obviously limited the depression of blood pressure during the standing exercise. The pressor mechanism of indomethacin might be regarded as a result of increased vasoconstrictivity by inhibiting the synthesis of prostaglandins.
We used a pulsed Doppler technique to examine the flow velocity pattern in the right ventricular outflow tract in 33 adults. In the patients with normal pulmonary artery pressure (mean pressure less than 20 mm Hg, 16 patients), ejection flow reached a peak level at midsystole (137 +/- 24 msec, mean +/- SD), producing a domelike contour of the flow velocity pattern during systole. In contrast, the flow velocity pattern in patients with pulmonary hypertension (mean pressure greater than or equal to 20 mm Hg, 17 patients) was demonstrated to accelerate rapidly and to reach a peak level sooner (97 +/- 20 msec, p less than .01); in 10 of the pulmonary hypertensive patients a secondary slower rise in flow velocity was observed during a deceleration, resulting in the midsystolic notching. The time to peak flow (acceleration time, AcT) and right ventricular ejection time (RVET) were measured from the flow velocity pattern. Either AcT or AcT/RVET decreased with increase in mean pulmonary artery pressure, and a very high correlation (r = -.90) was found between AcT/RVET and log10 (mean pulmonary artery pressure). The use of this technique permitted the noninvasive estimation of the pulmonary artery pressure.
The role of left ventricular (LV) relaxation in the determination of transmitral flow dynamics was studied with pulsed Doppler flowmetry and high fidelity tip manometry in various cardiac diseases. Study population consisted of 14 cardiac patients (pts) with sinus rhythm, including 4 pts with chest pain syndrome, 4 with myocardial infarction, 3 with effort angina and 3 with hypertrophic cardiomyopathy. The acceleration of early diastolic inflow velocity (AC), the peak of early diastolic inflow velocity (peak EFV ) and the deceleration after the peak (DC) were determined from the phasic transmitral flow pattern. Hemodynamic parameters, i.e., cardiac index, mean pulmonary wedge pressure (PWP), peak positive dP/dt and the time constant of isovolumic LV pressure decay (T) were measured during cardiac catheterization. Decreases in AC, peak EFV and DC were accompanied by prolongation of T with correlation coefficient of -.851 (p less than .001), -.808 (p less than .001) and -.697 (p less than .01), respectively, indicating that impaired LV relaxation slows down the early diastolic LV filling irrespective of underlying cardiac disease. LV filling pressure did not appear as a predominant factor affecting the early diastolic filling in the pts studied, as indicated by an insignificant correlation between any of these flow indices and PWP. Also, no significant relations were found between the flow indices and other hemodynamic parameters. These results indicate that LV relaxation plays a primary role in determining the extent of the early diastolic filling. Pulsed Doppler flowmetry provides a new approach to evaluate the impairment of LV relaxation noninvasively and sensitively in cardiac disease.
Regurgitant flows in valvular diseases were evaluated by a pulsed Doppler flowmeter combined with an electronic beam sector scanning echocardiograph. The apparatus which was newly developed by us allowed the simultaneous demonstration of a sample site on a two-dimensional echocardiogram with flow measurement. Doppler signals of regurgitant flow were recorded as uni-directional or bi-directional wide frequency band signals. The locations, where regurgitant flow signals were detected, were depicted on the corresponding two-dimensional echocardiogram. This procedure was referred to as "a flow mapping technique" for non-invasive visualization of the distribution of regurgitant flow. In 12 patients with mitral regurgitation due to mitral valve prolapse detected by the pulsed Doppler technique, the regurgitant flow was distributed to the opposite side of the prolapsing mitral leaflet. The transmission of the regurgitant murmur was well consistent with the direction of the regurgitant flow. In 14 patients with aortic regurgitation, the distribution of aortic regurgitant flow visualized by the flow mapping technique closely coincided with that obtained by cineaortography. Based on the distribution of the regurgitation, the severity of the regurgitation could be precisely evaluated by the Doppler technique. Regurgitant flow signals were detected in the right atrium in all 13 patients with tricuspid regurgitation diagnosed by right ventriculography. We found 4 patients who did not show Carvallo's sign but in whom were detected regurgitant flow signals by the Doppler technique. In all of them, tricuspid regurgitation was proven at surgery. These results indicate that the Doppler technique presented here has an obvious clinical advantage in detecting and evaluating regurgitant flow in valvular diseases.
In this study, transmitral flow velocity during the diastolic period was non-invasively measured to assess diastolic behavior of the left ventricle by pulsed Doppler flowmetry combined with electronic beam sector-scanning echocardiography. The velocity pattern was found to have 2 wave components: one appears in the early diastolic rapid filling phase (R wave) and the other in the late diastolic phase. The peak of the early diastolic inflow velocity (peak EFV), the deceleration rate of the R wave (DC), and the peak of the late diastolic inflow velocity (peak LFV) were compared in healthy subjects as the control, patients with hypertension, hypertrophic cardiomyopathy and definite old myocardial infarction. Normal peak EFV and DC, 61.3 +/- 6.7 cm/sec and 355 +/- 67 cm/sec2, respectively, were markedly reduced in patients with hypertension (50.0 +/- 10.0 cm/sec and 265 +/- 75 cm/sec2), hypertrophic cardiomyopathy (48.8 +/- 10.7 cm/sec and 205 +/- 78 cm/sec2), and myocardial infarction (46.1 +/- 12.0 cm/sec and 240 +/- 84 cm/sec2). Among all disease groups the DC was most significantly reduced in the hypertrophic cardiomyopathy groups. Normal peak LFV, 39.9 +/- 11.0 cm/sec, was significantly increased in patients with hypertension (54.3 +/- 10.7 cm/sec) and myocardial infarction (50.0 +/- 11.0 cm/sec), but not in patients with hypertrophic cardiomyopathy (42.0 +/- 8.4 cm/sec). The ratio peak LFV/peak EFV was significantly greater in all disease groups than in the normal group. These findings indicate that impaired early diastolic filling in all disease groups was compensated by enhanced atrial contraction in patients with hypertension and myocardial infarction, and by prolonged rapid filling in patients with hypertrophic cardiomyopathy. Left ventricular wall thickness was better correlated with DC in patients with hypertension (r = -0.76, p less than 0.01) than in patients in the other groups, which indicates that the left ventricular wall thickening is a more important factor in determining diastolic behavior of the ventricle in hypertension than in hypertrophic cardiomyopathy and myocardial infarction. Thus, the pulsed Doppler technique was proved to be useful in assessing ventricular diastolic events non-invasively.
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Pericardial constraining force is minimal in normal hearts; however, it is considered to be prominent in moderate to severe heart failure. Thus, effects of the pericardium on pulsed Doppler transmitral flow velocity pattern were examined in 17 dogs with acute left ventricular dysfunction. Left ventricular dysfunction with left ventricular end-diastolic pressure > or = 15 mm Hg was produced by injection of microspheres into the left coronary artery. Transmitral flow velocity pattern, left atrial and left ventricular diameters, and high-fidelity left atrial and left ventricular pressures were recorded before and after pericardiectomy. In five of the 17 dogs, mitral regurgitation with giant "v" wave of left atrial pressure occurred with reductions of left ventricular systolic pressure and peak rate of the left ventricular pressure fall (dP/dt) after pericardiectomy. In the other 12 dogs, peak early and late diastolic filling velocities increased with a decrease in left ventricular minimal pressure and increases in left arterial and left ventricular diameters and left atrial and left ventricular compliance after pericardiectomy. In these 12 dogs, left atrial to left ventricular crossover pressure, left ventricular end-diastolic pressure, and references for left ventricular relaxation did not change after pericardiectomy. Thus the release from pericardial constraining force in severe heart failure may increase chamber compliance of the left ventricle and left atrium and, in turn, increase peak early and late diastolic filling velocities through an increment in forward transmitral pressure gradient. Increased pericardial constraining force is a possible cause limiting left ventricular filling and hence cardiac output in heart failure.
Doppler-determined transmitral flow velocity pattern has been shown to depend on transmitral pressure gradient, and left atrial (LA) pressure has been considered to be important in determining transmitral pressure gradient in early diastole and peak early diastolic filling velocity (E). In recent studies in human beings, however, it was proved that E did not necessarily change with LA pressure. This may be because concomitant changes in other factors masked the effect of LA pressure. To investigate the relation between transmitral flow velocity pattern and hemodynamic parameters during preload intervention over the wide range of LA pressure, pulsed Doppler transmitral flow velocity pattern and high-fidelity LA and left ventricular (LV) pressures were simultaneously recorded during rapid volume loading to the LA. Data at three stages, at control, at moderate volume loading (the median LA-to-LV crossover pressure during the volume loading), and at advanced volume loading (the maximal crossover pressure during the volume loading), were compared with one another in 11 dogs. A mean value of E increased with the crossover pressure up to moderate volume loading but did not further increase at advanced volume loading. In the data pooled from all experimental stages in all dogs, the changes in E did not correlate with those in the crossover pressure, but correlated weakly with those in the difference between the crossover pressure and LV minimum pressure (r = 0.45, p < 0.05). E decreased at advanced volume loading in three of 11 dogs with a steep LA pressure drop in early diastole although the changes in the difference between the crossover pressure and LV minimum pressure in the three dogs were similar to those in the other eight dogs. The changes in a rate of LA pressure drop in early diastole associated with advanced volume loading inversely correlated with those in E (r = -0.79, p < 0.01). Thus, E may decrease with an extreme increase in LA pressure; this change may be due to an associated increase in a rate of LA pressure drop in early diastole. This finding suggests that at high LA pressure the increased rate of LA pressure drop in early diastole appears to decrease LV filling and hence to reduce stroke volume.