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Biomedical subjects

K Kiyoshige

Publications and source records attributed to K Kiyoshige.

At least 19 recordsLinked to original sources

Changes in left ventricular inflow and pulmonary venous flow velocities during preload alteration in dilated heart.

The aim of the present study was to assess the changes of left ventricular inflow (LVIF) and pulmonary venous flow (PVF) velocities during preload alteration in 30 patients with dilated heart (LV end-diastolic dimension > or = 6.0 cm) and impaired LV systolic function (% fractional shortening of the LV < or = 25%). We performed transesophageal pulsed Doppler echocardiography during lower body negative (LBNP, -40 mmHg) and positive pressure (LBPP, +40 mmHg) in 10 patients with dilated cardiomyopathy, in 20 with old myocardial infarction, and in 22 healthy controls. Eight of the patients showed a pseudonormalization (compliance failure) pattern, and 22 showed a decreased early diastolic wave and compensatorily increased atrial systolic wave (relaxation failure) pattern of LVIF in the control state. Mean pulmonary capillary wedge pressure (PCWP) was greater in the compliance failure group than in the relaxation failure group in the control state. LVIF in 6 of the 22 patients with the relaxation failure pattern changed to the compliance failure pattern during LBPP, and that in 3 of 8 patients in the compliance failure group changed to the relaxation failure pattern during LBNP. The 6 patients with a change from the relaxation failure to the compliance failure pattern showed significantly higher peak diastolic and atrial systolic PVFs during LBPP than in the control state, and significantly higher PCWPs in the control state than the 16 patients with no change in LVIF. These findings suggest that the compliance failure and relaxation failure patterns of LVIF are readily interchangeable in various hemodynamic conditions, and that pattern analysis of LVIF and PVF during preload alteration is useful for understanding the hemodynamic severity and for evaluating preload reduction therapy in the dilated heart.

Blood Flow Velocity↗

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↗

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↗

[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↗

[One family having 5 members with hypertrophic cardiomyopathy with similar pattern of left ventricular inflow and distribution of hypertrophy].

We examined, in one family, 5 cases of hypertrophic cardiomyopathy (HCM) with a similar pattern of left ventricular inflow (LVIF) and distribution of hypertrophy. Its clinical background and significance were discussed. Because a variety of morphologic expressions of HCM may be observed in the same family, distribution of left ventricular hypertrophy (LVH) varies in even first-degree relatives of the family. In all five cases in this study, however, LVH was localized between the anterior wall and the interventricular septum. On the other hand, typical pattern of LVIF in HCM is "decreased peak velocity and prolonged deceleration time of the early diastolic wave (E), and compensatory augmentation of the atrial contraction wave (A)". All of the five cases in this study had a pattern of three characteristic peaks of LVIF, which showed the mid-diastolic wave between the E and A waves. The above findings suggested that the myocardial characteristics of the five cases in this family were very similar, and could be important clues clarifying the mode of inheritance of HCM.

Adult↗

[Characteristics of jugular venous pulse and its genesis in Ebstein's anomaly].

To clarify the characteristics of the jugular venous pulse and its genesis in Ebstein's anomaly, 6 patients with Ebstein's anomaly whose mean age was 45 +/- 9 years, and 10 normal subjects with a mean age of 27 +/- 6 years were studied by phono-mechanocardiography and echocardiography. The parameters included the relative height of the jugular "c" wave, the relative timing of the upstroke (Q-Cu interval) and the peak of the jugular "c" wave (Q-Cpeak interval), the relative timing of the upstroke of the carotid artery pulse, the relative timing of tricuspid valve closure (Q-Tc interval), the excursion of the closing motion of the anterior tricuspid leaflet (TV excursion), the distance between the anterior mitral annulus and the septal tricuspid annulus (M-T distance), the area of atrialized right ventricle (ARV area) and the maximum area of the tricuspid regurgitant signal. Among 6 patients with Ebstein's anomaly, tricuspid regurgitation was predominant in 4 and mild in the remaining 2. The results were as follows: 1. A large jugular "c" wave was observed in 4 of the 6 patients. Two patients with large ARV area had giant "c" wave. 2. The interval of the upstroke of the carotid artery pulse and that of the jugular "c" wave was about 39.2 msec. 3. The Q-Tc interval was significantly longer and the TV excursion was significantly greater in the patients than in the normal controls. 4. There was only a weak positive correlation between the Q-Cpeak interval and the Q-Tc interval. No significant correlation was observed between the relative height of the jugular "c" wave and the TV excursion. 5. There was a positive correlation between the relative height of the jugular "c" wave, the ARV area and M-T distance. 6. No obvious correlation was observed between the grade of tricuspid regurgitation and the relative height of the jugular "c" wave. These results suggest that augmentation of the "c" wave of the jugular venous pulse is characteristic of Ebstein's anomaly and that it correlates closely with the severity of displacement of the tricuspid valve and the size of the atrialized right ventricle.

Adult↗

[Clinical significance of the click intervals for the diagnosis of dysfunction of the Medtronic-Hall prosthetic valve].

To investigate the clinical significance of click interval for evaluation of prosthetic valve dysfunction, 20 patients underwent Medtronic-Hall (MH) valve replacement (14 in the mitral position and 6 in the aortic position) were studied by simultaneous high-speed recordings of phonocardiogram, echocardiogram and/or Doppler echocardiogram. Two of the 20 patients, one in the mitral and the other in the aortic position, showed MH valve dysfunction. Eleven patients with normally functioning Björk-Shiley (BS) valve in the mitral position served as controls. Results were as follows: 1. There were usually 3 opening clicks (OC1, OC2, OC3) in patients with normally functioning MH valve in the mitral position. These 3 clicks coincided in timing with the beginning of opening, maximum opening and the end of sliding motion, respectively. Both OC1 and OC2 of the MH valve occurred in similar timing with those of the BS valve (A2-OC1 interval: MH = 65.4 +/- 11.8 msec vs BS = 72.3 +/- 17.2 msec; OC1-OC2 interval: MH = 31.2 +/- 7.7 msec vs BS = 27.3 +/- 6.1 msec). However, OC3 occurred significantly later in MH valve than in the BS valve (OC2-OC3 interval: MH = 32.3 +/- 7.5 msec vs BS = 16.4 +/- 3.8 msec, p < 0.01). 2. There were 2 closing clicks (CC1, CC2) in normally functioning the MH valve in the aortic position. These 2 clicks coincided in timing with the beginning and the end of the closing motion, respectively. Mean value of CC1-CC2 interval in 5 prosthetic patients with normal function was 31.0 +/- 9.6 msec. 3. A patient with malfunctioning MH valve in the mitral position showed a markedly prolonged OC1-OC2 interval, ranging from 66 to 140 msec, and she had multiple diastolic clicks after the OC2 phase. Prolonged OC1-OC2 interval was mainly caused by the delay of appearance of OC2, and it was thought to be due to temporary limitation of opening motion of the valve by valve thrombosis. 4. A patient with malfunctioning MH valve in the aortic position showed a markedly prolonged CC1-CC2 interval (100 msec), and he had a significant severe aortic regurgitation during this phase. At operation, fibrinoid thrombus was attached to the aortic annulus at the side of minor orifice of the valve. Closing motion of the valve was disturbed by this thrombus, and the completion of valve closure was markedly delayed.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

[Mitral valve prolapse associated with partial absence of commissural chordal insertion: report of two cases].

We reported 2 cases of mitral valve prolapse (MVP) associated with partial absence of the chordae tendineae. Case 1 was a 25-year-old man who was admitted to our hospital for further examinations of an apical pansystolic murmur (Levine 4/6) and the abnormal shadow on his chest radiograph. He was diagnosed as having grade 3 + mitral regurgitation (MR) by the Sellers classification and pulmonary varix by cardiac catheterization. Transesophageal echocardiography revealed MVP of the rough zone of the anterior mitral leaflet and MR blowing into the pulmonary varix. Case 2 was a 60-year-old man who was admitted to our hospital because of congestive heart failure and apical pansystolic murmur (Levine 4/6). Parasternal echocardiography revealed prolapse of both the anterior and posterior mitral leaflets and moderate MR. In both cases, absence of insertion of anterolateral commissural chordae was confirmed after surgery, and the abnormalities of chordal arrangement and insertion were considered as causes of MVP in these cases.

Adult↗

Vector U loop in patients with idiopathic cardiomyopathy.

The U loops of vectorcardiograms were recorded in 50 normal subjects, 10 patients with dilated cardiomyopathy (DCM group), and 83 patients with hypertrophic cardiomyopathy (HCM group). The HCM group was divided into three subgroups: those with obstructive hypertrophic cardiomyopathy (HOCM), nonobstructive hypertrophic cardiomyopathy (HNCM), and apical hypertrophy (APH). The spatial characteristics of the U loop were examined qualitatively and quantitatively and were correlated with echocardiographic findings. The magnitude of the U loop was significantly larger in the HCM group, especially in the APH subgroup, than in the normal subjects, but it was not larger in the DCM group. The maximum U vector was significantly displaced anteriorly and to the right in the DCM and HCM groups, especially the APH and HNCM subgroups. In the HNCM and APH subgroups, the magnitude of the U loop correlated significantly with the thickness of the posterior wall of the left ventricle, but not with that of the interventricular septum. These findings suggest that the U loop is related to hypertrophy of the apex and the posterior wall of the left ventricle.

Adult↗

Signal-averaging electrocardiogram in patients with diabetes mellitus.

In order to detect silent impairment of the heart due to diabetes mellitus, the signal-averaging electrocardiograms (ECG) of 21 healthy subjects and 22 diabetic patients without ventricular tachycardia were compared. The QRS duration in the signal-averaging ECG was longer in diabetic patients than in the normal subjects (87.3 ms vs. 114.5 ms, p less than 0.01). Moreover, late potentials in the terminal portion of the QRS complex were observed in 7 diabetic patients (32%), but in only one normal subject (5%, p less than 0.01). These findings suggested that patients with diabetes mellitus frequently have intraventricular conduction disturbances, presumably due to diabetic microangiopathy.

Adult↗

[Magnetocardiographic localization of an accessory pathway in patients with WPW syndrome].

The usefulness of magnetocardiography (MCG) in determining the location of an accessory pathway (Kent bundle) was examined by the isomagnetic map at the time of a delta wave, and by gated magnetic resonance imaging (MRI). MCG was performed at 36 points on the anterior chest wall in eight cases with Wolff-Parkinson-White (WPW) syndrome using a SQUID (superconducting quantum interference device) system with the second derivative gradiometer. Based on these records, isomagnetic maps during the QRS and T waves were constructed, and the depth of the accessory pathway from the coil was calculated mathematically. The locations of the accessory pathways were estimated using these data and the MRI findings. The locations of the accessory pathways thus determined were compared with findings obtained by body surface maps. A dipole directed towards the left was deduced, because the maximum was located more superiorly than the minimum in an isomagnetic map 10-40 msec after onset of the delta wave in cases with WPW syndrome, indicating an accessory pathway to be located in the right ventricle. A dipole directed towards the right was deduced, because the maximum was located more superiorly than the minimum in an isomagnetic map 10-40 msec after onset of the delta wave of cases with WPW syndrome indicating an accessory pathway to be located in the left ventricle. Assuming the electric current source is a single dipole, the location of a current dipole might be determined by positions of the maximum and the minimum in the isomagnetic maps. In the present study, the locations as determined by analysis of the isomagnetic map 40 msec after onset of the delta wave and the gated MRI were concordant with the findings obtained by body surface isopotential maps. Furthermore, some cases showed two opposing dipoles on the isomagnetic map at the peak of the T wave in lead II of the standard ECG leads; one directed to the left expressing normal repolarization; the other directed to the right presumably expressing repolarization of the myocardium which was excited by an impulse via the accessory pathway. The location of the current dipole as determined by analysis of the isomagnetic map at the peak of the T wave in lead II was nearly the same as the position of the current dipole as determined by analysis of the isomagnetic map 40 msec after onset of the delta wave.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Significance of T wave abnormality in hypertension studied by spatial velocity electrocardiogram and vectorcardiogram.

The ST-T wave abnormality in hypertension has been considered to be an indicator of poor prognosis, but its precise pathophysiological significance remains unclear. The present study was aimed to correlate the electrocardiographic (ECG) change in T wave and left ventricular characteristics studied by echocardiogram. The T wave abnormality in the ECG represented hypertrophy of the left ventricle or abnormality of systolic function, but it was difficult to differentiate either of them by conventional ECG. It was shown in this study that the anterior displacement of the vectorcardiographic T loop was related to the ventricular hypertrophy and that the abnormal shape or inscription of the T loop was more closely related to the ventricular dysfunction rather than hypertrophy. These results suggested that the vectorcardiogram and spatial velocity electrocardiogram were useful for analysis of the T wave abnormality and add important information in addition to the conventional electrocardiogram.

Aged↗

Vector U loop in patients with old myocardial infarction.

The U loop of the vectorcardiogram was examined qualitatively and quantitatively in 100 normal subjects and 67 patients with old myocardial infarction, using a direct-writing vectorcardiograph with memory function. In the control group, the U loop was directed to the left, anteriorly and inferiorly, and it was inscribed counterclockwise in the horizontal plane. In patients with anterior myocardial infarction, the U loop tended to be displaced to the right, and in patients with inferior myocardial infarction to the right and superiorly. The shape of the U loop in patients was also different from that of normal subjects. The maximum U vector was significantly smaller in magnitude both in patients with anterior and inferior myocardial infarction than that of normal subjects (p less than 0.01). In patients with ventricular aneurysm, the magnitude of the maximum U vector was significantly smaller and its direction was displaced more to the right and posteriorly than those without aneurysm (p less than 0.01). In standard 12-lead electrocardiogram (ECG), observation of the U wave in patients with old myocardial infarction was difficult, especially in the limb lead, because of the small size of the U wave. Therefore, vectorcardiographic observation may be more useful than electrocardiographic observation for the analysis of the U wave in patients with old myocardial infarction.

Adult↗

Vector U loop in patients with right ventricular overloading.

The U loop of the vectorcardiogram (VCG) was examined qualitatively and quantitatively in 126 normal subjects, 15 subjects with complete right bundle branch block (CRBBB group) and 58 patients with right ventricular overloading (RVO group), using a direct-writing vectorcardiograph with memory function. In normal subjects the U loop was directed similarly to the T loop, i.e., to the left, anteriorly and inferiorly. In the CRBBB group, maximum U vector was smaller, but its direction was not significantly different from that in normal subjects. In the RVO group, the U loop tended to be displaced posteriorly and to the left and was significantly greater in magnitude than that in normal subjects in the horizontal (P less than 0.01) and frontal (P less than 0.001) planes. In the RVO group, a good correlation was found between the direction of maximum U vector and right ventricular systolic pressure. In some cases of the RVO group, the U loop was the only abnormality suggesting right ventricular overloading. These findings suggest that abnormality of the U loop is a good indicator in a diagnosis of right ventricular overloading.

Adolescent↗

Agammaglobulinemia in a pregnant woman.

A case of common variable immunodeficiency in a pregnant woman is presented. Lobar pneumonia developed in the sixth month of the pregnancy and her serum immunoglobulin levels were found to be extremely low. She was treated successfully with immune human serum globulin and antibiotics. She delivered a full-term baby without any troubles. Various immunologic studies were done in the peripheral blood of the patient and the neonate. Consequently, functional abnormalities of helper T cells were considered to be responsible for the hypogammaglobulinemia.

Adult↗