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International audience; We describe the first ever implementation of a clock-based, multi-stage emulsion shifter in an accelerator neutrino experiment. The system was installed in the neutrino monitoring building at the Japan Proton Accelerator Research Complex as part of a test experiment, T60, and stable operation was maintained for a total of 126.6 days. By applying time information to emulsion films, various results were obtained. Time resolutions of 5.3–14.7 s were evaluated in an operation spanning 46.9 days (yielding division numbers of 1.4–3.8$\times10^{5}$). By using timing and spatial information, reconstruction of coincident events consisting of high-multiplicity and vertex-contained events, including neutrino events, was performed. Emulsion events were matched to events observed by INGRID, one of the on-axis near detectors of the T2K experiment, with high reliability (98.5%), and hybrid analysis of the emulsion and INGRID events was established by means of the multi-stage shifter. The results demonstrate that the multi-stage shifter can feasibly be used in neutrino experiments.

Precise neutrino--nucleus interaction measurements in the sub-multi GeV region are important to reduce the systematic uncertainty in future neutrino oscillation experiments. Furthermore, the excess of ${\nu_e}$ interactions, as a possible interpretation of the existence of a sterile neutrino has been observed in such an energy region. The nuclear emulsion technique can measure all the final state particles with low energy threshold for a variety of targets (Fe, C, H${_2}$O, and so on). Its sub-$\mu$m position resolution allows measurements of the ${\nu_e}$ cross-section with good electron/gamma separation capability. We started a new experiment at J-PARC to study sub-multi GeV neutrino interactions by introducing the nuclear emulsion technique. The J-PARC T60 experiment has been implemented as a first step of such a project. Systematic neutrino event analysis with full scanning data in the nuclear emulsion detector was performed for the first time. The first neutrino event detection and its analysis is described in this paper., Comment: 26 pages, 29 figures, 4 table, prepared for submission to PTEP

A 79-year-old man with primary chylopericardium associated with large granular lymphocytosis was followed for more than 26 years. Except for development of dyspnea on exertion during the past four years and more recently cough with sputum production, he has remained largely asymptomatic over this interval. Based on detailed examinations of cellular and humoral immunity, we speculate that increased natural killer cell activity and an increased number of large granular lymphocytes circulating in his peripheral blood represent a reactive response to production of various cytokines secondary to persistent loss (? chyloptysis) and sequestration of central lymph.

A case of early gastric plasmacytoma in a 66-yr-old woman is reported. The demonstration of monotypic IgM lambda immunoglobulin in plasma cells infiltrating the gastric antrum contributed the histological diagnosis. Genetic analysis of the tumor cells confirmed the presence of a monoclonal neoplastic population of plasma cells in the tumor. Monoclonal immunoglobulin (IgM lambda) was demonstrated in serum, not by conventional immunoelectrophoresis, but by a highly sensitive immunofixation electrophoresis technique. Serum monoclonal immunoglobulin disappeared after subtotal gastrectomy. The value of immunofixation electrophoresis of serum protein and DNA analysis of tumor cells was emphasized for the diagnosis of gastric plasmacytoma.

This is a report of a case of coronary and cerebral embolism occurred in a patient with mitral steno-insufficiency. Clinical diagnosis of coronary and cerebral embolism was made by evidences of left hemiplegia and myocardial infarction shown by electrocardiogram. Clinical diagnosis was confirmed at autopsy and postmortem coronary angiography disclosed the location of the coronary embolus.

Ferromagnetic oxide glass were obtained by rapid-quenching in the ternary system of (Fe 2 O 3 ) x -(CaO) y - (B 2 O 3 ) z . Specimens with x more than 0.65 were not glassy but crystalline. The maximum value of magnetization at room temperature, 19.5 eμ/g, was observed for x:y:z=0.55:0.15:0.3. The specimen heated once above the crystallization temperature lost its magnetization. The measurement of magnetic properties, Mossbauer spectra and DTA suggested this glass would be a new type amorphous magnetic material.

To evaluate the significance of left ventricular (LV) hypertrophy in patients with dilated cardiomyopathy (DCM), 50 patients seen between 1976 and 1983 were studied echocardiographically. We categorized the patients as four groups according to the degree of LV dilatation or hypertrophy. Group consisted of 17 patients with mild to moderate LV dilatation without hypertrophy (LV end-systolic I dimension: Ds less than 60 mm, LV wall thickness at end-systole: WTs less than 15 mm). Group II, 12 with mild to moderate LV dilatation and hypertrophy (Ds less than 60 mm, WTs greater than or equal to 15 mm). Group III, eight with marked LV dilatation and hypertrophy (Ds greater than or equal to 60 mm, WTs greater than or equal to 15 mm), and Group IV, 13 with marked LV dilatation without hypertrophy (Ds greater than or equal to 60 mm, WTs less than 15 mm). Twenty patients had LV hypertrophy and 30 patients were without LV hypertrophy at the start of this study. New York Heart Association functional classes, cardiothoracic ratio and ECG findings at the first study did not show any statistically significant differences among the four groups. During the prospective follow-up of 2.7 years in average, eight patients died of congestive heart failure including five of Group IV, and three of Group I who had progressive LV dilatation. Three patients of Group I, II and III died suddenly. Ambulatory ECGs showed life-threatening ventricular arrhythmias in all 32 patients studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular (LV) flow dynamics were analyzed by pulsed Doppler echocardiography in patients (pts) with dilated cardiomyopathy (DCM). Subjects consisted of five normal controls, 27 pts with DCM, five with myocardial infarction and five with valvular heart disease. The equipment used was a two-dimensional echocardiograph ( Toshiba SSH- 11A ) coupled with a pulsed Doppler flowmeter ( Toshiba SDS-10A). The long-axis plane through the left ventricle was obtained from an apical transducer position and Doppler flow signals were recorded at the apex (point A), the middle portion (point B), the inflow portion (point C), the portion near the mid-IVS (point D) and the outflow portion (point E) of the left ventricle, respectively. Left ventriculography was performed in all subjects, and ejection fraction (EF), the ratio of the short-axis to long-axis distance in end-diastole, percent shortening of the long axis and percent shortening of the short axis of the left ventricle were measured. Doppler signals of an ejection flow were recorded at points A, B, D and E in the normal controls, while in 27 pts with DCM Doppler signals of an ejection flow were detected only in two pts (7%) at the point A, in three pts (11%) at the point B, 16 pts (59%) at the point D and 27 pts (100%) at the point E. Twelve pts (44%) had abnormal Doppler signals with wide-band spectral pattern at the point C in systole. Toward flow signals in early diastole were recorded at the points A, B, C and D in the normal controls, while in pts with DCM the signals were visualized in only three pts (11%) at the point A, in 27 pts (100%) at the points B and C, and 10 pts (37%) at the point D. EF in pts with DCM was lower than that of the normal controls (36 +/- 11 vs 65 +/- 5%, p less than 0.005). The ratio of the short-axis to long-axis distance of the left ventricle was higher in pts with DCM compared with that of the normal controls (0.82 +/- 0.09 vs 0.60 +/- 0.02, p less than 0.005). Percent shortening of the long axis and the short axis was depressed in pts with DCM compared with the normal controls (11 +/- 5 vs 21 +/- 4%, p less than 0.02 and 15 +/- 6 vs 34 +/- 3%, p less than 0.001, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)

In order to evaluate left ventricular function of dilated cardiomyopathy, 24 patients and ten healthy subjects were studied by exercise echocardiography. The patients with dilated cardiomyopathy were classified into 3 groups according to the presence or absence of mitral regurgitation and the severity of left ventricular dilatation: Group I was consisted of five cases with mitral regurgitation. Group II was consisted of seven cases without mitral regurgitation who had marked left ventricular dilatation, where the left ventricular end-diastolic dimension index (DdI) was greater than 46 mm/m2 and left ventricular end-systolic dimension index (DsI) was greater than 40 mm/m2. Group III was consisted of 12 cases without mitral regurgitation who had moderate left ventricular dilatation, where the DdI was less than 46 mm/m2 or DsI was less than 40 mm/m2. The ergometer exercise tests were performed for 3 min at 25 watts in a supine position. There was no significant differences of exercise-induced increases in heart rate, elevations of systolic blood pressure and increases of rate pressure product, respectively, between healthy subjects and each group of dilated cardiomyopathy. In healthy subjects, both DdI and DsI were unchanged on exercise. In Group I, DdI was unchanged but DsI decreased (p less than 0.02), thus percent fractional shortening of the left ventricle (delta D) was increased (p less than 0.05). In Group II, both DdI and DsI were unchanged. In Group III, DdI was increased (p less than 0.05) while DsI was unchanged, thus delta D was increased (p less than 0.02). These results suggested that the left ventricle is able to respond to exercise by its further dilatation (increase of preload) in mild to moderate dilated cardiomyopathy (Group III). On the other hand, in cases with marked left ventricular dilatation (Group II), the further dilatation is not induced. The same was true in dilated cardiomyopathy with mitral regurgitation (Group I), where the left ventricle had almost the same size as in Group II, although changes in DsI and delta D were not evaluated precisely because of the associated regurgitation.

Two-dimensional echocardiographic examination was performed to investigate pathophysiological mechanism of mitral regurgitation due to papillary muscle dysfunction in 6 patients with myocardial infarction (anterior : 3, inferior: 2 and subendocardial: 1) and 13 patients with dilated cardiomyopathy. The patients were divided into 2 groups; Group I was 9 with mitral valve prolapse and Group II was 10 without mitral valve prolapse (MVP). In Group I MVP was observed in the posterior leaflet in 6 and in both leaflets in the remainder. The apical four-chamber view of all patients in Group II showed that the point of mitral valve coaptation displaced toward the apex of the left ventricle during systole and the both mitral leaflets were convexed toward the left ventricle. Follow-up observation in a patient with dilated cardiomyopathy revealed that the heart was not enlarged (CTR 50%), no murmur was heard and mild anterior mitral leaflet prolapse was observed in 1979, but, in 1981, CTR became 63%, and a grade IV systolic murmur suggesting mitral regurgitation was noted. Two-dimensional echocardiography revealed that mitral leaflets became convex toward the left ventricle and coaptation point of the mitral closure shifted to the apex of the left ventricle below the level of mitral annulus. Thus, the transition to Group II from Group I was suggested. Echocardiographic measurements revealed that left ventricular end-diastolic dimension was 71 +/- 11 mm in Group I and 74 +/- 10 mm in Group II, left ventricular end-systolic dimension was 61 +/- 11 mm in Group I and 62 +/- 11 mm in Group II, and anterio-posterior mitral ring dimension was 31 +/- 3 mm in Group I and 35 +/- 3 mm in Group II (p less than 0.05). In conclusion, it was suggested that two mechanisms of mitral regurgitation are present in papillary muscle dysfunction; 1) mitral valve prolapse and 2) shift of mitral coaptation point toward the apex of the left ventricle associated with marked dilatation of the mitral annulus.

Clinical examinations including echocardiography were performed for 14 acromegalic patients (five men and nine women, whose mean age was 48.6 years). Three of these had hypertension (HT) above 160/95 mmHg, three had diabetes mellitus (DM). Their cardiac sizes and functions were correlated with the durations of disease and plasma growth hormone (GH) levels. The incidences of HT and DM were also evaluated. Three of 14 patients (22%) had increased cardiothoracic ratios (greater than 55%). Electrocardiographic abnormalities were noted in three patients including two with left ventricular hypertrophy (LVH) and one with interventricular conduction defects with abnormal Q waves. By echocardiography (Table 2), nine patients (64%) were judged to be normal. The remaining five patients (36%) had abnormal echocardiograms. These included LVH (sums of the interventricular and posterior wall thicknesses greater than or equal to 25 mm) in two (25 mm in Case 10, 30 mm in Case 11), increased left ventricular end-diastolic dimension (EDD greater than or equal to 55 mm) in one (72 mm in Case 14) and both abnormalities in two patients (Cases 12 and 13). Two patients (Case 13 and 14), whose %FS were 17% and 22%, respectively, had definite evidence of congestive heart failure. Two patients (Case 11 and 13) met the diagnostic criteria for asymmetric septal hypertrophy. One patient with echocardiographic LVH and another who had increased EDD with LVH had histories of HT (Case 11 and 12). Plasma GH levels in patients with LVH were greater than 100 ng/ml (Cases 10 and 11). The left ventricular hypertrophy and/or increased EDD observed in these patients seemed related to the duration of acromegaly but not to the presence of DM. Myocardial biopsy of the right ventricle in two patients with congestive heart failure disclosed myocardial hypertrophy, myocardial fiber disarray, interstitial fibrosis and large nuclei.

Pulsed doppler echocardiography (PDE) was used to evaluate mitral regurgitation (MR) non-invasively and quantitatively in 156 patients including 51 of rheumatic valvular disease, 57 of mitral valve prolapse (MVP) or chordal rupture of the mitral valve (RCT), and 48 of ischemic heart disease (IHD) or dilated cardiomyopathy (DCM). The severity of MR was estimated three-dimensionally by a MR scoring system as follows: As an index of direction and extent of regurgitation, nine sampling sites were selected in the left atrium at the level of the mitral annulus. These include the anterior, mid, and posterior parts of each portion of the postero-medial, middle, and antero-lateral sides. The depth of regurgitation was graded by three degrees in the long-axis projection of the left ventricle; grade 1; MR signals localized within the level of the mitral annulus, grade 2; MR detected beyond the mitral annulus but not reaching the aortic valve level; and grade 3; MR detected beyond the aortic valve level in the left atrium. The MR score was comprised of the products of numbers of points at which MR signals were detected and the grades of the maximum depth. The MR scores correlated well with the severity of MR as determined by the left ventriculogram (LVG); the MR score was 4.0 +/- 1.6 (mean +/- S.D.) points in grade 1; 9.6 +/- 2.6 points in grade 2; 18.0 +/- 3.2 points in grade 3; and 23.0 +/- 1.7 points in grade 4 by LVG. Doppler mapping of the left atrium at the level of the mitral annulus suggested that the directions of MR varied with each disease and valvular lesion. Thus, these observations were helpful in the investigation of MR by PDE. We concluded that the above-mentioned MR scoring system proves a very useful method for quantitatively evaluating MR non-invasively.

We report a 26-year-old woman who survived fulminant hepatic failure but later developed permanent brain atrophy. After her recovery from fulminant hepatitis, her personality changed and mental abnormalities became obvious. Four years after the onset of fulminant hepatitis an epileptic attack occurred. At that time CT-scanning revealed generalized brain atrophy.

The purpose of this study was to investigate the relationship between exercise capacity and resting left ventricular function assessed by several non-invasive methods in patients with old myocardial infarction. Subjects were 25 male patients whose endpoint was either dyspnea or general fatigue at the symptom-limited maximal graded treadmill exercise test according to Bruce protocol. The indices obtained by non-invasive cardiac examinations included left ventricular fractional shortening (% FS), scintigraphic infarct size (% SIS) by 201Tl myocardial scintigraphy and PEP/ET (so-called Weissler's index). A significant correlation of exercise duration with % FS (r = 0.67, p less than 0.001) or with % SIS (r = -0.55, p less than 0.02) indicated that the more was impaired resting left ventricular function, the more was decreased exercise capacity. Also, a significant correlation of systolic blood pressure at the end-point in exercise test with % FS (r = 0.58, p less than 0.005) or with % SIS (r = 0.69, p less than 0.001) indicated that inadequate blood pressure response might be partially attributed to impaired left ventricular function during exercise. The response of heart rate at the Bruce protocol stage I correlated with % FS (r = -0.67, p less than 0.001) and with % SIS (r = 0.53, p less than 0.02), respectively. These findings may be interpreted as chronotropic compensatory mechanism for limited stroke volume during exercise in patients with imparied left ventricular function. Thus, it was concluded that resting left ventricular function assessed by non-invasive cardiac examinations may predict exercise capacity prior to the test to some extent. These informations can be utilized for the decision of the planning at cardiac rehabilitation and also for the guidance in daily activities. Additionally, low level exercise test with treadmill is considered to be valuable for screening cases with impaired left ventricular function in old myocardial infarction.

To evaluate the evolution of mitral valve prolapse (MVP) with increasing age, 158 patients were studied by two-dimensional echocardiography and 24-hour ambulatory electrocardiography (Holter monitoring). The patients were divided into seven age groups (25 patients ranging in age from 12 to 14 years, 21 from 15 to 17, 24 from 18 to 20, 24 from 21 to 30, 37 from 31 to 50, 8 from 51 to 60 and 19 older than 61). Each patient was echocardiographically graded as mild, moderate and severe MVP. Ventricular arrhythmia by Holter monitoring was graded as I, II, III and IV according to Lown et al. The following results were obtained. 1. Incidence of moderate and severe MVP was less than 10% in patients younger than 20 years, but increased with age. Incidence of left ventricular dilatation (left ventricular end-diastolic dimension less than or equal to 55 mm) and left atrial dilatation (left atrial dimension greater than or equal to 40 mm) were minimal in patients younger than 20 years, but increased with age, especially in patients older than 51 years. 2. Ventricular couplets or triplets (Lown grade IV) were found in less than 10% in patients in age from 15 to 17 years, 33% in patients from 18 to 20 years and showed no increase with age. The rate of ventricular tachycardia was over 150 beat per min (bpm) in five of nine patients (56%), and the sinus rate preceding ventricular tachycardia was from 65 to 140 bpm.

One hundred and five cases with idiopathic mitral valve prolapse (MVP) diagnosed by two-dimensional (2-D) echocardiography were classified into 5 groups according to the grade of prolapse (Fig. 1), 47 cases of which were followed prospectively for average 2.9 years. 1) Most of the cases with MVP of grade 3 or less showed normal left ventricular diastolic dimension (LVDd) and left atrial dimension (LAD) throughout the follow-up period, while the majority of the cases with MVP of grade 4 revealed increased LVDd and LAD. Thus the mitral regurgitation due to MVP seemed to be insignificant in cases of grade 3 or less, while it is significant in cases of grade 4. 2) During the follow-up period cases of grade 1, 2 and 3 showed the transition of the grade of prolapse each other. On the other hand, most of the cases of grade 4 at the initial examination did not show the change in its grade of prolapse. 3) Fifty-eight cases (55.2%) had symptoms such as chest pain, palpitation and dizziness, and various electrocardiographic abnormalities such as ST and T wave changes, prolongation of QT interval and arrhythmias were also frequently observed. However, the incidence of these symptoms and signs was independent from the grade of MVP. It was concluded that MVP with grade 4 or more is hemodynamically significant, while it was insignificant in cases of grade 3 or less. Therefore, those with symptoms and/or electrocardiographic abnormalities in cases with MVP of grade 3 or less will not require any treatment but only a follow-up observation.

A two and a half year follow-up study of segmental left ventricular wall motion was performed by two-dimensional echocardiography for 26 patients with dilated cardiomyopathy (DCM). Segmental analysis of left ventricular wall motion abnormalities (WMA) was performed using 11 segments obtained by short- and long-axis views of the left ventricle. Wall motion in each segment was classified and assigned a numerical score as normal (0), hypokinetic (1), severely hypokinetic (2), and akinetic or dyskinetic (3). Based on this categorization, a wall motion abnormality index (WMAI) was derived as an overall assessment of left ventricular asynergy. The intersegmental standard deviation of the wall motion abnormality score was used as an index of left ventricular asynergy (non-uniformity index: NUI). During the follow-up period, the wall motion abnormality index increased in all of the 26 patients (from 1.23 to 1.82, p less than 0.001), but the non-uniformity index did not change (from 0.72 to 0.73). When comparing the non-uniformity index among three groups classified according to the grade of wall motion abnormality, both at the initial and during follow-up studies, the moderate wall motion abnormality group (1.0 less than or equal to WMAI less than 2.0) had larger non-uniformity indexes (0.83, 0.84) than the other groups, and the severe non-uniformity index (greater than or equal to 0.9) was observed solely in the moderate group. In the follow-up study, these 26 patients were categorized in two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Eighty cases with mitral valve prolapse excluding the secondary prolapse of the mitral valve caused by known underlying diseases were studied by real-time ultrasoundcardiotomography and M-mode technic. It was thought that observation of the left ventricle with long axis sector scan was useful and sensitive technic to diagnose the mitral valve prolapse. By comparative study of M-mode technic and ultrasoundcardiotomography, echo sources and the mechanism of so called prolapse patterns such as pansystolic bowing, mid-systolic buckling and multilayered echoes were explained. Pansystolic bowing and mid-systolic buckling were considered as the reliable signs for diagnosis of anterior leaflet prolapse, but were not contributory to diagnose posterior leaflet prolapse and ultrasoundcardiotomographic technic was needed to detect the posterior leaflet prolapse. According to the mode of prolapsing findings by ultrasoundcardiotomograms classification of severity of mitral valve prolapse was undertaken and its grade was expressed as AmPn in which A and P designated prolapse of the anterior and posterior leaflet respectively and m and n indicated the grade of severity in number from zero to five.

Hypocalcemic crisis developed in a patient with acute alcoholic fatty liver. In addition to jaundice and marked hepatomegaly, the patient presented with hypocalcemic crisis associated with hypomagnesemia, low plasma 1,25(OH)2-vitamin D and undetectable plasma parathyroid hormone (PTH) concentration. Subsequent computerized tomographic scan and liver biopsy showed the presence of severe fatty liver. With the improvement of liver function, the serum calcium level increased, and was accompanied by normalization of plasma PTH, serum magnesium, and plasma 1,25(OH)2-vitamin D levels. Serial ethylenediaminetetraacetic acid infusion tests demonstrated the reversal of the impaired PTH secretion. Thus, hypocalcemic crisis in this patient appeared to result from transient hypoparathyroidism induced by magnesium deficiency.

Eighty-four cases with idiopathic mitral valve prolapse (MVP) were followed for 3.1 years in average (1 to 6 years). Left ventricular end-diastolic and end-systolic dimensions and/or left atrial dimension increased in 72.4% of the cases with severe grade of MVP, while in only 14.3% of the cases with mild grade of MVP during follow-up period. Incidence of ventricular arrhythmias was 70% including about 10% each of grade III, IVa, and IVb in Lown's classification. Repeated examination using 24-hour Holter monitoring showed ventricular arrhythmias of long duration in a majority of the cases, and 66.7% of the cases with III and IV in Lown's classification revealed IVa and IVb frequently including one case of sudden death occurred during follow-up period.

To investigate left ventricular function and the prognosis of patients with dilated cardiomyopathy (DCM), regional wall motion of the left ventricle of 38 patients with DCM was observed before and during dobutamine infusion (8 micrograms/kg X min) by two-dimensional echocardiography (2DE). The left ventricle was divided into 11 segments and the severity of wall motion abnormality (WMA) was classified into 4 grades, i.e. akinesis or dyskinesis (A), severe hypokinesis (SH), hypokinesis (H) and normokinesis (N), and numerical scores were assigned to each grade of WMA as follow; A: 3, SH: 2, H: 1, and N: 0. In the 38 patients with DCM, the number of segments with WMA was 8.3 +/- 2.9 (mean +/- SD). Among 418 segments in the 38 patients, we observed A in 71 segments, SH in 104 segments, H in 140 segments, and N in 103 segments. The WMA was not uniform in the left ventricle, and severe WMA was observed in the apex (WMA score: 2.0 +/- 1.0), while the grades of WMA in the lateral and posterior walls were mild (WMA score: 0.8 +/- 1.1) compared with those of other segments. The total sums of the WMA scores in 11 segments for each patient (TWMAS) were significantly greater in patients with severe heart failure (New York Heart Association [NYHA] functional class III or IV) than in patients with mild heart failure (NYHA class I or II) (22.0 +/- 5.2 and 9.9 +/- 4.9, p less than 0.001). TWMAS correlated with the cardiac index (CI) (r = -0.58, p less than 0.005) and pulmonary capillary pressure (PCP) (r = 0.68, p less than 0.001). In 242 segments of 22 patients, whose regional wall motion was observed before and during dobutamine administration, wall motion was improved by one grade in 82 of 170 segments with WMA before dobutamine infusion; i.e. regional wall motion changed from A to SH in six segments, from SH to H in 31 segments, and from H to N in 45 segments with dobutamine administration. According to the change in grade of TWMAS induced by dobutamine administration, 22 patients with DCM were classified into two groups: a good response group (% change of TWMAS greater than or equal to 40%), and a poor response group (% change of TWMAS less than 40%). The poor response group had ventricular tachycardia more frequently, more severe heart failure, lower CI and higher PCP than the good response group.(ABSTRACT TRUNCATED AT 400 WORDS)

This study was made to evaluate the usefulness of various non-invasive methods such as electrocardiography, echocardiography and 201T1 myocardial scintigraphy in the differential diagnosis of idiopathic congestive cardiomyopathy (CCM) and ischemic heart disease (IHD). Eighteen cases with CCM and 9 cases with IHD were subjected. For this study patients with IHD showing dilated cavity (LVDd over 66 mm) and diffuse hypokinesis of the left ventricle in the echocardiogram were selected. For echocardiographic study, cross-sectional sector-scan instrument, Toshiba SSH-11A was used, and 201T1 myocardial scintigraphy was performed using Toshiba jumbo gamma camera GCA-401. Cardiothoracic ratio of CCM and IHD were 59.6 +/- 6.3% and 58.3 +/- 6.3% in average, respectively. In CCM, mean LVDd was 76.0 +/- 5.6 mm and mean LVDs was 63.4 +/- 7.3 mm. In IHD, mean LVDd was 74.7 +/- 8.1 mm and mean LVDs as 63.2 +/- 4.6 mm. Both cardiothoracic ratios and echocardiographic findings showed no difference between CCM and IHD. Incidence of an abnormal Q wave in ECG was higher in IHD (2.72 leads per a case) than that in CCM (1.33 leads per a case). An abnormal Q wave in aVL was frequently (28%) observed in CCM but none in IHD. However, these ECG findings did not seem to be contributory to the differential diagnosis. Myocardial scintigraphic study revealed that 10 of 18 cases with CCM showed no perfusion defect or sparse uptake and others showed small and isolated defect in the apex or postero-lateral wall of the left ventricle, while 7 of 9 cases with IHD showed large perfusion defect over 15% in the anterior and inferior areas. However, small localized defects less than 14% in the apex were observed in both groups, 5 cases (27.8%) with CCM, and 2 cases (22.2%) with IHD, suggesting limitation of this method for the differential diagnosis.

In a total of 114 cases of hypertrophic cardiomyopathy (HCM), four cases were regarded to have dilated left ventricle and congestive heart failure. History of myocardial infarction was not present, and significant narrowing of coronary arteries was not detected in each case. The clinical manifestations were analyzed in the light of the differentiation from postmyocarditis cardiomyopathy (PMC: three cases) and hypertensive heart disease ( HHD : five cases). Representative case was a 47-year-old man with HCM, who showed congestive heart failure developed gradually over the last 20 years. The cardiothoracic ratio increased from 57% to 64% and high voltage of the precordial leads noted initially decreased gradually with normalization of ST-T changes. Meanwhile, a new abnormal Q wave appeared in aVL. The echocardiographic findings at the age of 47 were asymmetric septal hypertrophy and left ventricular enlargement. Myocardial biopsy of the right ventricle done at the same period revealed the marked progression of interstitial fibrosis as compared with that of 15 years ago. Clinical pictures demonstrated that PMC patients were younger than HCM or HHD patients. Abnormal Q waves were observed in three cases of HCM. In the remaining one, the Q wave was not discernible due to superimposed complete left bundle branch block. No abnormal Q waves were observed in cases of PMC and HHD . A high voltage of the left precordial leads with marked ST-T changes suggesting left ventricular hypertrophy was not seen in HCM with dilated left ventricle and HHD . Echocardiographically, the systolic anterior motion was absent in all cases. The left ventricular posterior wall in PMC and HHD was equally hypertrophied both at the apex and base, whereas in three of four cases of HCM, the apical region of the posterior wall was disproportionately hypertrophied. All cases of HCM and PMC showed asymmetric septal hypertrophy, while all the HHD cases except one showed concentric hypertrophy. In HCM, left ventricular end-diastolic dimension and left atrial dimension were increased to 60.0 +/- 6.1 mm and 45.3 +/- 9.4 mm, respectively, which were not different from those of PMC and HHD . Isometric relaxation time was prolonged to 100 msec or more in all cases of HCM, while in only one case of PMC it was prolonged and no prolongation was observed in HHD . Left ventricular wall motion revealed asynergy mainly at the hypertrophic apical area in HCM and PMC, whereas asynergy was found at the hypertrophic area, which was mostly apical, and also in the area without hypertrophy in HHD .(ABSTRACT TRUNCATED AT 400 WORDS)