In the successive myocardial imaging by thallium-201, the uptake by myocardial cells was assessed quantitatively. At a steady hemodynamic state, the second uptake was able to be predicted from the first uptake count and the ratio of the first and the second background counts. This predicted counts showed a high correlation with the actual counts (r = 0.987, p < 0.001). No significant difference was observed in the two counts. When heart rate was increased in six patients who were implanted a programmable pacemaker during the second myocardial imaging, the actual counts exceeded the predicted ones significantly (p < 0.001). An increase of the counts by 36% was observed in the average following the change of heart rate from 60 beats/min to 90 beats/min. Since the tissue level of uptake is dependent upon the blood level and the partition coefficient, this increase of myocardial uptake suggests an alteration in the partition coefficient.

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The concentration of plasma antithrombin III (AT III) and the biological activity of plasma alpha2-plasmin inhibitor (α₂ -PI) were measured in cases of mitral stenosis (MS) and rheumatic heart disease (RHD) without MS. Cases of MS showed the findings of the low levels of plasma AT III and and normal or a little higher levels of plasma α₂ -PI, that was not recognized in RHD without MS. This finding was interpreted to be hypercoagulable because of the acceleration of coagulation and of little or slight retardation of fibrinolysis. Besides, the influence of atrial fibrillation and chronic congestive heart failure on hypercoagulability in cases of MS was detected clearly, but the influence of them in cases of non-RHD was obscure. As the results, the severer the degree of MS, the clearer the hypercoagulable state. Therefore, the prethrombotic state existed in cases of MS, combined with blood flow disturbance due to atrial fibrillation or chronic congestive heart failure, endocardial damage resulted from rheumatic fever in an early stage and hypercoagulable state mentioned above in the present study. There was no significant difference between cases with and without thrombi in the degree of hypercoagulability in subjects with MS shown in the present work. It was concluded that the consumption of AT III caused the low levels of it in cases of MS, and that the low production of AT III in the liver rather than consumption caused the low levels of it in cases of non-RHD.

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The effects of PGI₂ and PGE₂, given in the same doses were compared as to renal hemodynamics and functions and renin release. The same experimental conditions were used for both compounds and experiments were carried out in pentobarbital anesthetized dogs. Adrenergic influences were excluded by renal denervation. Given intrarenally at doses of 0.1μg/min and 1μg/min, PGE₂ caused significant increase in RBF, UF and U_NaV, but had no effect on BP and GFR. Intrarenal infusion of PGI₂ at a rate of 1μg/min resulted in a significant increase of RBF and in a marked fall of BP. but only little change in GFR, UF and U_NaV. With a dose of 0.1 μg/min, the parameters remained the same. Intravenous infusion of PGI₂ (1μg/min) caused a significant fall in BP with no change in the other parameters. Both PGI₂ and PGE₂ had a similar effect on intrarenal hemodynamics, i.e., caused a progressively greater proportional vasodilation from superficial to deep cortex. Given intrarenally in a dose of 1μg/min, PGI₂ and PGE₂ increased renin release. But with a dose of 0.1μg/min and 1μg/min, i.v., renin secretion was not influenced. The effect of PGI₂ on systemic blood pressure was more potent than that of PGE₂, however, with regard to renal vasodilating action and tubular effects, PGE₂ was the more potent. Present data indicate that PGI₂ and PGE₂ stimulate renin secretion through a direct action on the juxtaglomerular cells.

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Comparative studies of the antihypertensive agents, guanfacine and clonidine, on their peripheral effects were performed using normotensive canine preparations. On the peripheral vascular beds, both drugs constricted cerebral, renal and femoral vasculatures, but there were no decreases in the renal blood flow. This vasoconstriction was blocked by phentolamine, and guanfacine was about 3 times less potent than clonidine. Both drugs contracted the canine nictitating membrane, and had no effect on the ganglionic transrnission in the cervical syrnpathetic ganglion. Qualitatively different effects were observed in their effects on renal function. Guanfacine slightly increased the urinary volume and Na excretion, while clonidine increased the urinary volume and K excretion. All these peripheral effects do not seem to be responsible for their hypotensive effect .

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A case report of a 32-year-old male with renovascular hypertension, suspected to be pheochromocytoma as a result of a tentative diagnosis, is given. The suspicion was based on the observation of high levels of urinary noradrenaline on several occasions with the sign of hyperreninemia. Reduction of the urinary noradrenaline levels by the administration of angiotensin converting enzyme inhibitor (SQ-14225) suggested that the high urinary noradrenaline probably resulted from hyperreninemia which reflected high plasma levels of angiotensin II. Radioisotope renography and intravenous urography strongly suggested a reduction of the right renal blood flow, and the final diagnosis of renovascular hypertension was obtained on the basis of renal arteriography. On the other hand, the possibility of a catecholamine releasing tumor was carefully excluded by angiography before undertaking surgical treatment. The affected kidney was transplanted autogenously into the abdominal cavity. The successful operation led to a decrease in plasma renin activity, blood pressure and urinary noradrenaline excretion. In the present case, we were thus unable to define at first whether the primary genesis of hypertension was related to the hyperactivity of the reninangiotensin system caused by renovascular stenosis or a noradrenaline releasing tumor.

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We observed a case of severe intravascular haemolysis following repair of subpulmonaic ventricular septal defect with pulmonic stenosis. In this case immunological studies and cardiac catheterization demonstrated haemolysis resulting from mechanical factors. When severe haemolysis and progressive anemia following intracardiac repair persists, inadequate intracardiac correction should be suspected and the second surgery is to be considered.

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(1) The ECGs Of 84 patients who survived corrective surgery for tetralogy of Fallot were reviewed. The overall incidence of sudden death during at least 5 years period of followup was 4%, mortality being highest in those with CRBBB and LAH (40%). (2) The ratio of leftward to rightward QRS forces projected on the X axis (Rs/Sx) is significantly decreased in postoperative T/F patients. (3) Twenty-seven patients who had corrective surgery for tetralogy of Fallot underwent cardiac catheterization postoperatively. LVEF was mildly, but significantly diminished and LVEDV was increased significantly, while peak dp/dt, Vpm and Vmax were significantly depressed. These findings indicate that patients who had corrective surgery for tetralogy of Fallot have impaired left ventricular function.

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Postoperative echocardiographic, hemodynamic and cineangiographic findings were obtained on 27 cases of complete transposition of the great arteries (TGA) which had undergone Mustard's procedure over two years ago. A majority of patients with TGA have abnormal right ventricular function as indicated by an increased right ventricular end-diastolic volume (RVEDV) and a low ejection fraction (RVEF). Despite this depressed RVEF, normal or increased RV output is maintained through an increased RVEDV. The postoperative right ventricular end-diastolic dimension (RVDd) averaged 275 ± 70% of normal and the left ventricular end-diastolic dimension (LVDd) averaged 75 ± 11% of normal. The postoperative ratio of RPEP/ RVET was greater (0.44 ± 0.06) than normal value (0.34 ± 0.06) for systemic circuit, whereas the postoperative ratio of LPEP/LVET was similar (0.23 ± 0.06) to normal value (0.22 ± 0.05) for pulmonary circuit. The ventricular cavity dimensions and ratios of PEP/ET were appropriate for the physiologic role of the ventricles rather than their morphologic identity. A variety of valve motion abnormalities were noted ;these included diastolic flutter of the mitral valve in 94% of patients, prolapse in 50% and systolic anterior motion (SAM) in 50%, while diastolic flutter of the tricuspid valve in 75% of patients, prolapse in 100% and SAM in 19%. Systolic flutter of the semilunar valve was found in half patients and paradoxical septal motion was found in all patients. Atrioventricular valve motion abnormalities presumably caused by the decrease of atrial volume or compliance or the increase of RV pressure were observed at high rate but at least until 8 years after Mustard's procedure, the function of those valves had been satisfactory. Echocardiographic dimensions or systolic time intervals (STI) were considered to be useful not only for the evaluation of LV performance but also for the evaluation of RV performance or dynamic status of pulmonary circulation after Mustard's operation for TGA. The finding of a great number of echocardiographic abnormalities in TGA suggests that these echocardiographic features are to be expected after Mustard's procedure.

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At the Heart Institute of Japan, Tokyo Women's Medical College, 474 aortic valve replacements (AVR) are performed using various kinds of prosthetic devices during the period of 1965, 5-1978, 12. Most popular valve prosthesis was Bjork-Shiley valve totalling 215. 56 cases were subjected to study of more than 5 years follow up. They carried operative mortality of 16.1% and late mortality of 7.1%. Thromboembolism was 5.4%. 3 patients delivered 4 normal full term babies. There were 4 reoperations for aortic orifice with successful outcome. Cardiothoracic ratio, left ventricular strain pattern on ECG, blood pressure, pulmonary artery wedge pressure, cardiac indices, ejection fraction, enddiastolic volume have post-operatively returned almost to normal in majority of cases. Actuarial survival curve beyond 6 years after AVR was 98% up to 9 years.

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