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Biomedical subjects

Y Koiwa

Publications and source records attributed to Y Koiwa.

At least 37 records · Page 2Linked to original sources
PubMed1992

Effects of mechanical vibration on left ventricular diastolic properties during global ischemia.

To examine the effect of mechanical vibration on ventricular relaxation and diastolic chamber stiffness under global ischemia, we studied eight coronary perfused, isolated, isovolumic canine left ventricles (LV). To produce varying degrees of impaired relaxation, graded coronary flow reduction and paced tachycardia were imposed. A mechanical 50-Hz, 2-mm-amplitude vibration was applied during diastole and was turned off during systole. Without diastolic vibration, the relaxation time constant of LV pressure (tau) increased with the severity of ischemia. The chamber stiffness index (K) from the diastolic pressure-volume relationship showed a slight increase during ischemia; tau decreased with diastolic vibration. The change in tau with vibration increased with ischemia and was dependent on vibration amplitude but not heart rate. The ratio of tau to the diastolic interval (DI, the time from peak negative rate of LV pressure change to end diastole) always decreased with vibration and was linearly correlated with K (r = 0.93; P less than 0.01). K decreased with vibration when tau/DI was greater than 0.3. We conclude that diastolic vibration improves impaired relaxation and chamber stiffness under myocardial ischemia.

Analysis of Variance↗
PubMed1992

Diastolic vibration improves systolic function in cases of incomplete relaxation.

BACKGROUND: Incomplete relaxation of the left ventricle (LV) affects LV filling, but the subsequent effect on LV systolic function remains unclear. We attempted to improve relaxation by applying oscillatory mechanical perturbation during diastole (diastolic vibration) and examined the extent to which systolic function improved. METHODS AND RESULTS: Using 10 open-chest canine preparations, pacing tachycardia and administration of propranolol were imposed to induce various levels of incomplete relaxation. Myocardial length perturbation was induced with an oscillator attached to the LV surface (50 Hz, 1-mm amplitude) and was restricted to the period from the beginning of isovolumic relaxation to end diastole. At resting heart rates, diastolic vibration caused an immediate decrease in the time constant (T) of LV pressure fall without any influence on heart rate, LV peak systolic pressure (peak LVP), stroke volume (SV), LV peak positive dP/dt, and total systemic vascular resistance. With pacing tachycardia, diastolic vibration increased both peak LVP and SV at 160 beats per minute (before) and 120 beats per minute (after propranolol), simultaneously decreasing both T and LV diastolic pressures and increasing end-diastolic segment length. The increase in peak LVP and SV caused by diastolic vibration correlated with the T/diastolic interval (r = 0.82), the assumed index of severity of incomplete relaxation. CONCLUSIONS: These results suggest that diastolic vibration accelerates the LV relaxation rate and that this increased relaxation improves systolic function through the Frank-Starling mechanism.

Animals↗
PubMed1992

Ventricular contractility evaluated by mechanical perturbation of the myocardium--experimental and clinical approach adopting small amplitude vibration input.

Small amplitude mechanical vibration has been reported to depress the function of the isolated left ventricle in an amplitude dependent manner. We examined, 1) contractility and preload dependency of the magnitude of functional depression (VID) by applying 50 Hz, 2 mm amplitude vibration to the epicardium of the canine left ventricle and 2) whether VID is present in the failing human ventricle. The magnitude of VID was independent of preload in the physiological range of LV volume showing peak LV pressure greater than 75 mmHg, and VID was correlated with Emax at each inotropic state. In the in-situ condition, VID appeared only in the failing condition with a sensitive increase at a mild level of heart failure. In a study during routine cardiac catheterization (n = 27), the presence of VID has been demonstrated in the human ventricle (n = 18). The magnitude of VID was correlated with ejection fraction (EF) as, VID in peak LV pressure (mmHg) = 80.6 - 110 x EF, r = 0.84, p less than 0.01 in patients with EF less than or equal to 0.7 (n = 14). Therefore, we concluded that VID could be a clinical tool for evaluation of mild heart failure.

Animals↗
PubMed1991

Vibration analysis of the human left ventricular posterobasal wall at the moment of the first heart sound emission.

We examined whether human left ventricular (LV) wall vibration at the first heart sound emission (LVvibr) could be a potential source of information about the left ventricular physical properties, as has been demonstrated by experimental forced vibration studies. LV posterobasal wall vibration in 51 subjects characterized by functional murmur (n = 13), mitral stenosis (n = 8), hypertrophic cardiomyopathy (HCM, n = 8), ischemic heart disease with old myocardial infarction (n = 12) and without prior infarction (n = 10), was detected with a miniature intraesophageal vibration sensor. Peak frequency, sharpness and peak power of LVvibr in patients with functional murmur and mitral stenosis were linearly related to the Q-vibration interval. HCM patients showed a higher peak frequency and sharper configuration in the power spectrum. However, differing from previous reports, we found no characteristic difference in configuration of power spectrum in patients with ischemic heart disease. These results suggest that human LVvibr possibly includes information demonstrated by experimental forced vibration analysis.

Adolescent↗
PubMed1991

[New method for estimating left ventricular myocardial elasticity by vibration analysis].

We solved numerical solutions of Advani-Lee's equation, which treats free vibrations of fluid-filled spherical shells, and forms the basis for non-invasive estimation of left ventricular myocardial elasticity. Numerical results showed that elasticity is approximated by E = 86.5.a2.f2 (E: elasticity (dyn/cm2), a: internal radius (cm), f: eigen-frequency (Hz)). To examine the accuracy of this theoretical equation in estimating elasticity, we made 7 spherical shells of silicone rubber, and compared the estimated elasticity by this equation with that by a standard stretch test. The elasticity calculated by Advani-Lee's equation and by stretch test proved to be nearly identical. Therefore, we concluded that we can estimate the elasticity of a spherical shell using this equation. We calculated the myocardial elasticity at the first heart sound emission in 25 normal persons with a simplified (approximated form of) Advani-Lee's equation. The mean elasticity in normal subjects was (7.04 +/- 2.46) x 10(5) dyn/cm2.

Elasticity↗
PubMed1989

The response of normal and failing heart to externally applied vibration in the canine open chest preparation.

We examined the left ventricular functional response to externally applied vibration using four canine open chest preparations. A sinusoidal 30 Hz vibration (2.7 mm in amplitude) was applied to the ventricular epicardium at each level of propranolol-induced myocardial depression. External vibration in control conditions induced no significant change either in peak left ventricular pressure (LVP) or in stroke volume (SV). With propranolol, 0.1 and 0.3 mg/kg, peak LVP and SV were depressed by the application of external vibration, even though there was no significant change of these values in the nonvibrating condition compared to control. We conclude that the ventricular response to vibration depends on the underlying myocardial viability.

Animals↗
PubMed1989

Effect of left ventricular volume on the magnitude of functional depression by external minute vibration.

We examined the effect of the left ventricular (LV) volume on the magnitude of the vibration induced functional depression (VID) using four canine cross-circulated isovolumically beating LV preparations. A sinusoidal, 50 Hz vibration (1.5 mm in amplitude) was applied to the ventricular anterior epicardium at different values of LV volume which was stepwisely increased by 1-2 ml from 0 to 30 ml. VID was estimated as the difference of the peak LV pressure between control and during external vibration. VID increased as an increment in LV volume when the volume was below 7-8 ml and when peak LV pressure was less than 70 mmHg. However, VID remained constant when the volume increased further. We concluded that VID was independent of LV volume at physiological range.

Animals↗
PubMed1989

The improvement of systolic function of depressed left ventricle by external vibration at diastole.

The left ventricular (LV) incomplete relaxation (IR) has been reported to play an important role in the pathophysiology of the congestive heart failure such as causing higher diastolic pressure and/or impeding the coronary perfusion during diastole. Therefore, using open chest canine preparations (n = 4), we examined 1) whether the minute external vibration during diastole could release IR and 2) what occurred to LV systolic function in this perturbation. LV failure with IR was induced by propranolol administration and, if necessary, by rapid atrial pacing up to 180 beats/min. When we applied a 50 Hz, sinusoidal vibration of 2.1 mm magnitude during diastole to the epicardium of LV with complete relaxation, there was no significant change in the ventricular function. However, the systolic functional improvement (3.8 +/- 1.1 mmHg elevation in LV systolic pressure) was observed when the vibration was applied to LV with IR. We concluded that external vibration at diastole could release IR and would be useful to improve the systolic function of the depressed heart with IR.

Animals↗
PubMed1989

Clinical demonstration of vibration-induced depression of left ventricular function.

In experimental studies, minute sinusoidal vibration has been reported to induce functional depression of the left ventricle and to be an index for evaluation of myocardial crossbridge kinetics. Therefore, to examine whether or not this vibration-induced functional depression could also be observed in the human ventricle, motion of the left ventricular (LV) wall or LV pressure was measured by echocardiography (n = 16) or by left heart catheterization (n = 4), in which 100 Hz, 2.07 mm-amplitude sinusoidal vibration was applied to the subject's precordium. In the echocardiographic study, left ventricular wall shortening did not change by vibration in nine healthy volunteers, but was depressed in two patients with aortic regurgitation (AR) and in one patient with ischemic heart disease (IHD). In measurement of LV pressure, the decrease in LV systolic pressure caused by vibration was obviously observed in two patients (AR and IHD) but was not observed in two patients with hypertrophic cardiomyopathy. These results suggest that we might be able to extend previously proposed experimental idea on early detection of the abnormality in myocardial crossbridge kinetics to the clinical setting.

Adult↗
PubMed1989

Human left ventricular wall vibration responded to precordial minute vibration.

We examined, noninvasively, the response of the left ventricular (LV) wall to precordially applied vibration in seven normal subjects. The LV posterobasal wall vibration was detected by an esophageal vibration sensor. Even though the amplitude of input vibration was maintained at a constant level, a sharp change in amplitude of the LV wall vibration was observed during the cardiac cycle, especially when 1) the subject was lying in a 45 degree left anterior oblique supine position, 2) the sensor was positioned at approx. 40 cm from the incisor teeth and 3) breath was at expiration. The pattern of this amplitude modulation changed with the input frequency. We concluded that the change in amplitude of output signal must have resulted from LV contraction and relaxation.

Adult↗
PubMed1988

Dependence of instantaneous transfer function on regional ischemic myocardial volume.

To obtain the instantaneous left ventricular transfer function curve (instantaneous TFC) under conditions of regional ischemia, sinusoidal accelerations ranging from 30 to 150 Hz were applied to a small area of the epicardium of cross-circulated isovolumic canine left ventricle, and the contralateral acceleration was measured under control and during regional coronary occlusion (n = 11). The TFC is the ratio of the output to input acceleration amplitudes. The instantaneous TFC was characterized as a single-peaked configuration under control coronary perfusion. However, TFCs progressively changed from a single-peaked to a double-peaked configuration during regional ischemia. To quantify this change in instantaneous TFC, we defined an index D as the mean squared difference of TFC during ischemia from TFC during control. Index D was linearly related to the percent mass of the ischemic region at 40 minutes after onset of ischemia. We conclude that 1) transfer function curves are sensitive measures of myocardial heterogeneity and 2) the fractional ischemic weight of the ventricle is a major factor in determination of the deformation in instantaneous TFC at the later stages of regional ischemia.

Animals↗
PubMed1988

The left ventricular vibration mode in the ventricular transfer function method and at the moment of the first heart sound.

Several investigators have aimed to clarify the patient's left ventricular (LV) physical properties by free vibration analysis of heart sound. Recently we have developed a transfer function (TF) method to calculate the LV viscoelasticity. To clarify whether this TF method and a clinical first heart sound (1 HS) analysis are based on the identical ventricular vibration mode analysis, we examined (1) the visualized LV vibration image in the TF method and (2) the quantitative relationship between the peak frequency of the 1 HS spectrum and that of TF curve in the early and late phase of the 1 HS. Isolated isovolumic potassium arrested canine left ventricles were used to visualize the vibration mode in describing the TF (N = 2). Examination of stroboscopically illuminated, slow-motion images revealed the oscillation of the ventricle to be of mode 2 behavior. To analyze the quantitative relation between the TF method and 1 HS analysis we used ten open-chest dogs. The correlation was good (r = 0.917) when the peak frequency of the TF curve at the early phase of the 1 HS was compared to the peak frequency of the 1 HS. We concluded that both the TF method and 1 HS analysis were based on the common, second-order ventricular vibration mode. Therefore, some information on the ventricular physical properties suggeted by the TF method could also be included in the clinical data obtained by 1 HS analysis.

Animals↗
PubMed1987

The degree of increment in plasma catecholamines in patients with mitral stenosis by mild exercise.

Although sympathetic excitation during mild exercise may readily occur in patients with mitral stenosis (MS), the degree of increment in plasma catecholamines has not been fully investigated. We imposed mild ergometric exercise (50 watts, 300 kg/min for 5 minutes) on five patients with mild MS (mitral valve area greater than or equal to 1.0 cm2) and eight with severe MS (mitral valve area less than 1.0 cm2) while they were undergoing cardiac catheterization. In patients with severe MS, total plasma catecholamine levels during exercise were remarkably higher (2821 +/- 783 [SEM] pg/ml) than in those with mild MS (957 +/- 113 pg/ml, p less than 0.05) and in seven control subjects (612 +/- 75 pg/ml, p less than 0.05). This marked increment could not be predicted by heart rate response, which did not differ between severe and mild MS (166 +/- 5 vs 153 +/- 10 bpm). In contrast with catecholamine change, the cardiac index in severe MS showed a very small increment. Results suggest that mild daily exercise can remarkably increase plasma catecholamine levels in severe MS, and this may accelerate various complications of this disorder.

Adult↗
PubMed1986

Measurement of instantaneous viscoelastic properties by impedance-frequency curve of the ventricle.

We developed a method for estimating the instantaneous viscoelastic properties of the left ventricle (LV). This impedance-curve method is based on the instantaneous impedance-frequency curve of the left ventricle generated by a rapidly oscillating mechanical impulse applied to the epicardial surface of the heart. The theoretical basis of the method and experimentally obtained instantaneous impedance-frequency curves were examined to evaluate the validity of our basic assumptions. Using these impedance-curve data, we calculated the instantaneous viscoelastic properties of the LV during the cardiac cycle. The impedance curve shows a configuration that is almost the same as the theoretical curve based on the assumption that an RCL (R, resistor; C, capacitor; L, inductor) parallel circuit is the electrical analog for the LV. The impedance curve varied moment by moment during the development of instantaneous LV pressure. The elastic and viscous coefficients, calculated from the impedance curve, increased with increase of LV pressure. We concluded that the impedance-curve method can delineate the instantaneous viscoelastic properties of the ventricle (especially of the ventricular myocardium).

Animals↗
PubMed1986

Regional myocardial volume perfused by the coronary artery branch: estimation in vivo.

Seven closed-chest dogs were anesthetized with intramuscular Innovar and a N2O/O2 gas mixture. Maximal coronary vasodilation was induced by intra-aortic injection of nitroglycerin (200 micrograms/kg) and continuous infusion of adenosine (1 mg/kg/min) into the main pulmonary artery. Superselective coronary arteriograms were obtained at varying distances along the left circumflex and left anterior descending coronary arteries during scans using the dynamic spatial reconstructor rapid tomographic x-ray scanner. At end-diastole the images of the coronary arteries and opacified myocardium were analyzed for cross-sectional area (CSA) of the coronary artery lumen and regional myocardial volume (Vdsr) perfused by that coronary artery. Postmortem regional myocardial volume (Vpath) was related to the volume perfused by the same artery measured in vivo by the dynamic spatial reconstructor as follows: Vdsr = 4.56 + 0.93 Vpath (r = .98, p less than .001). In addition, the cross-sectional area of the coronary artery supplying a volume of myocardium was related to that volume as follows: Vdsr = - 1.95 + 6.34 CSAmax (r = .88, p less than .001). This suggests that a maximally dilated coronary artery luminal cross-sectional area is linearly related to the volume of muscle it perfuses. We speculate that this relationship may be useful in expressing the physiologic significance of coronary arterial narrowing.

Adenosine↗
PubMed1986

The instantaneous impedance frequency curve of the ventricle with the regional ischemia.

We studied the feasibility of using the impedance frequency curve method (IFM) to detect the myocardial physical heterogeneity of a cross-circulated isolated canine left ventricle with regional ischemia. The curve changed from a single-peak configuration to a double-peak configuration after the LAD coronary flow cessation and returned to the single-peak configuration with the reperfusion of LAD coronary flow. We concluded that IFM can be a useful tool to describe the physical heterogeneity of the ventricular muscle under the regional ischemia.

Animals↗
PubMed1985

ST segment changes under occlusion of the proximal portion of major coronary arteries in the isolated canine heart.

We studied the mechanisms of ST segment displacement in the ECG recorded from the epi- and subendocardium of ischemic ventricles in the isolated and perfused canine heart. ST segment changes were observed in association with a relatively large area of ischemia produced by occlusion of the left anterior descending and septal arteries (LAD + Sept.) or of the left circumflex artery (LCx). Contrary to previous reports, we found that the amount of subendocardial ST elevation was not always greater than that in the epicardial ECG recorded at the center of ischemia. Also, in the non-ischemic area, the degree of the ST depression in the subendocardial record was nearly the same as the epicardial record. On the other hand, the degree of the epicardial ST elevation on the border zone was always smaller than that at the ischemic center, which seemed to be due to the broadness of the border zone. The amplitude of the ST depression in the non-ischemic area was greater when the recording electrode was near the ischemic border, which supports the solid angle theory. The degrees of both ischemic ST elevation and reciprocal ST depression in the LCx perfused area were always greater than in the LAD + Sept. perfused area. These results strongly suggest that ST segment displacement depends on the relative position of the recording electrode to the electric double layer which exists at the border between the ischemic and non-ischemic area.

Animals↗