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Biomedical subjects

A Iuchi

Publications and source records attributed to A Iuchi.

At least 55 records · Page 3Linked to original sources
PubMed1996

Peculiar patterns of aortic regurgitation and carotid pulse due to dysfunction of a Medtronic Hall prosthetic valve: a case report.

We describe a patient with dysfunction of a Medtronic Hall prosthetic valve showing peculiar patterns of aortic regurgitation and carotid pulse caused by valvular thrombosis. The aortic regurgitation was considered to be caused by a significant delay in prosthetic valve closure, manifested by a peculiar regurgitation pattern limited to early diastole, in association with widely split closing clicks and an abnormally low dicrotic notch in the carotid pulse. At surgery, fibrin thrombi were noted just below the prosthetic ring in the minor outflow region which restricted disc movement. The fibrin thrombi were removed and the valve was rotated 90 degrees. Following reoperation, all abnormalities disappeared.

Angiography↗
PubMed1996

[Evaluation of myocardial sympathetic nerve function in patients with mitral valve prolapse using iodine-123-metaiodobenzylguanidine myocardial scintigraphy].

Mitral valve prolapse (MVP) is closely related to myocardial sympathetic nerve function. This study evaluated the presence of impaired myocardial sympathetic nerve function by Iodine-123-metaiodobenzylguanidine (MIBG) scintigraphy in nine patients with MVP. For comparison, 15 healthy subjects without heart disease were investigated (control group). Single photon emission computed tomography (SPECT) and anterior planar myocardial scintigraphy were performed 15 min (initial images) and 3 hours (delayed images) after injection of MIBG (111 MBq). The location and degrees of reduced tracer uptake were evaluated. Myocardial MIBG uptake was quantified by uptake ratio of the heart (H) to upper mediastinum (M) on the anterior planar images (H/M). Percentage washout of MIBG in nine sectors of all oblique slices along the short-axis was calculated. The washout rates were higher at the inferoposterior and septal segments in patients with anterior leaflet prolapse, and at inferoposterior and lateral segments in patients with posterior leaflet prolapse. The bull's eye map showed increased washout rate in the apical and posteroseptal basal segments. There was no significant difference in the H/M ratio between MVP patients and the control group. These results indicate that MIBG can be used to evaluate localized myocardial sympathetic nerve function in MVP.

3-Iodobenzylguanidine↗
PubMed1995

Predisposing factors for severe mitral regurgitation in idiopathic mitral valve prolapse.

To elucidate predisposing factors for severe mitral regurgitation (MR) in idiopathic mitral valve prolapse (MVP), 124 MVP patients were classified into the following categories: 55 with isolated clicks (click group), 35 with a late-systolic murmur (late-SM group), and 34 with a holosystolic murmur (holo-SM group). Their clinical and echocardiographic findings were compared with those of 26 patients with spontaneous chordal rupture (rupture group). In 22 patients in the click group, 24 in the late-SM group, and 22 in the holo-SM group, follow-up studies were performed for a mean of 4.5 years (range 1 to 13.5). The mean age was youngest in the click group and oldest in the rupture group. The click and late-SM groups showed a female predominance, but the holo-SM and rupture groups showed a male predominance. There was no difference in the incidence of systemic hypertension among the 4 groups. Most patients in the click and late-SM groups had anterior leaflet prolapse. In the holo-SM and rupture groups, however, the incidence of posterior leaflet involvement was significantly increased. The incidence of thickened mitral valve increased in order of the click (8%), late-SM (21%), holo-SM (38%), and rupture (50%) groups. Six patients in the holo-SM group developed chordal rupture with severe MR during the follow-up period. In the click and late-SM groups, however, there were no complications and no development into a holo-SM. Thus, aging, male sex, posterior leaflet prolapse, thickened mitral valve, and holo-SM were found to be important predisposing factors for severe MR in idiopathic MVP.

Adult↗
PubMed1995

Effects of enalapril on left ventricular mass and diastolic function in essential hypertension: special reference to duration of hypertension.

Using M-mode and pulsed Doppler echocardiography, the effects of enalapril on left ventricular (LV) hypertrophy and diastolic dysfunction in essential hypertension and the relation between improvement in these two parameters and duration of hypertension were evaluated. The subjects, 30 previously untreated hypertensive patients, were divided into nonhypertrophy (18 patients) and hypertrophy (12 patients) groups. All patients received enalapril at a daily dose of 5 to 10 mg for 6 months. Left ventricular mass by M-mode echocardiography and LV inflow (LVIF) velocity by transthoracic pulsed Doppler echocardiography were measured before and after enalapril therapy. In the nonhypertrophy group, enalapril significantly increased peak early diastolic LVIF (E) velocity (P < .05), slightly lowered peak atrial systolic LVIF (A) velocity, significantly decreased their ratio (A/E) (P < .01), and significantly shortened both the deceleration time, from the peak of the early diastolic wave, and isovolumic relaxation time (P < .05 and P < .01, respectively). In the hypertrophy group, enalapril significantly increased E (P < .05), slightly lowered A, significantly decreased A/E (P < .05), slightly shortened the deceleration time and isovolumic relaxation time, and slightly decreased LV mass. The administration of enalapril correlated significantly and positively with the duration of hypertension and the rates of change in A/E and LV mass in all of the hypertensive patients (P < .01 and P < .05, respectively). These results suggest that long-term administration of enalapril to hypertensive patients improves LV diastolic hemodynamics regardless of the presence or absence of LV hypertrophy and that the effects are most remarkable in patients with the shortest duration of hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Evaluation of left ventricular diastolic hemodynamics from the left ventricular inflow and pulmonary venous flow velocities in hypertrophic cardiomyopathy.

We evaluated the characteristics of left ventricular diastolic hemodynamics in hypertrophic cardiomyopathy (HCM) by measuring left ventricular inflow (LVIF) and pulmonary venous flow (PVF) velocities in 62 patients with asymmetric septal hypertrophy and 34 normal controls. The patients were divided into four groups according to the LVIF pattern and left ventricular end-diastolic pressure (LVEDP): 1) the pseudonormalization group; 13 patients with the ratio of peak atrial systolic (A) to early diastolic (E) LVIF velocity (A/E) < or = 1 and LVEDP > or = 15 mm Hg, 2) the normal pattern group; 10 patients with the A/E < or = 1 and LVEDP < 15 mm Hg, 3) the relaxation failure group; 25 patients with the A/E > 1, and 4) the mid-diastolic wave group; 14 patients with a mid-diastolic wave. The peak early diastolic LVIF velocities in the pseudonormalization, relaxation failure and mid-diastolic wave groups were significantly smaller than in the control group. The deceleration time from the peak of the E wave and the isovolumic relaxation time were significantly prolonged in the relaxation failure and mid-diastolic wave groups. The peak diastolic PVF velocity in the relaxation failure and mid-diastolic wave groups was significantly decreased, and was significantly increased in the pseudonormalization group. The peak atrial systolic PVF velocity was significantly increased in all patients with HCM, particularly in the pseudonormalization group. LVEDP was the highest in the pseudonormalization group, followed by the mid-diastolic wave, relaxation failure and normal pattern groups, in that order. In conclusion, combined analysis of the LVIF and PVF provides useful information regarding various abnormalities of left ventricular diastolic hemodynamics in patients with HCM.

Adult↗
PubMed1995

The first heart sound in atrial septal defect with reference to atrioventricular valve motion and hemodynamics.

To clarify the characteristics of the first heart sound in atrial septal defect (ASD) and its pathophysiological basis, 17 patients with ASD associated with incomplete right bundle branch block (IRBBB) and 7 with isolated IRBBB were studied using phonoechocardiography and Doppler echocardiography. Fifteen of the 17 ASD patients also were studied following surgical closure of the defect. Indices were compared among the preoperative ASD, postoperative ASD, and IRBBB groups including: P-Q intervals, loudness of the mitral and tricuspid component of the first heart sound (IM, IT), end-diastolic closing excursions of the mitral and tricuspid valves (Mx, Tx), and mitral and tricuspid inflow velocities during early diastole and atrial contraction. There were no significant differences in the P-Q intervals among these 3 groups. IM was attenuated, and IT was accentuated in ASD compared with IRBBB. Postoperatively, IM was augmented in all but 1 patient and IT was attenuated in all patients. Mx was significantly smaller, and Tx was significantly larger in ASD than in IRBBB. Postoperatively, Mx was significantly increased and Tx was significantly reduced; the maximal mitral inflow velocity during atrial contraction was increased while the maximal tricuspid inflow velocity was significantly reduced. Thus, the first heart sound in ASD is characterized by an attenuated mitral component and an accentuated tricuspid component. Hemodynamic alterations and consequent changes in closing energies of the atrioventricular valves probably account for these features.

Adolescent↗
PubMed1995

[Transesophageal echocardiographic study on the mechanisms of mitral regurgitation in hypertrophic cardiomyopathy: comparison with sigmoid septum].

Transesophageal echocardiography was performed to elucidate the mechanisms of mitral regurgitation (MR) in 40 patients with hypertrophic cardiomyopathy with asymmetric septal hypertrophy, 15 obstructive and 25 nonobstructive, and the organic changes of the mitral leaflet were compared to those of 30 patients with sigmoid interventricular septum. Thirty subjects without cardiac diseases served as the control group. Transthoracic and transesophageal echocardiography were performed in all subjects to measure the following: left ventricular dimension, interventricular septal thickness and peak velocity at the left ventricular outflow tract by transthoracic echocardiography; the lengths and the thicknesses of the rough zone of the anterior and posterior mitral leaflets at mid-diastole and the distance between the tip of the posterior papillary muscle and the anterior mitral annulus by transesophageal echocardiography. The presence of systolic anterior motion of the mitral complex, contact between the anterior mitral leaflet and the interventricular septum during diastole, and the occurrence of mitral valve prolapse (MVP) were also investigated. The maximum area and timing of MR during systole was measured by M-mode color Doppler technique. The following results were obtained. 1. MR was observed in 35 (88%) of the 40 patients with hypertrophic cardiomyopathy. The maximum regurgitant area in the obstructive group was significantly greater than in the other groups, and the regurgitation was frequently pansystolic. 2. The lengths of both mitral leaflets at mid-diastole were significantly greater in both groups with hypertrophic cardiomyopathy than in the other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

[Changes in pulmonary venous and transmitral flow velocity patterns after cardioversion of atrial fibrillation].

The time course of recovery of left atrial mechanical function after electrocardioversion of atrial fibrillation was examined in 25 patients with atrial fibrillation by recording pulmonary venous and transmitral flow velocities and interatrial septal motion during atrial systole within a day (16 +/- 5 hours) and ten days after cardioversion of atrial fibrillation by transesophageal and transthoracic Doppler and M-mode echocardiography. There were 6 patients with hypertension, 4 with ischemic heart disease, 2 with alcoholic heart, 5 with dilated cardiomyopathy, and 8 without underlying heart disease. The peak velocities of the atrial systolic waves of the transmitral and pulmonary venous flow velocities (A and PVA, respectively) and first systolic wave (PVS1) of pulmonary venous flow, durations of both atrial systolic waves, and amplitude of interatrial septal motion during atrial systole increased significantly ten days after cardioversion compared with those measured within a day of cardioversion in all patients except the 5 patients with dilated cardiomyopathy. Peak velocity of the second systolic wave (PVS2) of pulmonary venous flow increased, and that of the early diastolic and diastolic waves (E and PVD, respectively) of transmitral and pulmonary venous flow decreased ten days after cardioversion compared with those within a day of cardioversion. These results suggested that active atrial systolic (A and PVA) and relaxant (PVS1) parameters obtained from transmitral and pulmonary venous flow velocities are good indicators of left atrial mechanical function after cardioversion of atrial fibrillation.

Adult↗
PubMed1995

Histopathologic studies of innervation of normal and prolapsed human mitral valves.

We evaluated the distribution of the nerves in valve tissue of humans to clarify the relationship between mitral valve prolapse and autonomic nerve dysfunction. We studied 15 autopsy specimens of normal mitral valve, 10 prolapsed mitral valves, five each of normal tricuspid, aortic, and pulmonary valves, and three prolapsed mitral valves obtained at cardiac surgery. Immunohistochemical studies utilized the avidinbiotin peroxidase complex (ABC) method and several nerve-related antigens: 1) S-100 protein, glial fibrillary acidic protein (GFAP), and neurofilament protein (NFP) as markers of glial and Schwann cells of the nervous system; 2) choline acetyltransferase (ChAT) to identify cholinergic nerve endings; 3) neuropeptide Y (NPY), a neuropeptide that is distributed in accordance with sympathetic nerves; and 4) calcitonin gene-related peptide (CGRP), a neuropeptide that is distributed in accordance with afferent nerves. Distribution of adrenergic nerve fibers was also examined by fluorescence method. Morphology of nerve endings of the normal mitral valve was studied by electron microscopy. In normal valves, distributions of S-100 protein, GFAP, and NFP immunoreactivities were clearly visible along the subendocardial site on the coaptation aspect of the base-to-body portion of each valve, regardless of the kind of valve. In contrast, there was only a scanty distribution of these reactivities on the physiologic coaptation area of the tip. In prolapsed mitral valves, there was no distribution of S-100-positive protein or other nerve-related antigens in areas of the valve with myxomatous degeneration. Distribution of CGRP, ChAT, and NPY immunoreactivities, and adrenergic fluorescence, were the same as those of the nerve-related antigens in both normal and prolapsed mitral valves. Electron microscopic study of the atrial aspect of normal mitral valves revealed numerous small axons with aggregations of small clear vesicles, indicating cholinergic features. The results suggest that the subendocardial site on the atrial aspect at the middle portion of the mitral valve is rich in nerve endings, including the afferent nerves, and that mechanical stimuli from this area caused by abnormal coaptation in mitral valve prolapse may produce an improper circuit in autonomic nerve function between the central and mitral valve nervous systems.

Adult↗
PubMed1994

Comparative phonocardiographic, echocardiographic and Doppler echocardiographic evaluation of normally functioning Medtronic Hall and Björk-Shiley mitral prosthetic valves.

Although data from cardiac catheterization and in vivo studies are available, phonocardiographic and ultrasonic characteristics of the Medtronic Hall valve in the mitral position have not been adequately established. Phonomechanocardiographic, echocardiographic and Doppler echocardiographic examinations were performed in 15 patients (Medtronic Hall group) with a Medtronic Hall mitral valve prosthesis to elucidate the phonocardiographic and ultrasonic characteristics of the normally functioning Medtronic Hall valve in the mitral position. These findings were compared with those obtained from 20 patients (Björk-Shiley group) with a normally functioning Björk-Shiley 60 degrees mitral valve prosthesis. Simultaneous recordings of the phonocardiogram and M-mode echocardiogram of the prosthetic valve in patients in the Medtronic Hall group revealed three opening clicks relating to disc motion. The timing of the three opening clicks correlated with the onset of disc opening, the completion of disc opening, and a notch which appeared about 30 msec after the completion of disc opening. Similar recordings performed in patients in the Björk-Shiley group revealed that the third opening click was detected in only half of the patients and that its timing was nearly twice as early as that noted in the Medtronic Hall group. The Medtronic Hall group had significantly shorter durations of the apical diastolic rumble and the slow filling wave on the apexcardiogram, as well as significantly reduced peak mitral inflow velocity during early diastole and shortened pressure half-time on the mitral inflow velocity curve. Transesophageal Doppler echocardiography demonstrated slight mitral regurgitation in all patients in both the Medtronic Hall and the Björk-Shiley groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Genesis of the Austin Flint murmur: relation to mitral inflow and aortic regurgitant flow dynamics.

OBJECTIVES: This study was designed to elucidate the genesis of the Austin Flint murmur. BACKGROUND: The Austin Flint murmur is an apical diastolic rumble associated with significant aortic regurgitation. The precise mechanism of the murmur remains unclear. METHODS: The relation between the Austin Flint murmur and mitral inflow and aortic regurgitant flow dynamics was evaluated nonivasively in 13 patients with moderate to severe aortic regurgitation and 15 control subjects using phonocardiographic and pulsed and color-coded Doppler echocardiographic techniques. The severity of aortic regurgitation was determined by color-coded Doppler echocardiography on the basis of the maximal distance of the regurgitant signal. RESULTS: The direction of aortic regurgitant flow was unrelated to the presence of the Austin Flint murmur. The severity of aortic regurgitation was greater in patients with than in those without this murmur. The peak mitral inflow velocity during early diastole (E) was significantly increased, and both peak mitral inflow velocity at atrial contraction (A) and the A/E ratio were significantly decreased in patients with the Austin Flint murmur compared with values in those without this murmur or in control subjects. However, the maximal amplitude of the Austin Flint murmur did not coincide temporally with the peak mitral inflow velocity. The murmur continued both after rapid mitral inflow had ended and during diastolic mitral regurgitation. CONCLUSIONS: The increased velocity of early diastolic mitral inflow in patients with the Austin Flint murmur is due to aortic regurgitation, but rapid mitral inflow is not an essential requirement for production of the murmur. In some cases, the Austin Flint murmur may be generated by aortic regurgitant flow alone.

Adult↗
PubMed1993

Assessment of left ventricular diastolic function and potential by quantitative analysis of left ventricular filling curves in patients with atrial fibrillation. A new algorithm for Doppler echocardiographic study.

To evaluate left ventricular (LV) diastolic function and potential, LV filling curves for 18 patients with atrial fibrillation (Af) were constructed and their positions and appearance were evaluated quantitatively by analysis of 95% maximal filling volume points and maximal curvature alteration points. The LV filling curves of group A (Af only) lay left superiorly, while those of group B (impaired LV diastolic function) were situated right inferiorly, all bending steeply. The LV filling curves of group C (mitral stenosis) bent slightly. The lowest normal filling volume points and compensation areas were calculated to evaluate LV diastolic function and were demonstrated to be very different in groups A and B. The lowest normal filling volume points of group C were similar to those of group A, but compensation areas were smaller, indicating a lower LV diastolic potential. It is concluded that the 95% maximal filling volume point, maximal curvature alteration point, lowest normal filling volume point and compensation area are effective indices for evaluating not only LV diastolic function but also the diastolic potential.

Algorithms↗
PubMed1993

[Evaluation of pulmonary venous flow patterns in left heart failure: a study using transesophageal Doppler echocardiography].

Pulmonary venous flow (PVF) patterns in left heart failure were evaluated using transesophageal pulsed Doppler echocardiography in 30 patients with dilated hearts (DH) and 30 normal subjects. Eighteen patients had myocardial infarction and 12 patients had dilated cardiomyopathy. The diagnostic criteria by using M-mode echocardiography were left ventricular end-diastolic dimensions (LVDd) of 5.5 cm or more and % LV fractional shortening (%FS) of less than 30%. Peak velocities of the first systolic (PVS1) and second systolic (PVS2) forward waves of PVF, %FS and total amplitude of mitral annular motion in the patient group were significantly decreased compared with the normal group. However, there were no differences in these parameters between the 22 patients (DH-1 group) with a mean pulmonary capillary wedge pressure (PCWP) of less than 18 mmHg and 8 patients (DH-2 group) with a PCWP of 18 mmHg or greater. Peak velocities of the diastolic forward wave of PVF and the early diastolic wave (D) of the LV inflow velocity in the DH-1 group were significantly decreased, and the peak velocity of the atrial contraction wave (A) of the LV inflow velocity was increased compared with those of the normal group. D of the LV inflow velocity, peak velocity of the diastolic forward wave, and peak velocity of the atrial systolic backward wave of the PVF in the DH-2 group were significantly increased compared with those of the DH-1 group. Significant positive correlations were observed between peak velocity of the diastolic forward wave and D or PCWP in the patient group, but the latter relationship was not linear. The A/D ratio of the LV inflow velocity was significantly decreased, and the ratio of the amplitudes of atrial contraction wave to total vertical deflection on the apexcardiogram of the DH-2 group were significantly increased compared with those of the DH-1 group. A patient with extensive myocardial infarction associated with development of severe LV dysfunction (PCWP = 23 mmHg) and a "pseudonormalization" pattern of LV inflow velocity demonstrated markedly increased peak velocities of the diastolic and atrial systolic forward wave, and decreased PVS2. However, the peak velocities of the diastolic and atrial systolic forward wave were decreased, and that of PVS2 was increased with fair improvement of LV dysfunction (PCWP = 10 mmHg) and with compensatory augmentation of the atrial contraction wave A of LV inflow velocity.(ABSTRACT TRUNCATED AT 400 WORDS)

Cardiomyopathy, Dilated↗