A Laser-Doppler-Velocimeter using an optical fiber and its application to local velocity measurement in the coronary artery.
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Biomedical subjects
Publications and source records attributed to G Tomonaga.
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A laser Doppler velocimeter with an optical fiber was developed to investigate point blood velocity in the arteries and was applied to the measurement of blood velocity in the canine coronary artery. Fundamental experiments revealed that the accuracy of this method was satisfactory, since an excellent linear relation was found between the known blood velocity and the Doppler shift frequency (r = 0.998). The fiber tip (0.1 mm diam.) was inserted into the proximal portion of the left circumflex coronary artery and was traversed across the vascular lumen to measure the point velocity at each sampling point. Detailed velocity profiles were than reconstructed sequentially in three dimensional coordinates, i.e., velocity, diameter and time. In general the velocity waveform showed a diastolic dominant pattern which is characteristic of coronary arterial flow. One peak in early systole and two peaks in early and in late diastole were commonly observed in the velocity waveform near the center-line of the vessel. The velocity profiles were flat in the axial region and declined abruptly near the vessel wall. These results indicate that the laser Doppler velocimetry with an optimal fiber proved to be an accurate and feasible method of evaluating the point velocity of coronary artery flow.
d-3-Acetoxy-cis-2,3-dihydro-5-]2-(dimethylamino)ethyl]-2-(p-methoxyphenyl)-1,5-benzothiazepin-4(5H)-one hydrochloride (diltiazem HCl) was orally administered to 9 patients with chronic congestive heart failure (Class IIb to III, NYHA) to examine whether the drug induces sodium retention and aggravates congestive heart failure. Renal hemodynamics and urinary electrolytes excretion were measured for 3 h after the medication in 6 out of 9 patients. Four of the rest of patients had received chronic administration of the drug for about 2 weeks. There was a significant increase in urinary sodium excretion without noticeable change in renal hemodynamics after diltiazem administration, demonstrating the presence of its direct inhibitory action on renal tubules. The increase in urinary sodium excretion was more marked in patients with heart failure than in those without. This difference in the response to diltiazem may be due to the functional constriction of renal cortical vessels in heart failure. This constriction may be related to renin-angiotensin system which diltiazem was reported to antagonize. The chronic administration of the drug did not induce sodium retention and edema. There was no deterioration of symptoms due to congestive heart failure such as dyspnea and body weight increase. It may be concluded that diltiazem does not aggravate congestive heart failure through its diuretic action and probably its systemic vasodilating action.
Dilitazem hydrochrolide, a potent coronary dilator, was administered in 18 patients to evaluate its effect on renal hemodynamics and urinary electrolyte excretion. Renal blood flow (RBF), glomerular filtration rate (GFR), and cardiac output were determined in 8 ambulatory patients by means of external counting of radioisotope dilution before and 3 or 4 weeks after the medication. Althoug RBF tended to increase after the therapy, there was no statistically significant change in RBF, GFR and cardiac output. Renal fraction of cardiac output (RBF/CO) showed a significant increase by 29.5% after the therapy, indicating that the renal vascular resistance decreased to a greater extent than the extrarenal vascular resistance. Standard renal clearance was performed in 10 inpatients whom 60 mg of dilitiazem was administered orally. Renal plasma flow (RPF) showed an average increase by 15% 3 hr after the administration of the drug, which was not, however, statistically significant. There was no certain trend for GFR and filtration fraction. Urinary sodium excretion (UNaV) began to increase one hr and reached its peak 2 hr after the medication in 9 out of the 10 patients. It may be concluded that diltiazem has a direct inhibitory action against the renal tubular reabsortion of sodium, although the participation of renal hemodynamics can not be denied.
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The left ventricular systolic ejection phase was cineangiographically analyzed in an attempt to evaluate left ventricular performance. Forty-eight patients were classified into five groups: (1) 9 controls; (2) 5 patients with PMD (congestive type) (COCM); (3) 9 patients with PMD hypertrophic type) (HCM), (4) 9 patients with ischemic heart disease (IHD); and (5) 16 patients with mitral stenosis (MS). The rate of volume change (deltaV/deltat) and the volume change as a percentage of stroke volume (deltaV/SV) in patients with COCM and IHD were lower in the early systole and higher in the mid-systole as compared with the control group. Normalized systolic ejection rate (NSER) and velocity of circumferential fiber shortening (Vcf) for the early and late systole were significantly lower in patients with COCM and IHD than in the control group. In two patients with IHD in whom normal indices of left ventricular performance and no asynergy were observed, NSER and Vcf were normal in the late systole but were significantly lower in the early systole. In all 48 patients, deltaV/deltat, deltaV/SV, NSER and Vcf were compared statistically with conventional ejection phase indices and isometric phase indices. delthV/SV for the midstystole showed a negative correlation with EF, MNSER and mVcf. NSER and Vcf for all three phases showed a good correlation with Vmax, max dp/dt and R-max dp/dt but a better correlation with EF, MNSER and mVcf. It was concluded that NSER and Vcf for the early systole were sensitive indices of left ventricular performance and may be utilized to detect subtle depression of left ventricular performance.
Thirteen patients with aortic regurgitation (AR) and 13 with mitral regurgitation (MR) were compared quantitatively from the standpoint of their vector-cardiograms (VCG). Vectorcardiographic parameters were also compared with left ventricular angiographic parameters. The QR time interval was longer and the magnitude of the spatial maximum QRS vector was larger in the AR group, but these differences were thought to be attributed to the differences in length of the left ventricular long axis and the left ventricular end diastolic volume (LVEDV). In the AR group, the ratio of the width to the long axis of the QRS loop in the horizontal plane correlated well with the length of the left ventricular long axis and the angle made by the axis from the middle of the aortic valve to the left ventricular apex and the horizontal axis in the lateral view of the angiogram. In the MR group, these correlations were poor.
The haemodynamic effects of a new anti-anginal drug, dilitazem HCl, were studied in 20 patients with angina pectoris. The 131I-dilution method was used. In two patients, one with atrial septal defect and the other with pulmonic regurgitation, heart catheterization was carried out. The drug exerted significant decrease in stroke volume, cardiac output, cardiac work, stroke work and cardiac output/circulating blood volume ratio. The patients who underwent direct cardiac catheterization disclosed no changes in Vmax and ejection fraction, but there were decreases in stroke volume. The decrease in cardiac work and stroke work after after diltiazem Hcl therapy was apparently due to diminution of venous return and prolongation of systemic circulation time. It is postulated that such a decrease leads to inhibition of myocardial oxygen consumption, which in turn has beneficial effects on angina pectoris.
Utilizing the pressure-volume relationship, the indices of left ventricular diastolic compliance, SV/EDP-DP, dV/dP, and dV/VdP, ventricular stiffness index, I/P(dV/dP), and myocardial stiffness index, I/S(dD/dS) were evaluated of seven patients with normal left ventricle, eleven patients with hypertrophic and seven with congestive type of primary myocardial disease. Myocardial stiffness index was obtained from the equation of S = aekD, where S is a wall stress, a; a constant, D; a length of short axis, K; a stiffness constant. The mean values and standard errors of the means of SV/EDP DP, dV/dP, dV/VdP, I/P(dV/dP), and I/S(dD/dS) for normal group are 16.7 +/- 8.7 (ml/mmHg), 16.03 +/- 6.98 (ml/mmHg), 0.1259 +/- 0.0447 (mmHg-1), 0.0059 +/- 0.0032 (ml-1) and 0.603 +/- 0.153 (cm-1), for hypertrophic type are 10.5 +/- 5.5 (ml/mmHg), 7.23 +/- 7.42 (ml/mmHg), 0.0599 +/- 0.0736 (mmHg-1), 0.0174 +/- 0.0097 (ml-1) and 1.3555 +/- 0.3395 (cm-1), and for congestive type are 17.5 +/- 3.4 (ml/mmHg), 3.91 +/- 2.13 (ml/mmHg), 0.0250 +/- 0.0239 (mmHg-1), 0.0308 +/- 0.0126 (ml-1), and 3.287 +/- 1.272 (cm-1). There were highly significant differences between normal and primary myocardial disease in each indices except SV/EDP-DP. I/P(dV/dP), and I/S(dD/dS) had highly significant differences between hypertrophic and congestive type, the latter is stiffer than the former. The compliance index was not sensitive enough to separate two types of primary myocardial disease.
Intrarenal distribution of blood flow was measured by the 133xenon washout curve in 33 patients with heart disease. Plasma renin activity and sodium concentration were also measured on the day when the xenon study was performed. The patients were divided into three groups according to cardiac index: Group I whose cardiac index showed higher than 3.50 1/min/M2, BSA, group II whose index ranged from 2.50 to 3.50, and group III who had lower than 2.50. Total renal blood flow was significantly decreased in group II (p less than 0.001), as compared with normal controls. The percents of the total renal blood flow supplied to component I decreased significantly in group I, II (p less than 0.05) and group III (p less than 0.01). The flow rate in component I decreased significantly only in group II (p less than 0.05) and group III (p less than 0.01). There was a significant increase in the percent distribution of component II in group II (p less than 0.05) and in group III (p less than 0.01). The flow rate of component II showed a slight increase in group I and III. The study of autoradiographs done in dogs with heart failure demonstrated that component I corresponded to a cortical area having a relatively faster flow rate, whereas component II corresponded to the cortical area which was perfused more slowly. Accordingly, component III indicated outer medulla. There was no apparent relation between intrarenal distribution of blood flow and plasma renin activity although the latter tended to be elevated in patients treated with diuretics. In view of the data available it was concluded that outer cortical as well as outer medullary blood flow are decreased in chronic congestive heart failure and that there is no apparent correlation between outer cortical flow and plasma renin activity.
A comparison of echocardiography with cineangiocardiography in estimating left ventricular dimensions and volumes was undertaken in 43 patients classified into four groups according to the pathophysiology of the left ventricle. There were high correlations between echographic and angiographic ventricular minor axis dimensions, however, when minor axis dimensions were more than 5.0 cm, there were underestimations of minor axis dimensions by echography. From the mean value of long-to-short axis ratio of the left ventricle at end-diastole and end-systole, the following equations were derived for calculating left ventribular volumes from echo dimensions alone: EDV equals 0.837 Dd-3, ESV equals 0.994 Ds-3. That these equations allowed relatively accurate prediction of volumes over a wide range of ventricular sizes was confirmed by comparison with Pombo's formula and Fortuin's formula for calculating left ventricular volume by echo dimensions alone. A comparison of echographic and cineangiographic ejection fraction (EF), relative changes in shortening of internal diameter (delta S), and the mean velocity of circumferential fiber shortening (mean Vcf) was made i; 33 patients with sinus rhythm. There were significant correlations between EF and mean Vcf by echocardiography, except one discordant patient with aortic insufficiency who showed decreased mean Vcg in the face of normal EF, all these results were confirmed by cineangiography. This discrepancy between EF and mean Vcf was ascribed to the prolonged ejection time which characterizes aortic insufficiency.
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Ultrasoundcardiograms (UCG) and radiocardiograms (RCG) were obtained from 50 patients with essential hypertension. They were classified into four groups according to the severity index of Veterans Administration Hospital. These echocardiograms were compared with those obtained from 20 normal individuals. Of the 50 patients with hypertension, ten had abnormal patterns of mitral valve echogram: two had shoulder formation of the A wave (A-A'), three had increased amplitude of the A wave (A greater than E), and five had systolic anterior movement (SAM) of the anterior mitral leaflet toward the ventricular septum. The former two groups were considered to have impairment of left ventricular (LV) function proven by UCG and RCG, however, the SAM group was considered to have hyperfunction with concentric hypertrophy of the left ventricle with thickened ventricular septum simulating that of idiopathic hypertrophic subaortic stenosis (IHSS). This was supported by the fact that SAM increased after inhalation of amyl nitrite and decreased after injection of propranolol. The descent rate of the anterior mitral valve decreased and the thickness of the ventricular septum increased with the severity of hypertension, indicating the LV compliance decreases as the severity of hypertension advances. A significant positive correlation was noted between stroke index (SI) obtained by UCG and RCG. There were no significant differences of LV dimensions and function indices measured by UCG and RCG among the groups classified according to the severity index of hypertension. This suggests that such factors as myocardial ischemia might play an important role in LV function as well as the grade of afterload due to hypertension.
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