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A Kitabatake

Publications and source records attributed to A Kitabatake.

At least 271 records · Page 15Linked to original sources

[Pulmonary arterial end-diastolic pressure noninvasively estimated by continuous wave Doppler echocardiography].

To estimate pulmonary arterial end-diastolic pressures noninvasively, we measured the pulmonary regurgitant flow velocity by continuous wave Doppler echocardiography in 17 patients with pulmonary hypertension (pulmonary arterial end diastolic pressure greater than or equal to 18 mmHg) and in 23 patients without pulmonary hypertension. Pulmonary regurgitation was successfully detected by continuous wave Doppler echocardiography in 14 of the 17 patients with pulmonary hypertension and in 14 of the 23 patients without pulmonary hypertension. The end-diastolic pulmonary artery-to-right ventricular pressure gradient was estimated from the Doppler-determined pulmonary regurgitant flow velocity by means of a simplified Bernoulli equation. The Doppler-determined end-diastolic pulmonary artery-to-right ventricular pressure gradient correlated well with the catheter measurement (r = 0.94). It also correlated well with the pulmonary arterial end-diastolic pressure (r = 0.92). Thus, continuous wave Doppler echocardiography was useful in estimating noninvasively pulmonary arterial end-diastolic pressures.

Adolescent↗

An increase in afterload augments ventricular relaxation rate in isolated perfused canine hearts.

The afterload dependency of relaxation rate was reappraised in isolated canine hearts both in isovolumic and isobaric contractions by using the reliable exponential method in which the asymptote LV pressure (P chi) is variable. This method provided a closer correlation (r = 0.999 +/- 0.001) between the measured LV pressure decay and the model estimate than the semilogarithmic method assuming P chi = 0 (r = 0.992 +/- 0.001). Time constants of isovolumic LV pressure decay obtained by the exponential method demonstrated a significant (p less than 0.01) decrease during volume loading both in isovolumic and isobaric contractions, indicating that the relaxation rate is augmented as afterload increases. In contrast, if we assume P chi = 0, the time constant of LV pressure decay was independent of peak LV pressure as previously reported. Thus, we conclude that the load insensitive relaxation rate implied by the semilogarithmic method (P chi = 0) may be erroneous due to an invalid assumption, ie, P chi = 0, but the relaxation rate is augmented as afterload increases both in isovolumically contracting and isobarically ejecting isolated canine hearts.

Animals↗

Loading sequence is a major determinant of afterload-dependent relaxation in intact canine heart.

To elucidate the role of loading sequence in afterload-dependent slowed relaxation in hearts in situ, the time constants (Texp from best exponential fitting method and TL from semilogarithmic method) of isovolumetric left ventricular (LV) pressure decay were studied in nine anesthetized open-chest dogs under the pharmacological blockade of autonomic nerve activity. An afterload change was imposed by clamping the ascending or descending aorta to make the peak LV pressure early or late in systole. During afterload interventions, in contractions with the peak LV pressure in late systole Texp and TL were significantly (P less than 0.05) larger than in those with the peak LV pressure in early systole in any comparable peak LV pressure range. Moreover, both time constants were directly correlated (P less than 0.01) with the time of peak LV pressure irrespective of peak LV pressure and clamp mode of aorta. In another protocol, marked differences both in Texp and TL were also observed between each of 25 pairs of contractions with different loading sequence but with comparable peak LV pressure and LV dimension (segment length). Thus afterload-dependent slowed relaxation in hearts in situ could not be attributed to an increased total load but to the altered loading sequence associated with an increase in afterload.

Animals↗

A new approach to noninvasive evaluation of aortic regurgitant fraction by two-dimensional Doppler echocardiography.

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.

Adolescent↗

Altered loading sequence as an underlying mechanism of afterload dependency of ventricular relaxation in hearts in situ.

Underlying mechanisms of afterload dependency of ventricular relaxation rate were studied in nine isolated canine hearts and nine open chest dogs. In isolated hearts with isobaric contraction, peak LV pressure was increased by volume loading with stroke volume unchanged, and in anesthetized open chest dogs the afterload was altered by a manual clamp of the descending aorta to various extent under the pharmacological blockade of the autonomic nerve activity. Ventricular relaxation rate was assessed by the time constant (T) of isovolumic LV pressure decay. In hearts in situ of open chest dogs, T was progressively (p less than 0.01) increased as peak LV pressure increased, whereas in isolated hearts T was decreased as afterload increased (p less than 0.05), indicating that peak LV pressure is not a major determinant of ventricular relaxation rate. Between these two heart preparations loading sequence of the heart during contraction was characteristically different; in open chest dogs, as afterload increased ejection timing was accelerated and the time of peak LV pressure (TPmax) was prolonged, whereas TPmax in isolated hearts was decreased and ejection timing was progressively delayed as an increase in afterload. Consequently, TPmax showed a high correlation with T irrespective of peak LV pressure. These results indicate that T is directly dependent on loading sequence mainly regulated by ejection timing. This finding was also confirmed in open chest dog experiments in which 20 pairs of contractions with comparable peak LV pressures and LV dimensions (end-systolic and end-diastolic lengths) but characteristically different loading conditions during contraction (early maximal loading vs late maximal loading) were obtained by the manual clamp of ascending aorta; in early maximal loading conditions (TPmax: 185 +/- 8 ms) T's (66 +/- 3 ms) were significantly (p less than 0.01) smaller than those (110 +/- 10 ms) in late maximal loading conditions (TPmax: 261 +/- 11 ms). A change in loading sequence associated with afterload interventions in hearts in situ may be due to a change in compliance in peripheral arterial system. We conclude that afterload dependency of ventricular relaxation rate observed in hearts in situ could be attributed to the accompanied changes in loading sequence of the heart probably due to a change in arterial compliance. The dependency of relaxation on loading sequence of the heart might be clinically important in evaluating the effect of cardiovascular agents on ventricular relaxation since these agents may largely affect the vascular compliance as well as muscular relaxation per se.

Animals↗

[Continuous wave Doppler echocardiography as a noninvasive evaluation of aortic regurgitation].

Continuous wave Doppler echocardiography permits measurement of high blood flow velocity, which is not obtained by conventional pulsed Doppler echocardiography. In this study, continuous wave Doppler echocardiography was used to measure aortic regurgitant flow velocity, and the utility of this method in evaluating aortic regurgitation (AR) was examined. Continuous wave Doppler recordings of the left ventricular outflow were obtained with the guidance of the long-axis two-dimensional echocardiogram from the apex in 20 patients with AR and 10 without AR. In 18 of the 20 patients with AR, Doppler signals of regurgitant flow were successfully detected. The recorded regurgitant flow velocity pattern had characteristic contours: the regurgitant flow was greater than 1.8 m/sec in velocity immediately after aortic valve closure, and gradually decelerated until the next ventricular systole. The Doppler half time index, which was the time profile to decline to 0.5 of the peak velocity, was significantly shortened in accordance with the degree of AR (p less than 0.01). Thus, continuous wave Doppler echocardiography is a simple, useful method for the noninvasive evaluation of AR.

Adult↗

[Intracardiac flow dynamic alterations with a prosthetic mitral valve studied by pulsed Doppler technique].

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)

Adult↗

Noninvasive evaluation of the ratio of pulmonary to systemic flow in atrial septal defect by duplex Doppler echocardiography.

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.

Adolescent↗

Ejection timing as a major determinant of left ventricular relaxation rate in isolated perfused canine heart.

In the present study, we attempted to test the hypothesis that ejection timing rather than peak left ventricular pressure is a primary determinant of ventricular relaxation rate. In cross-circulated isolated canine hearts instantaneous left ventricular volume was controlled by a servo-pump system. To eliminate the effects of end-systolic and end-diastolic volumes and ejection velocity on left ventricular relaxation rate, these parameters were clamped, and only the ejection timing (onset and end of ejection) was altered, keeping the duration of ejection unchanged. Left ventricular relaxation rate was assessed by time constants of left ventricular pressure decline during the isovolumic relaxation phase calculated by both a semilogarithmic method, assuming that the asymptote is zero, and a best exponential fitting method. In 25 runs, a pair of contractions with ejection timings which differed by 53.1 +/- 2.1 (SE) msec were imposed, while end-systolic and end-diastolic left ventricular volumes and ejection duration were unchanged. All pairs of contractions demonstrated early ejection resulted in significantly (P less than 0.001) slowed relaxation as indicated by a prolongation of the time constants of isovolumic left ventricular pressure decay (delta 4.2 +/- 0.7, sec and delta 15.4 +/- 2.1 msec by semilogarithmic plot and the best exponential fit respectively), although peak left ventricular pressures (104.6 +/- 2.4 mm Hg) were even lower than those (116.6 +/- 2.8 mm Hg) in contractions with later ejection timing. Furthermore, in seven experiments, the heart was allowed to eject at five different timings; onset and end of ejection were progressively delayed in steps of 20 or 30 msec.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Non-invasive estimation of transmitral pressure gradient and mitral valve area in mitral stenosis by an ultrasonic pulsed Doppler technique].

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.

Adult↗

Noninvasive evaluation of pulmonary hypertension by a pulsed Doppler technique.

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.

Adolescent↗

[Role of left ventricular relaxation on transmitral flow dynamics during early diastole: pulsed Doppler flowmetry].

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.

Adult↗

Detection and visualization of regurgitant flow in valvular diseases by pulsed Doppler technique.

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.

Adult↗

Transmitral blood flow reflecting diastolic behavior of the left ventricle in health and disease--a study by pulsed Doppler technique.

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.

Adolescent↗