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Biomedical subjects

T Masuyama

Publications and source records attributed to T Masuyama.

159 records · Page 9Linked to original sources

Relation between low serum cholesteryl-ester transfer activity and abdominal aortic calcification in normolipidemic elderly subjects.

We studied the relation between cholesteryl-ester transfer activity (CETA) and abdominal aortic calcification in elderly subjects. Compared with 10 young healthy subjects (mean +/- S.D. age, 27 +/-2 years) and to 26 elderly subjects without abdominal aortic calcification (79 +/- 7 years), 16 elderly patients with abdominal aortic calcification (82 +/- 6 years) had significantly lower levels of serum CETA. However, there were no differences in the levels of serum lipids and apolipoproteins, including total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol and apolipoproteins A-I, A-II, B, C-II and E, between the two elderly groups. When the two groups of elderly subjects were considered together, the level of serum CETA did not correlate significantly with any lipids and apolipoproteins. These results provide evidence that CETA may prevent the development of aortic calcification in normolipidemic elderly people.

Journal Article↗

Dynamic change in collateral flow associated with myocardial ischemia in humans.

BACKGROUND: This study sought to investigate how collateral flow changes during myocardial ischemia in patients. METHODS: Myocardial contrast echocardiography (MCE) and rapid atrial pacing were performed in 20 patients with angiographically evidenced coronary collaterals from the right coronary artery (RCA) to the occluded left anterior descending coronary artery. Sonicated contrast medium was injected into the RCA before and immediately after atrial pacing to determine the peak background-subtracted contrast intensity (PI) in the collateral territory (PIA) and its ratio to PI in the control territory (PI ratio) as parameters of collateral blood flow. Lactate production in the coronary circulation during pacing was determined to assess myocardial ischemia in the collateral territory. RESULTS: PIA showed a significant correlation with regional wall motion either before (r(squared)=-0.64, P<0.01) or after pacing (r(squared)=-0.65, P<0.01). Similarly, PI ratio was significantly correlated with regional wall motion either before (r(squared)=-0.54, P<0.05) or after pacing (r(squared)=-0.64, P<0.01). Rapid atrial pacing decreased both PIA and PI ratio significantly greater in patients with lactate production than in those without (PIA: -67+/-53 vs. -15+/-34%, P<0.05; PI ratio: -68+/-49 vs. -8.2+/-32%, P<0.05, respectively), while neither PIA nor PI ratio differ between the two groups of patients before pacing (PIA: 13.8+/-19. vs. 16.2+/-13.3U, P=0.75; PI ratio: 0.70+/-0.71 vs. 0.87+/-0.65, P=0.58, respectively). CONCLUSIONS: We concluded that (1) collateral flow determined by MCE was closely associated with regional cardiac function, and (2) not the amount of collateral flow at rest, but pacing-induced change of collateral flow seemed to be a determinant of regional ischemia in patients with coronary collaterals.

Aged↗

Transthoracic Doppler echocardiographic measurements of pulmonary venous flow velocity patterns: comparison with transesophageal measurements.

Recently, we and other groups showed that analysis of transthoracic pulmonary venous flow velocity patterns is useful in the estimation of left ventricular diastolic function and left atrial pressure; however, it is unclear whether transthoracic tracings, in contrast to transesophageal tracings, provide reliable quantitation of the abnormal pulmonary venous flow characteristics in patients with and without cardiac disorders. This study was attempted to validate transthoracic pulmonary venous flow measurements by comparing them with transesophageal measurements in eight normal volunteers and 17 patients with a variety of cardiac disorders. Transesophageal and transthoracic measurements of peak diastolic forward flow velocity, the ratio of peak systolic/diastolic forward flow velocities, and the peak reversal flow velocity at atrial contraction sampled in the right upper pulmonary vein showed good correspondence to each other. The flow velocities were higher in the right upper pulmonary vein than in the left upper pulmonary vein. Narrower spectral flow velocity patterns with higher velocities were obtained 1 to 2 cm distal to the orifice in the pulmonary vein than at the orifice. Thus transthoracic measurements of the pulmonary venous flow velocity pattern are feasible and accurate in patients and may be used to assess left ventricular function and hemodynamics as a substitute for transesophageal measurements.

Adult↗

Progressive intraventricular drop of early diastolic flow velocity reflects impaired active ventricular diastolic function in hypertensive heart disease: comparative study between early diastolic and atrial contraction phases.

Left ventricular (LV) diastolic function in the early diastolic phase includes both active and passive processes, but in the atrial contraction phase it includes only passive processes. To elucidate the relation between the intraventricular dispersion of the flow velocity in diastole and LV diastolic process, 31 normal volunteers and 12 patients with hypertensive heart disease were studied. In these subjects the flow velocity pattern at the mitral tip was recorded simultaneously with regional flow velocity patterns 1, 2, or 3 cm from the mitral tip toward the apex, respectively, with multigate pulsed Doppler echocardiography from the apical long-axis view with the guidance of Doppler color-flow imaging. Although the ratio of regional peak flow velocity/mitral peak flow velocity in the atrial contraction phase decreased from the mitral tip to the apex to the same degree in the normal volunteers and patients with hypertensive heart disease, there was a significant difference in the intraventricular dispersion of the early diastolic flow velocity between the two groups. These results suggest that the progressive intraventricular drop of the flow velocity in the early diastolic phase in patients with hypertensive heart disease may reflect the impairment of active rather than passive LV diastolic function.

Adult↗

Transthoracic Doppler assessment of pattern of left ventricular dysfunction in hypertensive heart disease: combined analysis of mitral and pulmonary venous flow velocity patterns.

Although mitral flow velocity pattern changes with the progression of left ventricular (LV) diastolic dysfunction, it lacks predictive value in individual patients because of pseudonormalization in the presence of congestive heart failure and many physiologic and pathologic contributors to the mitral flow velocity pattern. To determine whether analysis of pulmonary venous flow velocity patterns complements the information obtainable from the mitral flow velocity patterns in the evaluation of patterns of LV dysfunction of hypertensive heart disease in individual patients, the ratio of the peak early diastolic filling velocity/peak filling velocity at atrial contraction (E/A ratio) in the mitral flow velocity pattern and the ratio of the peak systolic forward flow velocity (S)/peak diastolic forward flow velocity (D) (S/D ratio) in the pulmonary venous flow velocity pattern by the transthoracic approach were determined in 107 hypertensive patients with and without congestive heart failure. Age-related normal values of the E/A and S/D ratios were determined in 61 normal subjects and used to judge the normality or abnormality of the patterns. Results of the study indicate that (1) although an increased mitral E/A ratio is strongly indicative of heart failure with normal LV systolic function, the mitral E/A ratio is frequently within the normal range in hypertensive patients with heart failure; (2) association of decreased pulmonary venous S/D ratios with a normal mitral flow velocity pattern indicates the presence of heart failure as a result of LV systolic dysfunction that is usually observed at the most advanced pattern of LV dysfunction; (3) mild LV diastolic dysfunction is likely to exist in patients with normal E/A ratios if the pulmonary venous S/D ratio is higher than normal value; (4) predictive accuracy in the detection of LV systolic and diastolic dysfunction would be improved if both mitral and pulmonary venous flow velocity patterns rather than the mitral flow velocity pattern alone were analyzed. In conclusion, analysis of pulmonary venous flow velocity recordings improves accuracy and reliability of the Doppler assessment of LV systolic and diastolic dysfunction, particularly in individual hypertensive patients with normal mitral flow velocity patterns.

Adult↗

Decreased and abnormal left ventricular filling in acute heart failure: role of pericardial constraint and its mechanism.

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.

Acute Disease↗

Peak early diastolic filling velocity may decrease with preload augmentation: effect of concomitant increase in the rate of left atrial pressure drop in early diastole.

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.

Animals↗

Doppler echocardiographic assessment of changes in pulmonary artery pressure associated with vasodilating therapy in patients with congestive heart failure.

Transpulmonic pressure gradient and pulmonary artery pressures can be estimated from the Doppler pulmonary regurgitant flow velocities by applying the simplified Bernoulli equation. In this study, continuous-wave Doppler echocardiography was used to assess changes in pulmonary regurgitant flow velocities associated with administration of vasodilators in 10 patients with congestive heart failure. M-Mode echocardiographic parameters such as left ventricular end-systolic and end-diastolic dimension and fractional shortening did not change with administration of vasodilators. Pulmonary regurgitant flow velocity at end diastole decreased from 1.9 +/- 0.6 to 1.3 +/- 0.3 m/sec (p less than 0.01), and Doppler-estimated transpulmonic pressure gradient at end diastole decreased from 16 +/- 11 to 8 +/- 4 mm Hg (p less than 0.01). Doppler-estimated transpulmonic pressure gradient at end diastole was compared with catheterization-determined pulmonary arterial end-diastolic pressure before and after administration of vasodilators in three patients, and there was a good agreement between these measurements. Thus noninvasive and sensitive assessment of the effect of vasodilators on pulmonary arterial end-diastolic pressure in patients with congestive heart failure is possible with continuous-wave Doppler echocardiographic measurement of pulmonary regurgitant flow velocities.

Adolescent↗

Variability of diastolic paradoxical jet flow in a patient with hypertrophic cardiomyopathy with midventricular obstruction: dissociation between systolic and diastolic intracavitary flow dynamics.

Variability of paradoxical jet flow in a case of hypertrophic cardiomyopathy with midventricular obstruction was examined. Propranolol decreased both peak diastolic paradoxical jet flow velocity and peak systolic velocity at the narrowing portion. Nitroglycerin decreased peak diastolic paradoxical jet flow velocity with an increase in peak systolic velocity at the narrowing portion. Thus the diastolic paradoxical jet flow is dynamic as well as the abnormal systolic flow; however, changes in these abnormal flow dynamics may not be necessarily in the same direction. Doppler echocardiography should be useful in assessing effects of interventions on the flow dynamics in patients with hypertrophic cardiomyopathy with midventricular obstruction.

Adult↗

Improvement in left ventricular diastolic filling by septal myectomy in hypertrophic cardiomyopathy.

Abnormalities in left ventricular diastolic function or filling are considered to be responsible for some of the symptoms in patients with hypertrophic cardiomyopathy. To clarify whether the abnormalities in left ventricular diastolic filling are improved by septal myectomy, 13 patients with hypertrophic cardiomyopathy and intracavitary pressure gradient were studied preoperatively and postoperatively by use of pulsed Doppler echocardiography. Peak early diastolic filling velocity (E), the ratio of peak early diastolic filling to peak atrial filling velocities (E/A ratio), and deceleration time were measured from the transmitral flow velocity pattern before and after septal myectomy. Although E and E/A ratio did not change after septal myectomy, deceleration time significantly shortened from 314 +/- 72 to 271 +/- 53 milliseconds (n = 10; p less than 0.05). Further, if seven patients with significant changes in heart rate (greater than 30%) or in the Doppler-determined severity of mitral regurgitation (more than one degree) were excluded (because these parameters may effect E and E/A ratio), there were also significant changes in E (81 +/- 21 versus 98 +/- 25 cm/sec, p less than 0.05) and in E/A ratio (0.84 +/- 0.17 versus 1.14 +/- 0.33, p less than 0.05). Because left ventricular systolic function has been demonstrated to remain constant or to decrease by most measures after septal myectomy, relief of some symptoms may be largely the result of the improvement in diastolic filling suggested by these criteria.

Adult↗

Left ventricular diastolic dysfunction in end-stage dilated cardiomyopathy: simultaneous Doppler echocardiography and hemodynamic evaluation.

Left ventricular diastolic dysfunction is an integral component of end-stage dilated cardiomyopathy. To better characterize this disorder we studied 15 patients undergoing catheterization during cardiac transplant screening evaluation. Pulsed-wave Doppler echocardiographic recordings of mitral inflow were obtained with simultaneous high-fidelity left ventricular and phase-corrected pulmonary capillary wedge pressures. Doppler-derived isovolumic relaxation times were within normal limits, despite a prolonged coefficient of relaxation (tau), and correlated with pulmonary capillary wedge--left ventricular crossover pressure. Peak velocity of early diastolic filling was similar to that reported in normal subjects and did not correlate with crossover pressure or tau. Early diastolic acceleration and deceleration times were shortened compared with reported normal values. Acceleration time correlated with mean negative dP/dt from mitral valve opening to left ventricular minimum pressure and with crossover pressure, and deceleration time correlated with mean dP/dt from left ventricular minimum pressure to the peak of the rapid filling wave. Late diastolic filling at atrial contraction was absent in 12 patients, all of whom had a significant early diastolic rapid filling wave and an elevated end-diastolic pressure. Despite an increase in pulmonary capillary wedge pressure during atrial contraction, the failing ventricles were unable to generate detectable forward transmitral flow. Poor cardiac pump function was shown by low left ventricular stroke volume, which correlated with the diastolic flow velocity integral. Thus, in end-stage cardiomyopathy, the transmitral flow velocity pattern is characterized by normal peak early filling velocity, low normal isovolumic relaxation time, shortened acceleration and deceleration times of early diastolic flow, decreased early flow velocity integral, and absent or decreased filling during atrial contraction. This pattern reflects interaction between elevated transmitral driving pressure and the compromised relaxation and compliance of a left ventricle functioning on an elevated pressure-volume curve.

Adult↗

Dobutamine stress ultrasonic myocardial tissue characterization in patients with dilated cardiomyopathy.

Although acoustic properties of the myocardium are different between patients with cardiomyopathy and normal subjects, the frequency of the abnormal properties in patients with cardiomyopathy is unknown. We assessed the frequency of abnormal acoustic properties of the myocardium detectable with integrated backscatter in patients with cardiomyopathy and attempted more sensitive ultrasonic tissue characterization by combining dobutamine stress testing in patients with cardiomyopathy with apparently normal acoustic properties of the myocardium at rest. The magnitude of cyclic variation of integrated backscatter and calibrated myocardial integrated backscatter at end diastole were measured in 36 normal subjects and 40 patients with dilated cardiomyopathy. Either one of the integrated backscatter parameters was abnormal in 30 of 40 patients with cardiomyopathy. Dobutamine stress ultrasonic tissue characterization was performed in 10 patients with cardiomyopathy with normal values of both integrated backscatter parameters and 10 normal subjects. Calibrated myocardial integrated backscatter did not change during dobutamine infusion in any subject. The magnitude of cyclic variation in integrated backscatter increased in normal subjects but did not change in patients with cardiomyopathy despite a comparative associated increase in the systolic wall thickening during dobutamine infusion. Abnormal acoustic properties are detectable at rest with myocardial integrated backscatter about in three quarters of patients with cardiomyopathy. A combination of dobutamine stress testing would provide more sensitive ultrasonic myocardial tissue characterization and may make it possible to detect subtle changes in the acoustic properties of the myocardium in patients with dilated cardiomyopathy. Therefore dobutamine stress ultrasonic tissue characterization may detect mild dilated cardiomyopathy.

Adult↗

Diagnostic performance of myocardial contrast echocardiography for detection of stunned myocardium.

Improvement in regional wall motion after acute myocardial infarction has been described up to 2 to 3 weeks after the acute event despite restoration of blood flow by early successful reperfusion therapy. The prospective identification of potentially reversible ventricular dysfunction caused by stunned myocardium has significant clinical implications. Twenty-seven patients with acute myocardial infarction underwent myocardial contrast echocardiography (MCE) before, immediately after, and 4 weeks after successful reperfusion therapy. MCE was performed by imaging a parasternal short-axis view during intracoronary arterial injection of 2 ml sonicated ioxaglate (Hexabrix-320). The contrast defect area and contrast-filled area before reperfusion were defined as the risk area and noninfarct area, respectively. The normalized gray level was defined as the ratio of the gray level in the risk area/gray level in the noninfarct area. In 21 patients, wall motion was akinetic or dyskinetic immediately after reperfusion, and 10 of 21 patients in whom wall motion recovered during the chronic stage were defined as patients with stunned myocardium. In patients who showed asynergic wall motion immediately after reperfusion, MCE predicted the recovery of left ventricular wall motion (stunned myocardium) during the chronic stage with a sensitivity of 77%, specificity of 100%, and predictive accuracy of 86%, when a normalized gray level of more than 0.4 was presumed to predict stunned myocardium. We conclude that MCE provided the prospective identification of potentially reversible ventricular dysfunction caused by stunned myocardium, and wall motion in the area of nonenhanced myocardium on MCE immediately after reperfusion is not expected to show reversible dysfunction.

Adult↗

Reduction of endothelial microfilament bundles in the low-shear region of the canine aorta. Association with intimal plaque formation in hypercholesterolemia.

To interrelate in vivo wall shear stress, endothelial microfilament bundle formation, and atherosclerosis localization, we used a mild abdominal aortic stenosis in 11 beagles to produce a range of wall shear stresses above and below the constriction. Six of the beagles were fed standard animal chow supplemented with 5% cholesterol and 10% coconut oil. Wall shear stresses, endothelial microfilament bundles, and intimal plaque localization were assessed along the stenosed aorta. Shear stress was determined in vivo from the near-wall velocity profiles with a 20-MHz, 80-channel, multigate Doppler velocimeter. Content of the microfilament bundles was quantified by planimetry of transmission electron photomicrographs. After 6 weeks, mean shear stress was higher immediately upstream from the throat of the stenosis than at the proximal site (46.1 +/- 7.3 dynes/cm2 versus 24.0 +/- 6.2 dynes/mc2, p less than 0.001) and was significantly lower immediately distal to the stenosis than at the proximal site (9.4 +/- 0.3 dynes/cm2, p less than 0.01). The microfilament bundle content increased immediately upstream from the throat of the stenosis and decreased immediately distal to the stenosis compared with the proximal site in both normocholesterolemic and hypercholesterolemic fat-fed beagles. Intimal plaques formed exclusively immediately distal to the stenosis in the hypercholesterolemic beagles. These findings suggest that a low shear-stress environment attenuates endothelial microfilament bundle formation, thus leading to a predilection for the initiation of atherosclerosis in atherogenic conditions such as hypercholesterolemia.

Actin Cytoskeleton↗

Subendocardial myocardial ischemia as assessed with myocardial contrast echocardiography in patients with ischemic heart diseases.

Myocardial contrast echocardiography was used to characterize changes in the regional and transmural myocardial blood flow distribution that were provoked by rapid atrial pacing stress in patients with coronary artery diseases. In patients with coronary organic stenosis, a decrease in the myocardial contrast-enhancement in the subendocardial half after rapid atrial pacing was associated with stress-induced chest pain and electrocardiographic ST-T changes. The decrease in the myocardial contrast-enhancement in the subendocardial half after rapid atrial pacing was not observed in patients without coronary stenosis or after coronary angioplasty. Thus, the finding was considered to reflect myocardial ischemia. Pacing-induced decreases in myocardial contrast-enhancement were observed in some patients with old myocardial infarction and significant resting coronary collaterals. In these patients, myocardial ischemia was considered to have developed at rapid pacing because collateral function was good enough to perfuse the infarct myocardium at rest, but was not good enough to prevent myocardial ischemia at stress. Thus, myocardial contrast echocardiography seems to be particularly useful in assessing myocardial ischemia at stress due to coronary stenosis in patients with angina pectoris and due to poor dynamic collateral function in patients with old myocardial infarction.

Angioplasty↗