In coronary artery disease, non-invasive measurement of left heart volume by compartment analysis of radiocardiogram with 1311-labeled human serum albumin (RCG) was assessed in 32 patients. Although left heart volume includes mean left atrial and ventricular volume, there was a good correlation between left heart volume and left ventricular end-diastolic volume by left cineventriculography (r = 0.94). Both thallium-201 (²⁰¹Tl) myocardial imaging and RCG were performed at rest in 87 patients and during bicycle ergometer exercise in 21 of these patients, the objective being to investigate the relationship between myocardial perfusion and left heart volume. Eightyseven patients were divided into subgroups after ²⁰¹Tl-myocardial perfusion images at rest were studied. Left heart volume, right heart volume and total blood volume were increased and stroke volume index was decreased in proportion to the size of imaging defects (p < 0.005, F > 4.07). New exerciseinduced imaging defects on myocardial images correlated with the increase in left heart volume by exercise (p < 0.001 ). These findings demonstrate the relationship between myocardial perfusion and left ventricular function, in the presence of bi-ventricular heart failure.

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In 16 patients on chronic hemodialysis, the cardiac catheterization was performed. They had received the hemodialytic treatment for 41 months in the average. All but two cases had cardiothoracic ratio above 50%. It was 58 ± 7% in all. The laboratory data, body weight, or the interdialytic body weight change was comparable with those of other patients with normal heart size. Pericardial effusion was denied by echocardiographic study. Cardiac index and the left ventricular stroke work index were higher than normal; 4.7 L/min/m² and 85 ± 31 g·m/m² respectively. Cardiac index was higher than 3.9 L/min/m² in 11 patients and left ventricular stroke work index was above 68 g·m/m² (= mean value of control). The pulmonary artery wedge pressure was 16 ± 6 mmHg and abnormally high in six patients (> 15 mmHg). The pulmonary artery wedge pressure was found to be correlated with the cardiac work (r = 0.53, p <0.02), and with the cardiothoracic ratio (r = 0.64, p < 0.02). The present study revealed a circulatory abnormality of pulmonary congestion which may be brought by an excessive load upon the heart in the renal failure patients. A further increase in the cardiac work by aggravation of anemia, retention of body fluid, or the elevation of blood pressure may easily result in an acute pulmonary edema. The reduction of the load by vasodilator may be useful for the relief of the acute rise of the pulmonary artery wedge pressure as suggested in the study of a small group in the present paper.

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Hemodynamic responses and behaviors of the renin-angiotensin-aldosterone system to a single administration of captopril (50 mg) were studied in 16 hypertensive patients (essential hypertension, n = 10 ; renovascular hypertension, n = 3; primary aldosteronism, n = 2; Cushing's syndrome, n = 1). In 10 essential hypertensive patients, the immediate blood pressure reduction caused by decreased total peripheral resistance after the administration of captopril was observed without changes of cardiac output and heart rate. Serum angiotensin converting enzyme activity and plasma aldosterone concentration significantly decreased, whereas plasma renin activity significantly elevated 2 hours after the administration of captopril. The close relationship between the pretreatment value of plasma renin activity and the maximum decrease in mean blood pressure in 16 hypertensive patients suggests that the depressor response to a single administration of captopril could evaluate the degree of angiotensin 11 dependency in the maintenance of high blood pressure in various types of hypertension.

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Fifty-seven patients with artificial pacemakers were studied from electrocardiograms (ECGs), vectorcardiograms, echocardiograms, and non-invasive techniques of systolic time intervals. Thirty-nine patients demonstrated a left bundle branch block (LBBB) pattern induced by transvenous right ventricular (RV) pacing, and 9 patients demonstrated a right bundle branch block (RBBB) pattern also induced by transvenous RV pacing. Perforation of the right ventricle or malpositioning of the catheter electrode was not recognized. Eight patients with epicardial left ventricular (LV) pacemakers showed a RBBB pattern and one showed a LBBB pattern. The maximal QRS vector of a RBBB pattern produced by RV pacing was directed leftwards and anteriorly, whereas that of a RBBB pattern produced by LV pacing was oriented rightwards and posteriorly. A rapid initial posterior motion of the left side of the interventricular septum (IVS) during early systole and/or anterior or flat motion of the IVS during the ejection period was almost exclusively indicative of RV pacing, regardless of the ECG wave form. There was one exceptional case in LV pacing, which showed a LBBB pattern with the same septal motion as that in RV pacing. However, the direction of the maximal QRS vector in this case was directed inferiorly, which is in sharp contrast to that in the RV pacing which was directed superiorly. There was no significant differences in systolic time intervals between a LBBB pattern and a RBBB pattern in RV pacing. Based on the hypothesis that the ECG wave form induced by epicardial LV pacing might be equivalent to that in a case of perforated right ventricle, the following conclusions can be drawn from the present study. (1) A RBBB pattern in RV pacing could be differentiated from perforation of the right ventricle. The following findings may suggest uncomplicated RV pacing: (a) the left and anterior orientation of the maximal QRS vector, and (b) a rapid initial posterior septal motion during the early systole and/or a paradoxical anterior septal motion during the ejection period. (2) A RBBB pattern in uncomplicated RV pacing does not require the repositioning of the catheter electrode. (3) A LBBB pattern with inferior orientation of the maximal QRS vector would suggest perforation of the right ventricle.

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Life tables have been calculated for cerebrovascular disease and ischemic heart disease in various occupational groups in Japan, and England and Wales. For cerebrovascular disease there are large occupational differences in both countries, and the experience of the lowest-ranking Japanese group (administrators and managers) is better than that of the highest-ranking group in England and Wales (miners). For ischemic heart disease the occupational variations within each country are less, and all Japanese groups fare better than any groups in England and Wales. Within each country mortality from cerebrovascular disease in different occupations has many positive and significant correlation coefficients with rates for stillbirth, and mortality from infections, cancers, etc. However, mortality from ischemic heart disease shows relatively less correlation coefficients with other diseases.

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1. Quantitative analysis of structural proteins from a minute amount of myocardial tissue was performed from 10 μ thick cardiac tissue slices weighing 2 to 5 mg by the extraction in glycerol solution and by sodium dodecylsulfate (SDS) gel electrophoresis, and these changes were compared with the histologic alterations in the striated structure of the adjacent cardiac slices in the experimental myocardial infarction in the dog. 2. Approximately 69 μg of structural proteins were obtained from 1 mg of the normal heart muscle. In the central portions of the myocardial infarction, reductions in myosin heavy chain (HC), light chain (LC) 1 and α-actinin were observed at 12 to 24 hours after the coronary occlusion followed by the decrease in myosin LC 2 at 48 hours. Those changes became intense at 72 hours to 7 days, but restored gradually at 14 to 28 days. 3. Alterations in the striated structure of cardiac muscle fibers of the adjacent tissue slices were found simultaneously with the changes in structural proteins. At 12 to 24 hours after the coronary ligation increase in eosinophilia and overstretch of cross-striation were observed. The findings of coagulation necrosis, loss of striation, fragmentation, swelling of A-band, etc. of the infarcted fibers were markedly observed at 48 hours to 7 days, but the histologic restoration of cardiac fibers was found with the recovery of the infarcted tissue at 14 to 28 days after the coronary ligation. 4. Changes in the compositions of structural proteins corresponded well to the alterations in the striated structure in chronology and in quantity.

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A case of a 19-year-old woman with coronary artery fistula was reported. She was asymptomatic throughout her life. Physical examination revealed a continuous murmur along the left sternal border. Echocardiograms and left ventriculograms showed mitral valve prolapse. Selective coronary arteriograms disclosed arteriovenous fistula between branches of the right, the left anterior descending and the left circumflex coronary artery and the main pulmonary trunk. We believe that this is the first case report of an unusual form of anomalous coronary-pulmonary artery communication: three main coronary vessels participate in the fistula.

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The rate of extracardiac malformation (ECM) associated with congenital heart disease (CHD) is high in neonates. 108 cases of 212 neonates with CHD had ECM (50.9%). Main ECMs Were digestive system anomalies (36.1%), chromosomal aberrations (26.8%), respiratory system anomalies (21.3%), CNS anomalies (13.0%), and others (2.7%). Single lesion of left to right shunt accounted for 77.2% (61/79) of CHD with ECM from other than chromosomal aberrations. The prognosis of neonates with CHD without ECM was also studied. Total anomalous pulmonary venous connection, pure pulmonary atresia (PPA), pulmonary stenosis (PS), hypoplastic left heart syndrome are not generally associated with ECM, but the prognosis is poor. Coarctation complex which is sometimes associated with ECM has a poor prognosis in neonates. There is an increase of the survival rate in the patients with hypoxemia, such as PPA or severe PS, extreme tetralogy of Fallot, and tricuspid atresia, which can be managed with prostaglandin E₁. PDA associated with respiratory distress syndrome is ideally treated with indomethacin. In recent years, mortality from PDA has decreased in neonates. The mortality rate during the neonatal period was 46.8% (5 1 /109): 37.5% (30/80) died before surgical interventions and 72.4% (21/29) died during or after surgery. Half of neonatal deaths from CHD occurred within 3 days of admission. Thus, early detection, early diagnosis, and early treatment of neonates with CHD is most important.

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In a total of 107 cases with transposition of the great arteries (TGA-s), 20 died preoperatively and 76 underwent surgical treatment: 11 palliative and 65 primary corrective surgeries, with hospital mortality 36.4% and 46.2% respectively. Of 31 survivors after Mustard operation, tricuspid regurgitant murmur and ECG abnormalities were recognized at 26.7% and 33.3% respectively in simple TGA, and 62.5% and 37.5% respectively in complicated TGA during an average follow-up of 4 years. Angiocardiogram, performed more than 2 years postoperatively, revealed decreased ejection fraction (EF) with compensatory increase of right ventricular end-diastolic volume (RVEDV): EF 0.43 ± 0.04, RVEDV 168 ± 41% of normal in simple TGA and 0.36 ± 0.12, 1 73 ± 55% in complicated TGA. In 3 long-term survivors of arterial switch operation (Stansel, Kaye), no serious complications were observed, and ejection fraction and echocardiographic findings of systemic ventricle showed an earlier normalizing than in Mustard operation: EF 0.65 or more when no VSD leakage and pre-ejection period (PEP)/ejection time (ET) 0.35 ± 0.05 after switch operation, 0.45 ± 0.05 in simple TGA and 0.47 ± 0.07 in complicated TGA after Mustard operation. From these long-term postoperative evaluations, our policy at present is to prefer arterial switch operation to Mustard operation in corrective surgery for TGA.

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The natural history of pulmonary vascular obstruction in VSD associated with PH was studied by measuring PVR before and after injection of tolazoline 1 mg/kg. Organic pulmonary vascular obstruction (PVO) was minimal in infancy, but increased linearly progressively with advancing age, and average rate of increase in PVR after tolazoline was 1 unit·m²/year. The rate of increase in PVR after tolazoline in Eisenmenger complex was variable and ranged between 0.7 to 4 unit·m² /year in most cases. Analysis of 7 cases of post-operative late death due to PVO revealed that usually these cases were over 5 years of age at operation, and pre-operative PVR was more than 12 unit·m² . Reduction of PVR was confirmed post-operatively in most of these cases whose pre-operative PVR before and after tolazoline were less than 8 unit·m² and 7 unit·m² respectively. Early surgical repair is indicated in VSD and PH to prevent progress of PVO.

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The long-term results of 1023 adult patients with congenital heart diseases, operated and non-operated, with atrial septal defect (ASD), patent ductus arteriosus (PDA), pulmonary stenosis (PS) and tetralogy of Fallot, were followed for up to 24 years, and the long-term results of operated and non-operated congenital heart diseases were compared. The survival rate of patients with operated isolated ASD was significantly higher than in patients with non-operated isolated ASD, and that of operated patients with VSD associated with other anomalies was also significantly higher than in non-operated VSD patients with such involvement. The survival rate showed no significant difference in the operated and non-operated patients with PDA, PS and tetralogy of Fallot. In all congenital heart diseases, there was a close correlation between the mean pulmonary artery pressure and the mortality rate both in operated and non-operated patients and a marked improvement of physical capacity of operated patients at the time of the last follow-up examination.

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The histories and medical courses were reviewed in 154 patients with congenital heart disease (CHD) ranged in age 40 to 77 years (mean 48.8 years) who had not yet undergone cardiac surgery. The CHD most commonly involved were atrial septal defect (ASD) (63.6%), ventricular septal defect (13.6%) and patent ductus arteriosus (8.4%). There were no cases of tetralogy of Fallot or of transposition of the great arteries in this study. Hemodynamic observations showed no significant correlation between the age and systolic pulmonary artery pressure in left-to-right shunt disease. Mortality due to cardiac failure was higher in patients whose systolic pulmonary artery pressure was over 50 mmHg. 91 patients had cardiac surgery and surgical mortality was 7% (6 Patients). There was one late ASD death, and 46% are in good condition (NYHA I). In patients without surgery, 27% (17 patients) died of cardiac failure except one, and 11% (6 Patients) are in good condition. Among factors affecting prognosis, pulmonary vascular changes are the most important, with arrhythmia and myocardial damage occurring with age, and complications like infective endocarditis and coronary sclerosis affecting prognosis adversely.

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Two hundred and seventy-eight patients with atrial septal defect of secundum type were operated on surgical closure of the defect. The patients were divided into 5 groups according to age at surgery, and preoperative complaints and laboratory findings were analyzed to evaluate natural history. As year passed, incidence of complaints increased. Cardiothoracic ratio (CTR), systolic pressure of the right ventricle (P_RVS), end-diastolic pressure of the right ventricle (RVEDP), mean pressure of the right atrium (P_RAm), ratio of pulmonary to systemic systolic pressure (P_PA/P_S), right ventricular dimension (RVD) and left atrial dimension (LAD) increased significantly, while frontal axis of the QRS complex, R_V1, S_V1 +R_V5 and LVD decreased. No chronological changes were seen in ratio of pulmonary to systemic blood flow (Q_PA/Q_S) and ratio of pulmonary to systemic vascular resistance (R_PA/R_S). The first and second decades of life were considered to be stable stages of the disease. Postoperatively, changes in the above-mentioned parameters were compared in each age group, and effects of surgical repair on natural history were evaluated. Of 265 survivors, 168 were followed-up for more than one year, the longest period being 22 years. CTR, frontal axis, R_Vl, P_RVS, RVEDP, P_PA/P_S and RVD decreased significantly, while S_Vl + R_V5, R_PA/R_S and LVD increased. No changes were seen in LAD. Surgical effects appeared most significantly in the first decade and least in the fifth or more. From these findings it would be concluded that corrective surgery should be best carried out in the first decade, at latest in the second, though not to be contraindicated by age alone. Otherwise, postoperative improvement of parameters delays or hemodynamical abnormalities may persist regardless of considerable clinical improvement.

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Cross-sectional echocardiography was performed on 77 patients with secundum atrial septal defect (ASD). Mitral valve prolapse (MVP) was recognized in 41 out of the 77 (53.2%); anterior MVP was found in 36 patients, three cases revealed posterior MVP, and two were diagnosed as having both anterior and posterior MVP. Pre- and post-operative study was carried out on 53 cases; anterior MVP decreased in incidence from 28 patients to 17 following closure of ASD, whereas posterior MVP remained unchanged, as did both anterior and posterior MVP. The left ventricular distortion ratio (LVDR) was measured in the short axis view in 45 cases. After the repair of ASD, the LVDR decreased both in end-systole and end-diastole (p < 0.01), that is, the left ventricle became more circular in configuration. Pre- and post-operatively, MVP patients revealed a significantly greater LVDR than those without it in end-systole, and post-operatively in end-diastole as well (p < 0.01). Prior to operation, the short axis area of the left ventricle (LVSAA) was statistically larger in patients with MVP than without it in end-diastole (p < 0.05). However, there existed no relationship between the presence of MVP and the pulmonic to systemic flow ratio, right ventricular dimension index, right ventricular systolic pressure and size of ASD at the time of operation.

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The incidence of arrhythmias in 3614 preoperative patients with congenital heart disease was 1.6 per cent. Pre- and postoperative serial ECGs in 186 patients with an isolated VSD and in 58 patients with TOF were reviewed. The incidence of CRBBB and CRBBB-LAH following VSD repair was 33% and 6.6%, respectively, and for TOF was 55% and 5.2%, respectively. Complete A-V block (CAVB) was seen in 2 patients following VSD repair, and none of TOF patients developed CAVB. Late cardiac or dysrrhythmic death was not recognized in our limited follow up period. The indications for surgery in membranous VSD should be determined more carefully, because the risk of the surgical damage to the conduction system is still higher. Moreover, we must keep in mind that damage to the A-V condution system may occur naturally even in a patient with small VSD. Finally, it can never be overemphasized that physicians must pay attention to the occurrence and course of postoperative arrhythmias.

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