To determine the value and limitations of vectorcardiograms (VCGS) for diagnosing multiple myocardial infarctions, correlations between VCG and angiographic findings were analyzed in 307 cases with severe asynergies due to coronary narrowings on left ventriculograms. While the presence of anteroseptal hypokinesis, corresponding to a non-transmural infarction of the anteroseptal wall, lowered the sensitivity of vectorcardiographic diagnosis for inferior and posterior myocardial infarctions, that of inferoposterior hypokinesis did not lower its sensitivity for anterior myocardial infarction. Severe asynergy, corresponding to a transmural infarction, reduced the VCG sensitivity for diagnosing myocardial infarction occurring in the opposite side of the left ventricle.

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The location and course of the atrioventricular (AV) conduction system were studied histopathologically in 6 hearts by sectioning serially, 4 having common AV orifice (CAVO) with complete or partial transposition of the great arteries (TGA) and 2 having ventricular septal defect of the persistent common AV canal type (VSD-C) with complete TGA. Two cases of CAVO with TGA and asplenia syndrome (Cases 1 and 2) had 2 discrete AV conduction systems, being posterior and anterior to the site of the defect, respectively. In these 2 cases posterior AV conduction system well developed, whereas the anterior one was hypoplastic. In another case of CAVO with TGA and asplenia syndrome (Case 3), only the anterior AV conduction system existed near the base of the great arteries. In the other case of CAVO with TGA and polysplenia syndrome (Case 4), the posterior AV conduction system was found to have a congenital interruption of the AV bundle of His. Two case of VSD-C with TGA but with no splenic anomaly (Cases 5 and 6) showed the posterior AV conduction system with communication-free accessory bundles. The posterior AV node, bundle of His and left bundle branch inevitably shifted postero-inferiorly, except in Case 3. The bundle branches were always distributed appropriately to their morphologically matched ventricles. The superiorly oriented vector in the mean frontal QRS axis in Cases 1, 5 and 6 seemed to be related to the postero-inferior displacement of the posterior AV conduction system, whereas those of the left-inferior oriented vector in Cases 2 and 3 were thought to be responsible for the excessively unbalanced size of ventricles. The complete AV block in Case 4 was correlated with the interruption of the bundle of His. The morphogenesis of the anterior AV conduction system was discussed in relation to the asplenia syndrome.

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A case with myopericarditis caused by type 3 ECHO virus was reported. The diagnosis was based on a significantly increased hemagglutination-inhibiting antibody titer (from 4 :6 to 4: 516) against type 3 ECHO virus in the acute and the convalescent phase. A 29-year-old male was hospitalized for chest pain and fever. The patient had congestive heart failure, pericardial effusion and temporarily appearing abnormal Q waves on his electrocardiogram in the acute phase all of which gradually improved within about 3 weeks. Cardiac catheterization performed on the 21 st day of hospitalization disclosed normal coronary arteries, but a partially hypokinetic region was found in the left ventricular free wall. A right ventricular endomyocardial biopsy study revealed histological features of a small number of mononuclear cell infiltrations, myocardial cell necrosis and early fibrosis associated with an increased number of fibroblasts and ultrastructural changes including myocytolysis, vacuolation in sarcoplasm and dissociation of some intercalated discs. The endomyocardial biopsy study, and the electrocardiographic and cineangiographic findings in this case suggest that viral infection may induce clinical signs of myocardial infarction in the heart with normal coronary arteries.

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The throat carrier rates of Group A streptococci and the antibody titers to 3 antigens of Group A streptococci, i.e., antistreptolysin O (ASO), antideoxyribonuclease B (ADN-B) and antistreptococcal polysaccharide (ASP) were followed up from October, 1980 through November, 1981 for the children living in a religeous organization in Kyoto, where epidemic infections of Group A streptococci had occurred from August to October, 1980. The recovery rate of Group A streptococci from the throat increased throughout the present study period, and the high carrier rate of Group A streptococci was maintained especially for first 8 months after the epidemic infection. Type 4 was present throughout the entire 13-month period. Although the ASO and ADN-B titers, both of which had initially risen, decreased during the present study period, the ASP levels peaked after about 4-8 months and decreased after 13 months. None of the children showed evidence of rheumatic fever with continuous observation.

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The distribution of ADN-B titers in healthy school children and in healthy adults were determined by the method of the Streptonase B. The upper limit of its normal titer value was 480 in children aged 9 and 10 and 240 in adults, and its diagnostic levels were 480 in children and 320 in adults. There were no close correlations between ADN-B and ASO or ASK.

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ASO titers of school children were studied during a period from 1975 to 1981, and the annual difference of this titer was investigated. As reported by many authors, the upper limit of normal ASO titer was 250 units and values of 333 units or more should be considered abnormal in our series of children, because 15 to 20% of the population had an antibody titer of 333 units or more. The upper limit of the normal titer was the highest in 1975 when 19.7% of the children showed more than 500 units, and the lowest in 1980 when 20.1% of the children showed more than 80 units. Thus, there was a six-dilution difference in the normal upper limit between these 2 years. We must consider the annual changes of the normal upper limit of streptococcal antibody titer in order to make an accurate diagnosis.

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To clarify the immunological mechanisms in poststreptococcal acute glomeulonephritis (PSAGN) and anaphylactoid purpura (AP), anti-streptococcal cell membrane (anti-SCM) and anti-human glomerular basement membrane (anti-GBM) titers in the sera of patients with PSAGN and AP were determined by passive hemagglutination with chromic chloride-treated sheep erythrocytes. Sodium lauryl sulfate (SLS) soluble SCM and collagenase soluble GBM were used as soluble antigens. Positive anti-SCM titers (> 1:8) were demonstrated in 10 of 14 patients (71.4%) with PSAGN and in 4 of 9 patients (44.4%) with AP without evidence of antecedent streptococcal infection had positive anti-SCM titers. No correlation was noted between anti-streptolysin O (ASO) titers and anti-SCM titers in patients with PSAGN or AP, but many patients with high ASO titers also had high anti-SCM titers. No positive anti-GBM reactions were detected in patients with PSAGN or AP. No cross-reactions were noted between SLS soluble SCM and collagenase soluble GBM.

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Eight children with myocarditis underwent a cardiac catheterization study and right ventricular endomyocardial biopsy. The degree of histological changes of the biopsy specimens correlated well with the severity of the clinical manifestations. Patients who had evidence of residual functional impairment had biopsy findings compatible with their clinical couuse.

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In order to clarify the prognosis of myocarditis and the relationship between myocarditis and idiopathic cardiomyopathy, 20 patients with myocarditis (one with Coxsackie B, one with rubella and 18 with idiopathic myocarditis) were followed up for a long period using echocardiography and Holter electrocardiographic monitoring. The follow-up period was 49.1± 39.3 months (mean ± SD). Subjects were classified into the following 4 groups according to their prognoses, left ventricular end-diastolic dimensions (LVDd) and the presence or absence of life-threatening ventricular arrhythmias : Group I with a fatal prognosis, Group II with LVDd &ges; 55 mm, Group III with LVDd < 55 mm but associated with life-threatening ventricular arrhythmias, and Group IV with LVDd < 55 mm and with no life-threatening ventricular arrhythmias. Patients of Group I (2 cases) had a marked left ventricular dilatation and a poor left ventricular and left atrial dilatation, and 2 of them had serious ventricular arrhythmias. All 3 patients of Group III had ventricular arrhythmia (ventricular tachycardias, coupled premature ventricular contractions and multifocal premature ventricular contractions, respectively), and 2 of them had asymmetric septal hypertrophy. All 10 patients of Group IV had no residual cardiac abnormalities. In conclusion, 50% of 20 myocarditis patients had residual cardiac abnormalities ; 6 patients (2 of Group I and 4 of Group II) were complicated by left ventricular dilatation, simulating dilated cardiomyopathy, and 3 (one of Group II and 2 of Group III) showed asymmetric septal hypertrophy, simulating hypertrophic cardiomyopathy.

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In order to clarify the sequelae of 11 patients who suffered from acute myocarditis of viral origin and were diagnosed by endomyocardial biopsy in the early and the convalescent stage of the disease, left ventriculograms were obtained from 17 to 167 (46.5 ± 41.2, mean ± SD) days after the onset of the disease were analyzed. The data were compared with the biopsy findings in the convalescent stage. The mean left ventricular ejection fraction (LVEF) was 57.5 ± 10.8% and in 3 cases the LVEF was less than 50%. In 2 cases, apparent asyneresis was observed. In all cases coronary arteriographic findings did not show significant stenosis. It is concluded that after viral myocarditis, increase in left ventricular end-diastolic volume, depressed ejection fraction and asyneresis occur in some cases and it can be said that a development from myocarditis to dilated cardiomyopathy occurs.

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We studied serial electrocardiographic changes in murine myocarditis due to encephalomyocarditis (EMC) virus. After taking control electrocardiograms using standard extremity and 2 precordial leads, 86 mice were intraperitoneally inoculated with a 0.1 ml of the M variant of EMC virus suspension containing 100 TCID₅₀. Electrocardiograms were recorded everyday from the 2nd to the 14th day, and thereafter once every 3-5 days until the 35th day. The cumulative incidence of myocarditis was 90% (77 out of 86). The control electrocardiogram showed a heart rate of 528 ± 87 beats/min (mean ± SD) and PR intervals of 0.03-0.05 sec, and significant rhythm or conduction disturbances were not found. Various electrocardiographic abnormalities, such as atrial (10%) and ventricular (21%) premature contractions, were noticed on the 4th to the 14th day. After 15-35 days arrhythmias still remained in 3 mice. The presence of arrhythmias in the chronic stage of myocarditis suggests that arrhythmias in some patients with no other clinical manifestations may be a sequela of the previous viral myocarditis. Thus, this study may contribute clinically to the clarification of the electrocardiographic characteristics in viral myocarditis.

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Inbred strains of BALB/c, C3H/He and DBA/2 mice were inoculated intraperitoneally with the M variant of encephalomyocarditis virus with a titer of 100 TCD₅₀ per 0.1 ml and followed up to the 8th month. Right ventricular aneurysms were noticed in 7 hearts of these 647 mice (1.1%) sacrificed from 8 to 10 months after inoculation with the virus. Myocardial fibers of the right ventricle were destroyed transmurally and fibrosis was found in the chronic stage. This study demonstrated that viral myocarditis may cause right ventricular aneurysms, albeit infrequently, suggesting a pathogenetic role of viral infection in right ventricular dysplasia or Uhl's anomaly.

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A 2-month-old female infant with pancarditis was reported. The patient died after a 26-day clinical course. The autopsy showed pancarditis, including inflammation in all 4 valves and chordae, fibrinoid vasculitis, pharyngolaryngitis and atrophy of the lymph nodes. Microscopic examination revealed proliferative inflammation in the endocardium, valve, myocardium, epicardium and coronary vessels. The histological findings suggested the etiology to be a rheumatic-type reaction at an extremely young age.

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During the past 3 decades, surgical treatment was performed on 75 cases with chronic exsudative or constrictive pericarditis, except for cases suffered from malignant tumor or trauma. Among 7 cases with chronic exsudative pericarditis, t underwent pericardiectomy and 2 had a fenestration of the pericardium. As for constrictive pericarditis, pericardiectomy was performed on 68 cases. Excellent surgical results were obtained. The ages of the cases with constrictive pericarditis, who underwent surgery, were significantly higher in the last decade, and the occurrence of pericardial tuberculosis significantly decreased in the last 2 decades. Although pericardiectomy has been performed for constrictive pericarditis without exception, it also plays an important role in the treatment of chronic exsudative pericarditis, especially for cholesterin or tuberculous pericarditis.

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Left ventricular internal dimension (LVIDd), aortic root dimension (AOD) and left atrial dimension (LAD) were measured echocardiographically in 688 normal children, ranging in age from 5 to 15. Lean body surface area (BSA) was calculated from height and lean body weight which was estimated from triceps skin fold thickness, upper arm circumference and body weight. Cardiac parameters (LVIDd, AOD, LAD) were well correlated with √^3(BSA) or √^3(lean BSA) (r=0.72 ∼ 0.89). Regression lines of LVIDd and AOD against √^3(BSA) or √^3(lean BSA) were compared between boys and girls. Statistically significant sex difference was observed in regression lines of LVIDd and AOD plotted against BSA (p < 0.005), but this difference disappeared when plotted against lean BSA. It is concluded that the sex difference of LVIDd and AOD corresponding to a similar BSA depended on the difference of lean body weight between boys and girls.

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An analysis of cardiac fatal cases from elementary, junior and senior high school students of Osaka revealed the following features : 1) The mortality rate of the cardiacs under the heart disease program is two times as high in senior high school students as in elementary school and junior high school students. The same rate for males is significantly higher than the rate for females. 2) The mortality rate according to types of heart disease is the highest among cardiomyopathy. This rate is followed by the rates for acquired valvular heart disease, for unoperated congenital heart disease and for operated congenital heart disease in that order. However, the actual number of fatal case is larest among those with congenital heart disease exceeding more than half of the total number of deaths. 3) Recently the mortality rate showes a decreasing tendency. The number of deaths due to chronic congestive heart failure has decreased, but sudden deaths have increased. 4) Sudden deaths are mostly encountered in morderate or severe cardiac cases. Therefore, it is mandatory to accurately locate the cases with high potentiality for sudden death and to place them under proper supervision. 5) In one third of the cases of sudden death, no significant physical or behavioral causes were found to trigger the death. It seems to be difficult to prevent all the sudden deaths, therefore, it is important to establish successful emergency programs.

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