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Biomedical subjects

K Fujitani

Publications and source records attributed to K Fujitani.

At least 73 records · Page 4Linked to original sources
PubMed1989

[Factors influencing exercise tolerance in patients with myocardial infarction as elucidated by Tl-201 myocardial scintigraphy].

Measurements of O2 consumption during treadmill exercise tests and Tl-201 myocardial scintigraphy were performed in 17 cases of myocardial infarction to elucidate O2 consumption at an anaerobic threshold ATVO2 as an adequate index of exercise tolerance, and the scintigraphic indices influencing the exercise tolerance. ATVO2 was obtained using the method of Wasserman and Davisand corrected by body weight. The scintigraphic indices such as the location, extent (residual myocardium), and severity (% uptake) of myocardial infarction were obtained from SPECT and bull's eye displays on Tl-201 myocardial scintigraphy. ATVO2 was correlated with theoretical VO2max as obtained by the predicted maximal heart rate (r = 0.56, p less than 0.01) and with left ventricular ejection fraction as obtained by radionuclide left ventriculography (r = 0.59, p less than 0.01). There was no significant difference between ATVO2 in cases of anterior wall infarction and those of inferior (and/or lateral wall) infarction. There was no significant correlation between % uptake and ATVO2. However, the residual myocardium showed a significant correlation with ATVO2 (r = 0.61, p less than 0.01). In conclusion, 1) ATVO2 is an adequate index of exercise tolerance and reflects cardiac function. 2) The extent of the residual myocardium is most strongly influenced by ATVO2 among the indices of myocardial damage as obtained by Tl-201 myocardial scintigraphy.

Adaptation, Physiological↗
PubMed1988

Structure-activity relationships of 4'-O-substituted 1-benzylisoquinolines with respect to their actions on the cell membrane of blood platelets and erythrocytes.

4'-O-Substituted 1-benzyl-2-methyl-6,7-dimethoxy-1,2,3,4-tetrahydroisoquinolines inhibited the collagen-induced activation (aggregation and ATP secretion) of rabbit platelets and transformed the shape of human erythrocytes in a dose-dependent manner. Both effects increased with increasing number of carbon atoms of the 4'-substituted hydrocarbon moiety. The incorporation of these compounds into the erythrocyte membrane was also dependent on the number of carbon atoms of the 4'-substituted radical. The most potent phenoxy derivative suppressed arachidonic acid release from membrane phospholipids but had no effect on arachidonic acid metabolism in platelets. This indicated that the effects are comparable to those of a natural bisbenzylisoquinoline, cepharanthine. These effects appear to be due to a perturbing action on the membrane lipid bilayer.

Adenosine Triphosphate↗
PubMed1988

Pulsed Doppler echocardiographic assessment of transmitral flow in pacing-induced angina pectoris.

We analyzed transmitral flow using pulsed Doppler echocardiography during anginal attack provoked by atrial pacing in 11 patients with coronary artery disease (CAD). Left ventricular (LV) filling period was divided into 4 time intervals (Tr1: the time interval to peak velocity of rapid filling (peak R), Tr2: the time interval from peak R to the end of rapid filling, Ts: the time interval of slow filling, Ta: the time interval of atrial contraction). The velocity in each interval was integrated by planimeter as IR1, IR2, IS or IA which indicates relative filling volume in each interval. During angina, IR1 was unchanged due to prolongation of Tr1 (82 +/- 21 to 102 +/- 23 msec, p less than 0.02), despite a decrease in peak R (54 +/- 11 to 43 +/- 11 cm/sec, p less than 0.005), while IR2 decreased (5.8 +/- 1.9 to 4.3 +/- 1.4 cm, p less than 0.005) and IA increased (6.7 +/- 1.4 to 7.3 +/- 1.3 cm, p less than 0.005). In conclusion, these results suggested that in acute myocardial ischemia in CAD a decrease in transmitral flow from the time of peak R to the end of rapid filling (IR2) reflected the impairment of the LV rapid filling, which was incompletely compensated by an increase in atrial contraction.

Adult↗
PubMed1988

Effects of left ventricular dysfunction on left atrial performance in previous myocardial infarction and during pacing-induced myocardial ischemia in angina pectoris.

This study aimed to evaluate acute and chronic response of left atrial function to left ventricular dysfunction in patients with coronary artery disease. We studied simultaneous measurements of left atrial volume by biplane cineangiography and left ventricular pressure at rest and after pacing in 59 patients with coronary artery disease and 11 normal subjects. At rest, 35 patients with previous myocardial infarction (MI group) had low left ventricular filling rate of the first third in diastolic time, large left atrial volume before contraction (LA pre-ACV) and large left atrial ejection volume (LAEV), compared with control group. Left atrial ejection fraction (LAEF), the ratio of LAEV to LA pre-ACV, was similar between both groups. LAEF was maintained within a wide range of values in accordance with left ventricular peak A pressure, except for 3 patients who had high values of left ventricular peak A pressure and low values of LAEF. After a right atrial pacing stress test, time constant was prolonged and mean emptying rate of left atrial volume during early diastole decreased in 11 patients with angina pectoris who had an increase greater than 5 mmHg in left ventricular end-diastolic pressure after pacing. In these group, LA pre-ACV increased, LAEF decreased and LAEV was unchanged. These results suggest that left atrial performance responds differently to acute and chronic left ventricular dysfunction in patients with coronary artery disease.

Angina Pectoris↗
PubMed1988

[Clinical significance of precordial ST segment depression during acute inferior myocardial infarction].

To investigate the mechanisms and clinical significance of precordial (V1-V4) ST segment depression during acute inferior myocardial infarction, stress thallium-201 scintigrams and coronary angiograms were obtained within four to eight weeks after the onset of myocardial infarction in 37 patients experiencing their first acute inferior myocardial infarction. Among 18 patients with precordial ST depression (group 1), 11 with concomitant disease of the left anterior descending artery (LAD) had positive results on exercise test, whereas in seven patients without LAD lesion, only two had positive exercise test (p less than 0.01). In 19 patients without precordial ST depression (group 2), 11 had severe stenosis in the LAD. However, among these 11 patients, only two had positive exercise tests. Patients with precordial ST depression demonstrated a higher frequency of positive exercise tests than those without it (p less than 0.01). On stress thallium-201 scintigraphy, a perfusion defect involving the inferior wall was present in all patients, but additional anterior wall ischemia was present in only five of the 18 patients in group 1. These five patients had chest pain on exercise tests and a severe stenosis greater than 90% in the LAD. There was no significant difference in the frequency of additional posterolateral wall infarction between groups 1 and 2. In 18 patients in group 1, sigma ST (total degrees of ST segment depression in leads V1, V2, V3, and V4 in the acute stage) was significantly greater in 11 patients with LAD lesion than in seven without (p less than 0.05), and sigma ST greater than five mm was observed in 12 of 13 patients who had additional anterior wall ischemia and posterolateral wall infarction on stress thallium-201 scintigraphy (p less than 0.05). Myocardial revascularization, such as aortocoronary bypass surgery or percutaneous transluminal coronary angioplasty (PTCA), was performed in six of the 18 patients in group 1 in the chronic stage, but in only one of the 19 patients in group 2. Thus, in patients with initial acute inferior myocardial infarction, those with precordial ST depression seemed to be a high-risk group. It was suggested that, during the early stage of myocardial infarction, this abnormality on electrocardiograms is related to the summation of effects of anterior wall ischemia and posterolateral wall infarction. Furthermore, the sigma ST evaluation is useful in differentiating a mirror image of inferior wall infarction from anterior wall ischemia and posterolateral wall infarction as the mechanism of precordial ST depression.

Angiography↗
PubMed1987

Noninvasive demonstration of underlying severe coronary disease in patients with vasospastic angina.

Dipyridamole test, isoproterenol test, and treadmill exercise test were performed in two groups of patients with vasospastic angina (Group 1: 10 patients with 70% or greater coronary narrowings, Group 2: 8 patients with narrowings less than 70%. The results were correlated with coronary anatomy. In Group 1, vasodilation of resistance vessels by dipyridamole elicited ischemic episodes in 9 patients and an increase in myocardial oxygen consumption by isoproterenol caused anginal attacks in 7 patients. None of patients of Group 2 showed positive responses to either drug. All patients of Group 1, and 3 patients of Group 2 gave positive responses to treadmill test. These observations show that several different mechanisms are involved in the pathogenesis of myocardial ischemia in patients with vasospastic angina. Pharmacological interventions have higher specificity than exercise tests in predicting coronary anatomy and are useful for the choice of therapy in the patients.

Adult↗
PubMed1987

Impaired right ventricular filling in old myocardial infarction.

To evaluate ventricular filling and interactions between right and left ventricles in patients with old myocardial infarction, right and left ventricular time-volume curves were analyzed from a cineangiographic study of 10 normal subjects (Group 1), 10 patients with old anterior myocardial infarction (Group 2) and 10 patients with old inferior myocardial infarction (Group 3). Volumes of both ventricles were calculated from each frame over an entire cardiac cycle using Simpson's method. From time-volume curves, peak ejection rates, peak filling rates and atrial kick rates were obtained for both ventricles and these parameters were normalized by end-diastolic volume. All patients were in sinus rhythm with heart rates less than 80 beats/min. There were no significant differences among the 3 groups in end-diastolic pressure of both ventricles and mean pulmonary artery pressure. Left ventricular ejection fractions were significantly lower in Groups 2 and 3 than in Group 1 (p less than 0.001, p less than 0.005, respectively), although there were no significant differences in end-diastolic volume indexes of either ventricle among the 3 groups. Peak left ventricular ejection rate and peak filling rates of the left and right ventricles were lower in Group 2 than in Group 1 (p less than 0.01, p less than 0.05, p less than 0.01, respectively) and peak filling rate of the right ventricle in Group 2 correlated with the peak filling rate of the left ventricle and left ventricular ejection fraction (r = 0.64, r = 0.64, respectively). Peak filling rate of the right ventricle in Group 2 correlated inversely with left ventricular peak negative dp/dt (r = -0.72), but no correlation was found between peak filling rate of the right ventricle and left ventricular end-diastolic volume index or mean pulmonary artery pressure. Peak ejection rate of the left ventricle and peak filling rates of both ventricles in Group 3 were lower than in Group 1 (p less than 0.02, p less than 0.02, p less than 0.01, respectively) and no correlation was found between peak filling rates of both ventricles. Wall motion of the right ventricular septal portion was slightly reduced in 5 patients in Group 2. In all patients in Group 3, right ventricular wall motion centering around the right ventricular diaphragmatic portion was reduced. These results suggest that in old inferior myocardial infarction, right ventricular wall motion abnormality results in impaired right ventricular filling, whereas in old anterior myocardial infarction, right ventricular filling is reduced indirectly due to impaired left ventricular filling.

Cardiac Volume↗
PubMed1987

[Hypertrophic non-obstructive cardiomyopathy assessed by dipyridamole thallium single photon emission computed tomography: comparisons with hypertrophic cardiomyopathy with a dilated heart].

Thallium-201 (Tl) single photon emission computed tomography (SPECT) after dipyridamole infusion (0.56 mg/kg) was performed in 23 patients with hypertrophic non-obstructive cardiomyopathy (HNCM) and in seven patients with HCM simulating dilated cardiomyopathy (HCM-DCM) to clarify the mechanism and clinical significance of decreased coronary vasodilatory reserve. The coronary vasodilatory reserve in the hypertrophied area assessed by SPECT was compared with the findings of echocardiography, left ventriculography and endomyocardial biopsy. 1. Eleven patients with HNCM had no perfusion defects in the hypertrophied area (group I), but the other 12 patients (52.2%) had such defects (group II). All seven patients with HCM-DCM had perfusion defects in the anterior or septal walls (group III). Redistribution was observed in 11 of the 12 patients in group II and in three of the seven patients in group III. 2. The regional washout rate was relatively low in the upper septum in group II and in the anterior wall and upper septum in group III. Thus, coronary vasodilatory reserve in the hypertrophied area was decreased in groups II and III. 3. Echocardiographically, the degree of hypertrophy did not differ between groups I and II, but the latter had significantly greater left ventricular diastolic dimension (42.3 mm vs 49.5 mm: p less than 0.05) and lower percent fractional shortening (%FS) (43.7% vs 35.6%: p less than 0.05). However, group III showed thinner left ventricular wall, much greater diastolic dimension (60.9 mm vs 49.5 mm: p less than 0.05), and lower %FS (24.0% vs 35.6%: p less than 0.05) than did those of group II. 4. On left ventriculography, those in group II showed larger left ventricular end-diastolic volume index (93.9 ml/m2 vs 79.7 ml/m2: p less than 0.05) than that of group I. Left ventricular ejection fraction showed the same tendency, but this was not statistically significant. 5. On endomyocardial biopsy, the specimens of the patients in group II had significantly higher percent fibrosis than did those of group I (11.4% vs 6.8%: p less than 0.05). These findings suggest that the mechanism of decreased coronary vasodilatory reserve in the hypertrophied area may be related to myocardial fibrosis, and this decrease may induce left ventricular dysfunction and compensatory dilatation.

Adult↗
PubMed1986

Hemodynamic effects of digoxin on congestive heart failure.

To assess the hemodynamic effects of digoxin (0.01 mg/kg) on congestive heart failure, we evaluated 19 patients with decreased contraction force of left ventricle (old myocardial infarction n = 9, and dilated cardiomyopathy n = 10, group 1) and 8 patients with mechanical impaired left ventricular filing (mitral stenosis n = 8, group 2). In groups 1 and 2, heart rate and pulmonary capillary pressure significantly decreased (p less than 0.05). In group 1, stroke volume increased, but not significantly. In group 2, stroke volume increased significantly (p less than 0.05). There were no significant changes in blood pressure and systemic vascular resistance in either group. We divided group 1 into two groups (group 1A: cardiac index increased more than 15%, group 1B: cardiac index increased less than 15%). In group 1A, cardiac index and % fractional shortening before digoxin administration were lower than in group 1B (1.97 + 0.27 vs 2.80 + 0.481/min/m2, p less than 0.001, and 10.9 + 8.0 vs. 19.5 +11.9%, p less than 0.05, respectively). These data suggested that digoxin exerted a positive inotropic effect with decreased pulmonary capillary pressure but cardiac index did not always increase in congestive heart failure.

Digoxin↗
PubMed1986

[Infantile optic glioma involving the whole optic pathway--a case report].

A case of infantile optic glioma involving the whole optic pathway is reported. The patient was a 4-month-old female. The mother noticed that the baby could not follow the object, although her physical development had been apparently normal only until three months after birth. On admission, she was lethargic, although no definite motor weakness was identified. The ophthalmological check revealed delayed bilateral pupillary light reaction and choked disks. Skull X-ray film showed the J-shaped sella and the enlarged bilateral optic canals. CT scan also revealed an isodensity mass in the suprasellar cistern and enlarged bilateral optic nerves. The lesions were enhanced homogeneously with contrast medium and extended toward both optic radiations. Lateral ventricles were mildly dilated. Cerebral angiography showed the upward shift of A1-portion of the bilateral anterior cerebral arteries and the backward shift of the basilar artery. No abnormal vessels were visible. A bifrontal craniotomy was performed to partially remove the suprasellar tumor. The histological diagnosis was optic glioma. The postoperative course was uneventful. The patient was discharged without any neurological deficits except poor visual acuity. Four months later, she suddenly fell into generalized convulsion. CT scan revealed the significant enlargement of residual tumor and ventricular dilatation. Surgical treatment of VP shunt was immediately performed on, and then irradiation of 4,000 rad of total dose to the tumor followed. The tumor size became definitively small. On a follow-up term of 15 months, the patient has been doing well.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral Angiography↗
PubMed1986

[Malignant familial cardiomyopathy with sudden death, typical asymmetric septal hypertrophy and dilated cardiomyopathy-like features].

Twenty-one members of a family were traced for three generations including the propositus, who had typical dilated cardiomyopathy (DCM)-like features. Clinical, radiological, electrocardiographic and echocardiographic examinations were performed for 13 of 16 still living. Five of 21 members died including three of sudden death. Among living 16 members, five had congestive heart failure, greater than grade III of the NYHA, and cardiomegaly on chest radiography in five. Left ventricular hypertrophy, abnormal Q waves, and ST-T changes were observed on electrocardiography in two, five and eight members, respectively. Echocardiography revealed asymmetric septal hypertrophy (ASH) in four, two of whom had systolic anterior motion (SAM) of the mitral valve. Two had features simulating DCM, and five had mitral valve prolapse. Among six patients with ASH or features simulating DCM, four had cardiac catheterization, coronary angiography and endomyocardial biopsy. None had significant coronary stenosis, but all had high left ventricular end-diastolic pressure (LVEDP) (23 +/- 7 mmHg). Endomyocardial biopsy showed moderate myocardial cellular hypertrophy, interstitial myocardial fibrosis, nuclear changes and myocardial disarrangement, with features characteristic of HCM. In this family with malignant HCM, patients had various clinical features including typical HCM, simulated DCM, DCM coexisted with mitral valve prolapse, and sudden death occurred frequently.

Adolescent↗
PubMed1985

The relation between left ventricular asynchrony, relaxation, outward wall motion and filling characteristics during control period and pacing-induced myocardial ischaemia in coronary artery disease.

To assess the relation between left ventricular asynchrony, relaxation, outward wall motion and filling in patients with coronary artery disease and normal systolic function, pressure measurements and left ventricular angiography were performed at rest and after pacing. Asynchrony and outward wall motion were quantified by segmental area-time curves. At rest, there were no differences in asynchrony and time constant between 10 patients with coronary artery disease and 10 normal subjects, while the early-filling rate was less in patients with coronary artery disease than in normal subjects. Six coronary artery disease patients with isolated left anterior descending disease displayed anterior outward wall motion which was less than that of normal subjects. In 10 coronary artery disease patients with pacing-induced angina, asynchrony increased, time constant prolonged and the early-filling rate decreased. In 6 coronary artery disease patients with isolated left anterior descending disease, anterior outward wall motion decreased after pacing. Thus, impaired early diastolic filling at rest in patients with coronary artery disease and normal systolic function may result not from asynchrony nor impaired relaxation, but from reduced regional outward wall motion of the affected area supplied by diseased coronary artery during early diastole. However, during ischaemia temporal asynchrony and impaired relaxation possibly add to left ventricular filling impairment in patients with coronary artery disease.

Adult↗
PubMed1985

Effects of left ventricular asynchrony on time constant and extrapolated pressure of left ventricular pressure decay in coronary artery disease.

To elucidate the effects of ventricular asynchrony with or without myocardial ischemia on the time constant of left ventricular pressure decay and asymptote, that is, the level to which pressure would decrease if isovolumic pressure decrease continued infinitely, left ventriculography and pressure measurements were investigated in 14 normal subjects and 25 patients with coronary artery disease. Ventricular asynchrony was quantitated by the segmental area-time curve. This study consisted of two parts. 1) After a right atrial pacing stress test, the time constant and asymptote remained unchanged in eight normal subjects. In 18 patients with coronary artery disease and pacing-induced angina, asynchrony increased, the time constant was prolonged (64 +/- 13 to 94 +/- 17 ms, p less than 0.01) and the asymptote decreased (-22 +/- 10 to -46 +/- 20 mm Hg, p less than 0.01) after the pacing. 2) During right ventricular pacing at 80, 100 and 120 beats/min in the patients, asynchrony increased and the time constant was prolonged (55 +/- 7 versus 70 +/- 10, 47 +/- 11 versus 66 +/- 19, 36 +/- 7 versus 53 +/- 13 ms, respectively, p less than 0.01 versus right atrial pacing), whereas the asymptote was unchanged in six normal subjects compared with the value during right atrial pacing at each pacing rate. In seven patients with coronary artery disease, right ventricular pacing at 80, 100 and 120 beats/min also produced an increase in the time constant, while the asymptote was unchanged. Thus, prolongation of the time constant of left ventricular pressure decay may result from ventricular asynchrony even in the absence of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗
PubMed1985

A comparison of two exponential models of the time constant during left ventricular isovolumic pressure decay in coronary artery disease.

To make a comparison of two exponential models of the time constant (Tw: Weiss's method, Tc: exponential analysis with a variable asymptote) during left ventricular (LV) isovolumic relaxation, we assessed LV pressure decay in 104 patients with coronary artery disease (CADpts) and 21 normal subjects at rest and after pacing, and investigated the hemodynamic determinants of these two models using forward-backward stepwise multiple regression analysis. At rest, Tw was prolonged as the left ventricular minimal pressure (LVPmin), the left ventricular end-diastolic pressure (LVEDP) and the end-systolic volume (ESV) increased (multiple regression coefficient: R = 0.87), whereas Tc was prolonged as ESV and regional wall motion abnormality (RWMA) increased (R = 0.72). Pacing-induced changes in Tw were augmented as LVPmin and RWMA increased (R = 0.75), whereas changes in Tc were augmented as RWMA increased (R = 0.63). Thus, the changes in Tw may be due to an increase in LVPmin rather than to any direct effect of ischemia on the relaxation rate. The relaxation rate can be evaluated more reliably by Tc than by Tw, irrespective of associated pressure changes during ischemia in CADpts.

Adult↗
PubMed1985

Exercise capacity correlating to exercise hemodynamics in coronary artery disease.

Forty-seven patients with coronary artery disease characterized by angina pectoris and/or old myocardial infarction underwent two maximal exercise tests, the supine ergometer test and the upright treadmill test, to study the relationship between exercise capacity and exercise hemodynamics. Subjects were divided into 3 groups: Group I (n = 19) achieved 25 or 50 watts, Group II (n = 15) achieved 75 watts and Group III (n = 13) achieved 100 or 125 watts. During ergometer exercise, the mean pulmonary capillary pressure elevated by 25.3 +/- 8.3 mmHg in Group I, 20.8 +/- 8.8 mmHg in Group II and 12.0 +/- 8.4 mmHg in Group III; the Group III value was significantly smaller than the other groups. The stroke volume index decreased by 3.6 +/- 8.8 ml/m2 in Group I, and increased by 10.9 +/- 8.7 ml/m2 in Group II and 10.7 +/- 14.7 ml/m2 in Group III. Thus, the impaired exercise capacity correlated with the abnormal exercise hemodynamics and its severity. In addition, the exercise capacity in the treadmill test was comparable to that in the ergometer test. It was concluded that the impaired exercise capacity in the both supine and upright exercise tests was well related to the development of abnormal exercise hemodynamics in patients with coronary artery disease.

Adult↗
PubMed1985

Hemodynamic effects of digoxin on congestive heart failure in old myocardial infarction, dilated cardiomyopathy, acute myocardial infarction and mitral stenosis.

The hemodynamic effects of digoxin (0.01 mg/Kg) on congestive heart failure were compared in 32 patients with old myocardial infarction (OMI) (n = 9), dilated cardiomyopathy (DCM) (n = 10), acute myocardial infarction (AMI) (n = 5) and mitral stenosis (MS) (n = 8). The responses of heart rate (HR) and pulmonary capillary pressure (PCP) to digoxin in OMI, DCM and MS were marked but different in each of these groups and no significant changes were found in patients with AMI. The responses of cardiac index (CI) to digoxin in patients with OMI and DCM in whom left ventricular myocardial contractile force was impaired were divided into 2 groups (Group 1: CI increased more than 15% and Group 2: less than 15%). In Group 1, both CI and percent fractional shortening (%FS) before digoxin administration were lower than in Group 2, i.e., 1.97 +/- 0.27 vs 2.80 +/- 0.48 L/min/m2 (p less than 0.001) and 10.9 +/- 8.0 vs 19.5 +/- 11.9% (p less than 0.05), respectively. In MS, CI increased after digoxin administration only in the 2 patients with low CI and rapid HR in the control state. These results indicate that the mode of hemodynamic response to digoxin is considerably different in various diseases. They further suggest that digoxin should not be used in the early phase of AMI, although digoxin was of great clinical benefit in patients with OMI and DCM through such mechanisms as its positive inotropic and negative chronotropic effects and lowering of PCP.

Adult↗